• Phlegmons and abscesses in anatomic regions (cheeks, orbits, zygomatic and temporal regions).
• Paramaxillar and paramandibular phlegmons.
• Phlegmon of the mouth floor.
• Parapharingeal.
• Phlegmon of the tongue.
• Phlegmon of the neck (lower than upper neck fold).

Spreading of phlegmons realize per continuitatem; through lymphatic vessels; through venous vessels; trough arterial vessels.

Clinical signs

General signs of severe intoxication are marked by nausea, anorexia, general sweating, increasing of pulse and breathing rate. Sometimes – thrombosis of face and neck veins. Significant leucocitosis in periferial blood, leukocyte shift, increasing of neutrophils, decreasing of eosinophils, ESR – up to 70 mm per hour. In more severe conditions of the patient lymphopenia develops (amount of leukocytes decreases to 10 %), against the background of which eosinophiles deplete, and amount of neutrophiles increases up to 80 % and more. It can be sign of toxic nephritis. Necrotic and gas phlegmons have the severest course. Thermoregulation disorders – body temperature arises to 39.5–40 °C. If general intoxication increases dramatically, and local inflammation is low it can evident about infiltration of infection through local reticuloendothelial barrier and regional lymphatic nodes, which indicates to decreasing of resistance and could be the basis for unfavorable prognosis.

Local signs rely on location:

1. Superficial phlegmons – presence of diffuse swelling is peculiar, swelling is tight and painful, skin hyperemia; skin cannot be folded, tensed and glossy; the face is asymmetric. There is a clinical case with typical signs of superficial phlegmon (Fig. 12.11).
2. Deep phlegmons (in pterygomandibular and parapharingeal space, in the depth of the tongue and so forth) skin changes and face asymmetry are absent or insignificant. Keep in mind the signs of inflammation by Halenus and Celsus: tumor, rubor, color, dolor, functio lease.

More or less significant disorder of mandible movement up to stiffness (trismus).Impairment and severe pain in mastication and swallowing, especially in pterygomandibular and submasseteric phlegmons, and in other cases, when masticatory muscles involved in inflammation.Impairment of articulation, speaking and breathing (as a result of swelling of oral cavity, trachea, vocal cords). Saliva becomes tough, viscous and it spits out with difficulties.

By clinical course phlegmons are divided to:

• 1 group – mild – phlegmons located in 1 anatomic region.
• 2 group – moderate – phlegmons located in 2–3 anatomic regions.
• 3 group – severe – phlegmons of the mouth floor, half of the face, and two different anatomic regions.

Course severity depends on microbiotic virulence and condition of the immune system.

In case of the anaerobic phlegmon of the mouth floor (Ludwig’s angina), the clinical course is of major importance. Anaerobic infection is marked by crepitation symptom (gases are accumulated in the subcutaneous fat and are cracking during palpation, resembling the creak of snow); necrotic mass is determined during draining of the nidus; muscles achieve the colour of the boiled meat; foul, grey substance is exuded, there is no pus.

Treatment consists of such principles: 1. Drain of abscesses and phlegmons via incision (under general anaesthetic) taking into consideration their localization, spreading of the n.facialis bacillus, natural folds of face, neck and creating of the favorable conditions for exudate outflow. 2. Draining of the inflammatory nidus. 3. In case of odontogenic origin of the disease – extraction of the affected tooth. 4. Bacterial examination for determining of the microflora antibiotic susceptibility. 5. General medical treatment (anti-inflammatory, antibiotic, detox, hyposensitive, fibrinolytic, immune therapy, desagregants – aspirin, trental, ticlid).

In case of the Ludwig’s angina:

Drain of the abscesses, phlegmons, infiltrates by means of section in the submaxillary, retromandibular, submental regions, joined by means of the perforated tube drainage.

Creating of the highest possible conditions for aeration of the wound, its dialysis with antiseptic liquid and oxidizing substances.

Prevention of the joining of the commonplace microflora.

Anti-inflammatory, antibiotic, detox, hyposensitive, fibrinolytic, immune therapy, desagregants – aspirin, trental, ticlid.

Antigangrenous serum (preventive dose, or therapeutic dose if necessary).

Wound draining to be carried out with drains, draining sorbents, dialysis.

Sorbents: uvesorb, carbovit, carbolong, enterosgel – per os, sorbilact, rheosorbilact (i/v).

There are some forms of dialysis: fractional, continuous, circulating, aspirating. Detoxication includes hemosorbtion – arteriovenous shunt, plasmasorption, lymphosorbtion. Blood processing by UV, helium – neon laser, infrared rays (for improvement of rheologic properties).

Wound management in postoperative period is distinguished by wound processing with pulsing current, vacuum processing of the wound, laser processing + photosensitive agents based on hematoporphirines – discharged oxigen amplifies antimicrobic effect, ultrasound wound processing, cryoprocessing, hyperbaric oxigenation.

Accelaration of wound healing is reached by preparations, which stimulate wound healing, physiotherapy, diet, primary delayed sutures (2–5 day), secondary delayed – on granulating wound – 7–10–12 days. Contraindications – fever, hematogenous osteomyelitis and immune disorders (diabetes mellitus, rheumatism, poliarthritis, nephritis, chronic radial disease.), hemo-, plasma-, lymphosorbtion.

Complications of the abcesses and phlegmons could be general: phlegmon of retrobulbal cellulae. Thrombophlebitis of facial veins, sepsis, mediastinitis, thrombosis of cavernous sinus (7.1 %), purulent basal meningitis (2.6 %), arachnoiditis etc.:

• in favorable course – in 13 % of patients;
• in unfavorable course – in 80 % of patients.

Pneumonia, pleuritis (metastatic – 14 %, kidney abscess – 7.1 %). DIC – syndrome of disseminating intravascular clotting.

Furuncle and carbuncle

Furuncle – acute purulo-necrotic inflammation of a hair follicle and surrounding tissues caused by pathogenic microorganisms, more often by staphylococcal infection.

Carbuncle – acute purulo-necrotic inflammation of several hair follicles which are close to each other, and sebaceous glands, and also extend to surrounding tissues (skin, hypoderm).

Predisposing factors to development of furuncles or carbuncles are skin pollution, microtraumas, especially after squeezing out of abscesses on a skin, increased perspire and increased fat production. Very often these processes arise in people suffering from hypovitaminoses, with carbohydrate metabolism disorders (diabetes), with parallel conditions (overheat, supercooling, etc.).

The most dangerous in the prognostic plan are furuncles and carbuncles which are situated in a site of the upper lip, mouth angles and infraorbital site. It is associated with the mesh structure of piogenic membrane, which surrounds furuncles and carbuncles, instead of formation of a solid “bank” as it is in the abscesses. Therefore squeezing of abscesses can lead to development of dangerous to patient’s life complications. There is clinical case of furuncle of the buccal region (Fig. 12.12).

Fig. 12.12. Clinical case of furuncle of the buccal region

Complication of furuncles and carbuncles can be divided on local and general.

Local complications:

1. Cheilitis (catarral, glandularis, impetiginous).
2. Phlebitis, thrombophlebitis.
3. Lymphangitis, serous and purulent lymphadenitis, periadenitis, adenophlegmons.
4. Inflammatory infiltrates, abscesses, phlegmons.
5. Osteomyelitis.
6. Different forms of an erysipelas.

General complications: sinus thrombosis; meningitis; different forms of a sepsis.

The main tasks of a doctor during the treatment of patients with furuncles and carbuncles are reduction of the terms and prevention of the development of local and general complications.

Erysipelas

Erysipelas (Greek spuamsAa – red skin) (also known as “Ignis sacer,” and “St Anthony’s fire” is an acute streptococcus bacterial infection of the dermis, resulting in inflammation and characteristically extending into underlying fat tissue.

Most cases of erysipelas are due to Streptococcus pyogenes (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Historically, the face was most affected; today the legs are affected most often.

Erysipelas infections can enter the skin through minor trauma, eczema, surgical incisions and ulcers, and often originate from strep bacteria in the subject’s own nasal passages.

Clinical forms distinguish: erythematous; erythematous bullous; erythematous hemorrhagic; bullous hemorrhagic.

Patients typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated raised edge (Fig. 12.13). It appears as a red, swollen, warm, hardened and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles, bullae, and petechiae, with possible skin necrosis. Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.

Fig. 12.13. The erythematous skin lesion

The infection may occur on any part of the skin including the face, arms, fingers, legs and toes, but it tends to favor the extremities. Fat tissue is most susceptible to infection, and facial areas typically around the eyes, ears, and cheeks. Repeated infection of the extremities can lead to chronic swelling (lymphangoitis). This disease is mainly diagnosed by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast. Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titre occurs after around 10 days of illness.

There are some severe complications: spread of infection to other areas of body through the bloodstream (bacteremia), including septic arthritis and infective endocarditis (heart valves); septic shock; recurrence of infection – Erysipelas can recur in 18–30 % of cases even after antibiotic treatment; lymphatic damage; necrotizing fasciitis; treatment.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition.

The maxillary sinusitis

The infectious-inflammatory disease characterized by involving in the inflammatory process of the sinus mucousa.

Distinguish rhinogenic, odontogenic, allergic or an extent maxillary sinusitis.

Odontogenic maxillary sinusitis according to different authors makes from 3 to 4.2 % of number of the admitted patients. Given statistical data concerning patients of the maxillofacial department as patients of the given group also can undergo treatment in ENT-department.

As a result of acute and chronic odontogenic inflammatory processes in the maxillary region there can be inflammation of maxillary sinus.

Comparatively frequent origin of odontogenic antritis is explained by the near location of apexes of the roots of the second premolar, first and second molar, more rarely – the third molar to the sinus (Fig. 12.14).

Fig. 12.14. The location of apexes
1 – saggital position, 2 – horizontal position

Sometimes apexes of the roots of these teeth are dissociated from the sinus by a thin bone plate, and on occasion – only by one mucus membrane (to 40 % cases). These anatomic features facilitate the breach of pus in the sinus cavity at acute purulent processes in the area of the second premolar and molars and explain possibility of connection of sinus with the cavity of the mouth during extraction of tooth with its next infecting by a mouth liquid.

A chronic process near the apexes of teeth, spreading toward the sinus, can entail thinning, up to complete disappearance of bone layer between the apex of tooth and sinus cavity and transition of inflammation to the mucous membrane of the sinus (Fig. 12.15).

Fig. 12.15. Complete disappearance of the teeth roots bone layer between the apex of tooth and sinus cavity

Also inflammatory process can extend to ossteomyelitic process or as a result of a suppuration of new growths of the upper jaw. An immediate cause of development of an inflammation is the microbic microflora. In odontogenic maxillary sinuitis staphylococcus is more often sown – both in a monoculture, and in microbic associations.

Odontogenic maxillary sinusitises divide into the acute, chronic, becoming aggravated chronic one. Among them is subacute, an initially-chronic sinusitis. And also they divide in opened (after perforation) and closed ones. Classification by pathologoanatomic signs: catarrhal; purulent; polypous; purulent-polypous.

Acute odontogenic maxillary sinusitis is difficult enough for differentiating from an aggravated chronic one. This proceeds and can come to an end with the treatment or transition into a chronic process. Often enough unique acknowledgement of the diagnosis is the absence of similar aggravations in the anamnesis. For a clinical picture odontogenic maxillary sinusitis are characterized by tearing pain, sense of weight in the infraorbital area, a pain can simulate that in a pulpitis, the body temperature is raises, depending on a type of reactivity. In the oral cavity causal tooth can be found, painful on percussion, an X-ray examination reveals destructive inflammatory process or cyst. On roentgenograms of the maxillary sinus opacity is observed. The maxillary sinus puncture makes it possible to finalise the diagnosis.

Local treatment consists of the creation of conditions for outflow of exudates from the maxillary sinus that is provided either by vasoconstrictive therapy or maxillary sinus puncture, and also in sanitation of odontogenic source by removal of a tooth or its endodontic treatment. It is also prescribed local and general antibacterial, hyposinsebilizating and anti-inflammatory therapy.

The chronic maxillary sinusitis often enough proceeds as initially-chronic inflammatory process.

The clinical picture of chronic odontogenic maxillary sinusitis is characterized by: a headache, heavy feeling in the maxilla with prevailing localization in the infraorbital area, passage of air or passage of a liquid from the oral cavity into the nasal one (at the closed forms), discharges from the fistula, discharges from the nose, presence of a causal tooth. It is typical to reveal the sinus opacity on the X-ray with primary localisation process in the bottom part of the sinus.

For making diagnosis we could use:

• X-ray examination including panoramic films.
• Electoodontodiagnostics.
• Endoskopic research of sinus.
• Spiral or cone-beam computer tomography.

It is necessary to differentiate odontogenic maxillary sinusitis follows with radix and other cyst, grown into the sinus (presence of a shadow, like a dome on the roentgenogram), malignant tumours. Maxillary sinusitis also can be accompanied with an odontogenic osteomyelitis, acting thus as its symptom. The treatment of chronic odontogenic maxillary sinusitis is similar. In inefficiency of conservative treatment, we have to provide the surgical one.

Surgical treatment is performed by the following operative approaches:

• Caldwell – Luc (Fig. 12.16).
• Wasmund – Neumann – Zaslavsky (a Figured incision with access to an alveolar shoot with possibility of plastic elimination of fistula).
• Evdokimov – apertures in an anterior wall maxillary sinus.
• Parch – bow-shaped.
• Trapezoid Novak – Peteru.

Fig. 12.16. Opening of the maxillary sinus:
a – incision of mucus; b – forming of the trepanation opening; c – scheme of location of the maxillary sinus and trepanation opening (1 – foramen infraorbital; 2 – a lower nasoturbinal; 3 – lower nasal path; 4 – alveolar process of the maxilla; 5 – trepanation opening; 6 – maxillary sinus); d – connection of the sinus with a lower nasal path; e – scheme of this connection (7 – opening which connects a sinus with lower nasal path); f – incision in the area of lower nasal path (8 – incision of mucus of the nose; 9 – the area of nasoturbinal is remote)

Thus formation of following flaps is possible:

• Muco-periostal flaps.
• Muco-periostal-bone flaps (V. O. Malanchuk).
• Muco-periostal-bone-adiposal flaps (V. A. Sukachyov).
• Muco-periostal flaps from the pallet.
• The overturning muco-periostal flaps.
• Bridge flaps.
• Multilayered flaps with use of GTR technique.

In the case of perforation of the maxillary sinus, the area of connection of the sine through the oral cavity passes in development of a stage of the connection, a fistula (at the presence of granulations) and anatomizes (at the presence of epithelium).

Approaches to treatment can be the following:

I. Oneself closing: in the case of absence an artificial body in the maxillary sinus; after ending over of acute inflammatory process; in a case of absence of an aggravation of chronic inflammatory process, without presence of polyps and the pathologically changed mucosa.

II. Plastic elimination of communication without sinusotomia:

In the presence of a punched aperture or fistula in a course without an maxillary sinusitis; in chronic, but not polyp inflammatory process; in presence of fibrous changed mucous membrane that probably can be assessed by endoscopic devices.

III. Plastic closing with sinusotomia, without formation of unnatural communication: after conservative treatment in removal of only changed mucous membrane; in endoscopical revision for estimation of a sinus – in the presence of single polyps

IV. Radical sinusotomia with formation of unnatural communication.

• At polypous changed mucousa in the maxillary sinus.
• Along with punching or presence of an foriegn body in a sinus (a root in maxillary sinus).

Sialadenitis

Sialadenitis means inflammatory processes involving the salivary glands. The process may be acute and may result in an abscess formation particularly as a result of bacterial infection. The involvement can be unilateral or bilateral as in viral infections.

Chronic sialadenitis may be nonspecific resulting from ductal obstruction due to sialolithiasis or external radiation or may be specific, caused by various infectious agents and immunologic disorders. The ductal obstruction or decreased salivary flow, allowing retrograde spread of bacteria throughout the ductal system. Blockage of the duct can be caused by sialolithiasis, congenital strictures, or compression by an adjacent tumor.

Etiology

Inflamation of the salivary glands (sialadenitis) can arise from various infectious and noninfectious causes. One of the more common causes of sialadenitis is recent surgery (especially abdominal surgery), after which an acute parotitis (surgical mumps) may arise because the patient has been kept without food or fluids and has received atropine during the surgical procedure. Other medications that produce xerostomia as a side effect also can predispose patients to such an infection. Most cases of acute bacterial sialadenitis are due to Stapfylococcus aureus, but they also may arise from streptococci or other organisms. Noninfectious causes of salivary inflammation include Sjogren syndrome, sarcoidosis, radiation therapy and various allergens.

The most common viral infection is mumps, although a number of other viruses also can involve the salivary glands, including Coxsackie A. ECHO, choriomeningitis, parainfluenza, and cyiomegalovirus (in neonates).

It may be subdivided temporally into acute, chronic and recurrent forms.

Clinical and radiographic features mumps (epidemic parotitis)

Mumps is a paramyxovirus infection that primarily affects the salivary glands. As with measles and rubella, the epidemiology has been affected dramatically by the MMR vaccine (measles-mumps-rubella vaccine). Before the advent of widespread vaccination, epidemics were seen every 2 to 5 years. Although most authorities assume that natural infection is associated with lifelong immunity, rare cases of recurrent mumps have been well documented in patients with a confirmed history of prior natural infection.

The mumps virus can be transmitted through urine, saliva, or respiratory droplets. The Incubation period usually is 16 to 18 days, with a range of about 2 to 4 weeks. Patients are contagious from 1 day before the clinical appearance of infection to 14 days after its clinical resolution.

Approximately 30 % of mumps infections are subclinical. In symptomatic cases, prodromal symptoms of low-grade fever, headache, malaise, anorexia, and myalgia arrive first. Most frequently, these nonspecific findings are followed within 1 day by significant salivary gland changes. The parotid gland is involved most frequently, but the sublingual and submandibular glands also can be affected. Discomfort and swelling develop in the tissues surrounding the lower half of the external ear and extending down along the posterior inferior border of the adjacent mandible. The enlargement typically peaks within 2 to 3 days, and the pain is most intense during this period of maximal enlargement. Chewing movements of the jaw or eating saliva-stimulating foods tends to increase the pain. Enlargement of the glands usually begins on one side and is followed by contralateral glandular changes within a few days. Unilateral involvement is seen in about 25 % of patients.

The second most common finding is epididymoorchitis, which occurs in about 25 % of postpubertal males, in those affected, the testicle exhibits rapid swelling with significant pain and tenderness. The enlargement can range from a minimal swelling to a fourfold increase In size. Unilateral involvement is most common. On resolution of the swelling, atrophy occurs in the affected testicle. Permanent sterility from testicular changes is rare. Less commonly, oophoritis and mastitis can be seen in postpubertal females. In addition, spontaneous abortion occurs In approximately 25 % of females who contract mumps during the first trimester of pregnancy.

Less commonly, meningoencephalitis, cerebellar ataxia, hearing loss, pancreatitis, arthritis, carditis, and decreased renal function may occur. Isolated changes such as orchllis or meningitis, may occur in the absence of salivary gland involvement, thereby making diagnosis difficult in nonepidemic settings. Mumps-related mortality is exceedingly rare and most frequently associated with mumps encephalitis.

The most frequently reported oral manifestation is redness and enlargement of Wharton’s and Stenson’s salivary gland duct openings. In addition, involvement of the sublingual gland may produce bilateral enlargements of the floor of the mouth.

The diagnosis of mumps can be made easily from the clinical presentation when the infection is occurring in an epidemic fashion; however. Isolated cases must be differentiated from other causes. Saliva, urine, or cerebrospinal fluid specimens can be obtained for culture.

The most frequently used confirmatory measures are demonstration of mumps-specific IgM or a fourfold rise of mumps-specific IgG titers when measured during the acute phase and about 2 weeks later.

Acute bacterial sialadenitis is most common in the parotid gland and is bilateral in 10 % to 25 % of cases. The affected gland is swollen and painful, and the overlying skin may be erythematous (Fig. 12.17). An associated low-grade fever may be present, as well as trismus.

Fig. 12.17. Sialadenitis. Tender swelling of the submandib­ular gland

A purulent discharge often is observed from the duct orifice when the gland is massaged (Fig. 12.18).

Fig. 12.18. Sialadenitis. A purulent exudate arising from Stensen’s duct

Recurrent or persistent ductal obstruction (most commonly caused by sialoliths) can lead to a chronic sialadenitis. Periodic swelling and pain occur within the affected gland, usually developing at mealtime when salivary flow is stimulated, unilateral, duct orifice is reddened and flow decreases, may or may not have visible/palpable stone. Depends on ethiology and pathogenesis, sialography demonstrates various types of changes either ductal or parenchyma gland’s tissue (Fig. 12.19; 12.20; 12.21).

Fig. 12.19. Chronic sialadenitis

Fig. 12.20. Chronic sialadenitis (interstitial form)

Fig. 12.21. Chronic sialadenitis (parenchymatous form)

Parotid sialogram demonstrating ductal dilatation proximal to an area of obstruction

In the submandibular gland, persistent enlargement may occur (Kuttner tumor), which is difficult to distinguish from a true neoplasm. Chronic sialadenitis also can occur in the minor glands, possibly as a result of blockage of ductal flow or local trauma. Subacute necrotizing sialadenitis is a recently recognized form of salivary inflammation that occurs most commonly in teenagers and young adults. The lesion usually involves the minor salivary glands of the hard or soil palate, presenting as a painful nodule that is covered by intact, erythematous mucosa. Unlike necrotizing sialometaplasia, the lesion does not ulcerate or slough necrotic tissue. An infectious or allergic cause has been hypothesized.

Histopathologic features in patients with acute sialadenitis, accumulation of neutrophils is observed within the ductal system and acini. Chronic sialadenitis is characterized by scattered or patchy infiltration of the salivary parenchyma by lymphocytes and plasma cells. Atrophy of the acini is common, as is ductal dilatation. If associated fibrosis is present, the term chronic sclerosing sialadenitis is used (Fig. 12.22).

Fig. 12.22. Chronic sclerosing sialadenitis. Chronic inflam­matory infiltrate with associated acinar atrophy, ductal dilatation, and fibrosis

Subacute necrotizing sialadenitis is characterized by a heavy mixed inflammatory infiltrate consisting of neutrophils, lymphocytes, histiocytes, and eosinophils. There is loss of most of the acinar cells, and many of the remaining ones exhibit necrosis. The ducts tend to be atrophic and do not show hyperplasia or squamous metaplasia. Chronic sialadenitis has been misinterpreted as other non-neoplastic entities and also overcalled as several different types of neoplasms, both benign and malignant (Table 12.2).

Treatment and Prognosis

The treatment of acute sialadenitis includes appropriate antibiotic therapy against S. aureus (eg, oxacillin, 250 mg, a 1st-generation cephalosporin, or clindamycin), modified according to culture results. With the increasing prevalence of methicillin-resistant S. aureus, especially among the elderly living in extended-care nursing facilities, vancomycin is often required and hydration, sialagogues (eg, lemon juice, hard candy, or some other substance that triggers saliva flow), warm compresses, compress with 10 % Dimeksid, gland massage, and good oral hygiene are also important. Surgical drainage may be needed if there is abscess formation. Although this regimen is usually sufficient, a 20 % to 50 % mortality rate has been reported in debilitated patients because of the spread of the infection and sepsis.

The management of chronic sialadenitis depends on the severity and duration of the condition. Early cases that develop secondary to ductal blockage may respond to removal of the sialolith or other obstruction. If sialectasia is present, the dilated ducts can lead to stasis of secretions and predispose the gland to further sialolith formation, if sufficient inflammatory destruction of the salivary tissue has occurred, surgical removal of the affected gland may be necessary.

Subacute necrotizing sialadenitis is a self-limiting condition that usually resolves within 2 weeks of diagnosis without treatment.

The treatment of mumps is palliative in nature. Frequently, nonaspirin analgesics and antipyretics are administered. In an attempt to minimize orchitis, bed rest is recommended for males until the fever breaks. Avoidance of sour foods and drinks helps to decrease the salivary gland discomfort. As with measles and rubella, the best results come from prior vaccination, thereby preventing the infection.

Physiotherapeutic procedures for treatment chronic forms of the sialadenitis consists of: magnet-therapy, UHF (ultrahigh frequencies), ultrasound, electrophoresis (hydrocortisone 0.25 %, trypsin 0.01). Gland massage – 2–3 times a day, everyday.

Arthtritis

Arthritis can occur in a chronic, low-grade form or an acute inflammatory form. In addition, it can occur as a degenerative condition, associated with either overuse or aging, or it can occur as an autoimmune disease, such as juvenile rheumatoid arthritis. Most cases are chronic degenerative joint disease and are successfully treated with non-surgical management. The cartilage of the jaw is specifically designed to absorb and cushion the stress associated with movement and chewing. In some patients, the cartilage may lose its elasticity and become stiff. This can occur due to premature aging of the joint or as a result of overuse, such as a patient who grinds their teeth.

Infectious arthritis: Infection of the TMJ may result from direct extension of adjacent infection or hematogenous spread of bloodborne organisms. The area is inflamed, and jaw movement is limited. Local signs of infection associated with evidence of a systemic disease or with an adjacent infection suggest the diagnosis. X-ray results are negative in the early stages but may show bone destruction later. If suppurative arthritis is suspected, the joint is aspirated to confirm the diagnosis and to identify the causative organism. Diagnosis must be made rapidly to prevent permanent joint damage.

Treatment includes antibiotics, proper hydration, pain control, and motion restriction. Parenteral penicillin, ampicillin, ceftriakson are the drugs of choice until a specific bacteriologic diagnosis can be made on the basis of culture and sensitivity testing. Suppurative infections are aspirated or incised. Once the infection is controlled, jaw-opening exercises help prevent scarring and limitation of motion.

Traumatic arthritis. Rarely, acute injury (e.g., due to difficult tooth extraction or endotracheal intubation) may lead to arthritis of the TMJ. Pain, tenderness, and limitation of motion occur. Diagnosis is based primarily on history. X-ray results are negative except when intra-articular edema or hemorrhage widens the joint space. Treatment includes NSAIDs, application of heat, a soft diet, and restriction ofjaw movement.

Osteoarthritis. The TMJ may be affected, usually in people > 50 yr. Occasionally, patients complain of stiffness, grating, or mild pain. Crepitus results from a hole worn through the disk, causing bone to grate on bone. Joint involvement is generally bilateral. X-rays or CT may show flattening and lipping of the condyle, suggestive of dysfunctional change. Treatment is symptomatic.

Rheumatoid arthritis. The TMJ is affected in > 17 % of adults and children with RA, but it is usually among the last joints involved. Pain, swelling, and limited movement are the most common findings. In children, destruction of the condyle results in mandibular growth disturbance and facial deformity. Ankylosis may follow. X-rays of the TMJ are usually negative in early stages but later show bone destruction, which may result in an anterior open-bite deformity. The diagnosis is suggested by TMJ inflammation associated with polyarthritis and is confirmed by other findings typical of the disease.

Treatment is similar to that of RA in other joints. In the acute stage, NSAIDs may be given, and jaw function should be restricted. A night guard or splint is often helpful. When symptoms subside, mild jaw exercises help prevent excessive loss of motion. Surgery is necessary if ankylosis develops but should not be done until the condition is quiescent.

For children who suffer from chronic arthritis, there are challenges of daily living that are associated with decreased range of motion, pain and inflammation. For many children, the complications of arthritis extend well beyond that of the arms, legs, feet, and hands, and even include the joints in the face, including the temporomandibular joint, TMJ. Children who suffer from complications associated with juvenile rheumatoid arthritis often develop complications involving pain when feeding. This pain is associated with arthritic complications in the TMJ. While some TMJ pain can be associated with infection in and around the mouth, most children experience the complication of feeding in direct response to the arthritic and associated arthritic effusions.

If child is complaining of pain in and around the jaw, or TMJ, and complications associated with feeding are becoming apparent, ask your child’s physician to run the diagnostic studies to determine if the complication is related to the development of arthritis in the temporomandibular joint. MRI is often the diagnostic tool used to confirm the development of arthritic conditions in children. With MRI of the head, your child’s complications of pain in the temporomandibular joint can also be confirmed.

Degenerative arthritis

Degenerative arthritis can be either primary or secondary. Primary disease is seen in old people and is a disease of wear and tear. Patients are usually asymptomatic, and when symptomatic, the complaints are usually mild. Secondary degenerative arthritis: This type of arthritis usually develops in people aged 20 to 40 after trauma or in people with persistent myofascial pain syndrome. When degenerative arthritis occurs, the cartilage may then splinter and fracture. Once this occurs, the joint will gradually become stiff and painful. The patient will often hear noise or grinding in the joint and may feel roughness or grating. Joint noise indicates that the cartilage and the disk are beginning to lose their normal smooth contour. Pain in the joint often indicates progression of the disease leading to destruction of the joint components. It is characterized by limited opening of the mouth, unilateral pain during jaw movement, joint tenderness, and crepitus. When it is associated with the myofascial pain syndrome, symptoms wax and wane. Diagnosis is based on X-rays, which generally show condylar flattening, lipping of the joint with osteophyte formation, spurring, or erosion of the articular surface of the condyle. Unilateral joint involvement helps distinguish secondary degenerative arthritis from osteoarthritis.

Treatment of degenerative arthritis is similar to that of myofascial disorders and early internal derangements. NSAIDs, such as ibuprofen, and muscle relaxers with a soft diet are the primary treatment. Bite appliances are added as necessary. When conservative medical management fails to improve symptoms after a 3–6 month trial, surgery is considered. Surgical intervation includes removal of any surgical capsular abnormality, including osteophytes, until the joint space is smooth. A condylar shave is when the entire cortical plate is removed. It should be avoided if possible, as resorption of the condyle is a known complication.

Physical findings which support an initial diagnosis of temporomandibular arthralgia include:

Complete absence of molar teeth in any one quadrant.

Deviation of the jaw to the painful side on wide opening.

Reproducibility of the pain by pressure below the ear forward in the direction of the mandibular condyle.

Reproducibility of the pain by pressure from within the membraneous ear canal forward in the direction of the mandibular condyle, typically by reversing a laryngeal mirror and pressing with the round end of the handle in the ear canal.

Reproducibility of the patient’s complaint of “ear pain” by inserting two tongue blades between the opposite molars and instructing the patient to bite down hard on the tongue blades.

Diagnosis

There are two elements to diagnosis. The first is a comprehensive history and clinical examination. The second is a series of diagnostic studies.

In general, the diagnostic studies available for TM Joint diagnosis and evaluation are:

• X-rays of the TM Joints Skull.
• MRI (Magnetic Resonance Imaging).
• Computed tomography.
• Electromyography (studies of muscle function).
• Motion Performance Studies.
• Joint Vibration Analysis (a form of ultra-sound sonography).
• Diagnostic Study Casts of the Mandible Maxilla.
• X-rays of the Dentition.

Lymphadenites of maxillofacial area and a neck

Lymphadenitis is an inflammation of lymph nodes (Fig. 12.23), often combined with inflammation of lymph vessels.

Fig. 12.23. The lymph nodes of the maxillofacial area and neck

Lympadenites in submaxillary and mental areas as well as in the area of a neck can be characterized as odontogenic or non-odontogenic inflammatory processes. Odontogenic inflammatory processes in a periodontium, bones of a face, maxillary sinus, soft tissue of a face and an oral cavity inevitably result in penetration of infection to respective regional lymph nodes: submaxillary, mental, cheek, parotid, neck. As a result symptomatic lymphadenites develop in the aboved mentioned nodes and both nonspecific and specific lymphadenites can occur.

Acute attack of chronic periodontitis, periostitis and acute pericoronitis were considered to be the most frequent reasons of lymphadenitis. Serous inflammation of a lymph node usually developed on 1–3 day of primary disease while purulent fusion more often was observed on 3–6 day. It is noted that pathological process in primary odontogenic lesion can be curable while the inflammatory occurrences in regional lymph node continue to increase.

Acute odontogenic lymphadenites have been connected with pathological changes in the region of molar teeth and premolar teeth of lower jaw, less often – molar teeth and lateral cutters of the upper jaw. It caused more frequent affect of submandibular ganglion, submental, cheek and parotid lymph nodes, having been major collectors of lymph outflow from mentioned sites of lesion. Usually one lymph node was involved in inflammatory process, the increase in two region nodes areas wasn’t often observed.

Group of non-odontogenic lymphadenites comprises those which have no pathogenetic relation with the dental-maxillary system. They are so-called stomatogenic, rhinogenous, otogenous and other symptomatic lymphadenites, developing due to stomatites, gingivites, glossites, rhinites, inflammatory diseases of an ear. Regional lymphadenites quite often arise in connection with more or less expressed damage of skin or the mucous membrane of the mouth: at a site trauma an entrance gate for an infection are created.

Classification of the lymphadenitis including such forms: acute; serous; purulent; chronic; exudative; productive; traumatic; odontogenic; nonodontogenic; Infectious – Non-specific (acute, chronic); Specific (tuberculous; syphilitic; actinomycotic; viral; vaccinal).

Acute lymphadenitis

Acute inflammation begins with feeling of some awkwardness at head motion, pain in the area of the injured node or groups of nodes.

Both in serous and hyperplastic forms increased lymph nodes are well determined by palpation and under such conditions they are a little bit painful and have dense-elastic consistency. General disorders at the beginning of an inflammation can be absent or be of low-grade. The serous inflammation seldom turns into purulent process; it gradually calms down in compliance with the efficacy of the treatment of the underlying disease which has caused an inflammation of lymphatic vessels and regional nodes. The nodes gradually decrease in sizes, become less painful in some weeks, have usual form and a consistency. At adverse course of serous inflammation it can turn into purulent: in the field of the node infiltration appears (perilymphadenitis), the node becomes not mobile, commissures with other nodes forming with them a package, suppurates. The body temperature raises up to 37.2–37.8 °C. As for blood, there are changes characteristic for abscesses. The general state of health and of the patient is quite often abnormal: indisposition, weakness, loss of appetite, etc. Inflamed lymph node gradually fuses and causes formation of the sinus tract (with transition of disease into the chronic form) or adenophlegmon (see below). In acute purulent lymphadenitis its general parameters (changes in blood, urine, temperature reaction) can be shaded and can be explained as changes due to underlying odontogenic or nonodontogenic inflammation caused lymphadenitis.

Process of purulent fusion of the node can develop quickly – within several days, but sometimes slowly even after elimination of the underlying process on the face, the jaw and in the oral cavity. In the maxillofacial area the most often lymphadenites are those in submandibular nodes as they are the major nodes of the first stage on the way of lymphatic outflow from the given area. The second by frequency of occurrence are inflammatory processes in mental as well as in parotid and supramaxillar (buccal) nodes. Odontogenic lymphadenites developing on the background of acute or chronic leucosis usually have plural character, locating simultaneously on the face, in the submaxillary areas and the neck. In odontogenic source of infection localized on one side, lymphadenitis can be bilateral as in leucosis all protective immunologic mechanisms are significantly lowered.

Chronic lymphadenitis

Chronic nonspecific lymphadenitis develops as a result of attenuation of the acute process or it is caused by poorly virulent microorganisms. It is characterized by enlargement of lymph nodes to various sizes and restriction of their motion. Separate, clearly determined nodes, painless, but dense enough are palpated. The general state of health of a patient usually is not disordered. The purulence of lymph nodes in chronic nonspecific inflammation occurs seldom; it is a feature of transition of chronic process to the acute due to the flare-up of a dormant infection. If odontogenic or other source of infection “bombards” node during a long period of time, it is gradually decaying during a chronic inflammation and is replaced by granulation tissue; from time to time there are aggravations; the latter finally lead to skin perforation and formation of a fistula which is closed and cicatrizes with time. Then beside a fistula appears.

Chronic specific lymphadenitis has, as a rule, tubercular or actinomycotic ethiology and affects mandibular, submandibular, retromandibular and cervical nodes. Sometimes it is combined with injury of other lymph nodes of a body, including bronchial both retroperitoneal. Tubercular and actinomycotic chronic lymphadenites initially have similar courses, creating a picture of so-called hypodermic migrating granuloma of a face or mandibular area. Later actinomycotic lymphadenitis differs by greater tendency to suppuration and formation of fistulas. Course of tubercular lymphadenitis is variable and depends on a stage of disease, amount of injured lymph nodes, reactions of tissues surrounding a node, etc.

It is important to determine first of all, whether lymphadenitis is banal or specific.

In this connection it should be taken into account, that tubercular lymphadenitis is characterized by the absence of the inflammatory features in the oral cavity, jaws, face; rather slow and quite often bilateral increase of inflammatory process in lymph nodes, prolonged mild pyrexia, positive Mantoux test, sterility of pus obtained during a puncture. If chronic lymphadenitis has syphilitic ethiology, thus in the anamnesis or the objective status there are proofs of this disease (Wassermann test, availability of specific destructions of the nose, palate, soft tissue in the area of the pharynx, etc.).

The diagnosis actinomycosis of lymph nodes is determined on the basis of the characteristic anamnesis, infiltrate density, immunoreactions, findings of pathologo-histological or cytological examinations.

Differences between adenophlegmon and lymphadenitis include more extensive area of injury, skin tension and more expressed general disorders (see below).

Sialoadenitis (inflammation of parotid or submandibular salivary gland) is characterized by purulent or serous-purulent discharge from the efferent duct of the gland. If in chronic lymphadenitis there is infiltrate tuberosity, it is necessary to exclude a neoplasm. In such cases biopsy is indicated.

Syphilitic injury of a node is characterized by its significant induration and availability of corresponding findings and the objective status in anamnesis (see above).

Brill-symmers disease or giant follicular lymphoma is one of benign variants of lymphosarcomas. For many years it can represent asymptomatic increase of parotid, submandibular, mental lymph nodes, dense by touch and by that supposing chronic nonspecific lymphadenitis or reactive follicular hyperplasia.

Giant follicular lymphoma (known also as medullar lymphosarcoma by WHO classification 1976) is diagnosed only by histologic study. As in this disease occurs generalization (injury of the nearby and remote lymph nodes with involving of the skin, a hypodermic layer, tonsils, internal organs, bone marrow), it is necessary to not hesitate with radical removal of palpated nodes and their careful histological examination.

Differential diagnostics of LAP (lymphoadenopaties)

Local (regional) LAP:

• Local infections bacterial (pharyngitis, mild otitis, ethmoiditis, frontitis, an antritis, an abscess and caries of teeth).
• Viral (disease of “the cat’s scratch”, a tuberculosis, children’s infections, etc.).
• Fungous (actyinomycaosis, candidiasis) lymphogranulematosis (Hodgkin’s disease).
• Non-Hodgkin’s lymphomas (lymphoma of tonsiles, LN).
• Carcinoma (secondary).

Generalized (systemic) LAP:

• Infections bacterial (sepsis, tuberculosis, brucellosis, tularemia, syphilis, etc.); viral (measles, adenoviral infection, flu, AIDS, infectious mononucleosis etc.) fungoid (histoplasmosis, actinomycosis) protozoan (toxoplasmosis, listeriosis, leishmanioisis).
• Autoimmune diseases (rheumatoid arthritis, systemic red erythematosus, dermatomyositis, sclerodermia, nodular periarteritis, granulematous arterites, etc.).
• Benign tumor diseases (sinus histiocytosis with massive LAP, associated with infections, hemophagocytic syndrome, sarcoidosis).
• Malignant tumor diseases primary: LGM (Hodgkin’s disease). Non-Hodgkin’s disease (lymphoma of peripheral LN, skin lymphoma, malignant histiocytoses; metastatic: leukemia, neuroblastoma, rhabdomyosarcoma. Kaposi’s sarcoma, cancers of the lungs, bronchus and thyroid gland.
• Storage diseases (Gaucher’s disease, Niemann – Pick disease).
• Reactions to medicinal and chemical substances (serum sickness, medicamentous allergy, pollinosis).
• Other diseases.

Treatment

Treatment of acute serous and chronic lymphadenites should be conservative only when it is impossible to define a source (an entrance gate) of infection in the oral cavity, teeth, jaws, face, ENT-organs, etc. In such cases there are applied: dry heat, UHF-therapy, short-term novocaine-antibitics blockade. For the treatment of acute serous lymphadenitis inflammatory infiltrates A. A. Timofeev (1989) recommends daily novocaine nerve-blockade for 5 days of superior cervical and stellate sympathetic ganglions on a side of injury and after dissection of purulent lymphadenites – intramuscular infusion of the Lysozyme (200 mg 2 times a day on first three days, 100 mg 2 times a day the next 3 days) without combination with antibiotics. Blockades are useful because sympathetic fibres of cervical ganglions innervate smooth muscule elements being in a capsule and trabeculas of lymph nodes of the maxillofacial area and the neck that provides contraction of the latter and promotes pushing through of lymph to revehent vessels. In the inflammatory area nervous fibres are in a state of parabiosis the rate of which depends on the severity of the inflammatory process. Novocaine has antiparabiotic property.

It is very useful to apply warming compresses with 30 % solution of dimethylsulfoxide. If the source of infection is not revealed and suppuration of a node (or a package of nodes) occured, it is necessary to dissect the abscess and drain it. In some cases it is possible to manage with aspiration of pus and filling of the cavity of an abscess with a solution of antibiotics. If the source of an infection is revealed, it is necessary to eliminate it with antibacterial preparations or surgical intervention (removal of tooth with periodontitis, husking of festered cyst, removal of hanging inflamed hood above cutting tooth, treatment of antritis, osteomyelitis, periostitis, etc.).

If there is interrelation between suppurated lymph node and odontogenic source of an infection, it is as usually enough to eliminate the latter to stop lymphadenitis or perilymphadenitis. However, in some cases besides intervention on a tooth (its removal, replantation, apical resection etc.) it is necessary to do an incision throughout the mucogingival fold to dissect granular-inflammatory bundle from a tooth to the focus of suppuration in soft tissue. An incision throughout mucogingival fold is drained by rubber strip. As a result, entry of new portions of infection from dental-maxillary systems completely stops. If lymph node suppuration resulted in destruction and cicatricial deformation of the skin, it is necessary to dissect cicatrical changes of tissue, to remove whole granulation tissue both in the depth of the focus of injury and on the internal surface of the dissected skin, to rinse the wound and layer by layer to take it in.

Specific tubercular lymphadenitis should be treated in specialized medical establishments. Sanitation of the oral cavity is obligatory. Immunotherapy is successful for adenoactinomycosis as well as hypodermic form of actinomycotic injuries of the face and the neck; in case of lymph nodal suppuration dissection of the focus, scraping of granulations and administration of antibiotics (locally and intramuscularly) is indicated. However, it is necessary to remember, that a source of a specific infection quite often is gangrenous tooth. Therefore the treatment of specific lymphadenitis should be started with sanitation of the oral cavity.

Prevention of acute sharp and chronic limphadenitis consists of general and local anticarious actions: duly treatment of caries of teeth and its complications, elimination of non-odontogenic sources of infection (treatment of stomatitis, rhinitis, gingivitis, glossitis, otitis, furuncules, carbuncules, etc.), treatment of traumatic injuries of the mucous membrane of a mouth and skin of face, increase of resistance of human organism, etc.

Specific inflammatory processes

Actinomycosis, tuberculosis, syphilis: etiology, classification, clinical course, diagnostics, treatment.

Tuberculosis (tbc.)

Mycobacterium Tbc. (human – 92 %, bovine – 5 %, intermediate – 3 %).

Droplet type of transfer, contact, alimentary factor. Immunity and firmness of an organism to Tbc, premobid background, social conditions of a life of the patient. Tbc. bacilli are partially persist in a place of penetration, the others – are transferred by a current of a lymph to the nearest lymph nodes. Further duplication of microbacilli takes and granuloma is formed – Tbc tubercule. Tubercule (Tbc) decays with formation of the cheesy decay focus 4–8 weeks after an organism sensitizes to tuberculoprotein.

Tbc can affect any human system or organ, remaining thus systemic disease.

Tbc of the maxillofacial area can be primary, when there is no pulmonary focus and secondary – when active Tbc process occurs in lung, bones, etc.

Clinic

Tbc. injury of the maxillofacial area includes injuries of the skin, mucous membranes, hypodermic cellular tissue, jaws, lymph nodes and salivary glands.

Primary Tbc injury is usually formed in the region of lymph nodes amounts up to 60 %.

Classification including:

Hyperplastic (infiltrative) form – Tbc granulomas against the background of lymphoid tissue proliferation. Fibrous-cheesy form – cheesy necrosis numerous combined Tbc granulomas. Fibrous – cicatricial hardenings, development of a connecting fabric.

1. Tbc of jaws – secondary, with mucous, in hematogenous spread (lymphogenous) spread, Ro – in a jaw foci of exhaustion take place.
2. Tbc of salivary glands are rare, often in parotid, foci of necrosis appear.
3. Tbc of skin and hypodermic cellular tissue:

Primary Tbc (Tbc chancre) – erosion and ulcers with harden bottom; Tbc lupus – Tbc tubercule (lipoma) soft; scrofuloderma – intrascutaneous nodes sized 1–3 cm, dense; lupus verucosis Tbc – small, dense, painless node of pinkish-cyanotic color; milliary-ulcer Tbc – small yellowy-red nodes, ulcerating conjugate and superficial very painful ulcers are formed; disseminated milliary Tbc (milliary lupus) – small nodes are painless, they are ulcering, cicatrize or resolve; roseola tuberculitis – pinkish-brown papulae with drying up crusts; papulo-necrotic Tbc – small roundish paulae (2–3 mm).

Treatment

Dissection of the purulent foci,biopsy (incisional, excisional), sequestectomy, etc. Sanitation of the oral cavity. Systemivc treatment: PAS(A), phtivazid, rifampicin.

Syphilis (LuES)

It is caused by pale treponema. A venereal and domestic way of transmission.

It can be congenital, a superinfection – pale treponemas get into an organism (repeated infection of not cured patient) – overlay of syphilitic infection on the already available ones, clinically – erupt during the period when repeated infection occured.

Clinic consist of the primary, secondary and tertiary periods.

The incubatory period is 3 weeks and is completed with formation of primary syphiloma. Primary – a spot of red color or papulae – in the center is necrosis – an ulcer (hard chanre), 5–7 days after enlargement of regional lymph nodes – syphilitic scleradenitis 3–4 weeks after – polyadenitis painless.

Seronegative and seropositive period 6–7 weeks later.

Secondary – occurrence of roseolas, papulae, pustules (syphilides) on the skin and mucous membrane.During this period the greatest contagiosa occures. Sometimes periosteum is injured, more often on the lower jaw, thickening.

The tertiary period occurs 3–6 years later and is characterized by grumous tubercle and gummatous formations. In tubercle syphilide in dermal thickness rounded dense raised formation are detected.

Formation of grumous infiltrate, necrosis, ulcers is possible. Gumma is a painless node densely elastic consistence up to 1.5 mm in diameter, contains viscous substance – a deep ulcer, cicatrizes slowly – deformed scars. They are in the region of hard and soft palates in the thickness of the tongue, the back wall of the throat, the nose, frequently in nasal septum. Foraminous defects in bone are formed.

Dental treatment includes the following stages: antiseptic care of syphilitic elements. Sanitation of teeth.Surgical treatment of deformations after the performed course of treatment.

Actinomicosis

Radiant-fungoid diseases – is ray fungus. In 85 % maxillofacial area is affected. Ray fungus – saprophyte, mainly in stroma of dental calculus.

The entrance gate of an infection – carious teeth, pathological dentalgingival pockets, the mucous membrane of the oral cavity, pharynx, nose, throat, salivary glands. The incubation period – from some days up to 2–3 weeks, but sometimes it can last for months. Ray fungus can develop in friable cellular tissue, in tissue layers of muscles and organs, i.e. in good vascularized environment. Specific granuloma is formed. Robustova distinguishes the following forms of actinomycosis of the face, neck, jaws and oral cavity: cutaneous; hypodermic; submucosal; mucous; odontogenic actinomycosis granuloma; hypodermical-intermuscular; actinomycosis of lymph nodes; actinomycosis of jaw periosteum; actinomycosis of jaws; atinomycosis of the oral cavity, tongue, tonsils, salivary glands, maxillary sinus.

The diagnosis is verified by analysis reaction:

1) - negative reaction – only a site of needle prick is visible;

2) ? doubtful reaction – hardly appreciable pink erythema;

3) +? poorly positive – clear erythema;

4) + positive reaction – brightly-pink erythema up to dark red color;

5) + + strongly positive reaction – brightly-red erythema with skin edema, painful;

6) + + + systemic or local reaction – systemic or focal changes.

Treatment may consist of surgical: removal of teeth – an entrance gate of infection; surgical processing of infection foci, removal of neoplastic bone. Influence on specific immunity; increase of general resistance of organism; influence on accompanying purulent infection; anti-inflammatory, desensibilizing, symptomatic treatment, treatment of concomitant diseases; physical methods and exercise therapy.

Complications of inflammatory processes of the maxillofacial region and neck

Sepsis

Sepsis is a serious medical condition characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) and the presence of a known or suspected infection. Septicemia is a related but deprecated (formerly sanctioned medical) term referring to the presence of pathogenic organisms in the blood-stream, leading to sepsis. Severe sepsis occurs when natural immune response to an infection goes into overdrive, triggering widespread inflammation and blood clotting in tiny vessels throughout the body. One or more organs may stop working properly or fail. Sepsis can lead to a dangerous drop in blood pressure (septic shock).

Sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor drugs can be used. Artificial ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low-dose corticosteroids or activated drotrecogin alfa (recombinant protein C).

Severe sepsis occurs when sepsis leads to organ dysfunction, low blood pressure (hypotension), or insufficient blood flow (hypoperfusion) to one or more organs (causing, for example, lactic acidosis, decreased urine production, or altered mental status). Sepsis can lead to septic shock, multiple organ dysfunction syndrome (formerly known as multiple organ failure), and death. Organ dysfunction results from sepsis-induced hypotension (< 90 mm Hg or a reduction of > 40 mm Hg from baseline) and diffuse intravascular coagulation, among other things.

Bacteremia is the presence of viable bacteria in the bloodstream. These term says nothing about the consequences this has on the body. For example, bacteria can be introduced into the bloodstream during toothbrushing. This form of bacteremia almost never causes problems in normal individuals. However, bacteremia associated with certain dental procedures can cause bacterial infection of the heart valves (known as endocarditis) in high-risk patients. Conversely, a systemic inflammatory response syndrome can occur in patients without the presence of infection, for example in those with burns, polytrauma.

At higher risk for sepsis are:

• Very young people and elderly people.
• Anyone who is taking immunosuppressive medications (such as transplant recipients).
• People who are being treated with chemotherapy drugs or radiation.
• Patients who have no spleen.
• Patients taking steroids (especially over the long-term).
• People with long-standing diabetes, AIDS, or cirrhosis.
• Someone who has very large burns or severe injuries.

In addition to symptoms related to the provoking infection, sepsis is characterized by evidence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower-than-average temperature. The modern concept of sepsis is that the host’s immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by hemodynamic compromise and resultant metabolic derangement. Outward physical symptoms of this response frequently include a high heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute), elevated WBC count (above 12G) and elevated or lowered body temperature (under 36 °C or over 38 °C). Sepsis is differentiated from SIRS by the presence of a known pathogen. For example, SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. Without a known infection you can not classify the above symptoms as sepsis, only SIRS. This immunological response causes widespread activation of acute-phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

Definition of sepsis

Sepsis is considered present if infection is highly suspected or proven and two or more of the following systemic inflammatory response syndrome (SIRS) criteria are met:

• Heart rate > 90 beats per minute (tachycardia).
• Body temperature < 36 °C (97 °F) or > 38 °C (100 °F).
• Respiratory rate > 20 breaths per minute or, on blood gas, a PaCO2 less than 32 mm Hg (4.3 kPa) (tachypnea or hypocapnia due to hyperventilation).
• White blood cell count < 4.000 cells/mm3 or > 12,000 cells/mm3 (< 4 × 109 or > 12 × 109 cells/L), or greater than 10 % band forms (leukopenia, leukocytosis, or bandemia).

Fever and leukocytosis are features of the acute-phase reaction, while tachycardia is often the initial sign of hemodynamic compromise. Tachypnea may be related to the increased metabolic stress due to infection and inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic cellular metabolism.

To qualify as sepsis, there must be an infection suspected or proven (by culture, stain, or polymerase chain reaction (PCR)), or a clinical syndrome pathognomonic for infection.

The more critical subsets of sepsis are severe sepsis (sepsis with acute organ dysfunction) and septic shock (sepsis with refractory arterial hypotension). Patients are defined as having “severe sepsis” if they have sepsis plus signs of systemic hypoperfusion: either end-organ dysfunction or serum lactate greater than 4 mmol/dL. Other signs include oliguria and altered mental status. Patients are defined as having septic shock if they have sepsis plus hypotension after aggressive fluid resuscitation (typically upwards of 6 liters or 40 ml/kg of crystalloid).

Diagnosis

The medical history and clinical examination can provide important elements regarding the cause and severity of sepsis.

The identification of the causative microbe in sepsis can provide useful information. The exact causative organism is confirmed by microbiological culturing in the laboratory (blood cultures and cultures from suspected sites of infections). However, this is a slow process, as it takes a few days to grow up the cultures and correctly identify the pathogens. New molecular diagnostic tests are now available that use genetic material from the pathogen to quickly (within hours) provide results. However, current practice is to directly prescribe broad spectrum antibiotics to the patient.

The effects of the condition on the function of the organs should be documented to guide therapy. This can involve measurement of blood levels of lactate, blood gas sampling, and other blood tests. Because patients on the intensive-care unit are predisposed to hospital-acquired infections (especially related to the presence of catheters), they may require surveillance cultures.

Treatment

The therapy of sepsis rests on antibiotics, surgical drainage of infected fluid collections, fluid replacement and appropriate support for organ dysfunction. This may include hemodialysis in kidney failure, mechanical ventilation in pulmonary dysfunction, transfusion of blood products, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition – preferably by enteral feeding, but if necessary by parenteral nutrition – is important during prolonged illness.

During critical illness, a state of adrenal insufficiency and tissue resistance (the word “relative” resistance should be avoided to corticosteroids) may occur. This has been termed critical illness-related corticosteroid insufficiency. Treatment with corticosteroids might be most beneficial in those with septic shock and early severe acute respiratory distress syndrome (ARDS).

A number of different types of medications are used in treating sepsis, such as:

• Antibiotics. Treatment with antibiotics begins immediately – even before the infectious agent is identified. Initially “broad-spectrum” antibiotics are used, which are effective against a variety of bacteria. The antibiotics are administered intravenously (IV).
• Vasopressors. If the blood pressure remains too low even after receiving intravenous fluids, the patient may be given a vasopressor medication, which constricts blood vessels and helps to increase blood pressure.
• Activated protein C. People with severe sepsis whose organs are failing or who are at high risk of dying may receive a newer drug called activated protein C. This drug interferes with some of the body’s responses to severe infection, helping to curb the overactive inflammatory reaction, but it can cause serious bleeding.
• Others. Other medications include low doses of corticosteroids, insulin to help maintain stable blood sugar levels, and painkillers or sedatives.

People with severe sepsis usually receive supportive care. Depending on the condition, the patient may need mechanical ventilation (respirator) in case of breathing problems or dialysis for kidney failure.

Possible complications: death; disseminated intravascular coagulation; impaired blood flow to vital organs (brain, heart, kidneys); septic shock.

Mediastinitis

Mediastinitis is inflammation of the tissues in the midchest, or mediastinum. The mediastinum lies between the right and left pleura in and near the median sagittal plane of the chest. It extends from the sternum in front to the vertebral column behind, and contains all the thoracic viscera excepting the lungs.

Mediastinitis can be either acute or chronic. Acute mediastinitis is usually bacterial and due to rupture of organs in the mediastinum. As the infection can progress rapidly, this is considered a serious condition. Chronic sclerosing (or fibrosing) mediastinitis, while potentially serious, is caused by a long-standing inflammation of the mediastinum, leading to growth of acellular collagen and fibrous tissue within the chest and around the central vessels and airways. It has a different cause, treatment, and prognosis than acute infectious mediastinitis.

Before the development of modern cardiovascular surgery, cases of acute mediastinitis usually arose from either perforation of the esophagus or from contiguous spread of odontogenic or retropharyngeal infections. However, in modern practice, most cases of acute mediastinitis result from complications of cardiovascular or endoscopic surgical procedures.

Treatment usually involves aggressive intravenous antibiotic therapy and hydration. If discrete fluid collections (such as abscesses) have formed, they may have to be surgically drained. Chronic mediastinitis is usually a radiologic diagnosis manifested by diffuse fibrosis of the soft tissues of the mediastinum. This is sometimes the consequence of prior granulomatous disease, most commonly histoplasmosis. Other identifiable causes include tuberculosis and radiation therapy. Fibrosing mediastinitis most frequently causes problems by constricting blood vessels or airways in the mediastinum. This may result in such complications as superior vena cava syndrome or pulmonary edema from compression of pulmonary veins. Treatment for chronic fibrosing mediastinitis is somewhat controversial, and may include steroids or surgical decompression of affected vessels.

Meningitis

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be often caused by bacteria of odontogenic origin. Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.

The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia).

A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory. The usual treatment for meningitis is the prompt application of antibiotics. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation. Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly.

Clinical features

In adults, a severe headache is the most common symptom of meningitis – occurring in almost 90 % of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46 % of all cases of bacterial meningitis. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises).

Nuchal rigidity occurs in 70 % of adult cases of bacterial meningitis. Other signs of meningism include the presence of positive Kernig’s sign or Brudzinski’s sign. Kernig’s sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig’s sign, pain limits passive extension of the knee. A positive Brudzinski’s sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig’s and Brudzinski’s signs are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases.

People with meningitis may develop additional problems in the early stages of their illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing. Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk.

The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue getting trapped. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal positioning. Inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus).

The types of bacteria that cause bacterial meningitis vary by age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination). In adults, N. meningitidis and S. pneumoniae together cause 80 % of all cases of meningitis, with increased risk of L. monocytogenes in those over 50 years old.

In some proportion of people, an infection in the head and neck area lead to meningitis. Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. In these cases, infections with staphylococci are more likely, as well as infections by pseudomonas and other Gram-negative bacilli. The same pathogens are also more common in those with an impaired immune system.

Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is skull fracture, particularly fractures that affect the base of the brain or extend towards the sinuses and petrous pyramids.

Diagnosis

In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures.

The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap). However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated, as it may lead to brain herniation. CT or MRI scans are performed at a later stage to assess for complications of meningitis.

Treatment

Meningitis is potentially life-threatening and has a high mortality rate if untreated; delay in treatment has been associated with a poorer outcome. Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. Intravenous fluids should be administered if hypotension (low blood pressure) or shock is present. Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early, as well as admission to an intensive care unit if deemed necessary.

Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. The structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis.

Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place.

The results of the CSF culture generally take longer to become available (24–48 hours). Once they do, empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics. For an antibiotic to be effective in meningitis, it must not only be active against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningitis.

Adjuvant treatment with corticosteroids (usually dexamethasone) reduces rates of mortality, severe hearing loss and neurological damage. The likely mechanism is suppression of overactive inflammation.

Prognosis

Untreated, bacterial meningitis is almost always fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause and is about 19–37 % in adults. Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid, the severity of the generalized illness, decreased level of consciousness or abnormally low count of white blood cells in the CSF.

Cavernous sinus Thrombosis

Cavernous sinus thrombosis (CST) was initially described by Bright in 1831 as a complication of epidural and subdural infections. CST is usually a late complication of an infection of the central face or paranasal sinuses. Other causes include bacteremia, trauma, and infections of the ear or maxillary teeth. CST is generally a fulminant process with high rates of morbidity and mortality. Fortunately, the incidence of CST has been decreased greatly with the advent of effective antimicrobial agents.

Pathophysiology

The cavernous sinuses are irregularly shaped, trabeculated cavities located at the base of the skull. The cavernous sinuses are the most centrally located of the dural sinuses and lie on either side of the sella turcica. These sinuses are just lateral and superior to the sphenoid sinus and are immediately posterior to the optic chiasm. Each cavernous sinus is formed between layers of the dura mater, and multiple connections exist between the 2 sinuses.

The cavernous sinuses receive venous blood from the facial veins (via the superior and inferior ophthalmic veins) as well as the sphenoid and middle cerebral veins. They, in turn, empty into the inferior petrosal sinuses, then into the internal jugular veins and the sigmoid sinuses via the superior petrosal sinuses. This complex web of veins contains no valves; blood can flow in any direction depending on the prevailing pressure gradients. Since the cavernous sinuses receive blood via this distribution, infections of the face including the nose, tonsils, and orbits can spread easily by this route.

The internal carotid artery with its surrounding sympathetic plexus passes through the cavernous sinus. The third, fourth, and sixth cranial nerves are attached to the lateral wall of the sinus. The ophthalmic and maxillary divisions of the fifth cranial nerve are embedded in the wall.

This intimate juxtaposition of veins, arteries, nerves, meninges, and paranasal sinuses accounts for the characteristic etiology and presentation of CST. Staphylococcus aureus accounts for approximately 70 % of all infections. Streptococcus pneumoniae, gram-negative bacilli, and anaerobes can also be seen. Fungi are a less common pathogen and may include Aspergillus and Rhizopus species.

Mortality / Morbidity

Prior to the advent of effective antimicrobial agents, the mortality rate from CST was effectively 100 %. Typically, death is due to sepsis or central nervous system (CNS) infection. With aggressive management, the mortality rate is now less than 30 %. Morbidity, however, remains high, and complete recovery is rare. Roughly one sixth of patients are left with some degree of visual impairment, and one half have cranial nerve deficits.

Causes

• Most cases of septic CST are due to an acute infection in an otherwise healthy individual. However, patients with chronic sinusitis or diabetes mellitus may be at a slightly higher risk.

The causative agent is generally Staphylococcus aureus, although streptococci, pneumococci, and Cavernous sinus thrombosis.

Clinical signs

The early signs and symptoms of cavernous sinus thrombosis (CST) may not be specific. A patient who presents with headache and any cranial nerve findings should be potentially evaluated for CST. The most common signs of CST are related to the anatomical structures affected within the cavernous sinus.

• Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5–10 days. In as many as 25 % of cases in which a furuncle is the precipitant, it will have been manipulated in some fashion (eg, squeezing, surgical incision).
• Headache is the most common presentation symptom and usually precedes fevers, periorbital edema, and cranial nerve signs. The headache is usually sharp, increases progressively, and is usually localized to the regions innervated by the ophthalmic and maxillary branches of the fifth cranial nerve.
• In some patients, periorbital findings do not develop early on, and the clinical picture is subtle.
• As the infection tracts posteriorly, patients complain of orbital pain and fullness accompanied by periorbital edema and visual disturbances.
• Without effective therapy, signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. Eye swelling begins as a unilateral process and spreads to the other eye within 24–48 hours via the intercavernous sinuses. This is pathognomonic for CST.
• The patient rapidly develops mental status changes including confusion, drowsiness, and coma from CNS involvement and/or sepsis. Death follows shortly thereafter.

Other than the findings associated with the primary infection, the following signs are typical:

• Periorbital edema may be the earliest physical finding:
• Chemosis results from occlusion of the ophthalmic veins.
• Lateral gaze palsy (isolated cranial nerve VI) is usually seen first since CN VI lies freely within the sinus in contrast to CN III and IV, which lie within the lateral walls of the sinus.
• Ptosis, mydriasis, and eye muscle weakness from cranial nerve III dysfunction.
• Manifestations of increased retrobulbar pressure follow:
• Exophthalmos.
• Ophthalmoplegia.
• Signs of increased intraocular pressure (IOP) may be observed:
• Pupillary responses are sluggish.
• Decreased visual acuity is common owing to increased IOP and traction on the optic nerve and central retinal artery.
• Hypoesthesia or hyperesthesia in dermatomes supplied by the V1 and V2 branches of the fifth cranial nerve.
• Appearance of signs and symptoms in the contralateral eye is diagnostic of CST, although the process may remain confined to one eye.
• Meningeal signs, including nuchal rigidity and Kernig and Brudzinski signs, may be noted.
• Systemic signs indicative of sepsis are late findings. They include chills, fever, shock, delirium, and coma.

FBC, ESR, blood cultures, and sinus cultures help establish and identify an infectious primary source. Lumbar puncture is necessary to rule out meningitis.

A MRI using flow parameters and an MR venogram are more sensitive than a CT scan, and are the imaging studies of choice to diagnose cavernous sinus thrombosis. Findings may include deformity of the internal carotid artery within the cavernous sinus, and an obvious signal hyperintensity within thrombosed vascular sinuses on all pulse sequences.

Treatment

Cavernous sinus thrombosis has a mortality rate of less than 20 % in areas with access to antibiotics. Before antibiotics were available, the mortality was 80–100 %. Morbidity rates also dropped from 70 % to 22 % due to earlier diagnosis and treatment.

Recognizing the primary source of infection (i.e., facial cellulitis, middle ear, and sinus infections) and treating the primary source expeditiously is the best way to prevent cavernous sinus thrombosis.

Broad-spectrum intravenous antibiotics are used until a definite pathogen is found.

Vancomycin may be used if significant concern exists for infection by methicillin-resistant Staphylococcus aureus or resistant Streptococcus pneumoniae. Appropriate therapy should take into account the primary source of infection as well as possible associated complications such as brain abscess, meningitis, or subdural empyema. Anticoagulation with Heparin is controversial. Retrospective studies show conflicting data. This decision should be made with subspecialty consultation. Steroid therapy is also controversial and is not recommended by many sources. All patients with CST are usually treated with prolonged courses (3–4 weeks) of IV antibiotics. If there is evidence of complications such as intracranial suppuration, 6–8 weeks of total therapy may be warranted.

All patients should be monitored for signs of complicated infection, continued sepsis, or septic emboli while antibiotic therapy is being administered.

Complications of untreated CST include extension of thrombus to other dural venous sinuses, carotid thrombosis with concomitant strokes, subdural empyema, brain abscess, or meningitis. Septic embolization may also occur to the lungs, resulting in ARDS, pulmonary abscess, empyema, and pneumothorax.

Complications in treated patients include oculomotor weakness, blindness, pituitary insufficiency, and hemiparesis.

In order to treat an acute dentoalveolar infection as well as a fascial space abscess correctly, the following are considered absolutely necessary.

Take a detailed medical history from the patient. There are following indications for hospital admission: temperature > 38.3 °C, dehydration, threat to the airway or vital structures, infection in moderate or high severity anatomic spaces, need for general anesthesia, need for inpatient control of systemic disease and other.

The most frequent cause of death in reported cases of odontogenic infection is airway obstruction. Therefore, the surgeon must assess current or impending airway obstruction within the first few moments of evaluating the patient with a head and neck infection. Complete airway obstruction is, of course, a surgical emergency. In such cases insufficient or absent air movement in spite of inspiratory efforts will be apparent. In highly skilled hands one brief attempt at endotracheal intubation may be made, but a direct surgical approach to the airway by cricothyroidotomy or tracheotomy is more predictably successful. In such extreme circumstances the presence of infection overlying the trachea is less important than the absence of ventilation. Therefore, infection in the region of surgical airway access is not a contraindication to an emergency cricothyroidotomy or tracheotomy

Drainage of pus, when its presence in tissues is established. This is achieved by way of the root canal, with an intraoral incision, with an extraoral incision, and through the alveolus of the extraction. Without evacuation of pus that is with administration of antibiotics alone the infection will not resolve. Drilling of the responsible tooth during the initial phase of inflammation, to drain exudates through the root canal. In this way, spread of inflammation is avoided and the patient is relieved of the pain. Drainage may also be performed with trepanation of the buccal bone, when the root canal is inaccessible. In general, surgery for management of severe odontogenic infections is not difficult. Given a thorough knowledge of the anatomy of the deep fascial spaces of the head and neck, the surgeon should be able, by using appropriate anatomic landmarks, to use small incisions and blunt dissection without direct exposure and visualization of the entire infected anatomic space. Another important principle of surgical incision and drainage is the need to dissect a pathway for the drain that includes the locations where pus is most likely to be found.

On the management of deep fascial space infections of the head and neck there are two approaches to surgical drainage of deep neck infections. First strategy is to use parenteral antibiotic therapy as a means of controlling, localizing, or even eradicating the soft tissue infection. Failure of the medical approach is determined by patient aggravation, impending airway compromise, and the identification of an abscess by CT or clinical examination or both. Only then is surgical drainage undertaken. The expectant approach to management of severe odontogenic infections has not been supported by empiric investigation. The alternative strategy is the immediate establishment of airway security as necessary, and aggressive early surgical intervention. Identification of an abscess is not required before surgical intervention. This approach is predicated on the concept that early incision and drainage aborts the spread of infection into deeper and more critical anatomic spaces, even when it is in the cellulites stage.

Planning of the incision and steps so that:

• Antisepsis of the area with an antiseptic solution before the incision.
• Anesthesia of the area where incision and drainage of the abscess are to be performed, with the block technique together with peripheral infiltration anesthesia at some distance from the inflamed area, in order to avoid the risk of existing microbes spreading into deep tissues.
• Injury of ducts (Wharton, Stenson) and large vessels and nerves is avoided. Incision for drainage of a sublingual abscess is performed parallel to the submandibular duct and the lingual nerve. During cutaneous incisions, the course of the facial artery and vein must be taken into consideration, as well as that of the facial nerve movement of the fluid inside the abscess. If the incision is premature, there is usually a small amount of bleeding, no pain relief for the patient and the edema does not subside.
• Sufficient drainage is allowed. The incision is performed superficially, at the lowest point of the accumulation, to avoid pain and facilitate evacuation of pus under gravity. The incision is not performed in areas that are noticeable, for esthetic reasons; if possible, it is performed intraorally.
• Placement of a rubber drain inside the cavity and stabilization with a suture on one lip of the incision, aiming to keep the incision open for continuous drainage of newly accumulated pus. The advantages of drainage are the provision of two pathways for the egression of pus, placement of the incisions in healthy tissue in cosmetically acceptable areas, and the ability to irrigate the infected wound with unidirectional flow from one incision to the other. Wound irrigation is facilitated especially by the use of tube drain, which is noncollapsible and perforated.
• Removal of the responsible tooth as soon as possible, to ensure immediate drainage of the inflammatory material, and elimination of the site of infection. Extraction is avoided if the tooth can be preserved, or if there is an increased risk of serious complications in cases where removal of the tooth is extremely difficult.

Administration of antibiotics, when swelling is generally diffuse and spreading, and especially if there is fever present, and infection spreads to the fascial spaces, regardless of whether there is an indication of the presence of pus. Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a culture sample. These antibiotic choices are separated by severity of infection. Penicillin group of antibiotic continues to be a highly effective for uncomplicated odontogenic infections, owing to its low cost and low incidence of unwanted side effects. Most resistance to penicillin that occurs among the oral pathogens is due to synthesis of P-lactamase. Therefore, it is reasonable to use penicillin plus a P-lactamase inhibitor such as ampicillin-sulbactam or a penicillin plus metronidazole as alternative antibiotics for serious odontogenic infections. The penicillins and metronidazole have the advantage of crossing the blood-brain barrier when the meninges are inflamed. Clindamycin, on the other hand, does not cross the blood-brain barrier. Therefore, it is appropriate to use penicillin plus metronidazole or ampicillin-sulbactam when there is a risk of an odontogenic infection entering the cranial cavity. Few cephalosporins are able to cross the blood-brain barrier. Some third generation cephalosporins, such as ceftadizime, can do so. In addition, ceftadizime is effective against the oral streptococci and most oral anaerobes.Among the cephalosporins, therefore, ceftadizime is the alternative antibiotic of choice. A new fluoroquinolone antibiotic, moxifloxacin has great promise in the treatment of head and neck infections. Its spectrum against oral streptococci and anaerobes is excellent. Its absorption is virtually complete via either the oral or intravenous routes, and it penetrates bone readily. The tissue level of antibiotics determines their effectiveness. Those tissue levels are of course dependent on the antibiotic’s level in serum, through which the antibiotic must pass in order to achieve therapeutic levels in soft tissues, bone, brain, and abscess cavities. Administration of antibiotics by the oral route requires that the drug successfully navigate the vagaries of the highly acidic stomach, the chemical qualities of ingested foods, and the basic intestinal tract. Some antibiotics, however, are equally well absorbed intravenously and orally. The fluoroquinolones, such as ciprofloxacin and moxifloxacin, are the best examples of this. For this reason the fluoroquinolones are not given intravenously unless use of the oral route is contraindicated. Dosage intervals should not be changed from published guidelines by the surgeon. Nonetheless, the surgeon must be aware of the greater effectiveness of intravenous antibiotics over their oral counterparts.

Criteria for changing antibiotics: allergy, toxic reaction, or intolerance, culture and/or sensitivity test indicating resistance, failure of clinical improvement, given, removal of odontogenic cause, adequate surgical drainage (suggest postoperative imaging), other causes for treatment failure ruled out 48–72 h of the same antibiotic therapy. Medical supportive care for the patient with a severe odontogenic infection is composed of hydration, nutrition, and control of fever in all patients.

Chapter 13. Benign tumors and tumor-like lesions of the maxillofacial area and neck

Tumors and tumor-like lesions of the maxillofacial area are very numerous and have various clinical manifestation and gistogenesis. Some of these tumors may be found in other areas of the human body, but there are also specific neoplasms which occur only in the maxillo-facial area. Maxillofacial tumors originate from different tissues ectodermal, mesodermal, entodermal or mesenchymal. Maxillofacial area is more liable to the action of exogenous carcinogens.

Benign tumors and tumor-like lesions of the soft tissues

Fibroma

A fibroma, also referred to as an irritation fibroma, is by far the most common of the oral fibrous growths. Although the terminology implies a benign neoplasm, most if not all fibromas represent reactive focal fibrous hyperplasia due to trauma or local irritation. Although the term focal fibrous hyperplasia more accurately describes the clinical appearance and pathogenesis of this entity, it is not commonly used.

A fibroma may occur at any oral site, but most often it is seen on the buccal mucosa along the plane of occlusion of the maxillary and mandibular teeth. It appears as a round-to-ovoid, asymptomatic, smooth, firm, and sessile or pedunculated mass. The diameter may vary from 1 mm to several centimeters. The surface may be hyperkeratotic or ulcerated because of continued trauma.

Fibromas most often are observed in adults, but they may occur in individuals of any age. Females are affected twice as frequently as males.

The clinical differential diagnosis of a fibroma includes giant cell fibroma, neurofibroma, peripheral giant cell granuloma, mucocele, and benign and malignant salivary gland tumors.

Histologically, a fibroma is an unencapsulated, solid, nodular mass of dense and sometimes hyalinized fibrous connective tissue that is often arranged in haphazard fascicles. A mild chronic inflammatory infiltrate may be observed. The surface epithelium may be hyperkeratotic, either hyperplastic or atrophic, and it may be ulcerated. Conservative excisional biopsy is curative, and its findings are diagnostic; however, recurrence is possible if the exposure to the offending irritant persists.

A giant cell fibroma has a distinctive histologic appearance that sets it apart from a conventional fibroma. It appears as an asymptomatic sessile or pedunculated nodule that is smaller than 1 cm in diameter. Often, it has a bosselated or somewhat papillary surface. Most cases are diagnosed in persons aged 10–30 years, and no sex predilection exists. The most common site is the mandibular gingiva, followed by the maxillary gingiva, tongue, and palate.

The clinical differential diagnosis includes squamous papilloma, irritation fibroma, pyogenic granuloma, and peripheral giant cell granuloma.

Microscopically, a giant cell fibroma is an unencapsulated mass of loose fibrous connective tissue that contains numerous characteristic large, plump, spindle-shaped and stellate fibroblasts, some of which are multinucleated. These cells are easily observed in the peripheral areas of the lesion, whereas the more central areas contain typical fusiform fibroblasts. The surface epithelium is corrugated and atrophic; in contrast to an irritation fibroma, a giant cell fibroma has thin, elongated rete ridges. Conservative excisional biopsy is curative, and its findings are diagnostic. Recurrence is rare.

A peripheral ossifying fibroma is also known as a calcifying fibrous epulis or a peripheral fibroma with calcification. It is a reactive gingival lesion that is believed to arise from cells of the periodontal ligament or periosteum. Most often, it is located in the gingival papilla between adjacent teeth. A peripheral ossifying fibroma appears as a sessile or pedunculated mass, which is often ulcerated; generally, its diameter is less than 2 cm. Primarily, peripheral ossifying fibromas are seen in persons aged 10–20 years. Females are affected more often than males by a ratio of about 3:2. The maxillary gingiva is involved more often than the mandibular gingiva; usually, the anterior region is affected. Mobility and/or migration of adjacent teeth is occasionally observed. Microscopically, fibrous proliferation is accompanied by increased cellularity with plump, immature fibroblasts and variable amounts of calcified material. This material may be osteoid, cementoid, or dystrophic. In some cases, this characteristic pattern is only part of the pattern of a larger lesion that resembles an irritation fibroma or pyogenic granuloma. Surface ulceration is common. The clinical differential diagnosis of a peripheral ossifying fibroma includes inflammatory gingival hyperplasia, peripheral giant cell granuloma, pyogenic granuloma, peripheral odontogenic fibroma, and fibroma.

Treatment consists of excision down to the periosteum and the elimination of any local irritants. Care must be taken to maintain or reestablish acceptable gingival architecture and periodontal integrity. A recurrence rate of 16 % is reported. Even in cases complicated by recurrence, reexcision is generally successful, with the retention of the associated tooth.

A peripheral odontogenic fibroma is a rather uncommon neoplasm that is believed to arise from odontogenic epithelial rests in the periodontal ligament or the attached gingiva itself. The entity, formerly confused with peripheral ossifying fibroma, is currently considered to be the extraosseous counterpart of the central odontogenic fibroma of the World Health Organization type. A peripheral odontogenic fibroma appears as a firm, slowly growing, sessile, and nodular growth of the gingiva, most often on the mandibular buccal or labial aspect. It occurs in persons of a wide age range and affects both sexes equally.

The clinical differential diagnosis of a peripheral odontogenic fibroma includes inflammatory gingival hyperplasia, peripheral ossifying fibroma, and peripheral giant cell granuloma.

Microscopically, the tumor consists of an unencapsulated mass of interwoven cellular fibrous connective tissue that contains scattered nests or strands of odontogenic epithelium. Myxoid foci; calcifications; or osteoid, cementoid, or dysplastic areas are sometimes seen. The surface generally is not ulcerated.

Treatment consists of conservative excision performed with care to maintain or reestablish the gingival architecture and periodontal integrity. The tendency for recurrence is low.

Desmoplastic fibroma

A desmoplastic fibroma is considered to be the intraosseous counterpart of the soft-tissue fibromatosis. A desmoplastic fibroma appears as a firm,

painless, poorly demarcated mass that is either rapidly or slowly growing. Usually, it involves the tongue or buccal mucosa. The mass is locally aggressive, blends into surrounding structures, and causes resorption of the underlying bone when it is present.

The differential diagnosis of a fibromatosis includes low-grade fibrosarcoma, nodular fasciitis, reactive fibrous hyperplasia, fibrous histiocytoma, and neurofibroma.

Treatment consists of wide excision. The reported recurrence rate of 24 % for intraoral fibromatoses is considerably lower than the 50–70 % rate reported for fibromatoses of the entire head and neck region.

Myofibroma

Myofibroblasts have features of both fibroblasts and smooth muscle cells. Myofibroblasts have been identified in lesions other than myofibromas, but when they are the predominant cell type in a tumor, the terms myofibroma (if solitary) or myofibromatosis (if multicentric) are applied. The tumors are benign, and, although myofibromatosis is similar to fibromatosis in many ways, its behavior is less aggressive. Tumors of the myofibroblasts may occur in either sex and in patients of all ages, with a mean patient age of 26.6 years.

Myofibroblastic tumors are most common in the head and neck region, including oral and perioral sites, than in other areas. Intraoral lesions occur mainly on the tongue, lips, and buccal mucosa. Tumors also have been described in the dermis, soft tissues, viscera, and bone. Jaw lesions, usually mandibular lesions, generally appear as well-defined unilocular or multilocular radiolucencies. Oral lesions appear as firm submucosal nodules or exophytic masses with a diameter of 0.3–5.0 cm. Although lesions are most often asymptomatic, they may be tender or even painful.

The clinical differential diagnosis for oral myofibroma includes irritation fibroma, peripheral giant cell fibroma, neurofibroma, leiomyoma, and benign and malignant neoplasms of the minor salivary glands.

Treatment for oral myofibromas is conservative excision. The recurrence rate is low, and spontaneous regression is reported.

Juvenile nasopharyngeal angiofibroma (angiofibroma, nasopharyngeal fibroma, bleeding fibroma of adolescence, fibroangioma)

Juvenile angiofibroma (JNA) is a benign tumor that tends to bleed and occurs in the nasopharynx of prepubertal and adolescent males. The lesion originates in close proximity to the posterior attachment of the middle turbinate, near the superior border of the sphenopalatine foramen. A hormonal theory has been suggested because of the lesion’s occurrence in adolescent males. Other theories include a desmoplastic response of the nasopharyngeal periosteum or the embryonic fibrocartilage between the basiocciput and the basisphenoid. Etiology from nonchromaffin paraganglionic cells of the terminal branches of the maxillary artery has also been suggested.

Clinical symptoms

Nasal obstruction (80–90 %) – Most frequent symptom, especially in initial stages. Epistaxis (45–60 %) – Mostly unilateral and recurrent; usually severe epistaxis that necessitates medical attention; diagnosis of angiofibroma in adolescent males to be ruled out. Headache (25 %) – especially if paranasal sinuses are blocked; facial swelling (10–18 %); other symptoms – unilateral rhinorrhea, anosmia, hyposmia, rhinolalia, deafness, otalgia, swelling of the palate, deformity of the cheek. There are main signs: nasal mass (80 %); orbital mass (15 %); proptosis (10–15 %). Other signs including serous otitis due to eustachian tube blockage, zygomatic swelling and trismus that denote spread of the tumor to the infratemporal fossa, decreasing vision due to optic nerve tenting (rare).

Treatment include: hormonal therapy (the testosterone receptor blocker flutamide was reported to reduce stage I and II tumors to 44 %. Despite tumor reduction with hormones, this approach is not routinely used).

Radiotherapy (Some centers have reported 80 % cure rates with radiation therapy. However, concerns regarding potential effects of radiation make radiation therapy a nonuseful modality in most cases).

Stereotactic radiotherapy (e.g., Gamma knife) delivers a lower dose of radiation to surrounding tissues. However, most authorities reserve radiotherapy for intracranial disease or recurrent cases.

Surgical therapy include: a lateral rhinotomy, transpalatal, transmaxillary, or sphenoethmoidal route is used for small tumors (Fisch stage I or II). The infratemporal fossa approach is used when the tumour has a large lateral extension.

The midfacial degloving approach, with or without a Le Fort osteotomy, improves posterior access to the tumor. The facial translocation approach is combined with Weber – Ferguson incision and coronal extension for a frontotemporal craniotomy with midface osteotomies for access. An extended anterior subcranial approach facilitates en bloc tumor removal, optic nerve decompression, and exposure of the cavernous sinus. Intranasal endoscopic surgery is reserved for tumors limited to the nasal cavity and paranasal sinuses.

Neurofibroma

A neurofibroma is, like a schwannoma, derived from sheath cells. It actually may represent in many instances a hamartoma or a reactive process rather than a neoplasm. A neurofibroma is asymptomatic and rarely occurs as a single lesion. Most often neurofibromas are part of von Recklinghausen’s disease (Fig. 13.1). Quite often the tongue is involved, in some cases resulting in unilateral macroglossia.

Fig. 13.1. Neurofibromatosis I type (after 9 operations)

Also the possibility of hereditary neuropolyendocrine syndrome – consisting of mucosal neuromas, pheochromocytoma of the adrenal glands, and medullary thyroid carcinoma should be taken into account. In general, the mucosal neuromas in that syndrome are already present at childhood, being the first manifestation of the syndrome (Casino et al, 1981). In contrast to the schwannoma, a neurofibroma is not encapsulated.

Proliferating Schwann’s cells are haphazardly arranged, not showing the palisade arrangement of schwannomas. With a single neurofibroma, management consists of surgical removal (Fig. 13.2; 13.3). With multiple or massive involvement, surgical removal may be impossible to carry out and is indicated only when malignant changes are suspected. With von Recklinghausen’s disease, there is a 5 % to 15 % risk of malignant degeneration. This seems especially true for deeply located lesions (Maceri and Saxon, 1984).

Fig. 13.2. Planning before operation

Fig. 13.3. IV stage of the surgical treatment (made in our clinic)

Neurilemmoma

Neurilemmomas are benign encapsulated tumors of the nerve sheath. Their cell of origin is thought to be Schwann cells derived from the neural crest. These masses usually arise from the side of a nerve, are well encapsulated, and have a very unique histologic pattern. The benign lesion essentially manifests with cosmetic deformity, a palpable mass, and/or symptoms similar to a compressive neuropathy. Neurologic symptoms tend to present late. Symptoms can be vague, with an average interval of up to 5 years before the diagnosis is established. Neurilemmoma is the most common neurogenic tumor. The prevalence of these benign lesions is unknown. The cause for the growth of these neoplasms is unknown. Neurilemmoma can be associated with von Recklinghausen disease, and, when associated, multiple tumors often are present. Neurilemmomas affect persons aged 20–50 years. The head and flexor surface of the upper and lower extremities and the trunk are common locations in decreasing order. The mass is usually mobile in the transverse plane and tethered along the axis of the nerve from which it arises. Tenderness to palpation is often present; secondary neurologic symptoms may be present if the tumor is large. When involving the C7 nerve root, neurilemmoma has been described as a cause of thoracic outlet syndrome. Lesions in the sciatic nerve can mimic discogenic low back pain.

Differential diagnoses include the following: fibroma, neurofibroma, neurosarcoma, ganglion cyst, giant cell tumor of tendon sheath, lipoma.

Lipoma

A lipoma is a benign neoplasm composed of fat cells. Its cause is unknown. Trauma and metaplasia of perivascular connective tissue have been suggested as playing a role. Oral and oropharyngeal lipomas are rather rare. There is no predilection for sex. An oral lipoma rarely occurs before the second decade. A lipoma appears as a sessile, soft, and asymptomatic swelling (Fig. 13.4; 13.5; 13.6; 13.7; 13.8).

Fig. 13.4. Giant lipoma of the neck, frontal area

Fig. 13.5. CT scanning of the lipoma

Fig. 13.6. Planning the incision before operation

Fig. 13.7. Extraction of the tumor within capsule

Fig. 13.8. Macropreparation of the lipoma

When it is located superficially, a yellowish texture can be seen. In rare instances bilateral or multiple occurrence has been reported (Pisanty, 1976). Histologic examination of a lipoma shows a well-delineated mass of lobules of fat cells with fibrous septa interspersed between them. In rare instances one encounters a benign “infiltrative” lipoma, which should not be confused with a liposarcoma (Bennhoff and Wood, 1978). The distinction between a benign lipoma and a low-grade liposarcoma may indeed be difficult in some cases. When fibrous tissue is a substantial part of a lipoma, the term fibrolipoma can be applied. When vascularity is a prominent feature, the term angiolipoma is used.

Leiomyoma

A leiomyoma is a benign neoplasm composed of smooth muscle cells. The source of a smooth muscle tumor in the oral cavity is believed to be the walls of blood vessels or undifferentiated mesenchymal cells. Occurrence of a leiomyoma in the oral cavity is rare. In two reviews of the literature (Natiella et al, 1982; Praal et al, 1982) approximately 80 oral leiomyomas were collected. The majority of reported leiomyomas of the oral cavity and oropharynx were small, circumscribed, and asymptomatic swellings, covered with an apparently intact mucosa. They were either single or multiple. A leiomyoma is composed of whorls of smooth muscle cells. The diagnosis of leiomyoma can be difficult to make just from light microscopic examination. The tumor should be differentiated from fibromatosis and schwannoma on the one hand and leiomyosarcoma on the other hand. Management consists of surgical removal.

Rhabdomyoma

A rhabdomyoma is a benign neoplasm of striated muscle. It is an exceedingly uncommon tumor. The male-female ratio is more than 2 to 1. The mean age of patients with a rhabdomyoma is about 40 years. Although extracardiac rhabdomyomas show a preference for the head and neck, occurrence in the oral cavity and oropharynx is rare. The floor of the mouth is the most common site. Multifocal appearance is exceptional (Schlosnagle et al, 1983). The clinical presentation is a submucosal swelling without any specific signs or symptoms. A rhabdomyoma is a well-circumscribed tumor. Based on histopathologic characteristics and gross morphology, two types are recognized: fetal and adult. The adult type is composed of large, round or polygonal cells with a slight granular cytoplasm. The cytoplasm may contain lipod material. Cross striations may be found in just a few cells. The fetal type almost exclusively occurs in the first few years of life. Histologically that type is characterized by immature skeletal muscle in varying stages of developmental and undifferentiated mesenchymal cells. Differentiating a rhabdomyoma from a rhabdomyosarcoma may be difficult. Management of a rhabdomyoma consists of surgical removal.

Fibrous growths of the oral soft tissues are fairly common and include a diverse group of reactive and neoplastic conditions.

Fibrous overgrowth

Fibrous overgrowths or fibroepithelial polyps are relatively common in the mouth and are usually the result of trauma or frictional irritation. By contrast, fibromas, which are benign neoplasms, are extremely rare. They are most often seen in the cheeks or lips where such irritation from the dentition can be encountered (Fig. 13.9; 13.10).

Fig. 13.9. Fibrous overgrowths

Fig. 13.10. Fibroma of the of the palate sublingual area

Sometimes known as polyps, they may be semi-pedunculated or sessile in their attachment and are similar in colour to the surrounding normal tissue unless they have been traumatised frictionally, when they may show a whitened keratinised surface. They do not, however, have the cauliflower hyperkeratotic surface of the papilloma, being smooth-surfaced and hence easily distinguished from the papilloma.

Treatment is simple surgical excision. As, histologically, they are simple hyperplasias, there is no requirement to remove a margin of normal tissuenor to extend the excision deeply into the underlying tissues. A suture may be needed to ensure adequate haemostasis in the larger lesions.

Fibrous epulis

An epulis may be defined as a swelling or lump arising from the gingivae, and the fibrous epulis is the most common type. The lesion is basically a hyperplastic response to irritation to the attached gingivae. In some cases, the stimulus or irritant is very obvious, such as an overhanging restoration or subgingival calculus. In others, however, it may be more difficult to detect and only careful examination may reveal a small developmental defect in the enamel or dentine of the tooth at the gingival margin. Clinically, they present as smoothsurfaced, rounded swellings, normally pink in colour and often pedunculated in attachment (Fig. 13.11).

Fig. 13.11. Fibrous epulis

In older, more mature lesions, the surface may show stippling reflecting the attached gingival origin of the overgrowth.

Treatment is by surgical excision, with removal of any irritant focus found. The base of the wound is often dressed with a periodontal pack or if larger with a ribbon gauze impregnated with Whitehead’s varnish. This may be sutured over the raw surface.

Giant cell epulis

This epulis is sometimes known as a peripheral giant-cell granuloma and, as its name implies, the tissue consists of a mass of multinucleated giant cells in a vascular stroma. Many are seen in teenagers or adolescents and are usually found in the anterior regions of the mouth. They may represent an overgrowth of osteoclasts derived from the resorptive process encountered during the loss of the deciduous dentition. They can, however, arise in the older patient. These lesions are typically deep red or even purplish in colour and are often quite broadly based, unlike the paler coloured, often pedunculated fibrous epulis (Fig. 13.12; 13.13).

Fig. 13.12. Giant cell epulis

Fig. 13.13. X-ray examination of the giant cell epulis

If suspected of being a giant-cell lesion, radiographs should be taken to ensure that it is a peripheral and not a centrally, i.e. bony, originating lesion, which would appear as a radiolucent area. If it is a peripheral epulis then surgical excision with curettage or cautery to its base is normally curative. The base of the lesion can be covered by a periodontal pack if small, or a Whitehead’s varnish packing may be used for larger lesions. If a central giant-cell lesion is evident on the radiograph, it must be distinguished from the brown tumour of hyperparathyroidism by appropriate assessment of blood calcium, phosphate and parathormone levels.

Pregnancy epulis

This lesion is histologically indistinguishable from the pyogenic granuloma, being essentially a vascular overgrowth of granulation tissue. It may be related to an obvious focus such as calculus but it may equally arise from an extraction socket. Hormonal changes during pregnancy are believed to enhance the reactive tissue response to irritation and although many lesions remain small and do not require surgical intervention, some can grow alarmingly fast and attain considerable size even to the point of being traumatised by the opposing teeth. These lesions are therefore surgically excised with appropriate curettage or diathermy to their bases. If small they tend to resolve following the pregnancy.

Epulis Fissuratum (denture-induced hyperplasia, inflammatory hyperplasia, denture hyperplasia, denture-induced fibrous hyperplasia).

Epulis fissuratum is a hyperplastic reactive lesion, often with inflammatory and reparative phases. The histologic picture can be variable. Most frequently, a dense fibrous hyperplasia occurs, often with varying degrees of inflammation and vascularity. Because capillary proliferation is considerable, an overlap with pyogenic granuloma occurs. Mucous glands are often present in the specimen and may show a chronic sialadenitis. Occasionally, the glands may have an associated lymphoid hyperplasia and papillary ductal hyperplasia. The epithelium may be atrophic or hyperplastic and occasionally shows a pseudoepitheliomatous hyperplasia. Ulceration can occur. Infrequently, chondroid or osseous metaplasia can develop within the mass.

Treatment

Surgically excise the epulis fissuratum because even removal of the offending stimulus (ie, denture) will not result in complete resolution. In addition, correct the denture, otherwise the lesion will recur. Either make a new denture or reline the old denture.

Congenital (granular cell) epulis

The rare congenital epulis is typically present at birth as a smooth but prominent soft nodule, usually on the alveolar ridge. Females are predominantly affected and occasionally the mass is so large as to obstruct respiration.

Histologically, large pale granular cells with sharply-defined cell membranes are covered by epithelium which lacks pseudoepitheliomatous hyperplasia. Immunohistochemistry suggests that the origin is myogenous. Excision is curative but spontaneous regression is also seen.

Papilloma

A papilloma is a benign epithelial neoplasm composed of fingerlike projections of squamous epithelium. Some authors use the term squamous papilloma (Abbey et al, 1980). The cause is unknown, although a virus is most likely. The prevalence of oral papillomas is less than 0.1 % (Axell, 1976). Oral and oropharyngeal papillomas may occur as single or multiple, sessile, warty lesions, seldom measuring more than a few millimeters (Fig. 13.14; 13.15). When they involve the oropharynx, the soft palate and the uvula are the usual sites. The clinical differential diagnosis of a papilloma includes verruca vulgaris (Green et al, 1986), fibroepithelial polyp, focal epithelial hyperplasia, and condyloma acuminatum.

Fig. 13.14. Papilloma of the lower palpebra

Fig. 13.15. Papilloma of the tongue

The histology of a papilloma shows fingerlike projections of squamous epithelium above the level of the surrounding mucosa. In most cases a mild hyperorthokeratosis occurs. Epithelial dysplasia is not a feature of papilloma. Carcinomatous changes in a papilloma are exceptional, if indeed ever proven.

Squamous cell papilloma

This is not an uncommon lesion of the oral mucosa and may arise at virtually any site, but more commonly on palate, buccal mucosa or lips. It is a benign neoplasm of epithelial tissue and most squamous cell papillomata present as pedunculated (stalked attachment) lesions with characteristic white, hyperkeratinised, crenated surfaces, which can be likened to a cauliflower. They are normally small, usually less than 0.5 cm in diameter.

Treatment is simply excision at the base of the stalk.

Pyogenic Granuloma

A pyogenic granuloma is a benign, elevated, and capillary-rich lesion occurring on the skin and mucous membranes. When located at the gingiva of pregnant women, the term pregnancy tumor may be used. The pyogenic granuloma is thought to be the result of an overreaction to minor trauma rather than to infection. The pyogenic granuloma is a lesion that arises from a failure of normal healing causing an exuberant overgrowth of what is essentially granulation tissue. They may grow in relation to extraction sockets or from traumatic injuries to soft tissues, most often tongue or palate. They can be regarded as reactive lesions and obvious irritational factors may be evident clinically or from the patient’s history. Foreign bodies related to extraction sockets, such as fragments of filling material or indeed of small bony sequestra, may form the stimulus, whereas in soft tissues there is occasionally a history of self-medication with a variety of remedies that could be attributed as causal. Hormonal changes may be another cause. It has no predilection for sex or age group. An oral pyogenic granuloma most frequently involves the gingiva. The lower lip and the dorsal surface of the tongue are rather common sites as well.

The lesion is usually pedunculated or sessile, and the surface is often ulcerated. Clinically they appear as red or speckled-red overgrowths of tissue that closely resemble granulation tissue on visual examination.The size of the lesion’s diameter may vary from 0.5 to 2 cm or more.

Histologically a pyogenic granuloma does not consist of true granulomas. Large numbers of vascular spaces can exist together with numerous inflammatory cells, sometimes rising the question of whether one is dealing primarily with a vascular lesion with secondary signs of inflammation or with an inflammatory condition. Mitotic activity may be abundant and should not be mistaken as a sign of malignancy. Differential diagnosis: A very similar lesion may be attributed to a viral origin and is sometimes known as a viral wart. In these cases it is sometimes possible to see finger warts that have clearly been responsible for transmitting the virus to the oral cavity. Treatment is surgical excision with curettage or diathermy to the base of the lesions where appropriate attachment. Surgery is the management of choice. With the exception of the gingival lesions, recurrences of a pyogenic granuloma is rare.

Hemangioma, heamngiopericytoma and phlebectasias

A hemangioma is a benign lesion of blood vessels or vascular elements. Haemangiomas of the head or face are a frequent vascular pathology, consisting in an embryonic dysplasia that involves the cranial-facial vascular network (Fig. 13.16; 13.17).

Fig. 13.16. Hemangioma of the face, capillary form

Fig. 13.17. Big compound hemangioma of the face

Haemangiomas show clinical, morphological, developmental and structural changes during their course. The majority of oral and oropharyngeal hemangiomas seem to be of a developmental nature. In some instances lesions are probably a mixture of hemangioma and lymphangioma, leading to the term angiomatosis (Fig. 13.18).

Fig. 13.18. Systemic angiomatosis

In rare instances a hemangioma is located within the jawbones. Hemangiomas of the oral cavity are often present at birth or shortly thereafter. They have a strong preference for occurrence in the tongue and the floor of the mouth. A hemangioma of the tongue may affect just a part of the tongue or the entire tongue, producing macroglossia (Fig. 13.19; 13.20).

Fig. 13.19. Hemangioma of the mouth

Fig. 13.20. Hemangioma of the and oropharyngeal area tongue, cavernous form

The color of a hemangioma may vary from bluish to purple or fiery red. The texture of the mucosa may be more or less unchanged, showing only an increased vascularity on the surface; in other cases, however, there is a pebbly appearance. Pain is not a prominent feature, except in cases of traumatization or secondary inflammation. In severe cases loss of tongue mobility may occur. Bleeding, either spontaneously or from mechanical irritation, can be a serious problem. Angiography may be an aid in diagnosing a hemangioma.

A hemangioma may histologically consist of numerous irregular, blood – filled spaces, lined by endothelial cells and surrounded by connective tissue. When a large number of proliferating endothelial cells line small capillaries, the lesion is referred to as a capillary hemangioma.

In the case of large dilated blood sinuses, the term cavernous hemangioma is applied. A cavernous hemangioma and a lymphangioma may occasionally be indistinguishable from each other, both clinically and histologically. In the case of ulceration (and thereby the presence of inflammatory cells) distinguishing a hemangioma from a pyogenic granuloma may be impossible. When hemangiomas undergo regression, extensive sclerosis can occur, sometimes followed by calcification. Such concretions are called phleboliths. The majority of hemangiomas do not require treatment and regress spontaneously during childhood.

Therapeutic management of a large, persisting, or even growing hemangioma is a difficult problem. A conservative approach seems justified: that is, managing only the areas that produce bleeding. In large, diffuse lesions the use of cryosurgery or CO2 laser therapy does not seem to be effective. Injection of sclerosing agents has been advocated in the past but has not been shown to be effective. The technique of selective percutaneous embolization before surgery has emerged as a valuable adjunct to surgery in the management of such lesions (Braun et al, 1985; Thompson et al, 1979). Radiotherapy should be avoided because of possible late adverse sequelae.

A hemangiopericytoma is a complex neoplasm that should be regarded as malignant, not in the usual sense of a 5-year survival but over the lifetime of the host (Batsakis, 1979).

Occurrence in the oral cavity and the oropharynx is extremely rare (Morita et al, 1982). The clinical appearance is just a firm, usually well-circumscribed swelling of the mucosa. In patients above the age of 40 to 50 years, single or multiple, bluish, hemangiomalike changes may occur in the oral and lingual mucosa as the result of vein widening. These are so-called phlebectasias (Ettinger and Manderson, 1974). No treatment is required.

Management

The first-line treatment for capillary hemangiomas is simple observation. Since most of these lesions regress on their own, there is no need to intervene unless one of the above criteria is met. Corticosteroids, in various formulations, also have been used in the treatment of capillary hemangiomas. Topical steroid formulations, such as clobetasol propionate cream, can be applied topically to the lesion. The response to these treatments, even with the strongest corticosteroid formulations, is slower than other methods because several weeks are required to obtain a response. Systemic corticosteroids are used for amblyogenic life-threatening lesions.

Surgery

Laser surgery has been attempted to ameliorate capillary hemangiomas but still is controversial. The hemostatic effects of the carbon dioxide laser have been used with success to surgically remove these lesions. Other lasers used include the argon laser and NdYAG laser. The pulsed dye laser is only effective for very superficial lesions; its mechanism of action is too slow for sight-threatening hemangiomas. Overall, variable results have been seen with various laser modalities, and the risks of scarring and ulceration often deter its usage. Incisional surgical techniques also have had variable success. Surgical ligation of the hemangiomas produces equivocal results. Vascular embolization of the lesions should be used for large extraorbital hemangiomas only. Primary excision also has been advocated for infantile hemangiomas.The prognosis for cosmetic and visual recovery is excellent if treatment is instituted at an appropriate time and careful attention is paid to the visual development. Most lesions involute by age 5 years.

Lymphangioma

Lymphangiomas are rare congenital benign lesions occurring mainly in the head, neck and oral cavity. They consist in localized centres of abnormal development of the lymphatic system. Three theories have been proposed to explain the origin of this abnormality. The first suggests that a blockage or arrest of normal growth of the primitive lymph channels occurs during embryogenesis, the second that the primitive lymphatic sac does not reach the venous system, while the third advances the hypothesis that, during embryogenesis, lymphatic tissue lays in the wrong area.

Lymphangiomas are classified as microcystic (capillary lymphangiomas), macrocystic (cavernous lymphangiomas) and cystic hygromas according to the size of the lymphatic cavities incorporated. Cystic lymphangiomas have been reported, in the literature, to be present in up to 67 % of all cystic lymphangiomas There was presented the concept that cystic hygromas and lymphangiomas are variations of a single entity and that its classification is determined by its location in the head and neck. A commonly used classification classifies these lesions into capillary lymphangioma or lymphangioma simplex, cavernous lymphangioma, and cystic lymphangioma or cystic hygroma. When a lymphangioma is confined to fairly dense tissue, such as the tongue, it presents as a cavernous lymphangioma, but when it develops in the relatively loose fascia of the neck, a cystic lesion occurs. These three types are frequently found together in the same patient, depending on the severity of the disease. Cystic hygromas, however, account for approximately 90 % of the lymphangiomas in the head and neck region. Other common sites, outside the head and neck, include the axilla, shoulder, chest wall, mediastinum, abdominal wall, and thigh. Diagnosis is not difficult in most cases. The neoplasms are usually characterized by the presence of a soft, compressible, loculated and ill-defined mass, which is usually located in the posterior cervical triangle. The the tongue lesions are not attached to the skin or movable across deeper tissues, and readily transilluminate.

The anterior triangle of the neck has been indicated as the most common site. Cystic hygroma may be localized in the parotid area, and is the second most common congenital mass of the parotid area (Fig. 13.21; 13.22).

Fig. 13.21. Lymphangioma, cavernous form

Fig. 13.22. Lymphangioma of the tongue

Ultrasound, CT and MRI can be used to define the relationship of the lesion with the neighbouring structures and to help plan surgical strategies 10. US, which provides size and extension of the lesion, should be performed routinely. The clinical course of the pathology varies from a spontaneously regressing cyst to an aggressively invasive lesion. Spontaneous or traumatic haemorrhage of the cysts is the most common complication of the lesion.

Treatment

Surgical resection still remains the best treatment for lymphangiomas; other treatment options, such as sclerotherapy have been proposed as an alternative to reduce the impact and complications of surgery. Various products, such as sodium morrhuate, dextrose, tetracycline, doxycycline, bleomycin, ethibloc and OK-432 (picibanil), have been used as sclerotherapeutic agents. Apart from OK-432, the other agents were reported to cause perilesional fibrosis and thus to complicate eventual surgical excision.

Cysts of the soft tissues

Epidermoid and dermoid cysts are ectoderm-lined inclusion cysts that differ in complexity: Epidermoids have only squamous epithelium; dermoids contain hair, sebaceous and sweat glands, and squamous epithelium. Both arise from trapped pouches of ectoderm, near normal folds, or from failure of surface ectoderm. An epidermoid cyst is a cyst lined by epidermis without the adnexal structures in the fibrous wall that a dermoid cyst has. Sometimes the term dermoid cyst is used in a clinical way, using histologic subdivisions such as dermoid type, epidermoid type, and teratoid type. An epidermoid cyst may result from traumatic implantation of epithelial cells into surface epithelium, whereas in a dermoid cyst entrapment of epithelium during the embryologic phase seems to be the most likely explanation. Both the epidermoid and dermoid cysts rarely occur in the oral cavity and are even rarer in the oropharynx. Epidermoid and dermoid cysts may occur in the floor of the mouth, the lips, and the cheek mucosa (Fig. 13.23; 13.24; 13.25; 13.26).

Fig. 13.23. Epidermoid cyst of the face

Fig. 13.24. Incision for extaction of the cyst

Fig. 13.25. Extaction of the epidermoid cys

Fig. 13.26. Epidermoid cyst, macropreparation

Just a few cases of lingual involvement have been reported. The clinical aspect is not characteristic and merely consists of a cystic swelling. Stratified squamous epithelium without adnexal structures lines an epidermoid cyst. When adnexal structures (such as sebaceous glands) exist, a diagnosis of dermoid cyst can be made. In most instances epidermoid and dermoid cysts can be enucleated. Only in very large cysts must marsupialization be considered. Recurrence is rare (Fig. 13.27; 13.28).

Fig. 13.27. Dermoid cyst of the mouth floor

Fig. 13.28. Dermoid cyst of the neck

Congenital cysts and fistule of the neck may be divided into the midline or thyroglossal, and the lateral or so-called branchial cysts and fistulae.

The midline cysts and fistulae are fairly well accepted as arising from the thyroglossal duct. During the development of the human embryo the isthmus of the thyroid gland is derived from a bud of hypoblast which arises in the midventral portion of the floor of the pharynx. This bud migrates downward, forming the thyroglossal duct. Epithelial rests anywhere along the course of this tract may give rise to a cyst or a fistula. The fistula usually reaches the exterior following infection of a cyst by breakipg through the thin skin lining. It is very exceptional to see a midline fistula at birth; ordinarily they are secondary, resulting from infection of a cyst. Wenglowski does not believe in the thyroglossal tract theory, and states that these cysts and fistulhe always end in a blind sac at the level of the hyoid bone to which they may be firmly attached. He further states that the tract between the hyoid bone and the foramen cacum is never patent. In one case we shall see histological evidence of a sinus leading into the foramen cecum, and in another case clinical evidence of patency of the duct. A thyroglossal cyst may develop anywhere from the foramen caecum to the suprasternal notch.. They are far more frequent in the infrahyoid regions. We are taught that thyroglossal cysts are exactly in the midline but we occasionally see them off-centre, particularly those found at the level of the thyroid cartilage, which by its conFig.uration more or less pushes the cyst to one side. Thyroglossal cysts are more frequently observed in children, but may develop at any age. Both sexes appear to be equally affected. The clinical picture is that of a midline “lump or bump,” which may vary in size from a few millimetres to four or five centimetres. It is not adherent to the overlying tissues but moves in a vertical direction on swallowing. Forced protrusion of the tongue also moves the cyst, a sign distinguishing it from a dermoid cyst, which does not move. The picture may be complicated by infection which very often will result in a fistula.

Lateral or branchial cysts

If authors are in reasonable agreement regarding the pathogenesis of the midline cysts and fistule, this is not so in the case of the laterally placed ones (Fig. 13.29; 13.30; 13.31; 13.32).

Fig. 13.29. Lateral cyst of the neck

Fig. 13.30. Lateral cyst, macropreparation

Fig. 13.31. Midline fistule of the neck

Fig. 13.32. Extraction of the midline Fistule

Two distinct theories prevail. The first and oldest maintains that lateral cysts and fistule develop primarily from the branchial apparatus, particularly from the second and the third pouches. The second theory, formulated by Wenglowski and interpreted by Meyer, who reviewed this question in 1932, explains these abnormalities as arising from epithelial rests of the pharyngothymic duct. Arguments for and against every theory have been formulated, and it would be beyond the scope of this paper to go into this controversial subject. For the moment all that can be said is that this question still remains to be clarified. Unlike the midline fistuloe, the lateral fistula is frequently present at birth. Many, however, are acquired as a result of either an infection or an ill-advised incision of a cyst.

At birth the true fistula may consist of only a small dimple and remain as such for a number of years before starting to discharge. The discharge is usually serous until infection sets in, when it becomes purulent and causes irritation of the surrounding skin. The sinus opening is located along the anterior border of the sternomastoid muscle, anywhere from the ear above to the clavicle below. One can sometimes feel the sinus tract as a small subcutaneous cord running up along the anterior border of the muscle. The cyst is usually seen below the angle of the mandible, in front of or beneath the sternomastoid muscle. It develops at any age but is more common in the third decade, and presents itself as a slowly growing nontender mass. The growth may be so slow as to reach a considerable size before being noted by the patient. The cyst very often develops after an infection of the throat or surgical procedure on the throat such as tonsillectomy. Pain is an exceptional symptom unless there is an infection. Pressure upon surrounding structures may, in time, give rise to certain symptoms such as cough through irritation of the vagus nerve. Some authors have reported that congenital cysts and fistulae are more frequently observed in the female sex, but a review of the reported cases indicates that males are probably affected as frequently as females. Fistule are divided into three groups: the complete fistula extending from the pharynx, usually the tonsillar fossa, to the outside; the external fistula having only an external opening; and the internal fistula opening into the pharynx only. This last group is rare.

Diagnosois

The history and complete and careful examination of the patient will help in making the correct diagnosis of congenital cyst or fistula, which should not be confused with the following: dermoid cysts, cystic hygroma, lipoma, tuberculous adenitis, haemangioma, deep cervical abscesses, the various mycoses, carotid body tumour, adenopathies and metastatic carcinoma.

The treatment of these abnormalities is surgical and requires complete and careful excision of the lesion. For thyroglossal tract anomalies the excision must include the midportion of the hyoid bone and a core of tissue from the hyoid bone up to the foramen caecum. For lateral cysts, complete excision by careful dissection through a wide exposure is recommended in order to avoid injury to surrounding structures. Lateral fistule must be followed up to the end. In cases of complete fistula, some authors recommend inverting the stump into the pharynx, but this does not appear to be necessary. The stepladder incision is most useful.

Tumors and tumor-like lesions of salivary glands

Tumors of the salivary glands

According to the classification, developed by World Health Organization (1990) tumors of the salivary glands are grouped into epithelial, nonepithelial, and metastatic.

Over 90 % of salivary gland tumours are epithelial in origin. The WHO classification includes 32 types of epithelial salivary gland tumors, 14 of them are benign. A wide spectrum of histopathological forms is due to the diversity of cell types, composing the glands (acinar cells, ductal cells, and myoepithelial cells). Despite of wide diversity of histological types, their clinical signs and treatment modalities are very common. For this reason only the most common types of epithelial tumors are discussed in this chapter.

Benign nonepithelial tumors include lipoma, hemangioma, lymphangioma, neurinoma, sarcoma and other, located within the salivary gland. They are rare (less than 10 %) and occur almost only in the parotid gland.

In general, the major salivary glands have the higher incidence of tumors and the higher percentage of benign tumors (75–80 %) in comparison to minor glands, where malignances make up to 50 %. The parotid gland is the most typical site for the salivary neoplasms (up to 80 %). The overwhelming majority of them occur in the superficial lobe or tail of the parotis, and most of them are benign (pleomorphic adenomas are predominant).

Salivary gland tumors usually present as a slow growing, well-circumscribed, painless nodule associated with the salivary gland. In early stages, benign and malignant salivary gland tumors cannot be distinguished clinically, so malignancy should be suspected in most of the cases. Another problem is variety of localizations, where salivary gland tumors are observed. It makes the diagnosis and management of salivary gland tumors rather challenging.

The adequate approach for management of the salivary gland tumors demands an accurate histopathologic diagnosis. For this reason fine-needle aspiration and biopsy is often indicated. It can help to differentiate a tumor from lymphadenopathy as well as to indicate the type of salivary tumor. At the same time it is not 100 % sensitive or specific, and sometimes the interpretation of the fine-needle aspiration results is rather difficult. CT scanning, MRI and ultrasonic study are also useful for proper diagnosis. They help to indicate the association of tumor with the salivary glands, deep lobe involvement of the parotid gland and lymphadenopathy in the neck in cases of malignant salivary glands tumors.

Benign epithelial tumors of the salivary glands Pleomorphic adenoma

Pleomorphic adenoma (benign mixed tumor) is the most common benign salivary glands tumor, comprising 78–85 % of all salivary gland neoplasms. Pleomorphic adenoma arises from duct epithelium or myoepithelial cells and consists of epithelial and connective tissue components in varying degrees. In some cases myxoid tissue, cartilage or calcified zones can be seen microscopically. Pleomorphic adenoma is most commonly seen in the parotid gland. Most of the tumors arise from the tail or the superficial lobe, but the deep lobe can be involved (Fig. 13.33).

Fig. 13.33. Pleomorphic adenoma of the right and left parotid glands

For the minor glands, the most common site is the palate, followed by cheek, lip and pharynx (Fig. 13.34).

Fig. 13.34. Pleomorphic adenoma of the minor gland of the soft palate

Adults are predominantly affected. The tumors grow slowly. They usually range from 2 to 5 cm in greatest dimension (Fig. 13.35), although in some cases they may achieve a size of 15–20 cm. Pleomorphic adenoma is usually round or ovoid painless, well-circumscribed mass with smooth or lobulated surface.

Fig. 13.35. Pleomorphic adenoma of the left submundibular gland

The connective tissue capsule is thin, delicate and may be incomplete. It has occasional projections into the surrounding salivary gland tissue, which are considered to be the main source of the tumor recurrence (Fig. 13.36) There is an incidence of malignant degeneration in pleomorphic adenomas in 3–7 % of cases (usually in longstanding tumors).

Fig. 13.36. Pleomorphic adenoma of the parotid gland, macro-preparation

Treatment of pleomorphic adenoma is determined by its clinical and histological peculiarities: incomplete capsule and high recurrence rate. It usually includes complete surgical excision of the affected gland. If the parotid gland is involved, superficial or total parotidectomy with standard facial nerve dissection and preservation are the methods of choice. Attempts at enucleation of the tumor from within its capsule will inevitably leave viable tumor cell nests and predispose to the multifocal recurrence. This rate in cases of simple enucleation is 25–50 %.

Adenolymphoma

Adenolymphoma (Warthin tumor, papillary cystadenoma lymphomatosum, cystic papillary adenoma) is a benign tumor, which consists of epithelial and lymphoid structures. Adenolymphoma is the second most common salivary tumor, comprising 2–6 % of all salivary tumors. In the majority of cases it affects the parotid gland, especially the tail of the parotis (Fig. 13.37). In some cases (10 %) a bilateral localization is observed.

Fig. 13.37. Adenolymphoma of the right parotid gland

Adenolymphoma has a male predominance and usually occurs in the sixth and seventh decades of life. This lesion presents as a slow-growing, soft, painless mass with a smooth surface. It is well encapsulated and usually contains multiple cysts or one big cyst (Fig. 13.38).

Fig. 13.38. Adenolymphoma, macropreparation

The tumour is thought to arise from the entrapped salivary epithelial rests within developing lymph nodes. Malignant transformation is not typical. Recurrence rate in simple enucleation is 2–5 %.

The treatment of this lesion is surgical excision. In spite of low recurrence rate, a superficial parotidectomy is the treatment of choice, because the accurate diagnosis of adenolymphoma can be confirmed only by pathohistological investigation.

Oncocytoma (oxyphil adenoma)

Oncocytoma is a rare monomorphic salivary tumor, characterized by benign proliferation of oncocytes (cells of the salivary ducts). Oncocytomas are rather uncommon, they account for 1 % of all salivary gland tumors. Usually they are observed in patients older than 50 years (Fig. 13.39), more often in women than in men. The parotid gland is the most common site for this tumor (more than 80 % of cases). Another possible localization is the submandibular gland, while affection of the minor salivary glands is very rare. Oncocytomas manifest as small (less than 5 cm), firm or elastic, slow-growing, spherical, painless, masses, with a distinct capsule. The color of the neoplasm is dark red or brown. The prognosis in cases of radical excision is good. Recurrence rate is less than 10 %. Malignant transformation is uncommon.

Fig. 13.39. Oncocytoma of the right parotid gland

Other types of salivary gland adenomas are rare, less than 1 % of all salivary tumors. Among them canalicular adenoma, basal cell adenoma, intraductal papilloma and others. They usually manifest as small, movable, painless masses with a comparably smooth surface. They are seen mostly in older patients and have no specific clinical signs. The diagnosis in vast majority of cases is the result of pathomorphological investigation.

Malignant epithelial tumors of the salivary glands

Malignant salivary gland tumors are observed less frequently as benign. The vast majority of malignant salivary gland tumors occur in adulthood and there number significantly increases in older groups. Malignant tumors are more common in the submandibular gland and minor salivary glands: up to 50 % of tumors arising from these glands are malignant.

The etiology of malignant salivary gland tumors is not exactly known. However, long history of smoking, family predisposal, head and neck irradiation and long-standing benign tumors are considered to be important risk factors.

The six most common types of malignant salivary glands tumor are mucoepidermoid, acinic cell carcinoma, adenoid cystic carcinoma, adenocarcinoma, squamous cell carcinoma and malignant transformation of pleomorphic adenoma.

It is often hard or even impossible to differentiate benign and malignant salivary gland tumors, especially in early stages. In these cases histological approval of the diagnosis is necessary. At the same times there are clinical signs, perculiar to the malignant salivary gland tumors, which are of great importance (Table 13.1).

The treatment of the malignant salivary gland tumors is radical surgical excision, if the procedure is possible. Depending upon the size of the tumour, its localization and histology, this may require removal of the facial nerve and other surrounding structures, including the ear and petrous part of the temporal bone, and part of the mandible, neck dissection and limphadenectomy. Postoperative radiotherapy may be necessary. Radiotherapy can be used as mono therapy as a palliative treatment.

Mucoepidermoid tumor

Mucoepidermoid tumor is a malignant neoplasm arising from the ductal epithelium. It is considered to be the most common malignant salivary gland neoplasm, affecting both major and minor salivary glands. This tumor can have low-grade or high-grade malignant potential depending on its histology. The clinical aggressiveness of the tumor is determined by the ratio of mucus and squamous cells (tumors with a high mucous content tend to have a lower malignant potential).

Low-grade mucoepidermoid tumors behave like benign tumors. They are usually slow growing and nonmetastasizing. High-grade mucoepidermoid tumors can exhibit aggressive growth and invasion resulting in widespread metastasis to cervical lymphatic nodes, lungs, liver, bone, and, finally, death of the patient.

The most common clinical presentation is a slowly growing painless mass of several years duration clinically mimicking a pleomorphic adenoma or other benign tumor. Pain, tenderness or rapid enlargement are seen only in high-grade lesions.

Treatment includes radical surgical excision (adenectomy or block resection). If neck nodes are affected, then a typical neck dissection is also included. In tumors that are histologically high-grade malignances, postoperative radiotherapy is often applied. Prognosis depends on the histological type and stage of the tumor, with 5-year survival rate ranging from 20 to 90 %. Tumors of the submandibular gland have a worse prognosis than tumors of the parotid gland.

Acinic cell carcinoma

Acinic cell carcinoma is a rare low-grade carcinoma, arising from the boundary zone between the acinar and intercalated ducts. It is often considered as an intermediate tumor. Depending on its histological pattern, it can behave in a relatively benign or aggressive malignant fashion.

It is more common in males, and the most common site is parotid gland (80 %). Tumor manifests as a slow growing, well-localised lesion, that is not fixed to the surrounding soft tissue or skin. Pain symptom and facial nerve paresis are observed rarely in a small number of patients with this tumor. Treatment includes complete surgical excision and irradiation in certain cases. Prognosis is generally good, with a 5-year survival of over 80 %.

Adenoid cystic carcinoma

Adenoid cystic carcinoma is the most common malignancy of the submandibular gland and minor salivary glands. It is also the second most common salivary gland cancer overall.

There are three histological types of the tumor: tubular, cribriform and solid. Solid type has the worst prognosis. The tumor is also characterized by perineural spread, repeated recurrences and metastasis via the blood stream. Although this tumor is very slow growing, its relentless course, gives low long-term survival rates.

Clinically adenoid cystic carcinoma manifests as a slow-growing mass. Pain may be present but it is not an obligatory sign. Other symptoms include fixation to adjacent tissues and paraesthesia or paralysis associated with perineural invasion, typical to this tumor. Clinical and radiologic examination of this tumor frequently underestimates its true extent. Ulceration may occur in some cases, and it is more common in intraoral tumors.

Treatment includes wide excision and postoperative radio-therapy aimed to increase local control of the disease. In cases of pereneural invasion the facial nerve should be sacrificed. If neck nodes are affected then a neck dissection is also required.

Prognosis depends on histological type and also on the length of follow-up. Perineural spread is a bad prognostic sign for both local recurrence and distant metastasis. Although it is sometimes very difficult to cure adenoid cystic tumours, they tend to be very slow growing and the patient can live for many years, even in cases of lung and liver metastases.

The infiltrative nature of this lesion and the frequency of perineural involvement with spread along the nerve mandate wide resection margins, and follow-up of 15 to 20 years is required as late recurrences occur.

Adenocarcinoma and squamous cell carcinoma

Adenocarcinoma and squamous cell carcinoma of the salivary gland are very aggressive tumors, which usually occur in elderly patients. Signs and symptoms include a painful rapidly enlarging tumor, invading surrounding tissues with facial nerve palsy present in 50 % of cases. Ulceration of the skin and metastases are often seen at the late stages. The prognosis in these cases is poor, with 5-year survival rate of less than 35 %. Treatment includes wide surgical excision, often combined with neck dissection and postoperative radiotherapy.

Malignant change in pleomorphic adenoma

Malignant change in pleomorphic adenoma arises from a pre-existing pleomorphic adenoma. The parotid gland is the primary site of this tumor in more than 80 % of cases, followed by the submandibular and minor salivary glands.

The presence of malignancy often manifests by onset of new symptoms. Among them – sudden and rapid growth of an existing tumor, development of pain syndrome, paresis of the facial nerve. Malignant transformation is usually seen in long-standing tumors or in recurrences after inadequate excision. Local and distant metastases (to the lungs, bones, especially vertebral column, and liver) are often found in clinical examination.

Histologically, malignant change in pleomorphic adenoma is characterized by carcinomatous areas adjacent to the benign cellular picture of the remainder of the tumor.

Treatment is the same as for the other malignant salivary gland tumors. Prognosis is poor, especially in cases with marked facial nerve palsy. 5-year survival rate is 15–20 %.

Nonepithelial tumors of the salivary glands

Noepithelial tumors develop in the major salivary glands from soft tissue structures (nerves, blood vessel, lipoid, lymphatic or connective tissue). In some cases they spread to the salivary gland from the adjustment tissues. The parotid gland is the most common site for nonepithelial tumors.

The most common tumors of this group are hemangioma, lymphangioma, lipoma, fibroma, neurinoma, lymphoma.

Although the clinical signs and treatment strategies for salivary glands nonepithelial tumors in general correspond to the soft tissue tumors of other localizations, there are some peculiarities in this group.

Hemangiomas. Two forms of hemangiomas, capillary and cavernous, may develop in the major salivary glands. These are vascular tumors directly involving the parotid or submandibular glands. The capillary type is the most prevalent tumor of the parotid gland which may be present at birth or first seen in childhood. These hemangiomas have no capsule and are formed by purple, spongy, lobular masses that infiltrate salivary gland tissue. The salivary gland structure is largely replaced by angiomatous tissue among which glandular elements can be found. They commonly infiltrate neighboring structures, expanding through the capsule of the salivary gland. The diagnosis is made based on clinical features. CT scanning with intravenous contrast may be helpful in demonstrating the vascular nature of these neoplasms. Cavernous hemangiomas, which present in an older age group, usually do not show spontaneous regression and their treatment is a difficult problem. In majority of cases they require surgical resection of the affected gland, embolization, or both.

Lymphangiomas are mostly observed in infants and children. They are spongy, multiloculated masses with a yellowish or bluish surface and are formed by endothelial-lined spaces. Usually, they manifest as painless masses that may involve parotid glands, submandibular glands, or both. Diagnosis is made based on clinical findings. Surgical excision with preservation of the vital structures is the treatment of choice.

lipomas are relatively uncommon in the major salivary glands. They derive from the fat cells and manifest as soft, mobile, painful well-demarcated, bright-yellow masses. They are slow-growing tumors with an average diameter of 3 cm. Treatment is surgical excision. In rare cases adenectomy is preferable.

Lymphomas. The most common non-epithelial malignant tumor of the salivary glands is lymphoma. In some cases they develop as a complication of Sjogren’s syndrome or salivary lymphoepithelial lesion. In other cases salivary gland lymphoma is the first sign of widespread disease. Such a possibility must always be investigated since the prognosis is heavily dependent on the tumour’s stage. The presence of persistently enlarged or nodular parotid or submandibular glands, regional or generalized lymphadenopathy, pulmonary infltrates, hepatomegaly, vasculitis, or a monoclonal gammopathy may be signs of malignancy. If a diagnosis of lymphoma is made, chemotherapy appropriate for the stage and type of lymphoma must be administered.

Metastatic disease of the salivary gland

Carcinomas of different origin, melanoma and occasionally other tumours can metastasise to the salivary glands. Lymphatic nodes within the parotid gland are commonly affected. Metastases to the salivary glands can sometimes resemble primary salivary gland tumors. Diagnosis may depend on finding a primary tumor site or precise pathohystological examination. For patients with metastases to the parotid gland, all potential cutaneous and mucosal sites need examination. This includes fiberoptic examination of the nasopharynx and oropharynx. Particular care is necessary when inspecting potential cutaneous sites, since cutaneous malignancies may be small relative to the size of regional metastases, especially in cases of melanoma. Inconspicuous lesions hiding in the hair, behind the ear, nasal vestibule, and in the external auditory canal are easily overlooked.

Treatment depends on the histological type and stage of the primary tumor. In most cases of salivary glands methastatic affection the prognosis is poor in view of the tumor dissemination.

Tumor-like lesions of the salivary glands

Tumor-like lesions of the salivary glands include sialadenosis, oncocytosis (diffuse oncocytosis and focal adenomatous oncocytic hyperplasia), necrotizing sialometaplasia (salivary gland infarction), benign lymphoepithelial lesion (chronic myoepithelial sialadenitis), salivary duct cysts (mucoceles of the minor salivary glands of extravasation or retention type, cysts of the major salivary glands, ranula and dysgenetic polycystic disease of the parotid gland), chronic sclerosing sialadenitis of the submandibular gland (Kuttner tumour), and cystic lymphoid hyperplasia in AIDS. All these diseases in some cases can mimic the true neoplasm and are usually associated with higher risk for the tumor development.

Mucocele

Mucocele is a tumor-like lesion of the salivary glands, which is a result of obstruction of the salivary outflow tracts and extravasation of mucus into the surrounding tissues. Salivary ducts, especially those of the minor salivary glands, are occasionally traumatized, commonly by lip biting. Subsequent saliva production may then extravasate beneath the surface mucosa into the soft tissues. Saliva leaking from a damaged duct into the superficial surrounding tissues excites an inflammatory reaction. Over time, the pools of saliva form a rounded collection of viscous fluid, surrounded by compressed connective tissue without an epithelial lining. As it has no epithelial lining, mucocele is not a true cyst.

Mucoceles mainly affect the minor salivary glands, particularly of the lip. Other typical sites are buccal mucosa and sublingual gland (ranula). Retention cysts of the minor salivary glands are usually superficial and rarely larger than 1 cm in diameter. They manifests as rounded, soft, compressible mass. Later, they become hemispherical, fluctuant and bluish due to the thin wall. Cyst is filled with viscous clear yelowish or blue-gray mucus (Fig. 13.40). Patients may relate a hystory of cyst rupture followed by lession reccurence.

Fig. 13.40. Mucoceles of the anterior lingual gland

Ranula

Ranulas are large retention cysts occurring in the sublingual gland. Their pathogenesis and histological structure is usually the same as in other salivary retention cysts. The term “ranula” has its derivation traced to the oral anatomy of the frog.

The origin of a ranula is due to obliteration of one of the minor ducts of the sublingual gland, while the main excretory duct remains patent. Extravasation of saliva moves throughout the sublingual gland and into the submucosal space via hydrostatic pressure as the sublingual gland continues to produce saliva. The extravasated mucus can gradually spread around or through the mylohyoid muscle into the submental or submandibular spaces.

Simple ranulas are located above the mylohyoid muscle in the sublingual space. Complex or plunging ranulas develop when the lesion extends beyond the level of the mylohyoid muscle into the submandibular or submental space. Plunging ranula may be quite large and extend to the inferior aspect of the neck or the chest wall (Fig. 13.41).

Fig. 13.41. Plunging ranula of the right sublingual gland (superior and inferior parts)

The ranula clinically manifests as a painless mucus pseudocyst on the floor of the mouth. Usually they have 2 or 3 cm in diameter, but occasionally extend across the whole of the floor of the mouth. They are soft, fluctuant on bimanual palpation, painless and bluish in color. They usually enlarge slowly but may become large enough to elevate the tongue and interfere with speech or mastication.

The usual presentation of a plunging ranula is a soft, compressible mass in the submandibular or submental region. These may be initially misdiagnosed as sialadenitis or a salivary tumor. Transillumination of the mass may be feasible in the larger ranula. Intraoral examination should demonstrate an intraoral component combined with the cervical component.

Magnetic resonance imaging (MRI) in this cases can show herniation of the sublingual tissue and cystic material through the mylohyoid muscle. T1–weighted images are usually low enhancing while T2–weighted images are bright. The use of ultrasound of the neck in the evaluation of a plunging ranula may also reveal deficiencies in the mylohyoid muscle with herniation of the sublingual gland. With computed tomography (CT), a plunging ranula can be readily identified preoperatively as a cystic unilocular mass in the suprahyoid anterior neck.

Cysts of the parotid gland. Retention cists that occur in the parotid gland are more common in men often in their seventh or eighth decades. They present as a slow growing swelling in the affected gland, which on aspiration reveals a clear colored fluid. They also often completely disappear on aspiration. In the majority of cases the diagnosis is only made when the cyst is removed. It is not always easy to distinguish it from cystic form of adenolymphoma preoperatively.

Treatment of the salivary glands cysts

Treatment of a small superficial mucocele consists of excision of the mucocele and the associated minor salivary glands that contributed to its formation. If the damaged minor salivary gland has not been removed recurrence of the disease is very likely. An operation is usually performed under the local anesthesia. Infiltration or mental nerve block can be used. It is advised to delineate the boundaries of the mucocele first because the local infiltration of anesthetic may distort the anatomy.

An elliptical superficial incision through the mucosa is made around the mucocele. Careful dissection around the cyst may permit its complete removal. The regional associated minor salivary glands are also removed and sent for pathohistologic evaluation. Hemostasis is achieved with an electrocautery device and the wound is closed with absorbable suture.

The recurrence rates of mucoceles after surgical removal are not very high and usually they are caused by incomplete removal or repeat trauma to the minor salivary glands.

In cases of ranula different treatment modalities can be used. The usual treatment is marsupialization, in which a portion of the oral mucosa of the floor of the mouth is excised, along with the superior wall of the ranula. Subsequently, the ranula wall is sutured to the oral mucosa of the floor of the mouth and allowed to heal by secondary intention.

The preferred treatment for recurrent or plunging ranulas is excision of the ranula and sublingual gland via an intraoral or extraoral approach (Fig. 13.42).

Fig. 13.42. Planing and extraoral approach during the operation of the plunging anulas

In this cases the general anesthesia with nasal intubation is often required. An intraoral approach is made with an incision along the axis of the gland. The submandibular duct is identified, either by dissection or following cannulation with a probe to prevent its injury during the resection. The sublingual gland and the cyst are dissected in a subcapsular space. At the posterior pole of the gland the lingual nerve is identified as it crosses the Wharton’s duct and is preserved. The sublingual gland is dissected from anteriorly, and the final excision is the posterior pole after visualizing the lingual nerve. After completion of the dissection and removal of the gland, careful hemostasis is achieved. Closure of the wound is performed with absorbable sutures in a single layer.

Some patients plunging ranulas with may require an incision on the neck for exposure and excision of the ranula. This incision is performed 2,5 cm below the inferior margin of the mandible. The submandibular gland is identified and carefully mobilized away from the ranula. In addition to identifying the submandibular duct and lingual nerve during the dissection, in this cases care must be taken not to rupture the pseudocyst as the ranula is followed through the mylohyoid muscle. Completion of the posterior and inferior extent of the plunging ranula is performed after careful identification of the facial artery and veins to prevent bleeding in the operative site. After the cyst removal incision is closed by layered suture. In cases when adenocystectomy is performed the recurrences are rather uncommon.

Complications of the surgical treatment for retention cysts of the salivary glands include recurrence, injury of the lingual or hypoglossal nerves, Wharton’s duct injury, bleeding and development of infection.

Benign lymphoepithelial lesion

Benign lymphoepithelial lesion is the group of the diseases which manifest as a diffuse enlargement of all or part of the salivary glands, or as a disrete mass. Histologically, the lesion is composed of a diffused, well-organized lymphoid tissue and lymphocytic interstitial infiltrate with obliteration of the acinar structures. Benign lymphoepithelial hyperplasia is observed in Sjogren’s syndrome, Mikulich disease, some forms of chronic parotitis.

Sjogren’s syndrome

Sjogren’s syndrome is a multisystem disease with a variable presentation. Sjogren’s syndrome characterized by xerostomia (dry mouth), keratoconjunctivitis sicca (dry eyes), and an associated connective tissue disorder, most commonly rheumatoid arthritis.

Sjogren’s syndrome is an autoimmune disease with primary connective tissue affection and a variety of immunological signs. Histological changes in salivary glands include periductal infiltration by proliferating limphocites. Infiltration progressively spreads through the glandular tissue, causing the destruction of secretory acini. Finally the total lymphocytic replacement of the normal glandular elements is possible. A decreased function of both the major and minor salivary glands results in marked xerostomia.

Sjogren’s syndrome has a strong female predilection (9 : 1), with a mean age of 50 years. It affects 15 % of patients with rheumatoid arthritis, possibly 25–30 % of patients with lupus erythematosus and a variable proportion of patients with other connective-tissue diseases (Fig. 13.43).

Fig. 13.43. Sjogren`s syndrome, deformation of the joints are caused by polyarthritis

Generally, the first symptoms to appear are arthritic complaints, followed by ocular symptoms, and, late in the disease process, salivary gland symptoms. Main oral effects of Sjogren’s syndrome are discomfort, difficulties with eating or swallowing, disturbed taste sensation, disturbed quality of speech, predisposition to infection. All this results from decreased saliva secretion and xerostomia.

In the early stages, the mucosa may appear moist but salivary flow measurement shows diminished secretion. In established cases the oral mucosa is obviously dry and red in color. The tongue is typically red; its dorsum becomes lobulated with a cobblestone appearance.

With diminished salivary secretion the oral flora changes and candidal infections are common. They are the main cause of soreness of the mouth in Sjogren’s syndrome and cause generalised erythema of the mucosa, often with angular stomatitis. Plaque accumulates and there may be rapidly progressive dental caries. The most severe infective complication is suppurative parotitis.

Swelling of the parotid glands in Sjogren’s syndrome usually shows no inflammation and is rarely painful. But in cases of infection development (suppurative parotitis) parotid swelling becomes hot, tender with red, shiny overlying skin. Parotid swelling appearing years after the onset strongly suggests lymphomatous change. An increased incidence of malignancy, especially non-Hodgkin’s lymphoma, associated with Sjogren’s syndrome determines the significance of this condition to surgical practice. These patients should therefore be followed-up to rule-out a lymphoma.

Sjogren’s syndrome can also have serious ocular effects associated with decrease in tear secretion. Among them failure of foreign particles clearance from the cornea and conjunctiva, gritty sensation in the eyes and inflammation (keratoconjunctivitis sicca) with a risk of impairment or loss of sight.

The diagnosis of Sjogren’s syndrome is suggested by the patient’s complaints and by a variety of abnormal immunologic laboratory tests. The oral component of SS may be diagnosed using salivary flow rate studies and sialography, but the use of a labial minor salivary gland biopsy currently is considered to be highly accurate in aiding the diagnosis. The histopathologic changes seen in the minor glands correlate closely with those in the major glands: biopsy shows the periductal lymphocytic infiltrate.

Syalography shows the typical “snowstorm” appearance (so-called sialectasis). Imunological tests shows the increased levels of rheumatoid factor and Ro (SS-A) and La (SS-B) antibodies.

There is no specific treatment for Sjogren’s syndrome apart from symptomatic treatment and treatment of the underlying connective tissue disease present. As the salivary gland damage is irreversible, dryness of the mouth can be relieved to some degree by providing artificial saliva. Cholinesterase inhibitors such as pilocarpine are also recommended to stimulate salivary salivary flow from the remaining functional salivary gland tissue. All other factors contributing to the xerostomia (for example medications) are to be checked, symptomatic treatment for mucosal diseases and caries control are necessary. Regularly follow up for possible development of ascending parotitis or lymphoma is one of the main principles in Sjogren’s syndrome management.

Ophthalmological examination is particularly important to exclude keratoconjunctisitis sicca, which is symptomless in its early stages. The artificial tears and symptomatic therapy are prescribed for the dry eyes.

Mikulicz disease

Mikulicz disease is a rare pathological condition, characterized by gradual enlargement of salivary and lachrymal glands. Histologically the signs of benign lymphoepithelial hyperplasia are observed. Affection of eyes and salivary glands is not associated with any connective tissue disease. Mikulicz disease is more frequent in females than in males, and its peak incidence is in the fourth and fifth decades. Occasionally, both parotids are involved. Growth of this tumor is slowly progressive, and usually painless. In rare cases it gives rise to pain around the ear or the retromandibular area. There is no specific treatment for this condition. Symptomatic treatment and follow up observation is performed by oral surgeon, ophthalmologist and rheumatologist.

Sialosis (Sialadenosis)

Sialosis is a non-inflammatory salivary gland disease caused by metabolic and secretory disorders of the gland parenchyma, accompanied by recurrent, usually painless, bilateral swelling of the glands due to acinar enlargement. Histologically, there is hypertrophy of serous acini, oedema of interstitial connective tissue and fatty infiltration on the late stages.

Sialosis has an equal incidence in both males and females and occurs most commonly in the fourth to seventh decades of life. The disease is associated with some underlying conditions.

Sialosis often occurs in patients with a history of alcohol abuse. Gland enlargement has been also described in most endocrine diseases but it is particularly linked to diabetes mellitis. Other important endocrine conditions include thyroid disease, gonadal dysfunction and pregnancy. Sialosis is commonly seen in chronic starvation and is thought to be linked to the deficiency of proteins and vitamins. The nutritional causes of the sialosis are also cirrhosis, anorexia, kwashiorkor, and pellagra. Dysfunction of the autonomic nervous system can give rise to sialosis and this is most commonly seen in people taking drugs that affect the autonomic nervous system, such as some antihypertensive drugs. Other neurochemical causes include vegetative state, chronic intoxication with lead, mercury, iodine. In cases when the direct cause of the sialosis is not find out it is called idiopathic.

Clinical manifestation of the disease is usually associated with recurrent painless enlargement of both pairs of the major salivary glands, espetially the parotids and less commonly the submandibular glands (Fig. 13.44). Minor salivary gland involvement can be seen rarely.

Fig. 13.44. Sialosis of the right parotid gland

The persistence of sialosis is dependent on the severity and duration of the underlying disease.

The gland enlargement can persist from weeks to months. In some cases the infection process may arise in affected glands and alter the clinical picture.

The diagnosis is made upon the history and clinical appearance associated with an underlying cause. A parotid biopsy is needed occasionally, and histology will then show acinar enlargement.

The treatment for sialosis is usually conservative. It always includes the treatment for underlying disease, patogenetic and symptomatic therapy for salivary gland pathology. However even with treatment of the underlying condition, it is common for the parotid enlargement to persist. In this cases surgical treatment (parotidectomy) may be performed for cosmetic purposes.

Oncocytosis

Oncocytosis is a diffuse or multifocal proliferation of oncocytes within the major salivary glands. Oncocytosis occur usually in the sixth decade more frequently in males. The parotid gland is the most common (more than 80 %) site, while the remainder arise almost exclusively in the submandibular gland. Clinically oncocytosis presents as unilateral or bilateral salivary gland enlargement, typically of the parotid gland. Multifocal nodular oncocytic hyperplasia is far more common than difuse oncocytosis. Difuse oncocytosis presents as a difuse enlargement while multifocal nodular oncocytic hyperplasia has at least two nodules within the salivary parenchyma. In patients with oncocitosis the true neoplasms oncocytomas can arise rathe frequently. They may be solitary, bilateral, or arise in the setting of multinodular oncocytic hyperplasia. The pathogenesis of oncocytosis and is unclear, but is likely a progression from the age-related precursor of oncocytic metaplasia. The disease progress very slowly and no specific therapy is necessary in the majority of cases. Surgical interventions (salivary gland biopsy) are performed to rule out other tumors, especially malignant neoplasms.

Cystic lymphoid hyperplasia of salivary glands in AIDS

HIV-associated salivary gland disease includes lymphoepithelial lesions and cysts involving the salivary gland tissue and/or intraglandular lymph nodes. Young males are predominantly affected. Main clinical signs include xerostomia, cystic parotid gland swellings usually associated with generalised lymphadenopathy. The histological features are essentially similar to those of Sjogren’s syndrome, apart from gross cyst formation. However, autoantibodies typical of Sjogren’s syndrome are not revealed by immunological tests. The treatment HIV salivary gland cysts respond to highly active retroviral therapy. The symptomatic therapy for xerostomia is also necessary.

Kuttner tumor

Kuttner tumor, known also as chronic sclerosing sialadenitis, is a chronic inflammatory disease of the salivary gland. Clinically, it produces a firm swelling of the glands and may be difficult to distinguish from neoplasia. The disease is very rare and affects almost exclusively submandibular glands. The diagnosis can only be made histologically and should not be difficult if the pathologist is aware of the condition’s existence. Adequate treatment is excision of the mass, usually carried out diagnostically.

Cysts of the jaws

A cyst is a pathological cavity that is usually lined with epithelium and which contains fluid or semi-fluid. Most jaw cysts are epithelial and odontogenic origin. Usually they grow slowly and expansively. Initially cysts of the jaws are often symptom-free and in this stage they may be found by chance on routine radiography. Radiologically they form sharply-defined radioluciencies with smooth borders. They differ mainly in relationship to teeth, radiographic features and pathomorphology. Cysts are much more common than true neoplasms of the jaw bones Depending on their origin and pathomorphological characteristics they are classified as following.

A. Non-epithelial cysts:

• Solitary (simple) bone cyst
• Aneurysmal bone cyst

B. Epithelial Developmental cysts:

1. Odontogenic:

• Gingival cyst.
• Dentigerous (follicular) cyst.
• Eruption cyst.
• Odontogenic keratocysts.

2. Non-odontogenic:

• Nasopalatine duct (incisive canal) cyst Nasolabial cyst.
• Globulomaxillary cyst.

C. Inflammatory (radicular) cysts.

Aneurysmal bone cyst

Aneurismal bone cyst is a tumor-like lesion, associated with trauma or vascular disorders in bone; it is neither a cyst nor an aneurysm. Etiology and pathogenesis of this lesion are still unclear. Possible mechanisms for the formation of the aneurysmal bone cyst include alterations in local hemodynamics leading to venous engorgement, resorption, and replacement with connective tissue and osteoid; futile attempts at repair of a hematoma and microcyst formation secondary to cellular edema.

Aneurysmal bone cysts of the maxilla-facial area are very rare. They occur in jaws of people of all ages, but they are more common in younger patients. Aneurysmal bone cysts are more likely to occur in the mandible than in the maxilla. They may displace but usually do not resorb the teeth, nerve disturbances are not typical. The radiographic appearance is described as cystic, honeycomb, or soap bubble radiolucent lesion with eccentric expansion. Cortical bone may be thinned or destroyed, and a periosteal reaction may be present.

Histologically, the aneurysmal bone cyst reveals a fibrous connective tissue stroma with many cavernous or sinusoidal blood-filled spaces. Young fibroblasts are present throughout the stroma, and multinucleated giant cells are scattered throughout the lesion.

Treatment of the aneurysmal bone cyst includes complete removal with aggressive curettage of the underlying bone. Excellent exposure to facilitate this treatment is necessary because these lesions may bleed copiously, and timely but thorough removal of the lesion helps to decrease blood loss. Failure to completely remove all traces of the lesion carries a significant risk of recurrence. For recurrent lesions some authors recommend combination of excision with cryosurgery, while other authors advocate block resection followed by reconstruction with bone graft.

Traumatic bone cyst

The traumatic bone cyst also is known as solitary bone cyst, hemorrhagic cyst, extravasation cyst, simple bone cyst, and idiopathic bone cavity.

The traumatic bone cyst is a rare tumor-like lesion of the jaw bones. This cyst is not a true cyst in so far as it has no epithelial lining. The etiology of these cysts is not clearly defined, although several mechanisms have been proposed. The most accepted theory is that these lesions originate from intramedullary hemorrhage caused by trauma. In these cases, failure of organization of the blood clot occurs followed by subsequent degeneration of the clot, eventually leading to an empty bone cavity. Restricted venous drainage leads to increasing edema, which in turn causes continued resorption of trabeculae and expansion of the lesion in the spongious bone. Expansion of the cyst stops when cortical bone is reached, thus these lesions are not characterized by any cortical damage. The cyst cavity are generally either empty or filled with a small amount of straw-colored fluid. Histologically, they have a thin connective tissue membrane lining or no lining at all.

The lesion most commonly is found in young persons, and the mental area or body of the mandible is the most typical localization. Clinically they are usually asymptomatic and cause no expansion of the bone. In majority of cases they are found out on radiographs taken for other purposes as incidental findings. It is also not unusual that some patients are unable to recall any trauma to the involved jaw.

Radiographically, these lesions look as smoothly outlined radiolucencies that scallop around the roots of the of the lower molar and premolar teeth. They do not displace teeth or resorb roots, and the lamina dura is intact. In radiographic examination the outline of the radiolucency is less well defined than would be obtained from other cysts. They may range from very small (< 1 cm) to very large (involving most of the mandible). Any signs of cortical involvement are not typical.

Treatment includes surgical intervention to establish a diagnosis, which is made upon finding an empty cavity. A curettage of the cyst wall is than performed to fill the cavity with blood. Soft tissues are closed, and the lesion tends to heal without further intervention.

Nasopalatine cysts

Nasopalatine cysts are also known as cysts of the incisor canal. These cysts arise from epithelial remnants within or near to the nasopalatine foramen. They are classified as fissural cysts, and they are one of the most common types of fissural cysts of the jaws.

Clinical features

Presence of a midline anterior palatine swelling is the only usual clinical finding. They may become infected and in this cases nasopalatine cysts cause pain and overlying tenderness. These cysts grow slowly, but in some cases may grow to a considerable size. In many cases cysts are diagnosed through chance by radiographs of the teeth in this region. It can be difficult when such radiolucencies are found on routine radiographic assessment of the central incisors. The radiographic image of the nasopalayinal cyst is a round or inverted pear-shaped radiolucency with radio-opaque margins. When they are large, they can cause separation of the central incisor roots, but the laminae dura of the teeth remain intact.

If there is doubt whether the cyst is a radicular cyst related to one or other incisor, pulp testing can be carried out and close examination of the apices radiographically should show an intact lamina dura.

Treatment. Nasopalatinal cysts are treated by cystectomy. Enucleation is carried out with a palatal flap taken around the gingival margins of the premolars on one side to the premolars of the other. After enucleation, interdental interrupted sutures are used to replace the flap and in larger cysts. It is sometimes useful to have constructed a palatal plate from preoperative impressions to support the flap and prevent the formation of a painful haematoma.

Nasolabial cyst

This is a fissural cyst that is formed by cystic degeneration of epithelium from the lower part of the nasolacrimal duct during embryological development. Clinically, they may present as painless swellings in the nasolabial fold, where they may be palpated either externally on the skin surface or intraorally high in the buccal sulcus anteriorly. Radiographically, although they are not intrabony cysts they may, if they attain a reasonable size, cause a depression of the radio-opaque margin of the floor and lateral wall of the nose, which is best viewed by an oblique anterior occlusal radiograph. Treatment is surgical enucleation.

Globulomaxillary cyst

This cyst is a rare fissural cyst which develops between roots of the vital upper lateral incisor and canine teeth. Globulomaxillary cysts grow slowly, but in some cases may reach a considerable size. Clinically they are asymptomatic unless infected. On late stages they can be palpated as a firm swelling in the buccal fold caused by expansion of the cortical plate. Sometimes retention or displacement of the upper lateral incisor or canine is observed.

Radiologically globulomaxillary cyst appears as a lucent area, in shape of the inverted pear. Deviation of roots is typical signs, but the laminae dura of the teeth remain intact (Fig. 13.45).

Fig. 13.45. The globulomaxillary cyst

Treatment of choice for globulomaxillary cysts is cystectomy, with recurrence rate being very low.

Dentigerous cysts

These cysts are developmental odontogenic cysts, which arise when cystic transformation occurs in the epithelium of the dental follicle. Dentigerous cyst are seen around unerupted tooth, most commonly in the third molar areas both upper and lower. Other common associations are with maxillary canines, and mandibular second premolars. Although dentigerous cysts occur over a wide age range, they are most commonly seen in second and third decades of life.

The histologic features of dentigerous cysts may vary greatly depending mainly on whether or not the cyst is inflamed. In the noninflamed dentigerous cyst, a thin epithelial lining may be present with the fibrous connective tissue wall loosely arranged. In the inflamed dentigerous cyst, the epithelium commonly demonstrates hyperplastic rete ridges, and the fibrous cyst wall shows an inflammatory infiltrate.

Most dentigerous cysts are small asymptomatic lesions that are discovered incidentally on routine radiographs. Although some may grow to considerable size, move teeth and cause bony expansion that is usually painless until secondary infection occurs. These cysts grow slowly and cause bony expansion only at late stages. If the cortical layer is destroyed, a soft fluctuant swelling over the area of the unerupted tooth will develop. Large dentigerous cysts are often associated with the significant risk for pathologic jaw fracture.

Radiographic imaging and, sometimes, aspiration are the main diagnostic procedures for dentigerous cysts. Radiographically, the dentigerous cyst presents as a welldemarcated unilocular radiolucency, often with a sclerotic border (Fig. 13.46; 13.47).

Fig. 13.46. The dentigerous cyst

Fig. 13.47. The dentigerous cyst of the mandible of the mandible from the 45 tooth from the 32 tooth

Since the epithelial lining is derived from the reduced enamel epithelium, this radiolucency surrounds the crown of the tooth, which is projected into the cyst cavity. The radiographic differentiation between a dentigerous cyst and a normal dental follicle is based merely on size. A very large dentigerous cyst in the lower third molar area can displace the wisdom tooth and may require to be differentiated from other lesions such as a keratocyst or ameloblastoma.

Treatment

Treatment will either be enucleation along with extraction of the unerupted tooth or cystotomy (marsupialisation). Histopathologic examination of the cyst wall is obligatory in both cases. Cystotomy is the method of choice if it is hoped to encourage eruption of the buried tooth, but it is only possible if the tooth is in a satisfactory position in terms of its angulation and depth.

Cystotomy is also used in large dentigerous cysts when enucleation and curettage might otherwise result in neurosensory dysfunction or predispose the patient to an increased chance of pathologic fracture. The prognosis for most dentigerous cysts is excellent, with recurrence rate being very low.

Gingival cyst of the newborn

Gingival cysts of newborns originate from remnants of the dental lamina and are located in the corium below the surface epithelium. These structures generally occur as small multiple or solitary nodules. They are located on the alveolar ridges of newborns or young infants. Occasionally, they may become large enough to be clinically noticeable as discrete white swellings on the alveolar ridges. They are generally asymptomatic and do not produce any discomfort for the infant.

Histologically, the gingival cyst of the newborn is a true cyst with a thin epithelial lining. The cyst cavity is usually filled with keratin but may contain some inflammatory cells, dystrophic calcifications, and hyaline bodies.

Epstein pearls are similar lesion with which gingival cysts sometimes may be confused; however, the location and etiology of these lesions are somewhat different. Epstein pearls are cystic keratin-filled nodules found along the midpalatine raphe and are thought to be derived from entrapped epithelial remnants along the line of fusion.

No treatment is required for these lesions, which usually disappear either by opening onto the surface mucosa or through disruption by erupting teeth.

Odontogenic keratocyst

The odontogenic keratocyst is a distinctive form of developmental odontogenic cyst that deserves special consideration because of its specific histopathologic features and aggressive clinical behavior. Keratocysts derive from remnants of the dental lamina. They can be found anywhere in the jaws but the most common site is the angle of the mandible (Fig. 13.48).

Fig. 13.48. The odontogenic keratocyst of the angle of the mandible

Unlike other cysts of the jaws, their epithelium is a keratinising stratified squamous epithelium and their contents are therefore filled with desquamated squames and keratin, which form a foul-smelling semisolid cheese-like material. Odontogenic keratocysts grow in a neoplastic fashion and not in response to internal pressure. The thin and friable wall of the cyst usually can pose problems for removal in one piece intraoperatively.

The lesions grow in a multilocular bosselated fashion with daughter cysts which protrude into the surrounding bone. Because of this relationship, the recurrence rate reported in patients with odontogenic keratocysts is high, particularly if the original surgical treatment does not result in complete removal of the lesion.

Odontogenic keratocysts may be found in patients ranging in age from infancy to old age; however, most of cases are seen in people of the second and third decades of life. A slight male predilection is usually seen, and 60 to 80 % of cases involve the mandible, particularly in the posterior body and ascending ramus. In younger patients these cysts are commonly found as part of the basal cell nevus syndrome, also known as Gorlin – Goltz syndrome (Fig. 13.49). In this case multiple keratocysts are found in different parts of the jaws (Fig. 13.50).

Fig. 13.49. Gorlin – Goltz syndrome

Fig. 13.50. Panoramic x-ray, multiple jaw cysts

Clinical features

Odontogenic keratocysts are different from other jaw cysts; they are aggressive and can be difficult to remove. They can grow quite rapidly, and recurrences are frequent.

The active growth of keratocysts appears not to be evenly distributed, so the cyst does not expand uniformly as a sphere or oval-shaped lesion. Different rates of activity within areas of the lining probably account for the formation of locules, which, once the cyst has achieved a moderate size, will give rise radiographically to the typical multilocular appearance. On the late stages the cyst may reach a considerable size, causing the expansion and later on a destruction of the outer cortical plates. Lingual expansion is noted as well as buccal once.

Unless infected, these sometimes very large lesions are painless and do not exert sufficient pressure on vital structures such as the inferior dental nerve to cause paraesthesia of the lip and chin. When infected, however, they can become very painful, cause anaesthesia and may discharge into the mouth, with consequent bad taste and bad breath as additional clinical features.

Infection occurs mostly when the cyst is quite large and where soft tissue trauma results in bacterial contamination. It is not infrequent to find that with expansion the cyst communicates with the surface through the periodontal space of an adjacent tooth.

As with other cysts, the diagnosis of odontogenic keratocysus is based on clinical features, radiographic findings (Fig. 13.51) and the results of aspiration and biopsy. Two extraoral radiographic views at right angles to each other, such as an orthopantomogram and posteroanterior mandibular view, may be required with large keratocysts.

Fig. 13.51. CT scanning. Keratocyst of the maxilla growing to the left infratemporal fossa

Classically, the appearance is of a multilocular radiolucency with marked expansion of both buccal and lingual plates. Unerupted wisdom teeth may well be pushed into ectopic positions such as inverted high into the ramus of the mandible. The inferior dental canal may be difficult to see and may reflect the more active growth of these cysts around the canal with less evidence of significant repositioning as is seen with radicular cysts. Displacement or tilting of the teeth can be a feature, as well as the resorption of dental roots. In large or recurrent cysts the usage of computer tomography is recommended for accurate estimation of the cyst size and to define its extension outside the bone.

Aspiration will yield a “dirty” cream-colored semisolid material composed of keratinized squames. These can be confirmed histologically and provide good evidence that the lesion is a keratocyst.

Odontogenic keratocyst has variety of clinical and radiological manifestations and can mimic other jaw cysts and tumors. It belongs in the differential diagnoses of any radiolucency of the jaws. Because of this diagnosis of the lesion should be proved histologically in all cases.

Treatment

Adequate diagnosis and treatment of the odontogenic keratocyst is important because this cyst is recognized as being more aggressive than other odontogenic cysts, the odontogenic keratocyst has a higher rate of recurrence than other odontogenic cysts, and the association with nevoid basal cell carcinoma syndrome requires that the clinician examine a patient with multiple cysts of the jaws for physical findings that might diagnose this syndrome.

Like the treatment of most odontogenic cysts, the odontogenic keratocyst may be treated with enucleation and curettage and must be removed in one piece, which requires acceptable access and lighting. As such, many patients are suitably treated in an operating room setting under general anesthesia. This is particularly helpful when removing large cysts.

Keratocysts have a higher recurrence rate than other cysts and especially when they are large and multilocular. Enucleation is suitable for most keratocysts but may be difficult in large ones where, for example, they extend upwards into the vertical ramus of the mandible. Surgical access may be difficult and with the multilocular pattern of growth it may be impossible to ensure that the whole lining is removed. It is known that small clusters of epithelium known as microcysts, or satellite cysts can lie outside the epithelial lining may account for eventual recurrence. For this reason, in large or recurrent cysts enucleation with peripheral ostectomy and/or cryosurgery are recommended as a treatment of choice.

Cystotomy can be used particularly with large keratocysts where it can be sometimes effective. It may be appropriate in some cases to use the technique to reduce the size of the lesion before enucleating it. Whatever method is used, long-term (for years) follow-up radiography is imperative to ensure that there is no recurrence. The reported frequency of recurrence of the odontogenic keratocyst is approximately 30 %.

Gorlin – Goltz syndrome known also as the nevoid basal cell carcinoma syndrome, basal cell nevus syndrome, Gorlin’s syndrome is an autosomaldominant inherited condition that exhibits high penetrance and variable expressivity. It is caused by mutations in the PTCH tumor suppressor gene, mapped to chromosome 9q22.3 – q31. Affected patients may demonstrate the presence of multiple keratocists and skin lesions in the form of basal-cell naevi or carcinomas, and skeletal abnormalities affecting the vertebral column and the ribs.

Clinical signs of the syndrome include mild ocular hypertelorism, midface hypoplasia, relative frontal bossing and mandibular prognathism, mental retardation, schizophrenia, multiple basal cell carcinomas, calcification of the falx cerebri, rib anomalies (splayed, fused, partially missing,bifid), palmar pitting (the pits later develop into basal cell carcinoma), and multiple odontogenic keratocysts.

Other symptoms seen less commonly are epidermal cysts of the skin, spina bifida occulta of cervical or thoracic vertebrae, calcified ovarian fibromas, and short fourth metacarpals, kyphoscoliosis or other vertebral anomalies, medulloblastoma, meningioma, lymphomesenteric cysts, cardiac fibroma, fetal rhabdomyoma, cleft lip and palate, hypogonadism in males.

The most significant clinical feature is the tendency to develop multiple basal cell carcinomas that may affect both exposed and non-sun-exposed areas of the skin. Pitting defects on the palms and soles can be found in nearly two-thirds of affected patients. The discovery of multiple odontogenic keratocysts is usually the first manifestation of the syndrome that leads to the diagnosis. For this reason, any patient with an odontogenic keratocyst should be evaluated for this condition. Of patients with odontogenic keratocysts, 5 % have basal cell nevus syndrome. Early identification of these patients and their lesions is the key to improving long-term survival and quality of life.

Although the cysts in patients with the nevoid basal cell carcinoma syndrome cannot definitely be distinguished microscopically from those not associated with the syndrome, they often demonstrate more epithelial proliferation and daughter cyst formation in the cyst wall.

The treatment of the odontogenic keratocyst in patients with the nevoid basal cell carcinoma syndrome can be difficult owing to the large number of “recurrences” in these patients.

Radicular cysts

Radicular (periapical) cysts are pathological cavities, lined with epithelium, and contain fluid or semi-fluid material. They are the most common cystic lesions of the jaws and originate from the epithelial remnants of Malassez rests, which are stimulated after inflammation at the apices of nonvital teeth.

The usual etiology is a tooth that becomes infected, leading to necrosis of the pulp. Toxins exit the apex of the tooth, leading to periapical inflammation. This inflammation stimulates the Malassez epithelial rests, which are found in the periodontal ligament, resulting in their proliferation and formation of a periapical granuloma. Eventually, this epithelium undergoes necrosis caused by a lack of blood supply, and the granuloma becomes a cyst. The formation of an epithelial semipermeable lining to the cyst content, that allows fluids to enter the lumen by osmosis, leads to its gradual enlargement in response to hydrostatic pressure.

Hystologically, the epithelium of the cyst lining is a nondescript stratified squamous epithelium without keratin formation. Inflammatory changes may be observed in the cyst wall, and these changes, in turn, may lead to epithelial changes (eg, ulceration, atrophy, hyperplasia).

Clinical presentation. The majority of radicular cysts are asymptomatic, especially on early stages. The small lesions are not usually clinically detectable and most often are discovered as incidental findings on radiographic examination.

With continued growth, the cyst eventually approaches the surface of the alveolar bone and manifests as a buccal, lingual or palatal swelling. As the apices of most teeth lie closer to the buccal than the palatal or lingual plates, it is the buccal plate which is affected most commonly. Palatal expansion of the cyst is usually associated with an upper lateral incisor, reflecting the palatal inclination of its apex. This bony swelling (known as bony expansion) is the first real evidence of a cyst. On late stages the expansion of the cortical plate becomes thinned and may demonstrate a crackling sound (crepitus). If the bone is completely destroyed, the cyst is connected to the periosteum and the mucosa in this area looks bluish-red. The cyst in this case became a soft fluctuant (fluid-filled) on palpation.

Loosening or tilting of adjacent teeth is only encountered in very large cysts, and resorption of roots usually results from repeated infection of the cyst and is very uncommon. Unless a radicular cyst becomes infected, it will remain painless and vital structures will be gently moved aside to accommodate it. This can be seen clearly in larger mandibular cysts, which push the inferior dental canal downwards to the lower border of the mandible. No paraesthesia of the lip or chin will be noted unless the pressure within the cavity rises rapidly as with an acute infection.

In radicular cyst the decayed non-vital tooth responsible for the lesion is usually present. With large cysts occasionally this tooth elicits a rather hollow note on percussion. From time-to-time the teeth responsible for the formation of a radicular cyst may be extracted but the cyst remains and may well increase in size subsequent to the extraction. In this circumstance the name residual cyst is commonly used.

Acute infection can supervene at any time during this process of cyst evolution and in this cases pain as well as other symptoms which resemble an acute periodontitis or periostitis. The acutely infected cyst may bursts and discharges into the mouth with fistula formation.

Diagnosis of radicular cysts is based on clinical and radiographic examination, as well as aspiration of the contents of the cystic sac. It should be also confirmed hystologically after the surgical treatment of the lesion.

Radiographically, radicular cysts present as a round or oval-shaped osteolytic or radiolucent lesions surrounded by a well-defined radiopaque borders (looking as a thin white line of increased bone density) (Fig. 13.52). This radio-opaque surrounding is due to reactive bone sclerosis around the lesion in an attempt to wall it off. It is also associated with slow rate of growth typical to most radicular cysts. The affected tooth will show loss of its apical lamina dura. Very occasionally there may be the evidence of resorption of adjacent teeth and this reflects repeated acute episodes of infection within the cyst.

Fig. 13.52. Radicular cysts of the maxilla and mandible

Similarly, such infection can cause haziness in the sharp radio-opaque delineations of the margin of the cyst. In larger mandibular cysts there may be clear evidence of the inferior dental canal having been displaced downwards by the advancing lesion.

In maxillary cysts, penetrating into the sinus cavity, the signs of reactive sinusitis are often observed, as well as the semi-round shadow of the cyst, projecting to the sinus cavity (Fig. 13.53).

Fig. 13.53. CT scaning of the radicular cyst, penetrating into the sinus cavity

In addition to the clinical and radiographic examination, aspiration of the contents of the cystic sac may be a valuable diagnostic aid. This procedure is possible in the large cysts with little or no bony covering. Usually the fluid appears as straw-coloured in which a shimmer may be seen due to its cholesterol content. However, if the cyst has been infected, this characteristic appearance may be lost and the fluid may consist of pus or blood-stained pus.

Several treatment options exist for radicular cysts. Depending on the clinical situation cysectomy, cystotomy, plastic cystotomy can be used. Most lesions should be surgically removed (cystectomy) and histopathologically examined. The tooth, responsible for the lesion, should be treated endodontically or removed.

Diagnostic tests used in patients with the jaw cysts

Radiographs – intra and extra-oral views:

• Round or oval radiolucence with well demarcated sclerotic border typical for most of the cysts.
• Associated with non-vital decayed tooth (radicular cyst).
• Associated with the crown of unerrupted tooth (dentigerous cyst).
• Not associated with the roots of the teeth (fissural cysts).
• Multilocolar or unilocular lesion (odontogenic keratocysts).

Vitality testing of teeth (electroodontometry).

Aspiration of fluid contents:

• Straw-coloured fluid containing cholesterol crystal from most cysts.
• Air, some blood or serosanguious fluid from solitary bone cysts.
• Blood from aneurismal bone cyst.
• Pus from infected cyst.
• Pale, yellow fluid containing keratin from odontogenic keratocyst.

Biopsy of lining, provides definitive diagnosis.

Management of the jaw cysts

There are several approaches that can be used for surgical treatment of the jaw cysts.

The main procedures used for these lesions listed below.

1. Enucleation with primary closure (cystectomia) is the most common and generally the treatment of choice. It consists of removing the cyst lining from the bony walls of the cavity and repositioning the access flap. Any relevant dental pathology is treated at the same time.
2. Enucleation with packing and delayed closure is used when badly infected cysts, particularly very large ones, are unsuitable for primary closure.
3. Enucleation with primary bone grafting.
4. Cystotomy (marsupialization) – opening of the cyst to allow continuity with the oral mucosa. Healing is slower than with enucleation and a cavity persists for some time.
5. Plastic cystotomy – enucleation of the cyst followed by icertion of the mucoperiosteal flap into the bone cavity.
6. Operations for cysts penetrating into the maxillary sinus – usually include the formation of the anastomosis between the cyst cavity and the sinus and, sometimes, with the nasal cavity.

Among these numerous operation types two techniques are employed in clinical practice for the surgical removal of cysts most commonly: cystectomy (removal of the lining in total) and cystotomy (creation of a permanent opening into the cyst cavity). The vast majority of cysts are treated by cystectomy, with cystotomy (marsupialisation) tending to be reserved for certain categories of patients, usually with larger cysts.

Cystectomy (Parch II operation)

Cystectomy involves complete removal of the cystic sac and healing of the wound by primary intention. This technique is suitable for all small to moderate-sized cysts and the majority of large cysts. This is the most satisfactory method of a cyst treatment and is indicated in all cases where cysts are involved, whose wall may be removed without damaging adjacent teeth and other anatomic structures.

After taking a radiograph to determine the exact localization and size of the lesion, a trapezoidal flap is created, whose extent must ensure adequate access and visualization of the surgical field.

Root-treating and conserving the tooth causing the cyst may be worthwhile and surgery may therefore be preceded by endodontic treatment.

The surgical procedure for treatment of a cyst with enucleation includes the following steps:

• Reflection of a mucoperiosteal flap.
• Removal of bone and exposure of part of the cyst.
• Enucleation of the cystic sac.
• Care of the wound and suturing.

After reflection of the mucoperiosteum, the bone covering the lesion is evaluated. It may be normal, thinned, or completely destroyed. In normal bone, a round bur is used to remove a portion of the buccal cortical plate covering the cyst, and, depending on its extent, the created osseous window is than enlarged if necessary. The osseous window must be large enough so that all parts of the cystic cavity may be accessed and removed without particular difficulty.

If the bony wall is thinned or perforated, it is removed peripherally until it reaches compact bone. A curette is used for enucleation of small cysts, while for larger cysts, the broad end of a periosteal elevator is preferred, which is placed inside the cavity pressing gently between the cystic wall and bone, while the cyst is carefully grasped with forceps. The lining should be sent for histopathological investigation.

After removal of the cysts, a curette is used to inspect the cavity for the presence of remnants of the cyst. After irrigating with sterile saline the flap is sutured back to its anatomical position. If the tooth has been root filled, an apicectomy should be performed at the same time with retrograde sealing of the canal if appropriate.

The operation for all but very large cysts is usually carried out under local anaesthesia with or without sedation according to the patient’s preference. Postoperative complications are rare, although breakdown of the wound in large mandibular cysts can occur. The patient is normally recalled about 4–6 months postoperatively, when a radiograph should show evidence of bony infilling of the cyst cavity.

Cystotomy. This method is usually employed for the removal of large cysts and entails opening a surgical window at an appropriate site above the lesion.

The rationale of this treatment is the permanent destruction of the integrity (wholeness) of the cyst. This, in effect, depressurises the cyst cavity, stops its continued expansion and encourages a shrinkage of the lining by new bone formation around its periphery.

It is more suitable for large cysts where enucleation may endanger vital structures such as the inferior dental nerve or there is a risk of fracture during enucleation. The limited surgery involved is very suitable for outpatient care under local anaesthesia and it can therefore be particularly appropriate for elderly or medically compromised patients who would be at risk from a general anaesthetic.

In order to create the surgical window, initially a circular incision is made, which includes the mucoperiosteum, the underlying perforated bone, and the respective wall of the cystic sac. After this procedure, the content of the cyst is evacuated, and interrupted sutures are placed around the periphery of the cyst, suturing the mucoperiosteum and the cystic wall together.

Afterwards, the cystic cavity is irrigated with saline solution and packed with iodoform gauze, which is removed a week later together with the sutures. During that period, the wound margins will have healed, establishing permanent communication. Irrigation of the cystic cavity is performed several times daily, keeping it clean of food debris and averting a potential infection.

Healing of the wound is by secondary intention, and the epithelium of the cyst is thus transformed into oral mucosa.

Any decision to marsupialise a cyst cavity should be preceded by histological evidence that confirms the lesion as a cyst and this involves a small incisional biopsy or retrieving tissue from the cyst cavity at the time of the procedure.

With the lining no longer complete, the bone heals inwards around the cyst, reducing it progressively in size. In some cases cyst can be removed by enucleation when it has reduced to a more manageable size.

In some cases the plastic cystotomy is used after performing the cyst enucleation. The mucoperiosteal flap is then turned into the remaining cavity and fixed with iodoform gauze. This procedure is used in cases of severe injury of the muco-periosteal flap during the operation, its defect, infection development or breakdown of the wound after cystectomy of the large cysts.

Marsupialisation of a large cyst may take many months for healing to occur and the onus is therefore on the patient to maintain cleanliness by frequent irrigations of the cyst cavity, as described above.

In infected cysts two-stage treatment is used. On the first stage the cyst is drained via the vertical incision or using the special needles. Antibiotics are prescribed and endodontic treatment of the non-vital teeth associated with the cyst is performed. When the signs of acute inflammation resolve, the final surgical procedure (usually cystectomy) is performed.

Benign odontogenic tumors and tumor-like lesions of the jaws

Tumours or tumour-like wellings of the jaws can be odontogenic or nonodontogenic. Odontogenic tumors comprise a complex group of lesions of the jaws, derived from primordial tooth-forming tissues and presenting in a large number of histologic patterns. They are lesions of great importance to oral and maxillofacial surgeons. Many of them are true tumors derived from tooth-forming tissue, whereas some are developmental malformations or hamartomas. Odontogenic tumors may arise from epithelial or mesenchymal tissue. Like normal odontogenesis, odontogenic tumors demonstrate varying inductive interactions between odontogenic epithelium and odontogenic mesenchyme.

Odontogenic lesions arise from tissue with the potential for differentiation into tooth or periodontal ligament structures, and they are found predominantly at tooth-bearing sites. Variable but distinctive histological features of odontogenic lesions include formation of tooth-related extracellular substance, some of which may calcify and be visible on radiographs, and epithelial-mesenchymal interactions.

In general terms, odontogenic tumors tend to be more common in younger patients but can occur at any age. They originate in the jaws and usually are found in the tooth-bearing sites. They are often associated with impacted or missing teeth. The common sites for odontogenic tumors are the mandibular molar region and the maxillary cuspid region. Odontogenic tumors are usually slow-growing and asymptomatic. Pain is not a feature of benign tumors of the jaws but is a common symptom of malignant tumors of the jaws. The odontogenic tumors are expansile lesions and may expand the bony cortex, but usually do not invade or perforate it.

Most odontogenic tumors are essentially benign lesions but are rather aggressive and can infiltrate the adjacent bone. This form of bony infiltration is not the true invasiveness of malignant tumors but represents a clinical problem that the tumor can recur after surgical therapy if the bony margins still contain some of the tumor remnants. A block resection leaving the cortical lower border of the mandible intact is favored. These benign tumors are relatively unaffected by radiation, and the risk of radiation stimulating the development of a malignant tumor or of radiation necrosis is unwarranted for a benign tumor.

True malignant transformation of benign odontogenic lesions or the development of malignancy de novo from odontogenic tissues have both been reported, but such occurrences are extremely rare. In general, the less-differentiated odontogenic lesions (the immature ones) are more likely to have indistinct radiographic borders, invasive growth patterns, and relatively aggressive clinical behavior, while the mature or well-differentiated entities are more likely to produce recognizable extracellular product, to be well circumscribed, and to be self-limiting in terms of growth.

Odontogenic tumours have been classified by the WHO as shown in Table 13.2.

Ameloblastoma

Ameloblastoma is an epithelial tumor arising from the dental lamina, Hertwig sheath, the enamel organ, or the lining of dental follicles. Ameloblastomas are the most common odontogenic tumors of the jaws. This lesion occurs in both the maxilla and mandible, but the posterior mandible is the most common location. 70 % of all ameloblastomas develop in the posterior lower molar region, and often involve the ramus of the mandible. The lesion is distributed equally between males and females.

Ameloblastomas are usually first recognized between the ages of 20 and 40 years. They are rare in children in their first decade of life and relatively uncommon in the second decade and in old people (Fig. 13.54; 13.55).

Fig. 13.54. Ameloblastoma of the mandible, Left part

Fig. 13.55. Ameloblastoma of the mandible, Right part

Although ameloblastoma is not a malignant lesion, it is very aggressive and infiltrative. It does not metastasize but is stadely growing, persistent, and hard to eradicate.

Ameloblastomas are symptomless until the swelling becomes obtrusive. Therefore ameloblastoma is usually noticed as an incidental finding on radiographs taken for other purposes or its first symptom is painless bony expansion. Neurosensory changes are uncommon, even with large tumors.

Slow growth is the typical for ameloblastoma, but this tumor may reach a large size, leading to tremendous facial disfigurement.

Radiographically ameloblastomas usually appear as a rounded, cyst-like multilocular radiolucency with well-defined margins in the area of the lower third molar (however they may be found anywhere in the jaws). These lesions may be unilocular when small. Buccal and lingual cortical expansion is common, frequently to the point of perforation. Resorption of adjacent tooth roots is common (Fig. 13.56).

Fig. 13.56. Polycystic ameloblastoma of the corpus, angle of the mandible

Unicystic ameloblastomas (Fig. 13.57), most commonly seen in young patients, with about 50 % of these tumors being diagnosed during the second decade of life manifest as a unilocular radiolucency, mimicking a dentigerous cyst.

Fig. 13.57. Unicystic ameloblastoma corpus of the mandible

Pathogenetically, this type of ameloblastoma is considered to be less agressive.

Differentiation of ameloblastoma from non-neoplastic cysts and other tumours or tumour-like lesions of the jaws is not possible by radiography and clinical signs alone.

Histologic patterns of ameloblastoma are multiple and include follicular, acanthomatous,plexiform, granular cell, basdal cell and other variants. In all cases the neoplastic component is purely epithelial with a reactive connective tissue component. In folicular ameloblastomas, which is the most common and easely recognisable type, the stellate reticulum is located within the center of the islands and trabecule of odontogenic epithelial cells. Epithelial structures consist of a well-organised single layer of tall, columnar, ameloblast-like cells. Plexiform type of ameloblastomas consists mainly of thin trabeculae of small epithelial cells in a connective tissue stroma. The stellate reticulum is located outside of the odontogenic rest.

Acanthomatous ameloblastomas show squamous metaplasia of the odontogenic epithelium. Granular cell ameloblastomas are rare and consists the epithelium, which forms sheets of large cells with granular eosinophilic cytoplasm in the central areas of the tumour islands. Basal cell variant is the least common. It consists of basaloid cells predominantly in a trabecular patternt, with a strong resemblance to basal cell carcinoma. In this latter tumor stellate reticulum is not present in the central portions of the nests. The variety of the hystological patterns make it difficult to diagnose the ameloblastoma even for experienced hystologist.

Treatment. The diagnosis of ameloblastoma must be confirmed by biopsy in all cases. The treatment of ameloblastoma is surgical excision with wide free margins. In the mandible, 1 cm clear margins are considered the standard. This may be accomplished with block or segmental resection, depending on the relationship of the lesion to the inferior cortical border.

The maxillary ameloblastoma is not confined by the strong cortical plate found in the mandible. In addition, the posterior maxilla lies in close relationship to many vital structures. These factors make strong arguments for aggressive and definitive surgical treatment of the maxillary ameloblastoma.

Complete excision is curative but enucleation is usually followed by recurrence. Ameloblastoma tends to infiltrate between intact cancellous bone trabeculae at the periphery of the tumor before bone resorption becomes radiographically evident. Therefore, the actual margin of the tumor often extends beyond its apparent radiographic or clinical margin. Attempts to remove the tumor by curettage, therefore, predictably leave behind small islands of tumor within the bone, which are later determined to be recurrent disease.

Complete excision of a large ameloblastoma usually means total resection of the jaw. Appropriate reconstruction by the bone graft may be performed at the same time.

The single exception to this may be the unicystic ameloblastoma. Unlike other types of ameloblastomas, it is believed that this lesion can be removed with enucleation/curettage procedures alone. These lesions however may recur, and in this cases more aggressive treatment is required.

All patients with ameloblastoma, regardless of surgical treatment method or histologic type, must be monitored radiographically for several years. If necessary re-operation is performed. The patient must be warned of the necessity of regular follow-up and, possibly, of a further operation.

Odontomas

Odontomas are developmental malformations (hamartomas) of odontogenic epithelium and mesenchyme and not true neoplasms. Even when the morphology is grossly distorted (as in complex odontomas), structures which resemble the pulp, dentine, enamel and cementum can be found in normal hystologic relationships with one another. When odontoma became fully calcified on its late stages they stop growing and do not develop further. In some cases the “eruption” of odontomas is observed, like in normal teeth.

Odontomas are the most frequently occurring odontogenic tumors and usually found between ages 10 and 20 years. They affect the maxilla slightly more frequently than the mandible and are often recognised in early adolescence by the dense opacity of the enamel component in routine radiographs. When odontomas have erupted, infection develops and abscess formation is commonly observed. In some cases, odontomss displace teeth or block their eruption.

The main types of odontomas are simple odontomas, compound odontomas and complex odontomas. Simple odontomas are the malformations arising from one tooth germ. In this type of odontoma pulp, dentine, enamel and cementum have normal anatomical relationships with one another, and the form of this lesion is near to normal (Fig. 13.58).

Fig. 13.58. Simple odontomas

Morfological distorsion may affect only the crown or the crown and root together. They can pose both aesthetic and orthodontic problems. In cases where extraction is necessary; simple odontoma may cause difficulties due to its complex In some classifications this type of odontomas is not considered as tumors or tumor-like lesion. Other types of odontomas are compound, in which multiple small toothlike structures exist; and complex, in which irregular masses of dentin and enamel are present with no anatomic resemblance to a tooth.

Compound odontomas are predominantly seen in the anterior maxilla, whereas complex odontomas are typically seen in the posterior maxilla or mandible.

Compound odontomas

Compound odontoma consists of many (2 to 30) small, tooth-like structures massed together within an outer capsule. This structures (denticles) are probably produced by localized, multiple budding-off from the dental lamina and formation of many tooth germs (Fig. 13.59). It represents the product of both histodifferentiation and morphodifferentiation of odontogenic tissues, resulting in what appears as a cluster of multiple abortive teeth.

Fig. 13.59. Compound odontoma

It most commonly forms in the anterior part of the maxilla but may be located anywhere within the tooth-bearing segments of the jaws. In some cases it gives rise to a painless swelling and it is often responsible for preventing normal tooth eruption, thus it usually is discovered during adolescence. The odontoma may be small, with only a few tiny teeth, or it may be of considerable size and contain many denticles.

Histologically, compound odontomas approaches to normal tooth structure. The denticles are embedded in fibrous connective tissue, and have a fibrous capsule. In majority of cases the macroscopical examination is sufficient for diagnosis.

Radiographically compound odontoma consists of multiple tiny toothlike densely-calcified structures contained within a fine radiolucent rim.

Complex odontoma

Complex odontomas consist of an irregular mass of hard and soft dental tissues, having no morphological resemblance to a tooth and frequently forming a cauliflower-like mass. This developmental aberration results in a random laying-down of all the dental elements in a totally haphazard fashion.

Clinically, complex odontomas are usually detected in adolescence, but may escape diagnosis until late in life. They usually have a predilection for the mandibular molar regions; however, they can be found in other areas of the jaws. Typically, a hard painless swelling is present, but the mass may start to erupt and in these cases infection may develop.

Radiographically, when calcification is complete, an irregular radiopaque mass is seen containing areas of different radiopaq density. Enamel, dentine, cement and pulpal tissues are all represented and the radiographic image may reflect these different tissues with varying degrees of opacity and radiolucency. The radioopaque zone is surrounded by a thin, uniform, radiolucent rim. Distinct line of cortication usually separates lesion from normal bone (Fig. 13.60; 13.61).

Fig. 13.60. Complex odontomas

Fig. 13.61. Complex odontomas, macropreparation

Although this radiographic picture may have some resemblance to the radiographic picture of osteosarcoma, the association with a tooth, the clear demarcation of the lesions’ borders, and the lack of pain and/or swelling serve to delineate this very benign lesion from osteosarcoma.

Histologically, the mass consists of all the dental tissues in a disordered arrangement. Histodifferentiation but no morphodifferentiation is typical to this lesion. The epithelium in this lesion has involuted, leaving disorganized dental hard tissues in place. A mixed honeycomb presentation of enamel, cementum, dentin, and pulpal tissue is present. The pulp is usually finely branched so that the mass is perforated, like a sponge, by small branches of pulp.

Differential diagnoses of odontomas include focal sclerosing osteitis, osteoma, periapical cemental dysplasia, ossifying fibroma, cementoma.

The method of treatment used in all types of odontomas is surgical removal and curettage of the fibrous capsule. Being enucleated from bone these lesions do not recur.

Adenomatoid odontogenic tumour

The adenomatoid odontogenic tumor is a fairly uncommon benign tumor, but it usually can be easily identified from its clinical and radiographic appearance. These lesions are usually diagnosed in the second and third decades of life and make up from 3 to 7 % of all odontogenic tumors. This lesion was preveously believed to be a variant of ameloblastoma and was designated adenoameloblastoma. Now it is considered as a hamartomous lesion originating from the reduced enamel epithelium of the dental follicle. Its clinical features and biologic behavior permit distinction from the ameloblastoma.

Adenoamatoid odontogenic tumor has a predilection for the anterior region of the jaws. Most of the cases occur in the anterior maxilla, the second most common place of its occurance is the anterior mandible. Two thirds of the cases are associated with unerupted tooth (usually the canine). Females are affected about twice as often as males. Clinically, adenomatoid odontogenic tumours are usually found either in late adolescence or young adults.

Tumor has a limited growth potential and therefore it is considered as a hamartoma rather than a true neoplasm. Histologically it has a thick fibrous capsule filled with a proliferation of epithelial elements that form nodules and microcysts, resembling ducts cut in cross-section and lined by columnar cells similar to ameloblasts. Tubular or duct-like structures are characteristic for the adenomatoid odontogenic tumor. The product of the tumor cells, a pre-enamel matrix, is thought to degenerate and ultimately leave areas of dystrophic calcification and amyloid. When the lesion is bisected, the central portion of the tumor may be essentially solid or may show varying degrees of cystic change with intraluminal proliferation of tissue.

Clinical signs.

Adenoamatoid odontogenic tumor is generally asymptomatic but may present with mild swelling or in association with a clinically missing tooth. The tumour is most frequently sited in the anterior maxilla and forms a very slow-growing swelling. It also may be noticed by chance on a radiograph where it frequently simulates a radicular or dentigerous cyst. Most specimens are small, rarely exceeding 3 cm in diameter.

Radiographically this lesion generally appears as a well-demarcated radiolucency, which may contain radiopaque flecks, representsng calcified material. In 75 % of cases, it is associated with an unerupted canine and can be indistinguishable from a dentigerous cyst.

Treatment and Prognosis.

The treatment of choice for adenomatoid odontogenic tumor is simple removal. Owing to this lesion being encapsulated, it separates easily from the surrounding bone. If the tumor is completely removed at biopsy, the reccurences are very uncommon.

Melanotic neuroectodermal tumor of infancy

Melanotic neuroectodermal tumor of infancy (MNTI) is a relatively uncommon osteolytic pigmented neoplasm that primarily affects the jaws of newborn infants. In most patients (more than 90 %), tumor manifests in the first year of life, usually from age 1–6 months. Although MNTI is classified as a benign lesion, it is often clinically worrisome because of its rapid onset and alarming local growth rate. Often, sucking and feeding are impaired secondary to the swelling. The typical MNTI begins as a nonulcerated, lightly pigmented, blue or black lesion on the anterior aspect of the maxilla and rapidly expands to form a swelling or a tumescence that is cosmetically obvious to the parents of the infant. The intraoral lesion appears as a sessile, lobulated mass, often reaching 2–4 cm in diameter by the time of diagnosis. Bone destruction often occurs because of the intraosseous expansion of the tumor, which can displace or destroy the developing deciduous and permanent dentition. Although the lesion expands rapidly, the overlying mucosa remains intact.

Plain dental radiography, CT scanning, and MRI are used in diagnosis of MNTI. The radiographic appearance of the tumor is a well-circumscribed irregular radiolucency, although diffuse, ill-defined cases have also been reported. The bone is destroyed as the tumor advances. Although a few cases have been described as multiloculated, most MNTI are unilocular. CT scanning with intravenous contrast is often used to delineate the margins of osseous involvement. Additionally, MRI with gadolinium contrast can be used to evaluate the extent of the lesion. Most MNTI appear as typical soft tissue tumors with nonenhancing heterogeneous tissue density.

The fast-growing pattern of the lesion, in many cases suggests a clinical impression of infection or malignant neoplasm. So, if a differential diagnosis is established from the clinical and radiographic findings, histologic evaluation of a surgical specimen is necessary to determine the final diagnosis. Although the histologic appearance is characteristic, special immunohistochemical stains and electron microscopy may be necessary to make a definitive diagnosis.

Grossly, the tumor has a gray, hard, rubbery consistency with foci of blue- black pigmentation. Additionally, entrapped developing tooth buds may be noted in the specimen as MNTI grows in and around the odontogenic apparatus.

The histologic appearance of MNTI is unique and characteristic in that a distinct biphasic pattern exists. The peripheral borders of the tumor are faintly noted as a thin, delicate, fibrous layer. In majority of cases tumor shows local infiltration into the adjacent bone.

One portion of the lesion contains large polygonal cells arranged in sheets or alveolarlike structures. These large cells have pale abundant cytoplasm and pale nuclei with finely dispersed chromatin. They often contain the melanin pigment that gives the MNTI its blue-black clinical appearance. The central portion of the alveolar spaces contains the second smaller characteristic cell type. These cells are lymphocytelike or neuroblastlike with small, dark nuclei and little, if any, cytoplasm.

Treatment and prognosis. MNTI is benign tumor, which can be effectively managed by aggressive surgical excision. This treatment can usually be accomplished with a partial maxillectomy by using a Weber – Ferguson incision and a facial degloving approach. Teeth, developing teeth, and the adjacent bone must be sacrificed when they lie near the borders of MNTI. It is recommended, that 5 mm margin of healthy tissue should be included in the surgical specimen.

The possibility of local recurrence in patients with MNTI remains a significant problem. The average recurrence rate is 15–20 %. The recurrent lesions, possibly secondary to inadequate excision or multicentricity, usually become apparent within the first year after surgery. In instances of inoperable recurrence or where clear margins are impossible to obtain, radiation therapy and/or chemotherapy can be used.

Although MNTI is an aggressive benign tumor, malignant variants have been also reported, ranging from 1.5 % to 2.1 % of total MNTI. Metastatic spread of MNTI occurs infrequently, in less than 5 % of malignant cases. Management of these rare cases is different with poor prognosis.

In all cases of MNTI postoperative care by monitoring the patient with physical and radiographic examination at monthly intervals for the first postoperative year is obligatory. Reconstruction of the affected jaw may be challenging. Permanent reconstruction of the maxillary alveolus and missing dentition in some cases is delayed until the growth is completed, often in the teenage years. In the interim, transitional removable partial dentures may be necessary. The skills of an orthodontist, prosthodontist, oral surgeon, and/or dentist may be required, based on the extent of the missing structures, to correct any functional and cosmetic deformity.

Calcifying (GHOST CELL) odontogenic cyst

The calcifying odontogenic cyst, or Gorlin cyst, is not actually a cyst but rather a true neoplasm with cystic tendencies.The are rare with no age, sex, or location predilections (it can be found anywhere in the jaws). It is a benign neoplasm but may undergo a malignant transformation.

If is not discovered as an incidental finding on radiographs, the earliest clinical presentation is a localized swelling. If not treated, the tumor may become quite large.

On radiographs, the appearance is usually nondescript radiolucency but it may be multilocular or contain flecks of calcification. Occasionally roots of adjacent teeth are eroded.

Hystologically the lining of cystic areas consists of squamous epithelium with cuboidal or ameloblast-like basal cells. Calcifying odontogenic cyst appears somewhat similar to the ameloblastoma, with masses of keratinized squamous epithelial cells. However, these cells have no nuclei and are called ghost cells. The ghost cells typically calcify in patchy fashion, and where this keratin-like material comes into contact with connective tissue it excites a foreign body reaction. More simply, this lesion represents enamel epithelium that has a tendency to mature but is unable to form enamel. Thise epithelium is more mature than in ameloblastoma, and, accordingly, the lesion have less growth potential.

Treatment and Prognosis

Calcifying odontogenic cysts are surgically removed by simple enucleation and rarely recur after excision.

Calcifying epithelial odontogenic tumour

The calcifying epithelial odontogenic tumor is a benign infiltrative tumor. It is derived from the stratum intermedium and has a lower growth potential than ameloblastoma. No cases of malignant transformation are reported. This rare neoplasm can occur at any site in the upper or lower jaw but is most commonly found in the mandibular molar/premolar region. It causes painless expansion of the affected area and in 50 % of cases it is associated with an unerupted or impacted tooth. Radiographs show a radiolucency, which may be multiloculated, and there may be areas of radiodensity within the central area of the radiolucency. Demarcation of the tumour from normal bone is not always clear.

Treatment

The treatment of this lesion is complete surgical excision. Because the lesion is locally invasive into the surrounding bone it is treated by a localised resection with a small margin of normal bone around it to reduce the chance of recurrence. The average recurrence rate for calcifying epithelial odontogenic tumor is 4 %. The lesion is slow growing and requires long-term follow-up monitoring for recurrence (at least 5–10 years).

Ameloblastic fibroma

Ameloblastic fibroma is a true mixed tumor arising from a combination of 2 embryonic tissues (epithelial and mesenchymal). This tumour is important in the differential diagnosis of ameloblastoma.

The ameloblastic fibroma tends to affect young persons in the first two decades of life. The posterior mandible is the most common site of the tumor. Ameloblastic fibroma is benign and grows expansively rather than invading surrounding tissues. It is slow-growing and usually asymptomatic, but eventually expands the jaw. The malignant change of the tumor is possible, though very rare. Approximately 45 % of ameloblastic fibrosarcomas develop in the setting of a recurrent ameloblastic fibroma. Radiographically, either a unilocular or multilocular lesion is observed most often in the posterior mandible. The radiographic appearance is identical to that of unicystic ameloblastoma, and both lesions should be differentially by diagnosed because they affect similar age groups and have similar clinical and radiographic appearances. Hystologicaly tumor is formed by both epithelium and connective tissue. The epithelial component of this lesion is almost identical to that of ameloblastoma. It consists of ameloblast-like or cuboidal cells surrounding others resembling stellate reticulum or more compact epithelium. The epithelium is sharply circumscribed by a basal membrane and forms islands in a loose but cellular, fibromyxoid connective tissue, which resembles the immature dentine papilla. It is a immature, cellular, homogenous connective tissue without much dense collagen. The epithelial and connective tissue components grow together inside a capsule.

Treatment and Prognosis

Ameloblastic fibromas do not infiltrate bone and separate readily from their bony walls. It is effectively treated by an enucleation and curettage surgery. But, if the tumor enucleation is incomplete, recurrence follows. Although recurrence is rare under the circumstances, resection should be reserved for recurrent lesions.

Odontogenic myxoma

The odontogenic myxoma is an uncommon benign infiltrative lesion of the jaws, which derive from dental ectomesenchyme.

These tumors are slow growing with a potential for aggressive behavior and a high recurrence rate after subtherapeutic removal. They occur over a wide age range, but most frequently in the second and third decades of life.

Clinically, young people are predominantly affected. Although the tumor can occur anywhere in the jaws, there is a slight predilection for the posterior mandible. If odontogenic myxoma is left untreated, it is invasive and destructive. The tumour gives rise to a fusiform swelling, erode bone and enlarge to form multilocular, radiolucent regions with scalloped margins or a soap-bubble appearance that can be very difficult to differentiate from other multilocular lesions such as ameloblastoma or odontogenic keratocysts. It may displace or cause root resorption of teeth in the area of the tumor. Although not pathognomonic of the odontogenic myxoma, the radiolucent defect may contain thin wispy trabeculae of residual bone, which are often arranged at right angles to one another in a “stepladder” pattern.

Histologically odontogenic myxoma resembles the dental papilla of the developing tooth. Histologically, the tumor is composed of haphazardly arranged stellate, spindle-shaped, and round cells in an abundant loose myxoid stroma that contains only a few collagen fibrils. The margins of the tumour are illdefined and peripheral bone is progressively resorbed. In some patients the tumor may have a greater tendency to form collagen fibers; such lesions are designated fibromyxomas.

Treatment and Prognosis

Odontogenic myxomas should be treated with resection with 1.0 cm bony linear margins as confirmed with a specimen radiograph. These tumors are not encapsulated and can infiltrate widely the surrounding bone such that complete removal by curettage is nearly impossible. Recurrences occur although with somewhat less frequency than with ameloblastoma.

Tumours and dysplasias of cementum

Cementoblastoma

Cementoblastoma is a true neoplasm of cementum neoplasm of cementum. Cementoblastoma is a benign neoplasm which forms a mass of cementum-like tissue as an irregular or rounded mass attached to the root of a tooth, usually a mandibular first molar. The lesion is usually asymptomatic, though occasionally the associated tooth may be slightly sensitive to percussion.

They are slow-growing and the jaw is not usually expanded. The tumor only rarely causes gross bony swelling and pain.

Radiographically, there is typically an opaque sunburst mass attached to the apex of a tooth with a thin radiolucent margin. The lession may be rounded or irregular in shape. Resorption of related roots is common, but the tooth remains vital (Fig. 13.62).

Fig. 13.62. Cementoblastoma from the 44 and 47 teeth

The tumor should be differenciated from sclerotizing (condensing) osteitis, a common lesion resulting from low-grade periapical irritation that stimulates bone growth. Although the most usual location for this lesions is the same, condensing osteitis does not obscure the periodontal ligament space and tends to be more irregular in outline.

Hystologically cementoblastoma consists of plump cementoblasts separated by cemental partitions. Cells are therefore enclosed within the cementum, and in the irregular spaces are many osteoclasts and osteoblast-like cells. The tumor is surrounded by a broad zone of unmineralised tissue and a connective tissue capsule.

Treatment. Removal of attached tooth and tumor is the method of treatment. Cementoblastomas are benign, and, if completely excised and the tooth extracted, there are no recurrences. Incomplete removal leads to continued growth.

Cemento-osseous displasias

Lesions formerly categorised as cementomas consists a group of the tumor like lesions which are now categorized as cemento-osseous displasias.

They are non-neoplastic proliferations originated from cementum and periodontal ligament origin. In this condition there is a disordered production of bone and cementum-like tissue in the jaws. They may occur singly or may affect many teeth in the dentition. Most of them are asymptomatic and are usually diagnosed by radiographic appearance. In the early stages they cause radiolucency, which later mineralises into cement-like tissue. The teeth affected are vital throughout this process.

There are three forms of cement-osseus displasias including periapical, focal, florid osseous dysplasias, and familial gigantiform cementoma, which are probably variants of the same pathologic process differentiated only by clinical and radiographic features. Histologically the three types of cemento-osseous dysplasia are indistinguishable, showing new woven bone trabeculae and/or zones of cementum-like material, which often blend into the cortical bone. A fibrous tissue stroma is also present with a very little inflammatory component. The etiology of these lesions remains unclean, but local trauma may play some role.

Periapical Cemento-osseous Dysplasia. Periapical cemento-osseous dysplasia presents as circumscribed lesions in periapical areas associated with vital teeth. Anterior mandible is the most common localization. Radiographically the lesions can be radiolucent, of mixed density, or radiopaque, depending on their stage of development.

Focal Cemento-osseous Dysplasia. Lesions of focal cemento-osseous dysplasia have a predilection for middle-aged females and present as nonexpansile radiolucencies with associated opacities, often in edentulous areas of the mandible. They frequently occur in sites of previous dental extractions and may represent some type of abnormal healing following dental extraction. Since they are usually asymptomatic, cases are often noted on routine panoramic radiographs. They are normally well circumscribed and rarely exceed 2 cm.

Florid cemento-osseous dysplasia presents as a painless nonexpansile lesion often involving two or more

Jaw quadrants. Radiographically, florid cemento-osseous dysplasia appears as multiple radiopaque, somewhat irregular lobular masses without a radiolucent border, located in tooth-bearing areas, wich can be mistaken for chronic osteomyelitis. Radiographically it appears as confluent radiopaque masses in. Lesions may be associated with superimposed infection and osteomyelitis, and have also been associated with idiopathic bone cysts. Histologically they have an unencapsulated proliferation of cellular fibrous tissue with trabeculae or woven bone and calcification. More mature lesions may become acellular and avascular with coalescent sclerotic bone masses. Many patients are partially or totally edentulous when the condition is first discovered. Therefore of dysplasia is usually asymptomatic unless they become infected, but can expand the jaw. Cortical expansion in this cases is usually of limited degree.

Familial Gigantiform Cementoma. Familial gigantiform cementoma represents a rare autosomal dominant variant of osseous dysplasia usually involving multiple quadrants with variably expansile lesions, often in the anterior mandible (Fig. 13.63).

Fig. 13.63. Familial gigantiform cementoma of the mandible (by H.O. Sedano)

This particular form of osseous dysplasia has no racial predilection. The lesions often evolve during childhood and can grow rapidly. Treatment is usually surgical and symptomatic and is limited to cosmetic recontouring.

Ossifying Fibroma

Ossifying fibroma (cemento-ossifying fibroma) usually presents as a well-demarcated mixed radiolucency/radiopacity with smooth and often sclerotic borders. The lesions are usually solitary and most commonly occur in the mandible. Histologically they contain a relatively avascular cellular fibrous stroma with reticular bone trabeculae and cementum-like zones.

The ossifying fibroma is probably a true neoplasm wich occurs usually in the third and early in the fourth decades. Growth rates of this tumor are variable.

The treatment is surgical: the lesions are easily enucleated at surgery, although there is recurrence, the rate of which varies from 10 to 50 %. When present in the craniofacial complex, treatment may have to be more aggressive to protect the vital structures and in some cases include the partial resection of the affected bone.

Benign non-odontogenic tumours of the jaws

Almost any type of bone tumour can arise in the jaws but most of them are considerably more common in other parts of the skeleton. However, neoplasms derived from bone itself are relatively infrequent in the jaws. Benign nonodontogenic lesions of the jaws represent a mixed group of tumors, which in many cases are difficult to classify (Table 13.3). The main types of them are fibro-osseous displasia, osteoblastoma and osteoid osteoma, benign tumors of bone-forming cells,synovial chondromatosis and osteochondroma, lesions containing giant cells,vascular malformations, Langerhans cell histiocytosis, nonodontogenic cysts ofthe jaws,neurogenic tumors, Paget’s disease, and tori.

Osteoma

Osteomas are benign tumors consisting of mature compact or cancellous bone. They may arise on the surface of bone (periosteal osteomas) or centrally within the bone (endosteal osteomas). They are often discovered in the form of a painless hard swelling or as asymptomatic radiopacities.

Osteomas are discovered in all age groups, more commonly during the fifth decade of life. Males appear to be affected more frequently than females (Fig. 13.64; 13.65).

Fig. 13.64. Osteoma of the frontal bone

Fig. 13.65. Osteoma of the mandible condylar with lateral displacement of the jaw

Periosteal osteomas usually present as asymptomatic slow-growing bony masses. Endosteal osteomas are usually asymptomatic and are noted on routine radiographs. Radiographically they appear as well-circumscribed round or oval-shaped radiodense masses (Fig. 13.66).

Fig. 13.66. CT scanning, frontal plane (the same patient)

In cancellous osteomas bone trabeculae with irregular orientation are seen. Histologically they consist of either dense compact bone with sparse marrow spaces or lamellar trabeculae of cancellous bone with fibrofatty marrow spaces. Osteoblastic activity is often predominant.

Gardner’s syndrome is an autosomal dominant condition in which patients have intestinal polyposis, multiple osteomas (usually endosteal), fibromas of the skin, epidermal cysts, impacted teeth, and odontomas. The condition is important because the syndrome exhibits multiple intestinal polyposis and these polyps have the potential for malignant transformation. Urgent referral to a gastroenterologist is therefore needed.

The associated osteomas are often found in the jaws, particularly in the angle region of the mandible, as well as the facial bones and long bones. It has been suggested that any patient with multiple mandibular osteomas should be investigated for the possibility of Gardner’s syndrome. If the diagnosis is confirmed, a prophylactic colonectomy should be performed.

Treatment of osteomas is surgical excision. Asymptomatic cases may be followed up clinically and radiographically without treatment. If the swelling is interfering with function, it can be surgically removed. Following excision, recurrences are very rare. 3-D reconstruction and stereolithographical model using CT scanning can be used for planning of the operation (Fig. 13.67).

Fig. 13.67. 3-D reconstruction and stereolithographical model using CT scanning (the same patient)

Torus palatinus

The palatine torus appears as a bony hard swelling along the midline of the palate. It can be discrete or may be large and lobular. It usually occurs in the second or third decade of life, and has a tendency to grow throughout life. If torus palatinus is large, it may require surgical removal because of its interference either with speech or feeding or with prosthetic reconstruction. The common surgical approach is via a double Y-shaped incision and subsequent bone removal. The bone is virtually always solid cortical bone and is actually fairly difficult to remove. The recommended technique is to make a number of vertical cuts in the bone with a fissure bur. Then the intervening ridges of bone can be snapped off and a final smoothing of the residual bone carried out, taking care not to perforate through into the nasal cavity. It may be advisable to insert a dressing plate after the procedure to prevent excessive hematoma formation and possible recurrence of the torus.

Torus mandibularis

Mandibular tori are bony exophytic growths that present on the lingual aspect of the mandible opposite the bicuspids or premolars. In most of the cases they are bilateral. They manifest in the second or third decade of life and tend to grow with age. Larger tori may require surgical removal because they interfere with tongue positioning, speech, and prosthetic reconstruction, as well as with oral hygiene around the lower posterior teeth (Fig. 13.68).

Fig. 13.68. Mandibular tori

If surgical removal is required, it is carried out via an extensive gingival margin incision with a possible lingual releasing incision, followed by removal of the bone. This is carried out by making a number of vertical cuts with a fissure bur, and then snapping off the intervening ridges of bone with a periosteal elevator. The residual irregularities are then smoothed with a larger bur. If mandibular tori are on a fairly narrow neck they can be removed totally by mallet and chisel. Recurrence of tori after surgical excision is not typical.

Osteoblastoma and osteoid osteoma

Osteoblastoma and osteoid osteoma are benign tumors arising from the bone tissue. They considered as the variants of the same neoplastic lesion.

The osteoblastoma represents large and more aggressive tumor which occurs in the maxilla-facial area very rarely. In the head and neck, the mandible is the most common site. Clinically osteoblastoma grows rapidly and the main clinical sign is pain, which is generally localized to the lesion itself. Most cases of osteoblastoma occur in the second decade of life. Males appear to be affected more commonly than females.

Radiographic features are variable, usually consisting of a combination of radiolucency and radiopacity. The lesions dimensions are more than 2 cm. They are well circumscribed radiographically with a thin radiolucency surrounding the variably calcified contents.

The histologic appearance shows irregular trabeculae of osteoid and immature bone within a predominantly vascular stromal network. There are various degrees of calcification present. Stromal cells are generally small and slender.

The osteoid osteoma represents a smaller version of the osteoblastoma. It is normally less than 2 cm in diameter clinically and radiographically. It occurs in the second and third decades of life with a male predominance. Pain is also the major clinical feature. Classically, the pain is worse at night and is relieved by acetylsalicylic acid. If the lesion is located near the cortex, it may produce a localized tender swelling. Radiographically the lesion again shows a well defined mixed radiolucency/radiopacity with a small radiolucent rim around the lesion, which is walled by sclerotic bone.

Histologically it resembles the osteoblastoma with a rich vascular stroma, trabeculae of osteoid and immature bone. The bone is rimmed by layers of active osteoblasts. Histologically it is impossible to differentiate it from the osteoblastoma.

Treatment of the osteoblastoma and osteoid-osteoma is surgical excision either with curettage or local resection. Recurrences are rare but have been reported. In these cases more aggressive treatment such as en bloc resection is often necessary.

Chondroma

Chondroma is a benign tumor of mature cartilage. The occurrence of these lesions in the jaws is extremely rare. Most cases appear in the mandibular condyle or anterior maxilla, suggesting that these lesions may arise from cartilaginous remnants. The chondroma presents as a painless slowly progressive swelling, which may result in mucosal ulceration. The gender distribution is equal, and most tumors occur under the age of 50 years. Radiographically they present as irregular radiolucent lesions, although foci of calcification may occasionally be present. Resorption of tooth roots has been reported. Histologically, chondromas consist of hyaline cartilage, but the cells are irregular in size and distribution. Calcification or ossification may develop.

Chondromas of the maxillofacial area are often misdiagnosed with low-grade chondrosarcomas. They also have a high potential to malignant transformation. Because of this the method of choice in treatment of maxilla-facial chondromas is en-block resection of the affected bone. Excision should include a wide margin of normal tissue to ensure the radical removal of the neoplastic tissue.

Giant Cell Tumor and Central giant-cell granuloma

The giant cell tumor is the tumor commonly found in the long bones and its manifestation in the jaws is comparably rare. This lesion is an aggressive tumor originating from the monocitic and macrophage system. Histologically it is very similar to the central giant cell granuloma, except that the giant cells are larger with more nuclei, and they are more evenly spread throughout the lesion and not as focally placed as in the central giant cell granuloma.

Clinically anterior mandible and upper premolar regions are commonly affected. In the mandible, the presence of a tumour may give rise to expansion of the outer and/or the inner cortical plates of the bone (Fig. 13.69; 13.70).

Fig. 13.69. The giant cell tumor of the mandible

Fig. 13.70. The giant cell tumor (lytic form) of the mandible

In the maxilla the cortical expansion is less significant. There may be mobility of related teeth and resorption of their roots. Occasionally, the soft tissue of the giant cell tumor may grow through the upper border of the alveolar process and appear as a dark red or mass under the oral mucosa. The lesion is usually non-painful but may be tender to palpation (Fig. 13.71).

Fig. 13.71. The giant cell tumor of the right maxilla (CT scanning)

Central giant-cell granuloma is an endosteally originating resorptive process causing a cyst-like lesion filled with a very vascular fibrous tissue rich in multinucleated giant cells. Its clinical and radiographical appearance in the jaws may be exactly the same as in the giant cell tumour. The diagnosis is therefore made on histological grounds.

Treatment of the giant cell tumor and central giant cell granuloma is usually performed by local curettage. However the recurrence rate after local curettage is high, and the appropriate treatment is in doubt. In the same cases the bony walls of the cavity are frozen with liquid nitrogen after curettage in an attempt to prevent the recurrence.

Some authorities advocate local resections in cases of large or recurrent lesions.

Hemangioma of the jaws

Hemangeomas and vascular malformations can occur anywhere in the body including jaw bones. True hemangioma is a neoplasm of vascular endothelium and is normally present at birth, often enlarges, and then frequently involutes. The vascular malformation generally is not present at birth, appears later, and does not involute. Vascular malformations can take a number of forms. The most practical classification is to divide them into high-flow and low-flow vascular malformations. The high-flow vascular malformations are either arterial lesions or arteriovenous fistulas. The low-flow malformations are mainly venous in nature. The clinical significance of a vascular malformation is that a central high-flow vascular malformation can cause torrential hemorrhage when surgical intervention ensues. This has been fatal on occasion.

Many of these lesions are asymptomatic and may even be difficult to detect preoperatively on radiographs. If there is a clinical presentation, it is often a slow-growing asymmetric expansile lesion of the jaw, and if it is high flow, it may be associated with a bruit. Radiographically jaw haemangeoma may appear as an irregular poorly defined soap bubble-type lesion, which may cause resorption of the roots of teeth and does not normally cause nerve involvement.

Diagnosis is usually confirmed by computed tomography. In some cases a diagnostic needle aspiration can be carried out preoperatively. If bright red blood under pressure is encountered it is patognomic to high-flow vascular malformations.

Since the radiographic and clinical appearances of a vascular malformation are not diagnostic, the differential diagnosis normally includes a number of odontogenic and nonodontogenic lesions, including the central giant cell granuloma, the aneurysmal bone cyst, ameloblastoma, odontogenic keratocyst, and odontogenic myxoma. All of these lesions should undergo needle aspiration prior to biopsy or surgical treatment to rule out a highflow vascular malformation. When a vascular malformation is suspected or diagnosed, selective angiography is normally performed via a femoral approach.

Treatment

If a vascular tumor of jaw is diagnosed, treatment includes preoperative embolization followed by wide resective surgery. The embolization can involve a number of materials, including muscle, polyvinyl, pellets, and platinum coils, which are inserted via the angiography catheter or on direct puncture. On entering the lesion they unwind and expand.

Postembolization angiography carried out immediately after the embolization normally shows a diminution in blood flow to the lesion. However, because of the powerful angiogenic effect of these lesions (probably by production of angiogenesis growth factor), reestablishment of smaller collateral vessels usually occurs within a few days, and it is often impossible to reembolize these smaller collateral vessels. Therefore, definitive surgery should be carried out within a small number of days after embolization. Definitive surgery normally takes the form of resection under hypotensive anesthesia with adequate resuscitative measures available. Following resection appropriate reconstruction can be performed. Other approaches such as injection of a variety of substances into the lesion including glue, fibrin gel, and platinum coils, for example, have been attempted.

Neurogenic tumors of the jaws

Neurilemmoma (schwannoma) is a benign tumor of the nerve sheath. Although usually found in the soft tissues, it can occur in bone, where it usually exists as a well-defined radiolucency. Histologically lesions are well encapsulated and predominantly of spindle cells showing either an Antoni A (spindle cells arranged in palisaded whorls and waves) or Antoni B (spindle cells with a more haphazard appearance). Following biopsy to confirm the diagnosis, treatment usually consists of surgical excision. Recurrences are rare.

Neurofibroma

Neurofibromas derived from the fibrous elements of the neural sheath and may exist as solitary lesions or as part of generalized neurofibromatosis or von Recklinghausen’s disease. Although most commonly reported in soft tissues, neurofibromas occur in bone affecting most commonly in the inferior alveolar nerve, where they appear as a fusiform swelling in continuity with the inferior alveolar canal. Other bone changes associated with neurofibromatosis can include cortical erosion from adjacent soft tissue lesions or medullary resorption from interosseous lesions. In cases associated with the inferior alveolar nerve, pain or paresthesia can result.

The normally recommended treatment following biopsy is localized excision. The lesions are often vascular, and extensive blood loss has been reported from surgical management of mandibular lesions.

Tumor-like lesions of the jaws

Hyperparathyroidism

Hyperparathyroidism is a pathological condition associated with overproduction of parathormone. Primary is caused by hyperplasia or adenoma of the parathyroid glands. Secondary hyperparathyroidism is due to the conditions that reduce calcium levels in the blood, such as chronic renal disease. Increased levels of parathormone mobilise calcium from the bony skeleton and raises the plasma calcium level.

Post-menopausal women are mainly affected. The major symptoms result from renal damage which leads formation of renal calculi, hypertension or other cardiovascular disease. In the bone, however, where the jaws can be affected, cyst-like spaces known as “brown tumours” may develop. The bone in these tumours is resorbed by vascular fibrous tissue with multinucleated giant cells in profusion.

The mandible is more commonly affected by such lesions than the maxilla. In the mandible, the presence of a brown tumour may give rise to expansion of the outer and/or the inner cortical plates of bone. Occasionally, the soft tissue of the brown tumour may grow through the upper border of the alveolar process and appear as a dark red or purplecoloured mass under the oral mucosa. The lesion is usually non-painful but may be tender to palpation.

Histologically, the cyst-like areas are foci of osteoclasts in a highly vascular stroma. Extensive haemosiderin deposits cause the lesion to appear as a brown tumour.

Radiographically, the main effects are thinning of bone trabeculae, subperiosteal resorption of the bone of the fingers and resorplion of the terminal phalangeal tufts. In severe disease, a well circumscribed radiolucent cyst-like areas often with a multiloculated appearance are a typical but rare finding. Alveolar bone may also be resorbed but reforms with treatment. The out-line may have a scalloped margin lamina dura surrounding the cyst is less defined than is normally found in a true cystic lesion.

In patients with hyperparathyroidism there are characteristic changes in blood chemistry and multifocal involvement of different bones. Biochemical findings in primary hyperparathyroidism include raised plasma calcium (2,8 mmol/1 or more), low plasma phosphorus (less than 0,8 mmol/1), elevated levels of parathormone in plasma, raised plasma alkaline phosphatase (over 100 IU/1). Blood chemistry examination is essential in patients same histological picture of osteoclastic proliferation. Occasionally, bone lesions cause pathological fractures. The increased excretion of calcium leads ultimately to renal calcmosis or stone formation and renal damage.

Treatment and Prognosis

Primary hyperparathyroidism is normally treated surgically by removal of an adenoma of the parathyroid gland. The bone lesions usually resolve spontaneously following this surgery. For secondary hyperparathyroidism the renal failure should be treated if possible. Bone lesions may respond to oral administration of vitamin D, whose metabolism is abnormal as a result of the renal disease.

Paget’s disease of bone (osteitis deformans)

Paget`s desease is characterized by irregular resorption of bone with subsequent redeposition which disrupt normal bony architecture. It is a slowly progressive bone condition of unknown etiology, predominantly affecting males over the age of 50 years, which causes bone distortion and weakening. Bone resorption and replacement becomes rapid, irregular, exaggerated and purposeless. The changes progress erratically but the ultimate result is thickening of affected bones without localised swellings.

During the resorptive phases, areas of bone may be severely resorbed, leading to distortion under normal weight bearing function. There may be pain in the bones, large vascular regions in the medullary spaces. In the formative phase, occlusion of bony foramina can prove a problem and the relative avascularity following redeposition of bone can then make infection in bone more difficult to manage. Since closely adjacent parts of the bone may show different stages of the disease, a common result is the patchy area of osteoporosis and of sclerosis.

The cause of the disease is unknown. One of the possible mechanisms is the delayed or slow reaction to a myxovirus or other virus stimulus in both osteoblasts and osteoclasts. A genetic factor may also be involved.

Bones most frequently affected are sacrum, spine, skull, femora and pelvis. Vertebral column and lower limbs in severe cases are unable to deal with the forces and deform as a result. The disease may be widespread and is usually symmetrical, but sometimes a single bone is affected.

In the uncommon severe form, the main features are an enlarged head, thickening of the weight-bearing long bones, and tenderness or aching pain which can be severe and almost intractable. The vault of the skull is more often affected than the facial skeleton, and the maxilla considerably more frequently than the mandible.

When the jaws are affected, the alveolar process becomes symmetrically and grossly enlarged. The classic presentation used to be a patient whose hat no longer fitted correctly, or in whom false teeth, particularly the maxillary denture, did not fit owing to bone swelling. There may also be gross and irregular hypercementosis of teeth, which may become fused to sclerotic areas of the bone (Fig. 13.72; 13.73). Attempts to extract affected teeth may succeed only by tearing away a large mass of bone. Severe bleeding or osteomyelitis of ischaemic bone may follow. Narrowing of foramina can occasionally cause cranial nerve deficits and severe headaches.

Fig. 13.72. Pagets desease (by H. O. Sedano)

Fig. 13.73. Pagets desease, irregular hypercementosis of teeth

Sarcomatous change has been reported in 5 to 15 % of patients with Paget’s disease, which should be considered a premalignant condition.

The main radiographic features are lower density of the bone in the early stages and sclerosis in the later stages. Radiographs show patchy areas of radiolucency interspersed with radio-opaque density. The term “cotton wool” is often used to describe these changes in the skull and maxilla of affected patients. Hypercementosisi observed around the roots of teeth, as well as loss of lamina dura and obliteration of the periodontal ligament space. Root resorption has also been noted.

The main histological changes are the irregular pattern of reversal lines, many osteoblasts and osteoclasts (often abnormally large), fibrosis of the marrow spaces and increased vascularity. Bone biopsy show irregular areas of resorption or evidence of previous resorption in the form of reversal lines. These are heavily staining haematoxilin lines, which denote the boundary of previous resorptive activity. Their irregular pattern characteristically produces a mosaic appearance in the bone. In the late stages, affected bones are thick, the cortex and medulla are obliterated and the whole bone is spongy in texture.

Blood samples may show very high levels of alkaline phosphatase that may reach 700 u/1with normal values for calcium and phosphate.

Treatment and Prognosis

Treatment of the Pagets disease is both systemic and local. Systemic treatment includes the usage of calcitonin and bisphosphonates to inhibit bone resorption. Calcitonin can be taken either subcutaneously or by nasal spray and is more effective for reducing bone pain and osteolysis, but can cause nausea and an unpleasant taste. Calcitonin is also given preoperatively to reduce bleeding from the highly vascular bone and may help to relieve cranial nerve deficits.

Bisphosphonates can be given orally or by injection. They have a direct effect on hydroxyapatite crystals, which make the bone less receptive to resorptive activity and hence reduce the rate of turnover. Treatment causes stabilization of the bone and a lowering of the raised alkaline phosphatase levels.

Local treatment is directed to cosmetic and/or functional recontouring of bone. It should be noted that the bone of Paget’s disease is often vascular, and bleeding during recontouring can be extensive. However, healing is often delayed owing to the intervening sclerotic areas of bone.

Dental problems may be encountered in the form of excessive bleeding if the area of the jaw affected is undergoing active resorption, and infection can be a complication where the bone has reformed and become relatively avascular. Added to these problems may be hyper cementosis of the roots resulting in large-rooted teeth that may be difficult to extract conventionally. Prophylactic antibiotics are often prescribed for extractions if the bone is sclerotic.

Fibrous dysplasia

Fibrous dysplasia is a developmental hamartomatous disease of unknown etiology. It may represent developmental arrest in a benign fibro-osseous proliferation that lacks the ability to fully differentiate. In fibrous dysplasia a replacement of normal bone by an immature bone with extensive vascular fibrous tissue elements is present. In majority of cases this condition manifests in children. The abnormality may affect many bones (polyostotic) or one bone (monostotic), and the maxilla is far more commonly affected than the mandible. Two rare variants are also identified, one being cherubism and the other Albright’s syndrome, which is a form of polyostotic fibrous dysplasia with additional features of skin pigmentation and precocious puberty in females. Fibrous dysplasia is usually self-limiting and tends to “burn out” on completion of skeletal growth (Fig. 13.74). It can, however, cause quite marked disurement in severe cases and in the polyostotic form can encroach on bony foramina leading to compression of nerves.

Fig. 13.74. Fibrous dysplasia of the maxilla and the mandible (diffusive form)

The jaws are commonly associated with all forms of fibrous dysplasia. In the jaws the onset is usually during the first and second decades, and it produces painless swelling of the involved bones.

In the monostotic form, the usual presentation is a painless enlargement of the jaw on the affected side. Buccal and palatal aspects of the alveolar bone may be enlarged and expanded and this may cause spacing between the teeth compared to the unaffected side. The occlusion, however, is seldom significantly affected other than the spacing and the teeth erupt normally and are not unduly mobile. The overgrowth can usually be seen as a facial asymmetry with fullness of the cheekbone and nasolabial fold.

Classically, the radiographic appearance shows a weak opacity without clearly defined borders and a fine orange-peel texture and an eggshell-thin cortex of expanded bone. The degree of radiopacity depends on the amount of lesional bone which may give a predominantly radiolucent or more sclerotic appearance. The key feature is that the margins merge imperceptibly with the surrounding normal bone (Fig. 13.75).

Fig. 13.75. Fibrous dysplasia, deformation of the alveolar ridges, adentia, displacement of the teeth (the same patient)

In its cranio-facial form the maxilla, zygoma, sphenoid, frontal bones, nasal bones, and base of the skull can be involved. Expansion can cause compression of nerves and blood vessels. The optic canal can be narrowed by fibrous dysplasia, although it seems unlikely that any associated vision loss can be relieved by orbital decompression.

Typically lesions undergo periods of activity and periods of quiescence. When they are active, they are often symptomatic in that the patient may perceive a throbbing or discomfort, the swelling increases, and the lesions appear hot on a bone scan and can mimic osteomyelitis. In a quiescent phase they may be totally asymptomatic.

The diagnosis is normally made on three grounds: the age of the patient and clinical features described; the radiographic appearance and the histopathology. Radiographs of the affected bone or bones typically show a granular appearance that has been likened to ground glass. There is an obvious excess of this abnormal bone and it merges with the normal appearance of bone without a clearly defined separation.

A bone biopsy will generally show loose cellular fibrous tissue containing slender trabeculae of woven bone of variable shape which merge imperceptibly into surrounding normal bone. Osteoblasts are scattered throughout the substance of the trabeculae rather than surrounding them. Some lamellar bone or calcified spherules and occasional loose foci of giant cells can also be seen.

Bone biochemistry is usually unhelpful, with calcium, phosphate and alkaline phosphatase levels within normal limits. The alkaline phosphatase level, which is a measure of osteoblastic bone formative activity, may be raised if the sample is taken during an active growth phase of the child, and its relevance is therefore almost impossible to determine.

Although not normally recognized as a premalignant lesion, sarcomatous change has been noted in fibrous dysplasia. Early cases appear to have been associated with the use of radiation therapy for treatment, but cases of spontaneous sarcomatous degeneration have been noted. Additionally, some cases have been difficult to diagnose and may have represented a low-grade osteosarcoma from the outset. For operation planning CT scanning, 3 D reconstruction of the facial scull’s bones is used frequently (Fig. 13.76).

Fig. 13.76. CT scanning, 3-D reconstruction of the facial scull’s bones

Albright’s syndrome comprises polyostotic fibrous dysplasia, skin pigmentation and sexual precocity. Polyostotic fibrous dysplasia involves the head and neck region in up to 50 % of cases. A jaw lesion may then be the most conspicuous feature and polystotic disease may not be suspected initially. In a young girl in particular, investigation for other skeletal lesions and pigmentation may therefore be indicated. Skin pigmentation consists of brownish macules which frequently overlie affected bones and appear especially on the back of the neck, trunk, buttocks, or thighs, but hardly ever on the oral mucosa.

Treatment

The disease is self-limiting, but grossly disfiguring lesions may need to be excised. If the lesions are asymptomatic, a biopsy diagnosis alone may be adequate without carrying out any definitive treatment. Surgical treatment should be also limited during an active phase because the lesions are vascular and can bleed quite profusely. Treatment is best reserved for quiescent periods, at which time cosmetic recontouring is the normal treatment of choice. In some cases more aggressive surgical procedures including mandibular and maxillary resections are used.

Cherubism

Cherubism is a familial genetically dominant condition regarded as a form of fibrous dysplasia. It is characterised by an increased width and fullness of the angles of mandible bilaterally (Fig. 13.77). The bone itself is immature in these regions with areas of vascular fibrous tissue. Affected family members often have multiple lesions mainly affecting the facial bones. Because of the involvement of the maxilla and orbital floor, the face has a rounded appearance and the eyes tend to look upward, giving the patient a cherubic appearance. The genetic defect in this condition has been identified on chromosome 4p16.3. Like other genetic diseases, many non-familial cases are seen as a result of new mutations.

Fig. 13.77. Cherubism (child 6 years old)

Expression is variable, with some patients having subclinical lesions discovered only on radiographs and some having extensive and clinically obvious lesions.

The onset is typically between the ages of 6 months to 7 years, but rarely is delayed until late teenage or after puberty. Typically, symmetrical swellings are noticed at the age of 2 to 4 years in the region of the angles of the mandibles and, in severe cases, in the maxillae. The symmetrical mandibular swellings give the face an excessively chubby appearance. The alveolar ridges are expanded and the mandibular swellings may sometimes be so gross lingually as to interfere with speech, swallowing or even breathing, but the rapidity of progress is variable. Expansion of the maxillae may also cause stretching of the skin and some retraction of the lower lids. Maxillary involvement can also cause the palate to assume an inverted V shape.

Teeth are often displaced, and in active periods the lesions are extremely vascular. Despite lack of inflammation, there is frequently cervical lymphadenopathy, due to reactive hyperplasia and fibrosis.

This is typically seen in the early stages and may completely subside by puberty.

Radiographically the lesions appear honeycombed and can be very extensive. The angles of the mandible are particularly involved but the process extends towards the coronoid notch and sometimes also forwards along the body. The lesions simulate multilocular cysts as a result of fine bony septa extending between the soft tissue masses. Panoramic radiographs help to determine the extent of the disease but it is more clearly visualised by CT scanning.

Histologically the lesions are very similar to central giant cell granuloma, with focal accumulations of giant cells in a spindle cell matrix. Perivascular cuffing is often present, and in some cases can be used to differentiate the two lesions.

Treatment of cherubism is usually conservative and expectant and into the teenage years is devoted to trying to aid eruption of the teeth, which is often abnormal. Later it is directed toward cosmetic recontouring of the affected bones. The lesions normally become less active and less vascular toward the end of the second decade and into the third decade, and it is at this time that most cosmetic remodeling is carried out. If disfigurement is severe the lesions respond to curettage or to paring down of excessive tissue but, in the early stages the recurrence rate is high.

Langerhans cell histiocytosis

Langerhans cell histiocytosis is the term currently employed for what was previously known as histiocytosis X, and before that the three separate conditions Letterer – Siwe disease, Hand – Schuller – Christian disease, and eosinophilic granuloma. Letterer – Siwe disease represent the acute disseminated form of Langerhans cell histiocytosis, whereas Hand – Schuller – Christian disease represents the chronic disseminated form, and eosinophilic granuloma represents the chronic localized form.

The cells of origin of this disease have now been identified as the Langerhans cells, which are dendritic cells in the skin and mucosa that have a macrophage-like function. At the present time what causes these cells to proliferate in a clonal fashion with phenotypic evidence ofactivation and give rise to Langerhans cell disease is unknown. Some studies suggested that it may have some of the properties of a tumor or have a viral etiology.

The acute disseminated form usually affects young children. It is multisystem in nature, affecting the skin, bones, and internal organs (especially lungs and liver), and is frequently fatal. Treatment is chemotherapy.

The chronic disseminated form of the disease is classically associated with a triad of punched-out bone lesions (often affecting the skull and jaws), diabetes insipidus (owing to posterior pituitary involvement), and exophthalmos (owing to deposits in the posterior orbit). This normally affects an older age group, often in the second and third decades but sometimes much older.

The treatment of the chronic disseminated form of the disease is variable. and for well-circumscribed lesions can consist of local curettage. However, for more aggressive forms, chemotherapy is frequently employed as well. Low-dose radiation therapy has also been used on isolated lesions, and it does remain one of the very few indications for low-dose radiation therapy.

The chronic localized form of the disease (eosinophilic granuloma) is commonly found in the jaws and usually shows as a well-defined radiolucency, often in the bicuspid region and more frequently in the mandible. The bone lesions often affect the jaws. Although they usually appear as fairly well-defined punched-out radiolucencies, they can also be less well defined and can affect the apices of the teeth only and lead to a possible differential diagnosis of periapical infection. A frequent aspect of presentation is loose teeth; radiographically they often appear as “floating teeth”. Treatment usually consists of aggressive local curettage, and the recurrence rate is low.

Chapter 14. Malignant tumors of the maxillofacial area and neck

Cancer means a malignant tumor of epithelial origin. Approximately 5 % of all malignant tumors fall on cancer of vermilion border and oral mucosa. The most frequently affected areas are red border of the lip (posterior area), tongue (lateral surface) and floor of the mouth. The majority of patients with cancer of vermilion border and oral mucosa are men at the age older than 40 years.

The majority of patients with cancer suffered previously from some of the diseases of oral mucosa and vermilion border called precancerous diseases. The reasons of their occurence are traumas, in particular chronic ones, smoking, betel and tobacco chewing, alcohol consumption. Traumas are considered to be external factor of cancerogenesis. Cancer is often associated with proliferative processes, benign tumors, chronic inflammatory diseases accompanied by erosions and chancres. Precancerous disease exists for a long time (from several months to decades), then it can transform into (not necessarily) cancer. Prompt diagnostics and treatment of precancerous diseases eliminates threat of cancer development or enables to undertake timely, more efficient and harmless treatment.

With respect to probability of malignization there are obligate and facultative pretumor processes. Obligate precancers cause cancer development in different periods if not treated in time. In the majority of cases they are cancer in situ from the very beginning. Facultative precancers cause cancer not always.

Classification of pretumor processes of oral mucosa

With high frequency of malignization (obligate): morbus Bowen.

With little frequency of malignization (facultative):

• verrucuos and erosive leukokeratosis;
• polypapilloma;
• erosive ulcerous and hyperkeratotic forms of erythema centrifugum and lichen acuminatus;
• postradial stomatitis.

Classification of pretumor processes of red border

With high frequency of malignization (obligate):

• verrucous precarcinoma;
• limited precancerous hyperkeratosis;
• abrasiva praecancerosa cheilitis Manganotti.

With little frequency of malignization (facultative):

• leukokeratosis;
• keratoacanthoma;
• cutaneous horn;
• papilloma with cornification;
• erosive ulcerous and hyperkeratotic forms of erythema centrifugum and lichen acuminatus;
• postradial cheilitis.

Morbus Bowen

Bowen was the first to describe this disease in 1912. From the very beginning it appears to be cancer in situ.

Clinical presentation. The affected area is as a rule single hyperemic bright red spot, smooth or with velutinate surface due to small papillary projections. The central area resembles leukokeratosis with pit-and-mount surface or lichen acuminatus with cornification focuses on hyperemic background. Due to atrophy of mucosa, the focus falls in slightly compare to surrounding areas, slightly bleeding erosions can appear on it. The affected area is from 1–2 mm to 5–6 cm, its contours are not smooth but rather distinct. Induration in its basis is not determined. If lesion is localized on the tongue, lingual papillae at affected area disappear. Regional lymph nodes are not palpable as a rule. Subjective sensations are minor but in cases of erosions tenderness can be present. Clinical presentation of Morbus Bowen on oral mucosa is not always apparent. The disease can manifest only by the small area of hyperemia or resemble leukokeratosis without evident inflammation. The disease may be present for indefinite time, in some cases invasive growth advances and traumatization accelerates this process, in other cases the disease remains at stage of cancer in situ. The diagnosis must be confirmed by histological study. Pathomorphologically morbus Bowen is characterized by signs of intraepithelial epidermoid cancer: polymorphism of spicular layer cells up to atypia, increase of mitosis number, its impairment, presence of giant cells, multinuclear cells, acanthosis, and in several cases hyperkeratosis and parakerathosis. The basal membrane and basal layer are preserved. There is small infiltration with lymphocytes and plasmocytes at the upper part of stroma.

Differential diagnostics includes leukoplacia, lichen acuminatus, chronic traumatic affection.

Praecancer verrucosus

It was described by A. L. Mashkilleison in 1965. It appears almost in all cases on the lower lip and resembles painless semiround node with verrucous surface 4–10 mm in diameter. The color of the node is from nearly normal coloring of vermilion border to stagnant red one. At the top the node is covered with hardly removable grey scaly crusts. The lesion is located on intact vermilion border but the signs of the small hyperemia may be present in some cases.

Histologically the signs of limited epithelium proliferation are revealed due to expansion of belemnold layer, in some cases hyperkeratosis and parakeratosis, polymorphism of cells of belemnold layer of different manifestation rate, even violent one. Basal membrane is preserved. Transfer into invasive cancer type appears quickly – in 1–2 months after beginning of disease. Differential diagnostics must be performed with papilloma and verruca. The diagnosis is confirmed by histological examination.

Hyperkeratosis praecancrosa circumscripta

The lesion is polygonal cornification locus not bigger than 2 mm. The affected area in majority of patients is covered with the mucous coat, often falls in slightly but it can be a little bit raised with flat surface covered with thin closely placed scaly crusts, which can not be removed by scraping. Palpation reveals superficial lamellar induration. Background changes are absent; this cancer type appears more rarely on the background of non-specific inflammation.

Histological examination reveals the limited acanthosis area, cells discomplement and polymorphism is often seen as well as hyperkeratosis on the surface. Differential diagnostics is carried out with leucoplasia and lichen acuminatus. Malignization occurs after some months or years.

Cheilitis abrasiva praecancrosa Manganotti

This type of precancerous lesions was identified and described by Manganotti in 1933. It occurs predominantly in men over 50 years. Traumas, insolation, herpes may cause the emergence of this disease.

Clinical presentation. Unlike low-grade limited or expanded chronic catarrhal inflammation of the lower lip one or rarely several red anabrosis with flat surface are seen. They can be sometimes covered with tight blood-tinged or serous crust, which is hard to remove. Anabrosis uncovered with scab tends to bleed. Induration at the base of the lesion is absent. Anabrosis can be hardly treated with ointments and applications of topical medications. Existing for a long time they can epithelize but then they appear again at the same or other areas. Histologically the deficiency of epithelium is observed as well as inflammatory infiltration in underlying connective tissue. Epithelium on the anabrosis edges is in the state of acanthosis or is atrophic. Epithelial bundles deviate deep into stroma. In some areas acanthocytes demonstrate different rate of discomplement and atypia. Cytological examination can reveal the signs of dyskariosis of epithelial cells, inflammatory elements but more often only inflammation. The process lasts from 1–2 months up to many years. If not treated it undergo malignization, which manifests clinically by induration of the anabrosis base and surrounded areas, emergence of papillary projections on the surface of anabrosis, its bleeding and cornification around the anabrosis. The diagnosis is confirmed by revelation of atypical cells in scrapes from the diseased area or by results of histological examination. The differential diagnostics must be performed with anabrosis forms of leukoplasia, lichen acuminatus, erythema centrifugum, vesicular fever, herpes iris, actinic cheilitis, herpetic anabrosis.

Treatment. It is necessary to remove properly all local irritators, and then oral cavity sanation must be executed including adequate prosthesis, smoking and consumption of irritating food must be forbidden, removal of insolation is also recommended. It is necessary to reveal and to treat accompanying diseases of other organs and systems. Vitamin A is prescribed intraoraly (solution of retinol acetate in oil 3.44 % or solution retinol palmitate in oil 5.5 %) 10 drops 2–3 times per day, as well as other polyvitamins. Applications with oil solution of vitamin A are prescribed topically, in case of baseline inflammation – ointments with corticosteroids and antibiotics. Nonsurgical therapy must not be carried out for more than 1 month. The best results are achieved by surgical removal of focus in the limits of healthy tissues. Only in case of Manganotti cheilitis the nonoperative treatment is permitted. The treatment of all types of obligate precancer is surgical procedure – full dissection of the diseased area in the limits of healthy tissues followed by immediate histological examination. Dissected tissue is surveyed by means of preparation of serial sections. Operation must be preceded by oral cavity sanation and removal of irritators. If operative treatment is impossible, radiation therapy is required.

Cornu cutaneum

Cornu cutaneum is limited hyperplasia of the epithelium with strong hyperkeratosis that resembles horn taking into account its appearance and solidity. It occurs on vermilion border, more often on lower lip, and is characteristic for people over 60, it is nontender. Its color is grey or grey-braun, diameter is up to 1 cm, length is up to 1 cm. Cutaneous horn is a long lasting disease (for years). Emergence of inflammation and induration around horn base, intensification of cornification are the main signs of its malignization. The diagnosis is confirmed after removal of lesion and its histological examination. Surgical treatment is removal of cutaneous horn in the limits of healthy cells.

Keratoacanthoma

Keratoacanthoma is epidermal benign tumor that develops quickly and regresses spontaneously (Fig. 14.1). The disease occurs on vermilion border, rarely on tongue. Keratoacanthoma appears as a grey-red solid papule with choanoid deepening in the center filled with horn mass that can be easily removed. The tumor grows rapidly and in a month it reaches its maximum dimensions (2.5 × 1 cm).

Fig. 14.1. Keratoacanthoma of the lower lip

Keratoacanthoma is nontender, movable and do not infiltrate surrounding tissues. In 6–8 months the tumor either regresses spontaneously and disappears leaving a scar or becomes malignant one and causes cancer. Keratoacanthoma must be distinguished from verrucous carcinoma and precancer. Cancer has firmer texture, solid base, after removal of horn masses bleeding emerges. Surgical treatment of keratoacanthoma is ligatory.

Skin cancer

Skin cancer is the most common tumor in European population. In the majority of cases it can be revealed even at early stages without any special diagnostic procedures so people begin treatment in more than 90 % of cases. Despite the fact that ultraviolet sun beams do not always cause skin carcinoma, in people with insufficient melanin pigmentation of skin the beams with wave length of 290–320 nm are the main, and very often the single, cause of the disease. This means that carcinoma develops more often on open skin areas. Genetic factors play also an important role in the development of skin cancer (cancerogenese). Such rare heritable diseases as albinism, xeroderma pigmentosum, syndrome of nevoid basal cell epithelioma are conditions that are also associated with increased risk of skin cancer development. Usage of effective sun-protective means by these patients contributes to decrease of disease risk. Chemical carcinogens, in particular inorganic compounds of arsenic and some organic hydrocarbons, belong to independent or additional reasons of skin cancer, especially its epidermoid type. Pathogenetic mechanisms of carcinoma development at ultraviolet irradiation and effect of chemical substances are similar. Ionizing radiation including simple X-rays and rays with wave length 0.1–0.3 nm and also gamma-rays have cancerogenic effect. Skin cancer as well as cancer of other organs develops more often under conditions of immune insufficiency, for example in lymphomas and immunodepressants treatment.

It was proved that influence of ultraviolet rays on skin is accompanied with immune insufficiency as a result of:

• destruction of activating lymphocytes Ia-antigens at the surface of lymphoid cells;
• failure of immune response;
• induction of suppressor lymphocytes;
• disappearance of functionally active Langerhans cells from epidermis (these cells play an important role in contact dermatitis development and other types of retarded hypersensitivity reaction). Despite the fact that any type of skin cells can be subjected to malignant transformation the basal-cellular and planocellular carcinomas develops more commonly.

Basal-cellular carcinoma. This type of cancer embraces more than 75 % of all skin tumors. It develops from epidermis and its cells are similar to intact basal cells. The slight tends to ordinary differentiation into keratin-producing squamous cells is commonly observed. Although these tumors metastasize very rarely, they show high local invasiveness and if effective and immediate treatment is not carried out, they can spread on the surface and ingrain deeply into underlying structures including nerves, bones, brain. Like the majority of cancer types the skin carcinoma is characterized by its indolence so it is often underestimated during long period. Typical basalcellular carcinoma appears to be an uninflamed papule with smooth wax surface that looks transparent at first sight. As a rule telangiectatically enlarged vessels can be seen near it. The tumor may contain certain amount of melanin pigment in form of small dots. These papules exulcerate and incrustate.Ulcers can reepithelize, the patient takes it incorrectly as good signs. Basal-cellular carcinoma can occur in other forms including subtle infiltration lesions not protruding over skin surface or fibrosis lesions resembling scars. In order to verify the diagnosis it is necessary to perform ordinary biopsy. Probably the patient with one canceromathose papule has other co-existing or developing ones in the forthcoming years. Some patients consult a doctor when they notice multiple primary basal-cellular carcinomas. Despite the absence of any visible skin alterations preceding the development of basal-cellular carcinoma, it is usually characteristic for persons who have got stigmas on skin areas exposed to sun or X-ray irradiation. The treatment depends on dimensions, depth and localization of tumor, sex, age and patient’s condition and, of course, abilities and qualification of a doctor. Judging by its cosmetic effect, no intervention can be compared with simple tumor resection (of course, if it is sufficient). Curretage (scraping) and electrocoagulation of minor basaliomas (as well as treatment with X-rays) provide total recovery of more than 95 % patients. Similar results can be achieved by cryodestruction of tumor tissue with liquid nitrogen, by the way this method is cosmetically more reasonable. Better results (recovery in nearly 99 % patients) can be achieved by tumor resection layer-by-layer under microscopic control (Mouh’s method). It is recommended in cases of reluctant and recurrent carcinomas not exposed to effect of other treatment means. Local chemotherapy using 5-fluorouracil is not recommended as a routine method of treatment of basal-cell carcinomas but it can turn out to be efficient in multiple superficial lesions. Immunotechniques of treatment are under exploitation. The patients must be aware of effect of ultraviolet rays in development of malignant skin tumors and methods of protection. It should be recommended for them to wear clothes which protect them from effects of sun beams, to avoid the influence of direct sun beams, in particular at midday, and to use special sun-protective means with protective action coefficient 15. After appearance of every new basal-cell carcinoma, it is necessary to carry out examination of the patient 1–2 times a year during 5 years. In 97 % cases it anticipates in the form of metastases and only in 3–5 % cases new basaliomas emerge on places of its former focuses. It is necessary to take into account the fact that patients with skin carcinoma have the higher risk of development of additional tumors.

Epidermoid carcinoma

This type of carcinoma also develops from epidermis but shows apparent planocellular differentiation and ability to produce keratin. These tumors are characterized by different predisposition to metastasis depending on their dimensions and localization, volume and depth of infiltration and also on the fact whether it develops from premalignized focus (scar tissue on places of burns, chronically inflamed skin areas) or from normal epidermis. Typical epidermoid skin carcinoma resembles solid nontender papule or red patch with apparent superficial cornific scaly crusts that can be ulcerated and covered with crusts. Relatively undifferentiated epidermoid carcinoma does not produce enough keratin so at its surface crusts can be absent. Unlike basal-cell carcinomas the epidermoid skin cancer usually develops from preexisting focus of actinic (sun or solar) keratosis. These precancer keratosis appear to be squamate scabrous red patches on skin areas chronically exposed to insolation. Despite the fact that only a small part of actinic keratosis advance to skin cancer, the most malignant type of epidermoid carcinoma develops from them. This type of epidermoid carcinoma metastasizes rarely (less than 2 % of all cases). Nevertheless, due to potential danger of malignant transformation of sun keratosis, it is recommended to remove them, particularly in persons of juvenile age. At present it is thought that applications of 5-fluoruracyle (1–5 %) in form of ointment or lotion (fomentation) are the most effective ones and as a result of this treatment scars usually do not transform into skin cancer.

Cryosurgical method of treatment using liquid nitrogen is also effective but it is fraught with high risk of cicatrisation. Epidermoid skin cancer developing in mucous coats, mucocutaneous areas, at places of burn scars, chronic ulcers, in atriums or in nearly healthy skin tends to metastasize. At the in situ stage epidermoid skin carcinoma is known under the name of Bowen disease. Despite the fact that epidermoid cancer in situ can develop as a result of chronic influence of sun beams, it is predetermined more frequently by preceding (accidental or due to therapeutic procedures) contact with inorganic compounds of arsenic, moreover from the moment of contact to disease development 10 years may pass. These patients have increased risk of respiratory, urogenital and gastrointestinal carcinoma development. The patients with epidermoid skin cancer must be carefully examined in terms of metastases revelation in order to work out the adequate treatment modality. If metastases are absent, the tumor is treated in the same manner as basal-cellular carcinoma. In this case it is more preferred to resect skin lesion or to use radio therapy to suppress potential metastases. In case of major local or metastatic lesions systemic treatment is used, sometimes local perfusion is applied.

Patients with epidermoid skin cancer should be warned to avoid ultraviolet irradiation and they should be under supervision of doctor at least during 5 years to control local recurrences, development of additional primary focuses and sometimes metastases in internal organs.

Cancer of oral mucosa and cancer of vermilion border

Malignant tumors of mouth and guttur tunica mucosa make total of nearly 5 % of all human tumors. They occur in men more frequently than in women, more commonly at the age 40–60 years.

Etiology

It is suggested that in the majority of cases cancer develops within pathologically changed tissues. As a rule it is long-lasting inflammatory processes of various etiology and dyskeratosis belonging to so called precancer. Such bad habits as smoking, abuse of strong drinks, consumption of “nasa” in Middle Asia and chewing of betel leaves in India, play an important role in development of pathological processes in mouth cavity. We can also mention such factors as chronic mechanical trauma caused by destructed crown of tooth, sharp edge of filling or poor quality prosthesis. Nutrition plays a definite role in development of pretumor conditions. Insufficient content of vitamin A in food or failure of body accessibility cause changes in cornification processes. Systematic consumption of very hot and spicy food is also harmful to oral mucosa.

In the majority of cases cornific epidermoid cancer, rarely non-squarmous one, develops on vermilion border and in oral mucosa. The clinical course of early cancer forms depends on preexisting diseases and tumor growth (exophytic, endophytic, mixed forms). At first cancer can proceed without serious consequences but in cases of tongue localization severe, irradiating pain often appears. Authors distinguish papillary, infiltrative and ulcerous forms of the oral cancer judging by external view at the beginning of disease.

Papillary form. At first a limited induration in form of papillose excrescence on wide base or on pedicle appears. Its surface is covered with papillary projections and horn masses (Fig. 14.2). Palpation reveals superficial infiltration around its base. Tumor grows in scope and depth, necrotic changes develops rather quickly in the center resulting in ulcer formation.

Fig. 14.2. Cancer of the tongue papillary form

Infiltrative form of the cancer is the most unfavourable one (Fig. 14.3). At the beginning of disease nontender induration emerges, it is often located under the mucous layer. Infiltrate grows, necrotize in the central areas and typical cancer ulcer occurs.

Fig. 14.3. Cancer of the tongue infiltrative form

Ulcerous form is the most common one because in the majority of cases a tumor begins to decay at early stage and resembles anabrosis and then ulcer. At the beginning of invasive growth the cancer is characterized by induration around an ulcer in form of roller and in its base being revealed by touch. At primary stage the induration is minor or it is not even revealed clinically, then due to rapid growth of tumor it increases reaching sometimes stone-like density.

At later stages the differentiation of forms is not possible, ulcerous infiltrative growth prevails (Fig. 14.4).

Fig. 14.4. Cancer of the tongue ulcerous form

As a rule an ulcer has raised twisted solid edges, irregular grainy bottom covered with grey-yellow fur or grey necrotic fur in the oral cavity; on vermilion border an ulcer is covered with solid grey fur or bloody grey crusts in case of bleeding. Inflammatory processes in surrounding tissues may be evident or clinically absent. Traumas caused by sharp edges of teeth, prostheses, consumption of hot food, smoking, burning etc. speed up the growth of tumor. It is forbidden to use burning means for ulcers of any etiology but it is dangerous in cases of malignant tumors in particular. After appearance of cancer metastases into lymphatic nodes they gradually consolidate, increase and then infiltrate surrounding tissues. Tongue cancer gives metastases very early; probably it is due to its high mobility.

Cancer of the oral cavity and vermilion border belongs to cancers of visual localizations that facilitates its diagnostics, enables to undertake examination and palpation of diseased area without special equipment (Fig. 14.5).

Fig. 14.5. Cancer of the oral cavity and vermilion border

Using stomatoscope you can observe earlier morphological changes. Clinical diagnosis must be confirmed with morphological investigations – the cytological or histological method. The cytological method of investigation enables to make a correct diagnosis in 90–95 % cases. The material for the cytological investigation is taken by means of scraping or puncture. Differential diagnostics of cancer must be carried out with respect to leukoplasia, benign tumors, traumatic and trophic ulcers, specific diseases (tuberculosis, syphilis, and leprosy), ulcers at lichen acuminatus and other chronic inflammatory processes.

Cancer of the buccal mucosa has the same histological presentation as in case of tongue cancer and oral cavity cancer. However, malignant tumors of minor salivary glands can rarely occur in this area. The buccal mucosa often became infiltrated by tumor secondarily from the side of tonsils, lip and skin. At fist reference to doctor regional metastases are seen rarely, the exceptions are tumors localized in the retromolar area and spreading onto tonsils and palatal arches.

Cancer of the palate mucosa – malignant tumors develop more frequently on the hard palate, they develops from minor salivary glands (cylindromatous carcinoma – cylindroma, adenocarcinoma). Composite tumors (polymorphous adenomas) occur rarely, their differential diagnostics is very often difficult even for histologists. Epidermoid cancer develops on the hard palate rarely. On the soft palate primary growths originating from minor salivary glands occur rarely and epidermoid cancer embraces the absolute majority of tumors. This morphological peculiarity of tumors of hard and soft palate impacts their clinical course.

Epidermoid cancer of the hard palate ulcerates rather quickly causing unpleasant feelings or pain. The patients usually consult a doctor when tumors are not very large.

New growths originating from minor salivary glands remain encapsulated for a long time sometimes becoming sizeable. These patients have the first and the main complaint – presence of tumor on the hard palate. With the increase of its size the pressure of the tumor upon the mucous coat increases and ulceration is commonly seen, then infection and aches develops. It should be noted that at early stage adenocarcinomas and composite tumors of hard have the same clinical picture with tendency to encapsulated growth for a long time. Then adenocarcinoma grows and destructs the underlying skeletal structures.

Cancer of mucous coat of alveolar edge of low and upper jaws

These new growths have almost always the structure of epidermoid cancer. They come out rather early because teeth become involved into the process, tooth ache appear. Treatment is often carried out when these aches appear, and a tooth can be even extracted. Improper tooth extraction caused the expansion of cancer growth into sockets and then into bone. At early stage a tumor is usually local one and bleeds when touching. The infiltration of underlying bone tissue (alveolar edge of low and upper jaw) occurs in several months and must be considered as late presentation of disease. The rate of tumor expansion in bone is determined by X-ray, but it should be taken into account that chronic diseases of teeth also cause presentation of demineralization of bone tissue. Depending on localization the gingival cancer spreads into the buccal mucosa, palate mucosa and oral cavity mucosa. Regional metastases occur early and are diagnosed in approximately one third of patients. Malignant tumors originating from minor salivary glands appear rarely.

Diagnostics

Clinical definition of epidermoid cancer of the oral cavity is based on peculiarities of this malignant tumor development (mentioned above) and does not cause any difficulties. It is necessary to determine the localization of tumor, its size, rate of expansion and clinical growth form. At present the rate of tumor expansion is determined visually and by touch.

Secondary affection of the facial skeleton by tumor is defined using X-ray method and scintigraphy. However in the infiltration of periosteum by tumor can not be determined by these methods so it must be considered as an affected zone. The aim of the morphological investigation is identification of tumor nature of biopsic material, histological structure of malignant growth, differentiation of epidermoid cancer, presence of tumor infiltration in surrounding tissues and vessels. All these features play an important role for prediction of disease progress and selection of treatment method. Cytological method plays an important role in differential diagnostics of minor tumors and precancer diseases.

As a rule, the diagnostics of regional metastases does not cause difficulties. In order to predict the disease progress and to select the most efficient treatment method it is necessary to estimate the amount of regional metastases and their localization in the corresponding groups of neck lymphatic nodes being defined by touch and using ultrasound scanning. Cytological investigation of punctates from metastatic node enables to make a correct diagnosis in 80 % of cases. Diagnostics of distant metastasis requires the examination of organs the most frequently affected by epidermoid cancer. The following examinations can be used: X-ray test, functional examination of liver (biochemical blood analysis, isotopic examination), ultrasound liver examination.

Treatment

Treatment of oral cancer can be divided into two stages: treatment of primary focus and treatment of regional metastases.

I stage – treatment of primary focus. In order to treat primary tumor the radiation, combined and surgical methods are used.

Radiation method. It is one of the most popular treatment methods for oral cancer. It is used for 88.7 % patients with tumors of oral cavity organs, and for 72.4 % – as an individual method. It is regarded as the main method of treatment at early stages of tumor development.

Gamma-ray teletherapy is used more frequently, intracavitary gamma teletherapy and their combination are used less frequently.

The results, according to native and foreign scientists are following: in case of primary cancer of the movable part of tongue corresponding to stages I and II (T1 and T2) the usage of different techniques of radiation therapy gave the possibility to cure 70–85 % and 38–56 % patients during 5 years respectively. In case of I stage of the oral cancer 53–66 % patients recover during 5 years, in case of II stage – 43–46 %, cheek cancer – 81 and 61 % respectively.

The results of radiation treatment of III stage cancer of the oral mucosa are worse – 16–25 %.

Combined method. At present the combined treatment of oral cancer is widely used, its main component is surgical operation. At the first stage of treatment the majority of specialists suggest gamma-ray teletherapy, at the second stage – operative treatment. The dosage of preoperative irradiation is 35–45 Gr. Favourable results of 5-year combined treatment for I and II stage cancer are comparable with results of radiation therapy along and reach 80–94 % and 39–65 % respectively. In cases of tumors of other localizations I and II stages 30–53 % patients with cancer of floor of the mouth recovered, 42,8 % patients with cancer of the mandibular alveolar bone and 94 and 65 % patients with cheek cancer respectively. In case of III stage disease the results of combined cancer treatment of any localization in the oral cavity make up 37 % recoveries during 5 years. This method is used as major one for treatment of locally advanced cancer. The main component is operation, its type depend on rate of primary tumor expansion, form of its development and its histological structure.

Surgical method

At present the half tongue electrocision is widely used in tongue surgery. This operation is conducted in case of I–II stage cancer as well as for the large tumors as a part of combined interventions (on 2 and more organs). Resection limits are not less than 2–4 cm of healthy tissues.

In case of locally advanced cancer of the movable part of the tongue and oral cavity bottom the combined half tongue electrocision is executed together with resection of oral cavity bottom (upon evidence – resection of the low jaw) with single-stage grafting of defects of tongue tissues and oral cavity bottom with musculocutaneous flaps.

II stage – influence on areas with regional metastases.

Regional metastases of cancer of the oral cavity of all localizations are observed in 23–40 %. The highest percentage of metastases in neck lymphatic nodes is identified in primary tumors with size 4 cm and more. In case of primary tumor 4 cm and more with morphologically confirmed metastases during 5 years only 17–20 % patients survive without recurrences and metastases. Regardless of the size of primary tumor with regional metastases 9–33 % patients survive, in their absence – 50–70 %. The most favourable treatment method of regional metastases is surgical method.

For this purpose fascial casing resection of neck dietary fibre and Crile operation are executed.

In order to avoid the development of regional metastases some radiologists use elective irradiation of areas of regional lymphatic outflow.

Dentists as well as doctors of any other specialization must demonstrate oncological suspicion when examining a patient. Regardless of the complaints that a patient has, the examination of the oral cavity and vermilion border is obligatory for a doctor. He must pay attention to any deviation from norm. Early evidences of cancer may not be evident for the patient but a doctor is obliged to reveal them as soon as possible. The term “oncological suspicion” means first of all particular oncological knowledge that enables a doctor to execute early and timely cancer diagnostics. This term also includes the knowledge of precancer diseases and their treatment, knowledge of organization of oncological assistance, chain of oncological treatment establishments, and immediate patient referral for treatment. In cases, that are difficult for diagnostics doctors should pay attention to possible growth of malignant tumor and make a diagnosis in as short period as possible. The treatment without proper diagnosis must not be conducted more than 7 days. It is required to remove local irritants, not to use means contributing to growth of tumor (burnings, physiotherapy etc.). In difficult cases a doctor must request assistance of more experienced specialists when examining a patient.

The treatment is conducted by oncologists. After cancer or precancer disease treatment patients must be at dispensary observation.

Malignant tumors of the jaws

Malignant tumors unlike benign neoplasms are more invasive, have a greater degree of anaptasia and have the ability to metastasize regionally to lymph nodes or distantly to other sites. Malignant tumors that arise de novo are termed primary tumors, and those that originate from distant tumors are termed secondary or methastatic.

Malignancies that commonly affect the jaws are carcinomas (lesions of epithelial origin), metastatic lesions from distant sites, sarcomas (lesions of mesenchymal origin), and malignancies of the hematopoietic system. Malignant tumors may occur at any age in either gender.

The following clinical signs are observed in malignant tumors: swelling, displaced teeth, loosened teeth over a short duration, foul smell, ulceration, presence of an indurated or rolled border, exposure of underlying bone, sensory or motor neural deficits, lymphadenopathy, weight loss, dysgeusia, dysphagia, dysphonia, hemorrhage, lack of normal healing, or pain with no demonstrable dental cause. Dentists must vigilantly watch for the possibility of malignancy in their patients. The risks of lack of attention to this possibility are delayed diagnosis, delayed treatment, increased need for aggressive treatment with added morbidity, and, in the worst case, premature death.

Diagnostic procedures in jaw malignences

The most informative imaging techniques in the head and neck are radiography and computerised tomography (CT), magnetic resonance imaging (MRI) and ultrasound.

Radiographic examination

Radiology has an important role in the management of the patient with cancer. First, diagnostic images may aid in the establishment of an initial diagnosis of a tumor. Diagnostic imaging also aids in the appropriate staging of disease from early small cancers to large cancers that have spread. Appropriate radiologic investigations assist the surgeon or radiation oncologist to determine the appropriate dimensions of the tumor so that it can be excised or irradiated adequately. Radiologic investigation has the potential to determine the presence of osseous involvement from soft tissue tumors and allow the practitioner to assess the presence of nodal disease and the outcome of treatment.

The following features may suggest the presence of a malignant tumor.

Location. Primary and metastatic malignant tumors may occur anywhere in the oral and maxillofacial region. Primary carcinomas are more commonly seen in the tongue, floor of the mouth, tonsillar area, lip, soft palate, or gingiva and may invade the jaws from any of these sites. Sarcomas are more common in the mandible and in posterior regions of both jaws. Metastatic tumors are most common in the posterior mandible and maxilla.

Periphery and shape

The typical appearance of the periphery of a malignant lesion is an ill-defined border with a lack of cortication and absence of encapsulation (a soft tissue or radiolucent periphery). This infiltrative border has uneven extensions of bone destruction. Fingerlike extension of the tumor occurs in many directions; this extension is followed by osseous destruction producing a region of radiolucency. Evidence of osseous destruction with adjacent soft tissue mass is highly suggestive of malignancy. Such a mass may exhibit a smooth or ulcerated peripheral border if cast against a radiolucent background. The shape of a malignant tumor of the jaw is irregular.

Because most malignancies do not produce bone nor do they stimulate the formation of reactive bone, the internal aspect is typically radiolucent in most instances. Occasionally residual islands of bone are present, resulting in a pattern of patchy destruction with some scattered residual internal osseous structure. Some tumors, such as prostate and breast metastatic lesions, can induce bone formation, resulting in an abnormal-appearing internal osseous architecture, whereas others, such as osteogenic sarcomas, can be productive in nature.

Effects on surrounding structures

Malignancy is destructive and often rapidly growing. The effect on surrounding structures mirrors this behavior. Rapidly growing malignant lesions generally destroy supporting alveolar bone so that teeth may appear to be floating in space.

Occasionally root resorption is present, this being more common in sarcomas. Internal trabecular bone is destroyed, as are cortical boundaries such as the sinus floor, inferior border of the mandible, follicular cortices, and the cortex of the inferior alveolar neurovascular canal. Because malignant tumors tend to grow rapidly, they invade by means of the easiest routes such as through the maxillary antrum or through the periodontal ligament space around teeth, resulting in, irregular widening with destruction of the lamina dura. Where the tumor has destroyed the outer cortex of bone, usually no periosteal reaction occurs; however, some tumors stimulate unusual periosteal new bone formation. Lesions such as osteosarcoma and prostate metastatic lesions as well as other tumors can stimulate the formation of thin straight spicules of bone, giving a sunburst appearance.

Plain radiography is widely available but the value of additional techniques should be understood. It is also advisable to request a formal radiologist’s report on radiographic films, whenever the radiographic features appear unusual or beyond the experience of the clinician.

Computerised tomography (CT)

CT is a cross-sectional radiologic imaging technique that is particularly useful in the evaluation of bone lesions. Not only can the density and margins of the lesion in question be evaluated with this technique but cortical expansion and fine internal details can often be more readily appreciated compared with plain film images. Use of contrast media has extended the utility of this technique in areas of soft tissue pathology. Furthermore, more recent designs such as spiral CT scanners have made data acquisition much more rapid and have reduced radiation dose to the patient while maintaining or improving resolution.

Magnetic resonance imaging (MRI)

MRI is a newer form of crosssectional imaging that does not expose patients to ionizing radiation. Although primarily used in the evaluation of soft tissue lesions, it is also capable of providing diagnostic information regarding bony lesions. Two distinct views are typically generated: T1 and T2.

Adipose tissue has the highest signal in the Tl-weighted image, and this view is often used for identifying anatomic structures. By comparison, the T2 image highlights tissues with high water content and is especially useful in depicting inflammatory processes and neoplasms.

Radionuclide imaging

Radionuclide imaging relies on the specific uptake of any one of several isotopes by various types of tissues or cells. Localization of the isotope is determined by examining the patient with a gamma scintillation camera.

The most commonly used isotope, Technetium-99m pertechnetate, can demonstrate areas of high metabolic activity. It is useful in identifying inflammatory conditions such as osteomyelitis, areas of active skeletal lesions of fibrous dysplasia or osteitis deformans, and metastatic disease.

PET (positron emissive tomography) scan

PET scan is the most recently developed cross-sectional imaging technology. This technique relies on the identification of metabolically active cells, such as metastatic deposits of squamous cell carcinoma, that exhibit preferential uptake of radionuclide-labeled glucose. In conjunction with CT/MRI, preoperative PET imaging of patients with head and neck cancer has lead to increased sensitivity and specificity for detection of oral cavity carcinoma, esophageal carcinoma, and clinically occult metastatic disease in the neck.

PET scans have proved particularly useful in the post-treatment follow-up by helping to distinguish altered anatomic landmarks or areas of fibrosis from recurrent tumor as well as the detection of distant metastases from head and neck primaries.

The technique is not recommended for neoplasms that are relatively inactive metabolically (eg, low-grade mucoepidermoid carcinoma). In addition, the lower limit of tumor mass detection by current technology is no better than that of CT/MRI, and false-positives owing to inflammatory changes are reported.

Osteosarcoma

Osteosarcoma is highly malignant neoplasm of bone in which osteoid is produced directly by malignant stroma. The three major histologic types are chondroblastic, osteoblastic, and fibroblastic osteosarcoma.

Osteosarcoma of the jaws is quite rare and accounts for approximately 7 % of all osteosarcomas. It is more common in young people under the age of 30 but can occur in older patients and a small number of people with Paget’s disease develop osteosarcoma as a rare complication. The age of presentation of the disease appears to be significantly older in the jaws than in other bones, and it may affect the maxilla or mandible. The most commonly reported symptom is rapidly growing swelling. Other signs are pain, movable teeth, and tenderness, erythema of overlying mucosa, ulceration, epistaxis, hemorrhage, nasal obstruction, exophthalmos, trismus, and blindness. Hypoesthesia is observed in cases involving neurovascular canals.

The mandible is more commonly affected than the maxilla. Although the lesion can occur in any part of either jaw, the posterior mandible, including the tooth-bearing area, angle, and vertical ramus, is most commonly affected. Osteosarcoma has an ill-defined border in most instances. When viewed against normal bone, the lesion is usually radiolucent with no peripheral sclerosis or encapsulation. If the lesion involves the periosteum directly or by extension, one may see the typical sunray spicules or trabeculae. Osteosarcoma maybe entirely radiolucent, mixed radiolucent-radiopaque, or quite radiopaque. The internal osseous structure may take the appearance of granular- or sclerotic-appearing bone, cotton balls, wisps, or honeycombed internal structures in areas with adjacent destruction of the preexisting osseous architecture. Whatever the resultant internal structure, the normal trabecular structure of the jaws is lost.

Effects on surrounding structures, widening of the periodontal membrane suggests osteosarcoma but is also seen in other malignancies. The antral or nasal wall cortices may be lost in maxillary lesions. Mandibular lesions may destroy the cortex of the mandibular canal and adjacent lamina dura.

If the internal structure is minimal or absent, fibrosarcoma or metastatic carcinoma may appear similar to osteosarcoma. If the osseous structure is visible, the practitioner should also consider chondrosarcoma. If spiculated periosteal new bone is present, prostate and breast metastases should be

considered. Comprehensive physical examination and laboratory tests assist in determining if the lesion is primary or metastatic. Benign tumors such as ossifying fibroma and benign conditions such as fibrous dysplasia may mimic osteosarcoma. The former conditions, however, are usually better demarcated and have a more uniform internal structine. Ewing’s sarcoma, solitary plasmacytoma, and even osteomyelitis share some of the radiographic characteristics of osteosarcoma.

Treatment and prognosis. The management of osteosarcoma is resection with a large border of adjacent normal bone. This may be possible in orthopedic cases but may be complicated by the presence of important adjacent anatomic structures in the head and neck. Generally radiation therapy and chemotherapy are used only for controlling metastatic spread or for palliation.

Carcinoma

Squamous cell carcinoma originatin in soft tissue

Squamous cell carcinoma, the most common oral malignancy, is a malignant tumor originating from the surface epithelium. It is characterized initially by invasion of malignant epithelial cells into the underlying connective tissue with subsequent spread into deeper soft tissues and occasionally into adjacent bone, local-regional lymph nodes, and ultimately to distant sites such as the lung, liver, and skeleton. Males are more commonly affected than females. Most squamous cell carcinomas occur in persons older than 50 years.

Squamous cell carcinoma appears initially as white or red (sometimes mixed) irregular patchy lesions of the affected epithelium. With time these lesions exhibit central ulceration; a rolled or indurated border, which represents invasion of malignant cells; and palpable infiltration into adjacent muscle or bone. Pain may be variable, and regional lymphadenopathy with hard lymph nodes that may or may not be tethered to underlying structures may be present. Other clinical features include a soft tissue mass, paresthesia, anesthesia, dyscsthesia, pain, foul smell, trismus, grossly loosened teeth, or hemorrhage. Large lesions can obstruct the airway, the opening of the eustachian tube (leading to diminished hearing), or the nasopharynx. Patients often report a significant weight loss and feel unwell. The condition is often fatal, if untreated.

Radiographically squamous cell carcinoma commonly involves the lateral border of the tongue. Therefore a common site to observe bone invasion is the posterior mandible. Lesions of the lip and floor of the mouth may invade the anterior mandible. Lesions involving attached gingiva and underlying alveolar bone may mimic inflammatory disease such as periodontal disease. Squamous cell carcinoma may erode into underlying bone from any direction, producing a radiolucency that is polymorphous and irregular in outline. Invasion occurs in one half of cases and is characterized most commonly by non-corticated border. Rarely the bolder may appear smooth, indicating underlying erosion rather than invasion. If bone involvement is extensive, the periphery appears to have fingerlike extensions preceding a zone of impressive osseous destruction. If pathologic fracture occurs, the borders show sharpened thinned bone ends with displacement of segments and an adjacent soft tissue mass. Surface carcinomas are capable of producing sclerosis in underlying osseous structures without frank invasion. The internal structure of squamous cell carcinoma in jaw lesions is totally radiolucent; the original osseous structure can be completely lost. Occasionally small islands of residual normal trabecular bone are visible within this central radiolucency.

Squamous cell carcinoma is discernible from other malignancies by its clinical and histologic features. Occasionally it is difficult to differentiate inflammatory lesions such as osteomyelitis from squamous cell carcinoma, especially when oral bacteria secondarily infect the tumor. Both osteomyelitis and squamous cell carcinoma are destructive, leaving islands of osseous structure that may appear to be consistent with sequestra. Evidence of profound bone destruction or invasive characteristics helps to identify the presence of a malignancy when a mixture of inflammatory changes and carcinoma exists. Osteomyelitis usually produces some periosteal reaction, whereas squamous cell carcinoma does not. In cases of osteoradionecrosis, the differentiation of this condition from squamous cell carcinoma requires advanced imaging or surgical exploration.

Treatment and prognosis. Oral squamous cell carcinoma is usually managed using a combination of surgery and radiation therapy. The choice of which modality to use depends on the location and severity of the tumor. Generally, if an adequate margin of normal tissue can be obtained, surgery is the usual treatment, followed by radiation treatment. Alternately, radiation may be used as the primary treatment followed by surgical intervention. Currently, the trend is to add concomitant chemotherapy as an adjunct to either radiation or surgical treatment.

Squamous cell carcinoma originating in bone

Squamous cell carcinomas that are encountered in the jaws, lack any continuity with the oral or antral mucosa, and occur in the absence of a primary carcinoma located elsewhere are termed primary intraosseous squamous cell carcinomas. These cases are assumed to arise from odontogenic epithelium.

They typically occur in elderly patients and tend to occur in the mandibular body region. Squamous cell carcinomas may also arise from the linings of odontogenic cysts. These neoplasms are rare and may remain silent until they have reached a fairly large size. Pain, pathologic fracture, and sensory nerve abnormalities such as lip paresthesia and lymphadenopathy may occur with this tumor. It is more common in men and in patients in their fourth to eighth decade of life. The surface epithelium is invariably normal in appearance.

The mandible is far more commonly involved than the maxilla, with most cases being present in the molar region and less frequently in the anterior aspect of the jaws. Because the lesion is by definition associated with remnants of the dental lamina, it originates only in tooth-bearing parts of the jaw. The periphery of the majority of lesions is ill-defined. They are most often rounded or irregular in shape and have a border that demonstrates osseous destruction and varying degrees of extension at the periphery. The degree of raggedness of the border may reflect the aggressiveness of the lesion. If sufficient in size, pathologic fracture occurs, with its associated step defects, thinned cortical borders, and subsequent soft tissue mass. The internal structure is wholly radiolucent with no evidence of bone production and very little residual bone left within the center of the lesion. If the lesion is small, overlying buccal or lingual plates may cast a shadow that may mimic the appearance of internal trabecular bone. These lesions are capable of causing destruction of the antral or nasal floors, loss of the cortical outline of the mandibular neurovascular canal, and effacement of the lamina dura. Root resorption is unusual. Teeth that lose both lamina dura and supporting bone appear to be floating in space.

Treatment and Prognosis.

Primary squamous cell carcinomas are excised with their surrounding osseous structure in an en bloc resection. Radiation and chemotherapy may be used as adjunctive therapies. The 5-year survival rate is 30 to 40 %.

Malignant odontogenic tumors

Malignant odontogenic tumors are very rare. They arise from the epithelial components of the odontogenic apparatus: the rests of Malassez, the reduced enamel epithelium surrounding the crown of an impacted tooth, the rests of Serres in the gingiva, and the linings of odontogenic cysts. In general, all of these tumors exhibit typical microscopic features of malignancy and have the potential for either regional nodal or distant metastases.

Malignant ameloblastoma AND Ameloblastic Carcinoma

Malignant ameloblastomas have the histologic features of benign ameloblastoma but with signs of metastatic dissemination. The most common sites of metastatic disease are the lungs, followed by the cervical lymph nodes and visceral organs. Ameloblastic carcinomas are malignant epithelial odontogenic tumors that exist in the background of benign ameloblastomas. Hystologically ameloblastic carcinomas represents the signs of malignant lesions with hyperchromatism, pleomorphism, and high mitotic activity. The tumour is variable in its aggressiveness and spreads by local destruction of bone. If untreated, it will eventually spread into soft tissues and this may make it very difficult to eradicate surgically. Gradual swelling of the jaw is the usual initial symptom of this tumour, although it may be diagnosed through a radiograph before this becomes apparent. Loosening and displacement of teeth can occur, as well as pain or altered sensation. Malignant ameloblastoma is rare and in early stages radiologicaly and clinically resembles to benign ameloblastoma. The correct diagnosis therefore demands histological verification.

Metastatic Tumors of the jaws

Metastatic tumors represent the establishment of new foci of malignant disease from a distant malignant tumor. Metastatic lesions of the jaws usu ally occur when the distant primary lesion is already known, although on occasion a jaw metastatic tumor may reveal the presence of a silent primary lesion. Jaw involvement accounts for less than 1 % of metastatic malignancies found elsewhere, with most affecting the spine, pelvis, skull, ribs, and humerus. Most frequently the tumor is a type of carcinoma, the most common primary sites being the breast, kidney, lung, colon and rectum, prostate, thyroid, stomach, melanoma, testes, bladder, ovary, and cervix. Metastatic carcinoma must be differentiated from the more common locally invading squamous carcinoma. Metastatic disease is more common in patients in their fifth to seventh decade of life. Patients may complain of dental pain, numbness or paresthesia of the third branch of the trigeminal nerve, pathologic fracture of the jaw, or hemorrhage from the tumor site. The posterior areas of the jaws are more commonly affected. The maxillary sinus may be the next most common site, followed by the anterior hard palate and mandibular condyle. Frequently metastalic lesions of the mandible are bilateral. Metastatic lesions may be moderately well demarcated but have no cortication or encapsulation at their tumor margins; they may also have ill-defined invasive margins. The lesions are not round but polymorphous in shape. Both prostate and breast lesions may stimulate bone formation of the adjacent bone, which will be sclerotic. The tumor may begin as a few zones of osseous destruction separated by normal bone. After a time these small areas coalesce into a larger, ill-defined mass and the jaw may become enlarged. Lesions are generally radiolucent, in which case the internal structure is a combination of residual normal trabecular bone in association with areas of bone lysis. If the tumor is seeded in multiple regions of the jaw, the result is a multifoeal appearance (multiple small radiolucent lesions). In most cases a known primary malignancy is present, and the diagnosis of metastasis is straightforward. Multiple myeloma may be confused with metastatic tumors; however, the border of multiple myeloma is usually better circumscribed than in metastatic disease. When a lesion starts within the periodontal ligament space of a tooth, the appearance may be identical to that of a periapical inflammatory lesion. Odontogenic cysts, if secondarily infected, may have an ill-defined border giving a similar appearance to a metastatic lesion.

Treatment and Prognosis

The presence of a metastatic tumor in the jaw indicates a poor prognosis. If metastatic disease is present, the patient will usually die within 1 to 2 years. If the radiographic appearance is suspicious, an opinion from a dental radiologist should be sought and tissue submitted for histologic analysis. Nuclear medicine may be employed to detect other metastatic lesions. Isolated malignant deposits, if symptomatic, may be treated with localized high-dose radiation treatment. In the rare occasion that the jaw is the first diagnosed site of malignant spread, it is imperative that the patient be referred quickly to an oncologist so that anticancer treatment can be delivered promptly. This treatment may take the form of chemotherapy, radiation therapy, surgery, immunotherapy, and hormone treatment.

Multiple myeloma

Multiple myeloma is a malignant neoplasm of plasma cells. It is the most common malignancy of bone in adults. Single lesions are called plasmacytoma, and multiple lesions arc termed multiple myeloma.

Multiple myeloma is a fatal systemic malignancy. A patient with multiple myeloma is usually lacks any sign of bone reaction. The lesions have been described as appearing “punched out”. However, many appear ragged and even infiltrative. Some lesions have an oval or cystic shape. Untreated or aggressive areas of destruction may become confluent, giving the appearance of multilocularity. If the lesion is located in the periapical periodontal ligament space, it may have a border similar to that seen in inflammatory or infectious periapical disease. Soft tissue lesions have been reported in the jaws and nasopharynx. When visible on radiographs, they appear as smooth – bordered soft tissue masses, possibly with underlying bone destruction.

No internal structure is radiographically visible. Occasionally islands of residual bone, yet unaffected by tumor, give the appearance of the presence of new trabecular bone within the mass. Very rarely the lesions appear radiopaque internally.

Differential diagnosis

The most likely disease to be mistaken for multiple myeloma is the radiolucent form of metastatic carcinoma. Knowledge of a prior malignancy in a patient may help differentiate multiple myeloma from metastatic carcinoma. Osteomyelitis, if severe, may yield a radiologic picture similar to that of multiple myeloma; however, a visible cause for it usually exists. In addition, inflammatory lesions and infections in general cause sclerosis in adjacent bone, which multiple myeloma does not. Simple bone cysts may be bilateral in the mandible and therefore may be mistaken for multiple myeloma. They are usually corticated in part and characteristically interdigitate between the roots of the teeth in a much younger population. Generalized radiolucency of the jaws may be caused by hyperparathyroidism but is differentiated based on abnormal blood chemistry.

Management

The management of multiple myeloma is usually chemotherapeutic with or without autologous or allogeneic bone marrow transplantation. Radiation therapy may be used for treatment of symptomatic osseous lesions when palliation is required.

Surgical management of the jaw cancer

Maxillectomy

The maxilla can be resected by three distinct methods. These include a direct standard approach through an extended lateral rhinotomy incision, a lateral approach, and a transoral transpalatal facial degloving approach. The first (Weber – Ferguson) is the most common approach and utilizes a lateral rhinotomy incision with a limb of the incision extended inferior to the lower lid and then two centimeters beyond the lateral canthus of the eye. Making the incision three millimeters below the tarsal plate prevents postoperative epiphora. By rounding the incision near the medial canthus a persistent nasal cutaneous fistula is avoided. An upward extension in the medial canthal region is made if a maxilloethmoidectomy will be required.

The soft tissue flap is elevated allowing muscle attachment to remain to the maxilla, especially if a previous Caldwell – Luc has been performed. The orbital periosteum is then elevated and the orbital floor inspected for invasion by malignancy. If none is found the infraorbital fissure serves as the lateral margin of resection.

Lateral bony resection can occur through the malar eminence utilizing an oscillating saw. Another approach is to use a Gigli saw, separating the frontal maxillary process. A second osteotomy is then required through the zygoma. The decision on placement of this incision is based on the lateral extent of the tumor. Preserving the malar eminence allows a better cosmetic appearance.

Medially, the plane of the resection has been determined by the preoperative assessment of the extent of ethmoid involvement. When a combined craniofacial approach is not planned this osteotomy is made by a chisel approximately one centimeter below the frontal ethmoid suture. A chisel is used to continue the lateral rhinotomy incision through the nasal bone, and if necessary the entire nasal bone and skin complex can be swung to the contralateral side.

Preoperative assessment of the intranasal extent of tumor determines whether the incision is made on the ipsilateral or contralateral side of the septum. The hard palate incision is made close to the midline on the ipsilateral side when there is no evidence of tumor extension into the hard palate. The soft palate is preserved and remains attached. When posterior tumor extension toward the nasopharynx necessitates excision of a portion of the soft palate, the remaining palate should be re-approximated to any remaining buttress of bone or soft tissue in this area to avoid problems in swallowing and speaking.

The hard palate incision can be modified to allow for preservation of the premaxilla, thereby retaining the medial and lateral incisors. It is seldom possible to retain the canine tooth without compromising the resection. Preserving this small segment of premaxilla allows the prosthodontist to make an obturator which stays in position more easily.

By extending the skin incision laterally, and separating the coronoid process with the attached temporalis muscle from the ascending ramus of the mandible, it is possible to preserve a temporalis muscle flap for reconstructing the orbital floor. Because the coronoid bone remains attached to the temporalis muscle, it allows more secure placement of sutures into the muscle as it is pulled to the remaining ethmoid area, septum, or contralateral nose. Without this small portion of bone, sutures tend to tear through the temporalis muscle.

This lateral approach allows inspection of the pterygopalatine space and permits chisel placement under direct vision when separating the pterygoid plates from the skull base. Final chisel placement is determined by whether the posterior wall of the maxilla or pterygoid plates appear intact.

Complete separation of the specimen requires excising remaining soft tissue attachments and rocking the specimen so that the posterior orbital floor fractures between the inferior orbital fissure and the incision made in the ethmoids. Tumors confined to the maxilla or with early maxilloethmoid extension are removed en bloc by this method and rarely should there be positive margins.

The pathologist comes to the operating room to evaluate the surgical specimen. We have found that even then it is still difficult to evaluate the adequacy of margins. Thus a new set of margins is taken directly from the patient from the following areas: the remaining hard palate, ethmoid and posterior ethmoid, the base of the skull near the foramen ovale, the base of the skull and adjacent mucosal lining of the nasopharynx, and the nasal vault. Frozen sections are obtained and further resection is performed if required. It has been noted by other authors that if any of this tissue is unexpectedly found to be positive the prognosis is poor even though further resection is immediately performed.

A second approach is used for large tumors with lateral or posterior extension. This begins with a more limited lateral rhinotomy incision without extension of the infraorbital incision beyond the lateral canthus of the eye. A second skin incision is made down through the chin and then directly laterally. A midline stepped mandibulotomy is performed after drill holes are placed for reapproximation. In young patients with excellent dentition it is possible to split the mandible in the midline without a dental extraction. If dental viability is in question one of the incisors should be extracted. The mandible is swung laterally and the lingual nerve, hypoglossal nerve, and submandibular duct preserved. The soft tissues of the floor of the mouth are dissected laterally and the tongue medially. If required, a temporalis muscle coronoid process flap can also be preserved in this lateral approach.

Tumors with infratemporal fossa extension particularly require this approach. The lateral approach is also required when there is definite invasion of the pterygoid plates or when resection is planned for tumors which extend primarily into the pterygomaxillary or pterygopalatine fossa. The approach can also be used for select tumors with limited extension onto the lateral wall of the nasopharynx anterior to the region of the eustachian tube.

Main advantages of this approach are control of the blood supply to these regions and direct visualization of this area early, as opposed to the direct anterior approach where the full extent of the tumor is not appreciated until late in the procedure. Ligation of the internal maxillary artery can be performed through this lateral approach. Tracheotomy is necessary. This method is preferred to the lateral mandibulotomy approach to the infratemporal fossa, as it provides nearly equal visualization and has less associated morbidity. The midline mandibulotomy is repaired with Wurtzburg or Luer miniplates. The temporary maxillary prosthesis is placed in the patient, who is permitted to eat after a few days, when the swelling of the soft palate and pharynx has resolved.

A third approach, which involves a degloving of the central face, is used for more limited tumors of the inferior maxilla. Tumors ideally suited for this type of resection include those of the nasal septum, inverting papillomas, and tumors of low grade malignancy, particularly when located medially. The obvious advantage is that no skin incision is required. Combined craniofacial resections have been performed for some tumors using this approach.

Combined craniofacial resection is used when there is extension into the superior ethmoid and cribriform plate area. Tumors which arise primarily in the ethmoid or nasal vault area will develop early extension through the cribriform plate. Cribriform plate involvement is difficult to ascertain by either CT scan or polytomography, and impossible to ascertain by a routine sinus X-ray. The MRI scan is valuable in determining the extent of tumor to this area.

In most cases, better survival rates are reported when orbital exoneration is included as part of this procedure. The extension into the orbit is usually from the posterior ethmoid area and can be appreciated on the CT scan. Preservation of orbital contents when this occurs is occasionally possible, but the prognosis is poor because of recurrence with extension into the middle cranial fossa.

Prior to surgery a lumbar subarachnoid drain is placed and 50 to 75 cubic centimeters of cerebrospinal fluid is removed. A Foley urethral catheter is inserted, especially if mannitol may be necessary. The neurosurgical approach begins with a standard frontal craniotomy with a free bone flap and preservation of the galea or periosteum for the reconstructive procedure. The dura is inspected for invasion. If extension of the tumor through the dura into the frontal lobe is found the procedure is terminated at this point. The posterior walls of the frontal sinuses are identified and removed, as well as all frontal mucosa, and the contralateral frontal duct is plugged with muscle. Dural extensions into the cribriform plate area are elevated and tearing of the dura can be expected in this region as well as over the fovea ethmoidalis. These tears are later repaired by either primary suturing or using fascia lata or temporalis fascia.

Once established that the tumor is resectable, the head and neck surgeon commences his portion of the operative procedure. A lateral rhinotomy incision is made and the Weber – Ferguson extension of this incision made if needed. If there is known tumor extension into the orbit an orbital exoneration will be required. This simplifies the en bloc procedure. Should the tumor extend across the midline, the superior portion of the nasal septum and the cribriform plate on both sides and the extension into the opposite ethmoid cells can be included.

Together, the neurosurgeon and head and neck surgeon outline the area for the cranial fossa floor incisions. A small mastoid burr is useful for outlining these incisions; they are completed using a chisel. Incisions can extend back as far as the anterior wall of the sphenoid sinus. Additional traction on the brain at this point is usually difficult and may compromise the optic nerves. The incision on the contralateral side is placed to avoid entering the preserved orbit. Maxilloethmoidectomy is now completed from below in the standard manner.

The previously created galeal flap is now sutured to the remaining lateral and posterior dura. Only in cases of very large defects is cartilage or iliac crest bone interposed between the galeal flap and a split thickness skin graft placed from below. Generally the galeal periosteal flap is sufficient, but a temporalis muscle flap can also be swung to close this defect when orbital exoneration has been performed. Every effort is made to avoid placing artificial or nonvascularized material in this region to close the defect. The frontal bone is replaced and maintained by wire sutures. A split thickness skin graft is placed from below and packed into position with one inch iodoform gauze soaked heavily in an antibiotic ointment. It is further held in position by the previously made palatal splint. The remaining portion of the wound closure is similar to a standard maxillectomy.

This procedure is particularly effective for patients with tumors confined to the ethmoid or nasal vault superior to the region of the middle turbinate. By mobilizing the nasal bones to the contralateral side in resecting the medial portion of the maxilla, orbital floor, and orbital exoneration, the anterior portion of the posterior ethmoids can be removed en bloc.

Fortunately, much of what appears to be tumor in the posterior ethmoids and sphenoid sinus by CT scan turns out to be chronic hyperplastic sinus mucosa without tumor extension. If there is obvious invasion and involvement of the sphenoid sinus, adequate tumor resection is seldom feasible.

Mandible resection and reconstruction in mandibular cancer

When tumor approaches or only superficially involves the mandible, a marginal resection may be carried out. The resection can be beveled so that the mucosal reflections of both the cheek and the floor of mouth are included, while the inferior alveolar nerve is spared. No bony reconstruction would be required in such a case.

More deeply invasive tumors may be treated with a more radical marginal resection, leaving only a strut of the lower or posterior border to maintain the continuity of the mandible. In such a resection, the entire inferior alveolar nerve may be removed. If the remaining strut of bone is thin, a bone graft may be needed to prevent pathologic fracture. This is technically far simpler than grafting a discontinuity defect.

When mandibulectomy is necessary, the remaining mandibular fragments are subject to displacement into the area of discontinuity by scar contracture and by the unopposed pull of the muscles of mastication. Appropriate management of these fragments will prevent much of the disability that results from such surgery and will facilitate later reconstruction.

In lateral mandibulectomy, it is usually possible to retain a portion of the ascending ramus, including the condyle. The posterior line of resection should be oriented vertically, from sigmoid notch to angle, rather than horizontally across the ramus in these cases. When the mandible is divided horizontally, the insertion of the temporalis muscle is retained. The unopposed pull of this muscle displaces the fragment superomedially beneath the zygomatic arch. This makes it technically difficult to retrieve later during reconstruction. When the mandible is divided vertically, the fragment remains almost in its natural anatomic position.

Immediate reconstruction of the resected oral mucous membranes with a soft tissue flap helps to maintain the separation of the mandibular fragments, prevents scar contracture, and replaces much of bulk that is lost when the mandible is removed.

In many cases, some form of internal, external, or dental fixation is very helpful in stabilizing the residual mandibular fragments. This is especially true in patients who retain a complement of useful teeth, which would otherwise be drawn out of occlusion. Internal fixation ranges from simple Kirschner wires or braided stainless steel wire to more elaborate bone plates. These should be used only as temporary spacers, as they will often loosen or fracture over time. External fixation consists of two bone screws in each fragment that are connected either by universal joints and connecting rods or by a bar of self-curing methyl methacrylate. Such devices are surprisingly trouble-free and can be maintained for years if necessary. The fact that they may be placed prior to the resection, and that they do not interfere with pedicle flaps, makes them extremely useful in certain cases. Dental fixation can range from simply wiring the remaining teeth together to utilizing appliances with flanges and guidance ramps to help prevent deviation of the remaining fragments.

The deformities and dysfunction that traditionally have been associated with oral cancer surgery result more from the resection of large areas of the mucous membrane than from mandibular resection. The problem is compounded by the practice of closing the surgical defect by drawing its edges together, thus approximating structures (for example, midline of the tongue and buccal mucosa) that are normally quite separate from one another. When bony reconstruction is to be carried out, adequate soft tissue lining and coverage are a necessary prerequisite. Satisfactory soft tissue reconstruction alone will, in many instances, provide patients with a very acceptable functional and cosmetic result after a major head and neck resection.

Numerous random flaps of oral mucosa, neck skin, and shoulder skin may be used to reconstruct surgical defects resulting from oral cancer resection. These flaps are thin. The blood supply may be unreliable, especially in irradiated patients. Multiple stages may be needed for their safe construction, transfer, and insetting. While these flaps largely have been replaced in practice by more versatile, reliable techniques, they retain their usefulness in certain individual situations.

Mucosal flaps have the advantage of providing the same sort of tissue as that which was resected. Their major drawback is the limited quantity of tissue available. Tongue and buccal mucosa are the most common donor sites. Tongue flaps are by far the most versatile mucosal flaps. Their excellent blood supply allows them to be elevated from the dorsal, ventral, or lateral surfaces. They may be based either anteriorly or posteriorly to reach small defects anywhere in the oral cavity. Their major drawback is the speech impediment that results from the use of moderately large-sized flaps.

Neck flaps are usually oriented vertically, with the base along the lower border of the mandible. If possible, platysma is included on the deep surface to increase the blood supply. The donor site may be closed primarily. The flap is turned under to provide oral lining. This leaves a controlled fistula, which is closed after three weeks when the base of the flap is divided.

Shoulder flaps are based on the nape of the neck. They have a limited arc of rotation, including the lateral face, neck, and posterior oral cavity. They should be delayed if extended beyond the mid-clavicle. The donor site cannot be closed, and requires a split-thickness skin graft.

Skin flaps that have a reliable vascular supply extending along their axis may be safely constructed with a large length-to-base ratio and thus have a wide arc of rotation. Such axial pattern flaps have found wide use in oral cancer reconstruction for many years. They generally lie well away from fields of radiation, are thin, well-vascularized, and versatile. Their major disadvantages are that a secondary procedure is usually required to divide the vascular pedicle, and that the donor site defect may be esthetically unpleasant. While they are no longer used as frequently as are newer techniques, they remain quite useful in certain specific clinical situations.

Recent advances in our understanding of the vascular anatomy of muscles have led to the development of techniques whereby a muscle may be detached from its origin and/or insertion and transferred into a defect. Since a significant part of the vascular supply of the skin overlying a muscle is derived from muscular perforators, composite flaps of muscle and skin may be transferred in a similar fashion. Such flaps have revolutionized soft tissue reconstruction of the head and neck because of their reliability and versatility. The muscle provides a highly vascular bulk of tissue to fill a defect. If skin is transferred as well, the entire surface overlying the muscle may be raised, or merely an island of skin, precisely tailored to fit a defect, may be safely used.

The transfer of tissue by microvascular anastomosis has achieved increasing success and popularity in recent years. Free flaps were initially directly derived from known axial pattern flaps. The newer free flaps have utilized larger vascular pedicles for more reliable anastomoses. The advantages of free flaps are that thin, pliable, nonirradiated tissues may be transferred in a single stage. The disadvantages include vastly increased operating time, potential donor site morbidity (especially for lower extremity or intra-abdominal donor sites), the need for specialized instrumentation, the requirement for personnel experienced in micro vascular surgery, and the fact that problems generally result in necrosis of the entire flap, whereas problems with pedicle flaps generally result in necrosis of superficial or distal portions of the flap.

In all cases of the mandibular resections osseous reconstruction of the mandible remains necessary for optimal functional and esthetic restoration of the face and the occlusion. A variety of implants, ranging from braided steel wires or mesh to metal plates and screws, to plastic or metalloplastic composites have been used to restore mandibular continuity. The advantage of these devices is that they do not require further surgery for a donor site. Their disadvantages are the possibility of soft tissue dehiscence, of fatigue and fracture of the implant, of loosening, and of pathologic fracture of the site of attachment to the host bone. Such devices are best used as temporary spacers prior to definitive osseous reconstruction. They may also be used in cases where medical considerations limit the length of the surgical procedure. Perhaps the best long-term results have been obtained with properly contoured plates and tapped, bicortical bone screws.

Bone derived from the patient himself is the preferred material for osseous reconstruction. In the process of autogeneic bone grafting, the graft assumes both an active and a passive role. Some cells with osteogenic potential survive the procedure and act with cells from the recipient site to produce new bone. The remainder of the bone dies, but acts as a template which is eventually resorbed and replaced by viable new bone.

Cortical bone grafts are resorbed and revascularized very slowly. Only a few surface cells survive the surgery, and there are few open spaces through which tissues of the recipient site may enter the graft. Large interior areas of these grafts may remain nonviable for years, making them subject to stress fracture, irregular remodeling, and clinical failure. Solid cortical grafts of rib or iliac crest are best avoided.

Cortico-cancellous bone grafts are split in such a way that one surface contains a mechanically sound cortical plate, while the opposite surface contains cancellous bone that presents a large surface area which favors survival of osteogenic cells, rapid revascularization, and remodeling. Corticocancellous grafts can be placed with the usual techniques used for fracture fixation; however, they may be stabilized most conveniently with bone plates that obviate the need for intermaxillary fixation. Split ribs, partialthickness blocks of ileum, and inner table strips of calvarium make excellent cortico-cancellous bone grafts.

Cancellous bone grafts present a very large surface area which is rapidly revascularized from the recipient site. Grafted marrow contains many cells with osteogenic potential that survive the surgery. Thus the individual spicules of grafted bone are rapidly resorbed and replaced with viable new bone. Unfortunately, the spicules of grafted bone seek a dependent position in a large mandibulectomy wound. For this reason, they have been used most frequently in conjunction with a prosthetic trough that assumes the shape of the mandible. The trough is firmly affixed to the ends of the defect, and then packed with cancellous bone.

Composite flaps containing bone, either transferred on a vascular pedicle or transferred via microvascular anastomosis, generally present more risks than benefits. Contouring of the bone is not safely possible, and so they are appropriate to reconstruct only relatively short, straight segments of mandible. The blood supply to the bony segment is primarily periosteal, permitting little stripping for the purposes of fixation. Despite survival of periosteal blood vessels, portions of the bone undergo avascular necrosis and require slow remodeling and replacement. Donor site morbidity can be high. Despite the attractiveness of performing the entire reconstruction at a single operative session, superior results can still be reliably obtained by bringing in healthy soft tissues at an initial surgery followed by a bone graft at a second stage.

Successful reconstruction of the hard and soft tissues following oral cancer resection frequently leaves the patient with residual defects of both form and function. A number of secondary surgical procedures can be considered for those patients who desire further improvement.

In terms of the extraoral tissue, procedures such as defatting of flaps, revision of scars, nerve grafts, or muscle transfers to reanimate portions of the face, and many others are useful.

Intraorally, there may be a number of problems. If there are remaining teeth, but they are not in perfect occlusion, specialized dental prostheses may greatly improve function. Bone grafts are rarely covered by tight, immobile tissues, and are thus unable to support dental prostheses. Such grafts require ridge extension procedures, such as skin grafts, to enable dentures to be fitted. Often portions of the tongue, floor of mouth, cheeks, and alveolar ridge are reconstructed using insensate flaps or grafts. This renders the patient only minimally capable of supporting and functioning with a denture. Such patients, after several surgeries, may be able to wear dentures only for cosmetic purposes. One solution to this problem is the placement of osseointegrated implants to help stabilize the denture.

Chapter 15. Maxillofacial trauma

General characteristics, clinical peculiarities, diagnostics and treatment of soft tissue injuries

Types of injuries

Abrasions

Abrasions are a type of injury caused by shear forces that remove a superficial layer of the skin. These superficial injuries usually heal without scarring. It is important to determine whether foreign bodies which have been embedded in the wound can cause permanent “tattooing” of the soft tissue. Treatment consists in wound cleaning and covering with a thin layer of topical antibiotic ointment to minimize desiccation and secondary crusting of the wound. Reepithelialization as usual is complete in 7 to 10 days if the epidermal pegs have not been completely removed. If the laceration significantly extends into the reticular dermal layer, significant scarring is likely.

Contusions

Contusions are caused by blunt trauma that causes edema and hematoma formation in the subcutaneous tissues. The associated soft tissue swelling and ecchymosis can be extensive. Small hematomas usually resolve without treatment; hypopigmentation or hyperpigmentation of the involved tissue can occur, but is rarely permanent. Large hematomas should be drained to prevent permanent pigmentary changes and secondary subcutaneous atrophy. In case of infection formed abscess has to be drained and treated in a usual way.

Wounds

Wound is a type of injury when consistency of the skin or mucosa is impaired (cut, stabbed, lacerated).

Classification and clinical picture according to injure pattern and traumatizing object:

1. Cut wound

A sharp object causes these wounds. The surrounding tissues damage is not substantial. But the sharp object can go through covering tissues and affect internal organs and tissues. Damage of blood vessels and nerve trunks can lead to faint pain syndrome and massive bleeding.

2. Stab wound

Stab wound is caused by sharp pointed object and has the large depth and small area of the injured skin and mucosa.

The pain syndrome is slight, hiatus is absent, the external bleeding is absent, but hematoma can develop.

3. Contused wound

These wound caused with a blunt object. Before the skin rupture, the blunt object damages the deeper soft tissues or organs (muscles, bones).

A wide zone of smashed tissues around wound is peculiar. Contused wound causes pain syndrome, but there is no obvious external bleeding and can be infected easily. According to these complications contused woundsmore often heal by secondary tension.

4. Lacerated wound (Fig. 15.1)

A blunt object causes these wounds but this object is directed under the acute angle to the skin. We can observe a big separation and sometimes to scalp of the skin. According to this separation skin can necrotize. Sometimes this kind of wounds can be caused by fractured parts of bones.

Fig. 15.1. Lacerated wound

5. Crushed wound

The mechanism of this damage is equal to contused and lacerated wounds, but the degree of injury is maximal. Crushed wounds can be infected heal worse.

6. Slash wound

Slash wound caused by big and sharp object (like axe, saber). It has signs of incised and contused wound simultaneously. In this type of injury the internal organs and bones can be damaged very often. Necrosis of affected tissues can be observed. Pain syndrome is very strong. Bleeding not severe, but massive diapedesis hemorrhages are present.

7. Bite wound

Injury caused by animal or human bite. Bite wounds can be primarily infected with special infection. So, thorough wound irrigation and debridement are important in reducing infection and further complications.Animal and human bites are most often polymicrobial, containing aerobicand anaerobic organisms.

8. Mixed wound

These wounds may connect two and more kinds of wounds.

Principles of management

The initial examination involves evaluating and stabilizing the trauma patient. Any life-threatening conditions should be identified and managed immediately. The conditions of the airway, breathing, and circulation are еxamined, followed by a general neurologic assessment with particular attention to cervical spine and cranial injuries. Radiographs are used to diagnose fractures of the face, because, facial fractures are ideally treated prior to soft tissue repair. If repair of the facial bones is delayed, it is optimal to close the lacerations initially (Fig. 15.2). The wounds can be reentered and revised if needed to access the fracture site.

Fig. 15.2. Management of the lacerated wound (chain saw):
a, b – before treatment, c – after wound closure and suturing, d – a week postoperative

It is important to achieve hemostasis when stabilizing and evaluating the patient who has sustained trauma. Most bleeding will respond to application of apressure dressing. Occasionally surgical exploration and packing of the wound under general anesthesia may be indicated. In rare instances vessels in the neck may need to be ligated. Indiscriminate clamping inside the wound should be avoided because damage to important structures such as the facial nerve or parotid duct may result. It is unusual for bleeding from soft tissue injuries to the face to result in a shock state.

Lacerations involving the scalp can occasionally be difficult to control with pressure and may require clamping, ligation, or electrocautery. In soft tissue injuries not involving the face the length of time from initial injury to treatment is important. Secondary risk of infection increases with the lapse of time. Because of the rich vascularity of the face there is no “golden period” for suture repair of facial wounds. In fact healing of facial wounds is unaffected by the interval between injury and repair. Patients who are immunized and have received a booster injection within the last 10 years do not require tetanus prophylaxis if the wound is not tetanus prone. Tetanus-prone wounds are those with heavy contamination from soil or manure, devitalized tissue, or deep puncture wounds. If the wound is tetanus prone and the patient has not received a booster injection within 5 years prior to the injury, a 0.5 Ml tetanus toxoid boost injection should be given. If the patient has not received a booster within 10 years prior, they should receive a booster injection for any wound. Patients who are not immunized should receive both a booster injection and 250 units of tetanus immunoglobulin, followed by a full course of immunization.Treatment of soft tissue injuries involves early reconstructive procedures addressing both the soft tissue and the underlying bony injury in a minimum number of stages 6, 7. Occasionally it is better to delay soft tissue repair until the facial fractures have been addressed. In patients with large avulsion of tissue, definitive early reconstruction of the tissue loss with regional or microvascular flaps may be required. After adequate anesthesia has been obtained, the wound is thoroughly debrided. Nonvital tissue is conservatively excised in an attempt to salvage most ofthe tissue. Devitalized tissue potentiates infection, which inhibits phagocytosis. Repair of facial soft.

Tissue injuries can be performed under local anesthetic with dosage 0.5 To 2 %. It is usually administered with epinephrine 1:100,000. Lidocaine has a rapid onset of action, a wide margin of safety, and a low incidence of allergic sensitivity. One should avoid injecting directly into the wound when important landmarks could be dislocated and distorted. Regional nerve blocks are beneficial in minimizingthe amount of local anesthesia required and also prevent distortion of the tissues. Proper cleaning and good surgical technique are imperative in minimizing infection. Infections are rare when wound is closed so that no dead space, devitalized tissue, or foreign bodies remain beneath the sutured skin. Hydrogen peroxideis minimally bactericidal and toxic tofibroblasts even when diluted to 1:100. Diluted hydrogen peroxide is useful in the postoperative period in cleaning crusts away from incision lines in order to minimizes carring. Common methods for closing wounds include suturing, applying adhesives, and stapling. It is preferable to suture complex facial lacerations secondary to esthetic considerations. A layered closure is almost always necessary and eliminates dead space beneath the wound. If the deadspace is not obliterated, accumulation of inflammatory exudates may occur. This leads to infection, which in turn may cause tension across the epidermis. Tension can cause necrosis of the skin edges due to impairment of the vascular supply and may cause an increase in scarring. Injuries involving anatomic borders such as the vermilion of the lip must be reapproximated precisely. Examples of these landmarks include eyebrows, lipmargins, and eyelids. Lacerations should be closed by placing a suture in the centerof the laceration to avoid creating excessive tissue on the end of the laceration (dog-ear). Deep layers should be reapproximated with 3–0 or 4–0 buried resorbable sutures. The superficial skin isclosed with 5–0 or 6–0 suture. It is important to avoid causing puncture marks when grasping the wound edges. Margins should be undermined to allow slighteversion of the wound margin. Skin sutures should be removed 4 to 6 days after placement. Delayed primary closure may be necessary in some instances. Patients who may benefit from a delayed procedure include those with extensive facial edema, a subcutaneous hematoma, or those with woundsthat are severely contused and contain devitalized tissue. Secondary revision procedures are usually undertaken months later to allow for scar maturation.

Mandibular fractures. Etiology, pathogenesis, diagnostics and treatment. Complications of the mandibular fractures

Epidemiology

Mandibular fractures and dentoalveolar injuries are most commonly (80 %) the result of motor vehicle accidents, interpersonal violence and assault, other causes are sporting and industrial accidents, or falls. Most fractures occur in the mandibular body, angle, or condyle regions, with lower percentages in the mandibular ramus, coronoid and symphysis regions. The literature demonstrates that many patients with mandible fractures have more than one fracture location. This may be due to a number of variables such as direction and force of the blow, mechanism of injury, teeth present or not, among others.

Classification

The first step in the development of an appropriate treatment plan is to establish a clear understanding of the type of injury the patient has suffered, in order to provide an adequate surgical solution. A number of classification schemes have been presented to describe mandible fractures. Mandibular fractures are classified according to various parameters. The most useful is classification by the pattern of fracture present and by anatomic location.

Anatomic location (Fig. 15.3):

• Dentoalveolar fracture: any fracture that is limited to the tooth-bearing area of the mandible without disruption of continuity of the underlying osseous structure.
• Symphysis fracture: any fracture in the region of the incisors that runs from the alveolar process through the inferior border of the mandible in a vertical or almost vertical direction.
• Parasymphysis fracture: a fracture that occurs between the mental foramen and the distal aspect of the lateral mandibular incisor extending from the alveolar process through the inferior border.
• Body fracture: any fracture that occurs in the region between the mental foramen and the distal portion of the second molar and extends from the alveolar process through the inferior border.
• Angle fracture: any fracture distal to the second molar, extending from any point on the curve formed by the junction of the body and ramus in the retromolar area to any point on the curve formed by the inferior border of the body and posterior border of the ramus of the mandible.
• Ascending ramus fracture: a fracture in which the fracture line extends horizontally through both the anterior and posterior borders of the ramus or that runs vertically from the sigmoid notch to the inferior border of the mandible.
• Condylar process fracture: a fracture that runs from the sigmoid notch to the posterior border of the ramus of the mandible along the superior.
• Aspect of the ramus; fractures involving the condylar area can be classified as extracapsular or intracapsular, depending on the relation of the fracture to the capsular attachment.

Fig. 15.3. Percentage of mandible fracture site distribution. by V. A. Malanchuk, M. A. Gordijchuk, 2010

Pattern of fracture:

• Simple fracture: a simple fracture consists of a single fracture line that does not communicate with the exterior. Inmandibular fractures this implies a fracture of the ramus or condyle or afracture in an edentulous portion with no tears in the periosteum.
• Compound fracture: these fractures have a communication with the external environment, usually by the periodontal ligament of a tooth, and involve all fractures of the tooth-bearing portions of the jaws. In addition, if there is a breach of the mucosa leading to an intraoral communication or a laceration of the skin communicating with the fracturesite, edentulous portions of the mandible may be involved.
• Greenstick fracture: this type of fracture frequently occurs in children and involves incomplete loss of continuity of the bone. Usually one cortex is fractured and the other is bent, leading to distortion without complete section. There is no mobility between the proximal and distal fragments.
• Comminuted fractures: these are fractures that exhibit multiple fragmentation of the bone at one fracture site. These are usually the result of greater forces than would normally be encountered in simple fractures.
• Complex or complicated fracture: this type of injury implies damage to structures adjacent to the bone such as major vessels, nerves, or joint structures. This usually implies damage to the inferioralveolar artery, vein, and nerve in mandibular fractures proximal to the mental foramen and distal to the mandibular foramen. On rare occasions a peripheral branch of the facial nerve may be damaged or the inferior alveolar nerve injured in subcondylar fractures.
• Telescoped or impacted fracture: this type of injury is rarely seen in the mandible, but it implies that one bony fragment is forcibly driven into the other. This type of injury must be disimpacted before clinical movement between the fragments is detectable.
• Indirect fracture: direct fractures arise immediately adjacent to the point of contact of the trauma, whereas indirect fractures arise at a point distant from the site of the fracturing force. An example of this is a subcondylar fracture occurring in combination with a symphysis fracture.
• Pathologic fracture: a pathologic fracturis said to occur when a fracture results from normal function or minimal trauma in a bone weakened by pathology. The pathology involved may be localized to the fracture site, such as the result of a cyst or metastatic tumor, or as part of a generalized skeletal disorder, such as osteopetrosis.
• Displaced fracture: fractures may be nondisplaced, deviated, or displaced.
• A nondisplaced fracture is a linear fracture with the proximal fragment retaining its usual anatomic relationship with the distal fragment. In adeviated fracture, a simple angulation of the condylar process exists in relation to the remaining mandibular fragment, without development of a gap or overlap between the two segments.
• Displacement is defined as movement of the condylar fragment in relation to the mandibular segment with movement at the fracture site.The fragment can be displaced in a lateral, medial, or anteroposterior direction. In displaced fractures the articular surface of the condyle remains within the glenoid fossa and does notherniate through the joint capsule.
• Dislocated fracture: a dislocation occurs when the head of the condyle moves in such a way that it no longer articulates with the glenoid fossa. When this is associated with a fracture of the condyle, it is termed a fracture dislocation. Fracture dislocations are discussed more completely later in this chapter. The mandibular condyle may also be dislocated as a result of trauma without an associated condylar fracture. Dislocations can occur anteriorly, posteriorly, laterally, and superiorly.
• Special situations: other types of fractures that do not readily fit the above classification include grossly comminuted fractures or fractures.

Involving adjacent bony structures, such as the glenoid fossa or tympanic plate; open or compound fractures; and fractures in which a combination of several different types of fractures exist. Open fractures of the condyle are usually caused by missiles such as bullets.

Diagnosis

The diagosis of mandibular fractures must begin with careful history and clinical examination. Immediate attention should be given to problems associated with bleeding and airway compromise, which may threaten patient’s life.

In the diagnostic work-up phase, the lack of standardized ways to assess and characterize the nature and severity of the orofacial injury engenders variation in practice patterns. Symptoms of mandibular fractures include pain, malocclusion, numbness of the chin or lower lip, and abnormal lower jaw movement.

A careful history should be taken from the patient. What was the mechanism of the injury: fist, shod foot, baseball bat, fall, motor vehicle accident? Was the injury witnessed? Was there any loss of consciousness? Is there a previous history of facial trauma or fractures, either treated or untreated? Were there any pre-existing dental conditions such as deviated or limited opening of the mouth.

Clinical examination

The clinical examination should consist of inspection and palpation. It is best to proceed in an orderly fashion and to perform this evaluation as a component part of the entire head and neck examination of the trauma patient. The skin of the face and, in particular, the area around the mandible should be inspected for swelling, hematomas, and lacerations. Examination should first seek out intraoral and extraoral lacerations, abrasions, and ecchymoses. Common signs include sublingual hematoma; loose, avulsed, or fractured teeth; steps in the occlusal plane; or lack of complete intercuspation. The external auditory canal should be examined because displaced condylar fragments occasionally pierce the canal, causing it to fill with blood while the tympanicmembrane remains intact. Inability to open the mouth due to trismus (spasm of the masticatory muscles) or deviation of the chin to one side are also seen. Palpation anterior to the tragus will produce pain and reveal abnormal condyle motion in condylar neck fractures. Steps in the mandibular borders or mobile segments of the tooth-bearing alveolus suggest body fractures.

Patients often complain of the following:

• Pain or tenderness is often present at the site of impact with the possibility of a direct fracture, or at a distant site in the case of an indirect fracture.
• Difficulty chewing. Pain could be limiting mandibular function or there may be a malocclusion or mobility at the fracture site.
• Malocclusion. The patient may be able to tell the clinician about an alteration in the bite from normal; however, patients are not always reliable and may claim that the bite feels normal when it is not and vice versa.
• Numbness in the distribution of the inferior alveolar nerve. This usually indicates a displaced fracture in the region of the body or angle of the mandible on the affected side. A nondisplaced fracture often does not give rise to numbness in the distribution of the inferior alveolar nerve.

A common site for a laceration is under the chin, and this should alert the clinician to the possibility of an associated subcondylar or symphysis fracture. Typically, the patient who has suffered a fracture of the mandibular’s condyle will present with facial asymmetry. This is owing to the loss of the vertical height of the ramus on the side with the fracture, resulting in a shift of the mandible to the ipsilateral side.The best routine to evaluate facial fractures is to start at the top and work down, assessing the stability of the anatomic structures in a mediolateral fashion. It is best to begin the examination from behind the seated or supine patient. The clinician should palpate the movement of the condyle both over the lateral aspect of the joint and through the external acoustic meatus and observe the movement of the mandibule itself. If a unilateral condylar fracture is present, a subjective assessment can then be made between the palpable movement of one side compared with the other. Failure to detect the translation of the condyle.

Especially when associated with pain on palpation, is highly indicative of a fracture in this area. Palpation will frequently confirm tenderness over the lateral pole of the injured condyle with associated crepitation. However, in the case of fracture dislocations, the condyle may not be palpable. Any significant deviation on opening may be indicative of subcondylar fracture on the side to which the mandible deviates.To better evaluate this area, the fifth finger is placed in each acoustic meatus and the patient is asked to open and close the mouth. On opening, the mandible frequently shifts even more toward the side of the fracture as a result of decreased translation of the condyle on the injured side. As mentioned before, in unilateral fractures, there is deviation of the occlusion toward the fractured side, with prematureocclusal contact in the posterior region on that side. This results because the lateral pterygoid muscle on the fractured side pulls on the fractured segment and does not have any protruding influence on the mandible. The lateral pterygoid muscle on the contra lateral side is unopposed and thus causes deviation to the fractured side. The midlines no longer coincide, and there is an open bite in the body region on the contralateral side. This is often accompanied by fracture of the posterior dentition on the same side as the condylar fracture. If bilateral condylar fractures are present, the occlusion may not be deviated. The midlines are often coincident, and premature contact is present bilaterally on the posterior dentition with an anterioropen bite. The posterior dentition may be fractured on both sides in these situations. Often the patient with a fracture of the condylar process also has a limited range of motion. This limitation, however, is primarily caused by voluntary restriction as a result of pain. One has to keep in mind that any limitation of mandibular movement may also be a result of reflex musclespasm, temporomandibular effusion, or mechanical obstruction to the coronoid process resulting from depression of the zygomatic arch. Other less common findings include blood within the external auditory canal and, in the case of fracture dislocation, development of a prominent preauricular depression. Careful otoscopic evaluation of the external auditory canal is of particular importance in patients suspected to have suffered an injury at this level. Occasionally a fracture of the condylar process will produce a tear in thee pithelial lining of the anterior wall of the canal, which produces bleeding from the acoustic meatus. It is important to determine that this

Bleeding is not coming from behind a ruptured tympanic membrane, which may signify a basilar skull fracture. A detailed intraoral examination should be undertaken with good lighting and immediate availability of suction. The most common intraoral findings are malocclusion, fracture of the dentition, and decreased interincisal opening. Continuing with the systematic evaluationof the patient, it is suggested that examination of the soft tissues be undertakennext. The gingival tissue should be inspected for tears or lacerations. With the aid of a tongue blade, the floor of the mouth is examined; sublingual ecchymosisis almost pathognomonic of a fracture of the mandible. Next the dentition is examined for the evidence of broken teeth and forsteps or irregularities in the dental arch. The patient is asked to lightly bite the teeth together and to say whether the bite feels different from normal, following which the occlusion is inspected. Premature occlusal contacts are noted. The three causes of analtered occlusion in the trauma patient are a displaced fracture, a dental injury such as a displaced tooth, and a temporomandibularjoint effusion or dislocation. Ifthe patient is edentulous and hasintact dentures with him, these can be replaced in the mouth and the occlusion inspected. The mandibles hould then be grasped on each side of any suspected fracture and gently manipulated to assess mobility. If no fracture can be found but clinical suspicion remains high, the mandible may be compressed by applying pressure over both angles. This nearly always gives rise to pain at a fracture site. In the case of subcondylar fractures, firm posterior pressure on the chin will cause pain in the preauricular region.

Radiographic evaluation

To adequately screen for the presence of a mandibular fracture, at least two views at right angles to each other are necessary. The initial screening of patients could be effectively undertaken with a panoramic radiograph alone. 92 % Of fractures were seen on apanoramic radiograph alone, compared with only 66 % on a routine radiographic series without a panoramic view. However, in order to accurately visualize displacement it is recommened that the standard mandibular views consist of a panoramic radiograph, a posteroanterior mandibular view (Fig. 15.4), and reverse towne’s view. The latter view allows for visualization of the degree of medial or lateral displacement of the fracture and unveils injuries in which only subtle deviation is present, such as is seen in greenstick fractures, which are not readily evident on panoramic view. The panoramic radiograph usually requires the patient to be able to stand upright and also requires accurate patient positioning for good-quality films. In the severely traumatized patient, this may be difficult to achieve with some machines.

Fig. 15.4. Posteroanterior mandibular view of a 36-year-old male with parasymphysis (left) and angle (right) fracture

Further, mesiolateral displacement in the ramus and body and anteroposterior displacement in the symphyseal regions may also be difficult to visualize. The traditional lateral oblique views of the mandible can be used when panoramic films are not possible.They require accurate positioning of the patient and film to obtain useful views, particularly in the condylar area. A transcranial temporomandibular view may be a good addition in these circumstances. Accurate assessment of symphyseal fractures may be problematic with the standard views. A mandibular occlusal view is particularly useful in this scenario. It also aids in the assessment of the fracture of the lingual plate, particularly in very oblique fractures. Periapical views may also be necessary for evaluation of the teeth on either side of the fracture line to assess root fractures, periapical and periodontal pathology, and the relationship

Of the fracture line to the periodontal ligament of each tooth. If only one view is used, fractures can easily be missed.In the multiple-trauma patient for whom panoramic radiographs are not possible, lateral oblique views may be substituted. Other radiographic views that may be useful depending on the circumstances are posteroanterior mandibular, mandibular occlusal, and periapical. Linear tomographies of the temporomandibular joints can also be useful in the evaluation of fractures at the level of the condylar process. However, intracapsular fractures of the condylar head are often difficult to visualize accurately on plain films.The typical radiographic findings when a condylar fracture is present are the following: a shortened condylar-ramus length; the presence of a radiolucent fracture line or, in the case of overlapped segments, the presence of a radiopaque double density; and evidence of premature contact on the side of the fracture if the radiograph was taken with the patient in occlusion. If more accurate information of the involvement of the temporomandibular joint is required, axial and coronal computed tomography (CT) scans offer an excellent opportunity to study the fracture details.

Indications for CT scans are the following:

1. Significant displacement or dislocation, particularly if open reduction is contemplated.
2. Limited range of motion with a suspicion of mechanical obstruction caused by the position of the condylar segment.
3. Alteration of the surrounding osseous anatomy by other processes, such as previous internal derangement or temporomandibular joint surgery, to the degree that a pretreatment baselineis necessary.
4. Inability to position the multipletrauma patient for conventional radiographs.

(Ct scans may be the only useful radiograph that can be obtained).

Treatment

Mandibular fractures, once properly diagnosed, should be treated in a timely fashion. Coordination of treatment of the multiply injured patient by all involved services (general or trauma surgery, oral and maxillofacial surgery, otolaryngology, neurosurgery, etc.). Is critical to ensure optimal patient care. Most fractures can and should generally be treated within 48 h of initial presentation. Because many mandible fractures involve gingival tears extending to the teeth and alveolus, they are by definition compound into the oral cavity and prone to invasion by saliva and oral bacteria. Early immobilization of segments has been shown to reduce the risk of wound infections. Because of the high risk of bacterial contamination in mandible fractures, antibiotic treatment is a necessity in all compound mandible fractures both pre- and postoperatively. Teeth adjacent to fracture sites should be evaluated and assessed for their relative value for retention vs. Risk to treatment. Teeth in the line of the fracture that are periodontally compromised, mobile, or fractured beyond restorability should be removed prior to definitive treatment. These pose the risk of infection (and nonunion) as well as recuperative-phase pain to the patient. Partially fractured teeth in a patient with limited dentition may be useful to aid in closed reduction. In this situation, the tooth could be retained until the fracture treatment is complete before a final decision is made to remove or restore the tooth. Wisdom teeth (third molars) in the line of mandibular angle fractures can pose a significant infection risk. The decision to retain or remove these teeth is not simple, and should be made considering such factors: patient’s compliance and hygiene, interference with proper bony segment reduction, difficulty and risk of removal, relative bone available at the fracture site, open vs. closed reduction, and favorable vs. unfavorable fracture. Maintenance of proper oral hygiene, both pre- and postoperatively, is an important treatment adjunct in the management of mandible fractures. Loss of tissue barriers to bacterial invasion due to compound fractures in the line of teeth, gingival tears, hematomas, edema, and interference with natural cleaning mechanisms all increase infection risk. Proper oral hygiene using saline, peroxide, or medicated (chlorhexidine gluconate) rinses should be encouraged. Increased frequency of tooth brushing should be encouraged and the use of pulsatile irrigating devices is helpful in selected patients.

A proper diet and maintenance of nutritional status are additional requirement during postoperative care. Enduring 3–4 weeks of mandibular immobilization with maxillomandibular fixation (MMF) makes nutritional intake.

More difficult and weight loss is inevitable. However, a large selection of nutritional supplements is available to patients in liquid form that will minimize weight loss and malnutrition. Pre- and postoperative patient positioning and bedside suction devices can simplify the ability of patients to manage oral secretions and bleeding in the immediate postinjury or postsurgery period. Elevating the head of the bed to a 45 degree angle allows patients to clear secretions effectively. Postoperative steroids and the use of ice compresses can be effective at reduction of edema.

Closed reduction

Accurate reproduction of the pre-existing occlusal state of the patient is the cardinal rule in treatment of mandible fractures. Mandible fractures can be treated with a variety of techniques (open reduction, closed reduction, pin fixation, etc.) And with a wide variety of materials (wires, alloy plates, resorbable plates, lag screws, splints, etc.). However, proper treatment should be guided by using the simplest method to achieve the most predictable favorable result. If the principle of using the simplest method to achieve optimal results is to be followed, the use of closed reduction for mandibular fractures should be widely used. Therefore, the indications for closed reduction may simply be stated as all cases in which an open reduction is either not indicated or is contraindicated. Several conditions deserve specific mention. Grossly comminuted fractures are, as a general rule, best treated by closed reduction, because using open reduction techniques would jeopardize the blood supply to the small bone fragments and lead to an increased likelihood of infection. This category also includes gunshot wounds, which are particularly prone to infection. Fractures in the severely atrophic edentulous mandible represent a difficult clinical situation. On the one hand, there is limited osteogenic potential; the majority of the blood supply comes from the periosteum, so an open reduction further disrupts the blood supply. On the other hand, a stable, nonmobile reduction and fixation of these fractures is difficult with closed reduction techniques. Open reduction with limited dissection of the soft tissue and rigid fixation may be the preferred technique.

In situations where there is a lack of soft tissue overlying the fracture site, soft tissue flaps have to be transposed to cover a fracture site (particularly if a through communication exists between the skin and oral cavity). The presence of bone plates, screws, and wires may increase the likelihood of infection under these circumstances. Fractures in children involving the developing dentition are difficult to manage by open reduction because of the possibility of damage to the tooth buds or partially erupted teeth. Indications for closed reduction:

1. Minimally to moderately displaced simple or compound fractures.
2. Most condyle fractures.
3. Fractures in children.
4. Severely comminuted fractures or fractures in which overlying blood supply has been compromised.

Closed reduction of fractures of the mandible together with indirect fixation can be achieved by either the application of imf or by applying a technique to the mandible only. Simple, time-tested, and predictable closed reduction techniques for use in the four aforementioned categories are ivy loops and circumdentally affixed arch bars (Fig. 15.5).

Fig. 15.5. Arch bars application

Ivy loops, named for their proponent dr. Robert ivy, can be a simple and effective means of reducing and immobilizing minimally displaced favorable fractures in compliant patients with a stable occlusion (Fig. 15.6).

Fig. 15.6. Ivy loops application

A 24-gauge wire can be used to fabricate a loop on itself, and is affixed to teeth utilizing a needle driver, local anesthetic, and a wire cutter. Pigtails can be left on the wire ends to affix elastic or wire traction, elastics

Being preferred for patient safety. Ivy loops can be fixed to each dental quadrant singly or in pairs. Arch bar fixation is a time-tested and reliable technique that results in more stable fixation than ivy loops alone. Arch bars come in a variety of styles. The two force ends of the wire are tightened in a pigtail fashion over the bar under continuous apical pressure. Arch bar ligatures should typically run from the first or second molars to the canines. Anterior teeth can be utilized, when necessary, but caution should be used because wires have been known to orthodontically move incisors labially or rotationally. A smaller wire is recommended if anterior tooth ligation is needed. Reduction of segments should be with elastic or box wire traction of arch bars into an acceptable occlusion before definitive tightening of circumdental wires, proximal to the fracture site. Arch bars should be affixed tightly without evidence of vertical or horizontal mobility. Tooth-bearing fractures (symphysis, body) should, as a general rule, be reduced prior to non-tooth-bearing fractures (angle, ramus). Arch bars also provide a stable point of fixation for luxated mobile teeth and dentoalveolar segment fractures. Following closed reduction of fractures, it may be determined that a previously nondisplaced fracture, for example, in the angle, is now significantly displaced and nonreducible. In such cases, the practitioner will need to weigh the indications for open reduction and at times change the initial treatment plan. Closed reduction techniques demand patient compliance with maxillomandibular elastic traction (immobilization) for 3–4 weeks prior to release. Thus, patients with behavioral difficulties or those at risk for significant aspiration (alcoholics, patients with alzheimer’s disease) may require more predictable, definitive treatment or overtreatment to effect a more predictable outcome. Mobility at the fracture site has been shown to lead to malunion, nonunion, and osteomyelitis. Persistent trismus often results from prolonged maxillomandibular fixation; physical therapy is often useful to obtain a return to normal range of motion.

Principles of applying the arch bar and intermaxillary fixation:

1. Adapt the arch bar closely.
2. Use a cuspid wrap wire where indicated.
3. Avoid placing the wire across the intermaxillary stabilization lugs.
4. Use circumferential wires when single teeth stand alone, and intraosseous suspension or circummandibular wires in edentulous areas.
5. In the area of the fracture, reduction should be accomplished prior to stabilization of the arch bar on both sides of the fracture.
6. Tighten the wires with a continuous tension.
7. Direct the force apically when tightening the wires.
8. Tighten all wires in a clockwise direction.
9. At the end of tightening, turn only half a turn at a time.
10. Turn the end of the wire into the interproximal embrasure.

When imf is used it may be applied with either elastics or wires (Fig. 15.7). Elastics can be used for fracture reduction and for imf; however, they apply a constant pressure, which can lead to muscle spasm and pain, particularly in the masseter muscle, and they are difficult to keep clean. Wires, on the other hand, are easier to keep clean and are passive. However, they do loosen over time and may need to be tightened or replaced over the period of fixation.

Fig. 15.7. Intermaxillary fixation with elastics

Two other techniques categorized as closed reduction methods for treating mandible fractures apply to situations in which a dentate mandible opposes an edentulous maxilla, or vice verse. In the first case, the patient’s pre-existing denture can be modified with acrylic to fix an arch. This is then affixed to the maxilla by screw fixation at the pyriform rims, zygomatic buttresses, or palate. Pyriform rim wires or perialveolar wires can also be used. An arch bar is then affixed to the dentate mandible and a standard closed reduction is then performed using the maxillary denture as the occlusal basis for proper alignment followed by elastic traction fixation. Wires and /or screws are removed when the time treatment is completed. If a dentate maxilla opposes a fractured mandible with a limited number of teeth, a modification of the patient’s mandibular partial denture or fabrication of an acceptable splint can be performed in a similar way. This can then be affixed to the mandible via circummandibular wires, with care being taken to avoid wire proximity to the fracture site. Care should also be taken to avoid injury to the mental nerve as it exits the mandible and to the submandibular duct and contents of the floor of the mouth. A standard closed reduction can then be created via elastic traction fixation.

Open reduction

Indications for the open reduction:

1. Moderate to severely displaced simple or compound fractures.
2. Fractures nonreducible by closed means.
3. Fractures opposing an edentulous maxilla or nonoccluding maxilla.
4. Unfavorable fractures.

Excluded from these indications for special consideration are edentulous mandible fractures, mandible fractures in conjunction with panfacial fractures, and avulsive or pathological fractures. Open reduction techniques for treating mandible fractures are numerous, ranging from both intra- and extraoral approaches, with variations in materials such as wires, wire mesh, plates and screws, lag screws, eccentric dynamic compression plates (Fig. 15.8; 15.9).

Fig. 15.8. Fixation of fractured mandible with miniplate

Fig. 15.9. Postoperative view of fracture fixation by a miniplate on the superior border of the mandibular angle

Resorbable plates, and others. However, the basis for treatment by open reduction or closed reduction should be the same: reestablishment of an acceptable occlusal relationship for the patient in a predictable and safe fashion. In most cases requiring open reduction, a closed reduction is performed initially to approximate an occlusal relationship. A closed reduction serves to guide the practitioner in a functional as well as anatomical alignment of mandibular segments. With the occlusal relationship established, open reduction techniques then provide a means of rigidly or semirigidly immobilizing and maintaining bony segments in an acceptable position with or without compression. Bone edges approximated under compression are thought to undergo more rapid osseous healing. Extraoral approaches to the mandible include the submandibular or risdon approach, the retromandibular approach, the submental approach, the preauricular approach, and through existing lacerations. Each approach has its particular strengths and weaknesses. Intraoral access can be gained to most anatomical regions of the mandible via a vestibular incision in the mucosa or by a traditional Obwegesser is approach to the ramus and low condylar neck and coronoid regions. Extraoral approaches lend themselves well to the use of bone screws and rigid plating systems of all types, allowing wide visualization and the ability to place bicortical screws safely. Intraoral approaches are useful to access oblique fractures of the anterior mandible when lag screw fixation is desired and for placement of plates and screws (low condyle fractures) or border wires.

Wire osteosynthesis is a time-honored method for the treatment of mandible fractures. However, with the advent of rigid fixation techniques many practitioners now have limited experience in the use of direct transosseous wiring. In the case of a dentate mandibular fracture opposing a limited maxillary dentition, dental models can be utilized to fabricate acrylic splints with arch bars to establish a stable occlusal relationship. Long-term intermaxillary fixation is required when wire osteosynthesis is used as a treatment option due to the wire’s inability to limit multidimensional mobility at the fracture site during typical mandibular function. Wires can also be useful adjuncts to manipulate segments in conjunction with extraoral open reduction techniques. Rigidfixation techniques (or semirigid techniques) differ from wire fixation techniques in several important ways. Rigid fixation techniques maintain stability across a fracture site with an increased surface area (of device) to bone interface compared to wires and these techniques generally do not require prolonged intermaxillary fixation. However, there is a wide variety of alternatives to consider within this particular technique category: plate material and thickness, screw size and thread pitch, mono- or bicortical crews, tension band plates, neutral zone plates, compression plates, lag screws, reconstruction plates, wire meshes, and resorbable plates. Lag screws generate substantial cross-fragment compression and load sharing. The concepts of tension band plates, neutral zone (static plates), and compression plates are well documented in the literature. Compression plates (thicker bicortical-fixed plates) compress bony segments when placed across a fracture via eccentrically placed holes. This compression is believed to promote enhanced bony healing with no intervening callus formation. Tension band plates (smaller monocortical-affixed plates) resist tensile forces along the superior aspect of the mandible. Arch bars have been described as effective tension bands. Neutral or static bone plates (bicortical-fixed) do not offer compression across fracture lines. Wire mesh does offer some three-dimensional stability depending again on size and material. These meshes generally are indicated in avulsed or severely comminuted fractures requiring bone grafting. Resorbable plates and screws, currently under close scrutiny regarding biodegradation issues, still have considerable mechanical limitations over equivalent alloy plates and screws.

Fractures of the edentulous mandible are categorized unto themselves. The appropriate management option selected to treat the edentulous mandible fracture should take into consideration the age of the patient, the degree of functional disability postoperatively, the severity and type of fracture, and, most importantly, whether the mandible is edentulous and atrophic (pencil thin). Closed reduction technique using the patient’s existing dentures is indicated when MMF with splints will offer adequate segment control and reduction. Circummandibular wires are used to fix the denture or splint with an arch bar to the maxilla. The dentures or splints should be modified by placement of arch bars (or sections thereof) along the labial flanges and interocclusal keys should be developed occlusally to serve as occlusal stops to prevent sliding displacement. Since the blood supply to the atrophic mandible is nearly entirely supplied by the periosteum, open reduction techniques on these fractures should only done if closed reduction techniques (or biphasic pins) are unsuccessful.

Midfacial fractures. Etiology, pathogenesis, diagnostics and treatment. Complications of midfacial fractures. Management of complex craniofacial injuries and polytrauma

The maxillary bones are paired pyramidal bones that in many ways serve as the cornerstones of the facial skeleton. Each individual maxilla can be conceptualized as a 5-sided structure, the base of which makes up the lateral nasal wall. The remaining 4 sides of the pyramid are composed of the orbital floor superiorly, the alveolar ridge inferiorly, the front wall of the maxillary sinus anteriorly, and the anterior face of the pterygopalatine fossa posterolaterally. The maxilla forms the largest component of the middle third of the facial skeleton. It is closely associated with adjacent bones providing structural support for for occlusion and protection for the globes and brain. The whole midface represents the bridge between the cranial base superiorly and the dental occlusal plane inferiorly. In a transverse plane, it bridges the 2 zygomaticoorbital complexes. Midfacial skeleton contributes to form and function by establishing vertical facial height, providing anterior facial projection, and anchoring the maxillary dentition in establishing a functional occlusal relationship. It makes the maxilla a functionally and cosmetically very important structure. It consists of alternating thick and thin sections of bone that are capable of resisting significant force.

Midfacial fractures account for approximately 10–25 % of all facial fractures. They often result from high-energy blunt force injury to the facial skeleton. Typical mechanisms of trauma include motor vehicle accidents, altercations, industrial accidents and falls. Fracture of these bones is potentially life-threatening as well as disfiguring. Timely and systematic repair of these fractures provides the best chance to correct deformity and prevent unfavorable sequelae. Reestablishing continuity of the midfacial buttresses is the foundation on which maxillary fracture treatment is based.

There are horizontal and vertical buttresses or pillars of the midface that establish a relationship between the palate and alveolar process and the superior cranium and skull base region.

The major vertical buttresses of the midface include the zygomaticomaxillary, nasomaxillary and the posterior buttress. Zygomaticomaxillary buttress connects the lateral maxillary alveolus to the zygomatic process of the temporal bone. It transmits forces from the zygomatico-alveolar crest through the zygoma to the posterior aspect of the superior orbital rim and temporal bone. The nasomaxillary buttress reaches from the anterior maxillary alveolus to the frontal cranial attachment. It transmits force from the maxillary canine area through the lateral pyriform rim and frontal process of the maxilla and to the superior orbital rim. Posterior buttress involving the pterygoid plates connects the maxilla posteriorly to the sphenoid bone. It conducts force through the palatine bone to the pterygoid plates and sphenoid base. An additional unpaired midline support is the frontoethmoid-vomerine buttress. These pillars serve to diffuse the vertical forces of mastication over the broad cranial base. They are also effective shock absorbers for a vertically oriented impact to the facial skeleton.

The superior and inferior orbital rims and alveolar ridge constitute a group of weaker horizontal buttresses. While these structures provide some protection against horizontal forces, they can withstand much less force than the vertical buttresses. Therefore, vertical impact tends to be better absorbed within the facial skeleton, which resists fracture, while horizontal impact tends to overcome the weaker horizontal buttresses and shear through the vertical pillars. In a surgical approach to maxillary fractures, attempts should be made to restore the continuity of these support buttresses.

Between these structurally reinforced buttresses, the bone of the maxilla is usually thin. It covers the pneumatized maxillary sinus and forms the orbital floor. Due to this fact fractures of the midface in majority of cases result in orbital fractures.

The unique situation of the midface is its complexity of interaction of hard with soft tissue. Six cranial nerves are localized in the orbital area. Furthermore, in the midface, form, function, and esthetics are interdependent; even minor dislocations may be obvious to everyone. The complexity or simplicity of a fracture in the midface is not only based on the fracture morphology (ie, fragment size, number, dislocation) but on the degree of injury to the soft-tissue envelope.

Classification

Much of the understanding of patterns of fracture propagation in midface trauma originates from the experimental work of rené Le Fort. In 1901, he reported his work on cadaver skulls that were subjected to blunt forces of various magnitudes and directions. Le Fort considered several factors: the vectorof force overcoming the inertia of the face; the thickness of the bone and buttresses counteracting the mass, velocity, and point of application. He concluded that predictable patterns of fractures follow certain types of injuries. The recurring fracture patterns he described are still commonly utilized.

Three predominant types were described.

Le Fort I Fractures (Fig. 15.10A)

Le Fort I is also known as a horizontal maxillary fracture. It may result from a force of injury directed low on the maxillary alveolar rim in a downward direction. The fracture extends from the lower third of the nasal septum to the lateral pyriform rims, travels horizontally above the teeth apices through the base of the maxillary sinuses, crosses below the zygomaticomaxillary junction, and traverses the pterygomaxillary junction to interrupt the pterygoid plates. It separates the alveolar processes, palate, and pterygoid processes from the facial structures above. The superior two-thirds of the maxilla remain associated with the face. Fracture dislocations of segments of the alveolus may be associated with this fracture. The fracture lines of a Le Fort I fracture may be linear (simple) or comminuted (complex). With high-energy injuries, the palate may be split in the midline in addition to the Le Fort I fracture.

Le Fort II Fractures (Fig. 15.10B)

Le Fort II is also known as a pyramidal maxillary fracture. It may result from a blow to the lower or mid maxilla. Such a fracture has a pyramidal shape and extends from the dorsum of the nose at or below the nasofrontal suture through the frontal processes of the maxilla, inferolaterally through the lacrimal bones and inferior orbital floor and rim through or near the inferior orbital foramen, and inferiorly through the anterior wall of the maxillary sinus; it then travels underneath the zygomaticomaxillary buttress, across the pterygomaxillary fissure, and through the pterygoid plates. Various amounts of the pterygoid plates usually remain attached to the posterior maxilla. Thus, maxillary fractures at the Le Fort II level involve most of the nasal bones, the maxillary bones, the palatine bones, the lower two-thirds of the nasal septum, the dentoalveolus, and the pterygoid plates. The segments may be intact below this line of fracture, but they are most often comminuted.

Le Fort IІІ Fractures (Fig. 15.10C)

Le Fort III is also known as a craniofacial dysjunction because the entire mass of facial bones is separated from the cranial base. These represent the most superior pattern of the maxillary fractures. It may follow impact to the nasal bridge or upper maxilla. The fracture line begins at the frontozygomatic suture along the lateral aspect of the internal orbit along the sphenozygomatic suture line to the inferior orbital fissure, extends medially across the floor of the orbit up the medial wall of the orbit towards the dorsum of the nose where it crosses and proceeds to the opposite side in the same manner. Intranasally, a branch of the fracture extends through the base of the perpendicular plate of the ethmoid, through the vomer, and through the interface of the pterygoid plates to the base of the sphenoid. Various amounts of the pterygoid plates usually remain attached to the posterior maxilla. Le Fort III fractures are often associated with head injuries, dural tears with associated cerebrospinal fluid (csf) leaks, significant orbital trauma, and other fractures of the craniofacial skeleton.

Fig. 15.10. Anteroposterior and lateral views of the skull showing the Le Fort classification system of maxillary fractures:
A – Le Fort I fracture; B – Le Fort II fracture; C – Le Fort III fracture

In reality, the Le Fort classification is an oversimplification of maxillary fractures. It described the typical lines of weakness in the face using low-velocity impact forces directed against cadaver skulls. The amount of force impacted during a motor vehicle accident is much greater than Le Fort took into consideration during his work in the late XIX century. Pure Le Fort I, II, and III fractures are rare. In most cases, maxillary fractures are a combination of the various Le Fort types. Fracture lines often diverge from the described pathways and may result in mixed-type fractures, unilateral fractures, or other atypical fractures. Segmental alveolar fractures of the tooth-bearing region can occur without a Le Fort I. Fractures of the thin maxillary wall without buttress involvement are also common. Parasagittal fractures of the palate also occur, often in combination with typical midface fractures.

The range of combined midfacial/panfacial fractures is enormous. This is due to the variety in possible mechanisms which occur during impact leading to the midfacial injury. In general, low velocity trauma less often leads to severe midfacial fractures than high velocity trauma.

Unlike with fractures in other bones, maxilla is practically unaffected by muscle pull, muscle forces do not play a significant role in the final position of the broken bony segments. Instead, the basis for the patterns of maxillary fractures depends on location, direction, and energy of the impact result in different injuries. Second factor is the anatomy of the mid face which provides strength and support to protect against injury.

Clinical evaluation and diagnosis

Evaluation of the maxilla and facial bones should be undertaken only after the patient has been fully stabilized and life-threatening injuries have been managed.

After initial stabilization of the trauma patient, evaluation of the facial injuries should commence with reassessment of the patient’s airway neurological, visual, and cervical spine status. Oral bleeding, loose teeth, edema, or associated mandible fractures may lead to airway problems. Head injuries are often associated with midface fractures and csf leaks should

Be suspected in patients with Le Fort II or III type fractures. The presence and extent of other injuries in patients with multiple trauma may influence the timing of fracture repair and patient outcomes. Information regarding the mechanism of the injury may assist in determining a diagnosis. In particular, knowing the magnitude, location, and direction of the impact is helpful. High-energy trauma is oftern associated with concomitant injuries. A history of mental status changes or loss of consciousness should cause concern regarding intracranial injury.

A careful and thorough evaluation of the eye and orbit is paramount. Every patient with orbital fractures should have an examination that includes visual acuity testing, visual field testing, ocular motility, binocular vision, globe position, pupillary reaction, intraocular pressure testing. In some cases preexisting optical correction by glasses or contact lenses or ocular disorders such as cataract, glaucoma, and retinal disorders can compromise basic visual acuity testing.

During examination of the eyes and orbit, the integrity of the orbital rims, orbital floor and intercanthal distance are also examined. Unlike Le Fort II fractures, Le Fort III fractures are associated with lateral rim and zygomatic breaks. Visual changes may signify a disturbance of the optic canal, problems within the globe or retina, or other neurologic lesions. An increased intercanthal distance implies displacement of the frontomaxillary or lacrimal bones or avulsion of the medial canthal ligament. For extensive involvement of the orbit or globe, consultation with an ophthalmologist is necessary. The standard assessment of visual status can be performed in the conscious patient. In the unconscious patient only regular light reflex testing is performed.

Associated soft tissue injuries of the face need to be cleansed and evaluated regarding the need for early repair. Focal areas of swelling or hematoma may overlie an isolated fracture. Periorbital swelling may indicate Le Fort II or III fractures.

Intraoral assessment of the patient’s dentition and occlusion should begin with the examination of the palate and maxillary alveolus for loose or missing teeth, lacerations, bleeding, and abnormal mobility. The maxillary segment is displaced posteriorly and inferiorly. This may cause premature contact of the molar teeth, resulting in an anterior open bite deformity.

The maxilla and palate will often be unstable and mobile on bimanual examination with Le Fort fractures and the midface may have a characteristic retrusion with loss of projection.

Asymmetry of the nose, traumatic telecanthus, a flatnasal bridge, and a dish-shaped face can be noted. A global posterior retrusion of the midface creates a flattened appearance of the face in Le Fort II or Le Fort III fracture. Intraorally the examiner may see fractured teeth, vestibular ecchymosis and edema, palatal ecchymosis, mucosal lacerations and bleeding, steps or diastema in the maxillary teeth, and malocclusion. Finger palpation of the maxillary contour intraorally may provide additional information about the integrity of the nasomaxillary buttress, anterior maxillary sinus wall, and zygomaticomaxillary buttress.

The skeletal framework of the faceshould be carefully palpated to detect for bony irregularities, step-offs, crepitus, and sensory disturbances. In many patients with facial fractures the bone injury may be obscured with soft tissue swelling, ecchymoses, wounds, and hematomas. With respect to the maxilla, the alveolus should be palpated and any fractures or mobility noted. Mobility of the midface may be tested by grasping the anterior alveolar arch and pulling forward while stabilizing the patient with the other hand. The size and location of the mobile segment may identify which type of Le Fort fracture is present.

Nasal fractures and associated epistaxis are common inpatients with midface fractures. Examination of the nose starts with inspection for swelling or asymmetry, followed by palpation. Characteristic signs for nasal fractures are:

• Pain.
• Bleeding.
• Swelling.
• Compromised nasal airway.
• Crepitation.
• Palpable bony dislocation.

If the nasal airway passage is compromised the reason has to be investigated.

Nasal inspection using a speculum with appropriate light (headlights are recommended) allows for examination of the nasal cavity. If further clinical examination of more posterior or cranial parts have to be performed, additional nasal endoscopy may be indicated.

The nasal bones are typically quite mobile in Le Fort II fractures, along with the rest of the pyramidal free-floating segment. Intranasal examination may reveal fresh or old blood, septal hematoma, or cerebrospinal fluid rhinorrhea.

Clinical signs for midfacial fractures:

• Facial swelling (edema, hematoma, emphysema), and deformity.
• Subconjunctival bleeding (hyposphagma).
• Oronasal bleeding.
• Palpable and crepitating dislocated bony contour in the periorbital region.
• Displacement of the globe (hyper-, hypo-, eno-, exophthalmos).
• Displacement of the medial canthal tendon (depending on the degree of noe fracture).
• Compromised ocular motility.
• Double vision.
• Sensory deficit (hypoesthesia, anesthesia, paresthesia) of the trigeminal nerve.
• Localized pain.
• Occlusal disturbance.
• Csf leakage (in case of anterior skull base involvement).

Clinical signs of Le Fort I

In a recent injury there may be slight swelling of the upper lip, but there is none of the massive oedema of the face which characterizes Le Fort II and III fractures. Typically ecchymosis is present in the buccal sulcus beneath each zygomatic arch. The occlusion is disturbed and a variable amount of mobility may be found in the tooth-bearing segment of the maxilla. Some Le Fort I fractures are so mobile that the whole fragment drops and the patient.

May have to keep the mouth slightly open to accommodate the increased vertical dimension of the bite. This situation may result from a direct blow from a sharp object in the front of the mouth above the apices of the teeth. When this happens a soft-tissue laceration is often present, and in extreme cases the resulting down-fracture of the maxilla may be so gross that it may be possible to see directly into the nares and the maxillary antra through the upper lip.

Most Le Fort I fractures are not as mobile as this. Indeed, the impacted type fracture may be almost immobile and it is only by grasping the maxillary teeth and applying slight but firm movement, that a characteristic grate can be felt which is diagnostic of the fracture. The maxillary cheek teeth should be moved apart in the same way to make sure there is no associated midline split in the palate.

In the impacted type of fracture there may be damage to the cusps of individual teeth, usually in the premolar region, caused by the impaction of the mandibular teeth against them. Percussion of the upper teeth results in a distinctive “cracked-pot” sound, similar to that produced when cracked china is tapped with a spoon. This sign is present whenever there is a fracture of the central mid-face, but is particularly valuable in the diagnosis of Le Fort I fractures.

All possible variations of open and closed type fractures may occur and it is possible to see the condition unilaterally when it involves only one maxilla, the tooth-bearing portion being split along the median palatal suture. The complete Le Fort I fracture is often associated with a split in the palate, sometimes along more than one line so that each of two or more fragments may be mobile. Multiple alveolar fractures of this nature are frequently complicated by damaged or subluxed teeth.

Clinical signs of Le Fort II

The most obvious difference between the Le Fort II and III fractures, from the clinical point of view, is the detection of a step deformity in the bone of the infra-orbital margin. This is made more apparent when the zygomatic complex on each side is intact.

As the fracture line passes across the inferior orbital rim, there is likely to be associated injury to the infra-orbital nerve resulting in anaesthesia or paraesthesia of the cheek.

Similarly the fracture line in the orbital floor may result in limitation of orbital movement in an upward direction with diplopia and possibly enophthalmos.

Because the line of fracture is below the lateral attachment of the suspensory ligament of lockwood, alteration of the pupil level does not occur unless there is an associated fracture of the zygomatic complex.

Gagging of the occlusion and retropositioning of the maxilla as a whole will be noted on intra-oral examination, but when the maxillary teeth are grasped, it will be noted that the mid-facial skeleton moves as a pyramid, the movement being detected at the infraorbital margins and nasal bridge.

The Le Fort II fracture may be impacted in the same manner as the Le Fort I, in which case little or no mobility can be detected. There is frequently a midline or paramedian split in the pyramidal block. The passage of the fracture line across the zygomatic buttress gives rise to haematoma formation in the upper buccal sulcus on each side, opposite the first and second molar teeth.

Unless the fracturing force was applied directly to the nasal region, the comminution of this part of the pyramidal block is usually minimal. In the same way there is less danger of extensive associated fracture of the anterior cranial fossa in the region of the cribriform plate, and cerebrospinal fluid rhinorrhoea is therefore not a constant clinical finding. However, when a Le Fort II fracture is present, it must be assumed that a breach of the dura mater has occurred, even if overt leakage of cerebrospinal fluid is not detected.

Clinical signs of Le Fort III

Superficially the Le Fort III fracture appears very similar to the Le Fort II fracture, but it is usually obvious that the injury is very much more severe. It is, however, very unusual to find a Le Fort III fracture occurring in isolation:

• There is tenderness and often separation at the frontozygomatic sutures. The amount of separation may not be symmetrical in which case the facial skeleton will be tilted to the side opposite to the direction of the fracturing force.
• Separation of both frontozygomatic sutures produces lengthening of the face and lowering of the ocular level, due to the fracture passing above whitnall’s tubercle, removing the support given to the eye by lockwood’s suspensory ligament. As one or both eyes drop, the upper lid follows the globe down, producing unilateral or bilateral pseudoptosis described as “hooding” of the eyes.
• A complete fracture at the Le Fort III level cannot occur without fracture of each zygomatic arch. Coincident independent fracture of one or other zygomatic complex occurs almost invariably. The displacement of the zygomatic complex will be detectable by palpation, which will reveal flattening and a step deformity at the infra-orbital margin. The arch of the zygoma will exhibit tenderness and some deformity in a pure Le Fort III fracture.
• If a finger and thumb are placed over the frontonasal suture region, and the dento-alveolar portion of the upper jaw is grasped with the other hand, movement of the entire face can be demonstrated. As mentioned previously the zygomatic bones may often be independently mobile.
• Intra-orally there is gagging of the occlusion in the molar area, as in other fractures of the mid-face. When lateral displacement has taken place, the molar teeth will be found to be gagged on one side only with a posterior open bite on the opposite side, and deviation of the upper midline. The entire occlusal plane may have dropped, holding the mandible open, a dramatic but rather unusual finding.
• A very loose Le Fort III fracture is usually associated with disruption of the cribriform plate area, and this type of fracture may therefore produce a profuse cerebrospinal fluid rhinorrhoea. In this situation the possibility of an intracranial aerocele must be considered seriously, and serial radiographs of the skull should be taken during the first few days after injury.

Clinical signs of nasal complex fractures:

• Bruising of skin over nasal bones.
• Laceration of skin of bridge of nose.
• Bilateral medial orbital ecchymosis.
• Epistaxis.
• Deformity of nose.
• Crepitus of bones of nasal complex.
• Unilateral or bilateral telecanthus.
• Airway obstruction.
• Septal deviation.
• Septal laceration or haematoma.
• Cerebrospinal rhinorrhoea.

Imaging

Fractures are identified clinically and confirmed radiographically. In the past the waters’ view and lateral facial radiographs were used in identifying maxillary fractures and may still be used today in remoteareas without access to a computedtomography (CT) scanner.

Fine details of the fracture sites are difficult to visualize. Axial and coronal CT scans of the midface should be obtained if a scanner is available. If clinical evidence strongly indicates maxillary fracture (midface mobility and malocclusion with intact mandible), then CT imaging is a confirmatory test for maxillaryfractures. Important indications forct scanning are suspected orbital floor fractures (best diagnosed in the coronalview) and surgical planning. CT scans can also demonstrate the soft tissue differences of hematoma or edema of the subcutaneous tissue, muscle, and fat. For severe midface trauma or maxillary displacement the three-dimensional CT scan is available.

Radiological assessment with plain films has limited value and should be reserved for situations in which computed tomography (CT) is not readily available. CT scans have dramatically changed the evaluation of midface fractures and all patients with suspected midface fractures should be scanned. Besides axial CT scans, coronal imaging (true coronals when feasible or coronal reformats of axial scans) is frequently useful in better evaluating the extent of orbital fractures. Although the Le Fort classification system is still widely employed and useful for describing fracturepatterns, CT scans are better able to evaluate and delineate precisely the exact location and extent of fractures. Most fractures in this region are comminuted

And usually involve different components of pure Le Fort-type fractures. CT scans provide superior guidance for treatment planning.

Imaging in patients with midfacial fractures

To assess the individual extent and type of fracture, CT or cone-beam based radiological examination should be performed. It is strongly advised to obtain postoperative CT scans to assess the surgical result.

By obtaining CT axial fine slices, the surgeon can obtain excellent reformatted coronal, oblique parasagittal views. The surgeon can also obtain 3D views. Examination of the craniofacial skeleton vastly benefits from 3D imaging and interactive image analysis. The modern surgeon should be trained to use the dicom voxel data set for multiplanar and 3D image analysis. The modern surgeon should be able to use full radiological information and not a limited selection of print outs or digitized views.

The surgeon thus changes his or her former role as a consumer of radiological information to interpreter of this data set. Having implemented computer assisted fracture assessment, much more detailed preoperative information is available to the surgical team. Radiological information acquired intraoperatively can be compared with different data sets (obtained pre- and postoperatively) via image fusion.

If no adequate visualization software for the dicom data sets is available, then CT axial, coronal, and oblique parasagittal views of the midface for simple fractures, with 3D views for more complex fractures are recommended.

Cone-beam technology allows adequate determination of the hard tissue problems, but is not equivalent to ct technology in terms of soft-tissue assessment (eg. Retrobulbar hematoma). Further limitations of cone-beam technology are given by a more limited scanning region. Cone-beam technology is becoming more important for pre-, intra- (3D C-arm), and postoperative imaging. Because there is less exposure to radiation, cone-beam scan may be more suitable for follow-up.

Prior to ct imaging, 2D X-rays had been considered adequate for pre- and postoperative diagnostics in orbital floor fractures. One of the great weaknesses of 2D imaging is that in many cases the modality may reveal a fracture, but not the degree of fracture displacement. With the availability

Of CT imaging, the surgeon can better define fractures, as well the degree of fracture displacement and the need for reduction. Plain X-rays therefore should only be considered appropriate if ct is unavailable or if distinct information for hard-tissue structures involved such as dentition (dental X-ray, orthopantomogram) is required.

2D imaging can include:
• Water’s view (this was a plain X-ray used for visualizing sinus fractures before CT was available. This offers poor visualization of fractures and does not provide the surgeon with adequate information about fracture displacement).
• Orthopantomogram (opg) this is a standard view normally used for the mandible, but can also provide information regarding midface:
  • Lateral view (cephalic).
  • Submentovertex view (for zygomatic arch injuries).

MRI or ultrasound can be helpful in some specific questions related to soft tissues but is in most cases not included in standard diagnostic workup (one exception is optic nerve sheath hematoma detection).

2D imaging particularly lacks precision for the sagittal extent of the injury. Treatment for midfacial fractures based on 2D imaging risks underestimating the severity of the injury. This might result in later deformities such as enophthalmos or hypophthalmos which could have been avoided by 3D preoperative radiological examination.

Special scanning procedures might be necessary if the anterior or lateral skull base is involved and, particularly, for detection or control of CSF-fistula or aneurysms. Special fine slices may be considered for the petrous portion of the temporal bone, particularly in cases where there is paralysis of the facial nerve.

In the event of accompanying dental trauma with missing tooth parts or empty alveolar sockets, it is important to determine the location of the missing elements. For dislocations of teeth into the jaws, standard orthopantomogram (OPG) is helpful. If the missing tooth or tooth parts cannot be localized, additional radiographs of the upper and lower airways (including frontal and/ or lateral cervical X-ray, frontal and/or lateral chest X-ray) and/or upper and

Lower gastrointestinal pathway should be considered. Additional endoscopic measures may be considered in retrieving dislocated dental fragments.

Management of the maxillary fractures

Definitive surgery should not be undertaken until the patient has been stabilized regarding other life-threatening injuries.

Initial attention should be directed at establishing an airway and controlling hemorrhage as the patient may die of concomitant injury or failure to manage the sequelae of maxillary fractures. The most frequent cause of hemorrhage in Le Fort level fractures is a fractured septum. This bleeding may be managed by placing nasal packs including gauze packing. Bleeding from sites of laceration or abrasion may be controlled by tamponade.

In case of severe bleeding the following options should be considered:
• Compression: either by nasal packing, balloon tamponade, or direct compression.
• Electrocautery: if a clear bleeding source can be evaluated.
• Control and adjustment of blood pressure.
• Assessment of current medical treatment for anticoagulation.
• Interventional embolization when other methods fail.
• In some cases fracture reduction may be required to reduce bleeding.

There are also a variety of possible injuries affecting the globe that may require immediate treatment. Pressure increase in the periorbital region due to retrobulbar hematoma can cause significant injury of the neurovascular structures with eventual loss of vision. If a retrobulbar hematoma leads to a tense, proptotic globe, emergency decompression should be considered. Transcutaneous transseptal incisions may help evacuate the hematoma and release the periorbital pressure. Alternative methods such as transconjunctival pressure release and/or lateral canthotomy and inferior cantholysis should be considered according to patient condition. Special attention has to be paid to the posterior third of the orbit and the bony optic canal. Bony dislocations in these anatomical areas are more likely to be associated with traumatic optic nerve lesions.

Careful coordination with the anesthesiologist regarding airway management using nasal or oral intubation. In many cases nasal intubation may interfere with reduction of nasal and midface fractures, while oral intubation may hamper evaluation and restoration of occlusal relationships. In this cases submental/submandibular intubation and/or tracheostomy should be considered.

In midfacial fracture repair the time frame regarded appropriate for primary fracture treatment is limited to 2 weeks (not including accompanying complications requiring immediate treatment, such as dentoalveolar trauma or post-traumatic visual loss). As soon as the general condition of the patient allows, definitive treatment should be undertaken. After 2 weeks, the treatment is regarded as delayed and thus has to follow the protocol of secondary post-traumatic reconstruction.

Extensive maxillary fractures are usually associated with significant cosmetic and functional sequelae. Expeditious definitive therapy is needed to best correct these problems.

Treatment of midface fractures aims to restore preinjury facial appearance and occlusion by restoring anterior facial projection and vertical facial height. Fracture treatment should be customized to the extent and location of the fractures based on clinical evaluation and CT scan findings. Dental occlusion is the most important parameter in reestablishing facial contour, reduction of fracture, and obtaining postoperative chewing function. The most common means of placing the patient into maxillomandibular fixation is the application of arch bars. A second surgical principle is to achieve anatomical correct repositioning of all midfacial bones. The height, width, and projection must be reestablished. Successful reconstruction of midfacial fractures is obtained by reestablishing the midfacial buttresses. If available, dental casts, stereolithographic models, and/or premorbid photographs may be useful guides for treatment.

Nondisplaced fractures may require minimal treatment. Maxillary fractures isolated to the dentoalveolar process and involving bone should be manually reduced and rigidly fixated with arch bars and ligature wires.

Rigid fixation techniques in the dentate patient begin with fixation of the occlusion. This ensures that the patients maintain their preoperative occlusal status.

There are several techniques to providing mandibulo-maxillary fixation. The gold standard in mandibulo-maxillary fixation is the use of arch bars. However, there are various methods of mandibulo-maxillary fixation to be used in specific clinical situations. Strong consideration should be given to the repair of any mandible fracture before the maxilla is stabilized.

Common mandibulo-maxillary fixation methods are:
• Arch bars.
• Ernst ligatures.
• Ivy loops.
• Gilmer wiring.
• Stout wiring.
• Kazanjian buttons.
• Bone supported devices including intermaxillary fixation screws, hanger plates and interarch miniplates.

Arch bars are preferred for temporary fragment stabilization in emergency cases before definitive treatment. They are used as a tension band in combination with rigid internal fixation or for long-term fixation in conservative treatment. The method is also used for fixation of avulsed teeth and alveolar crest fractures.

Before placing the arch bars the occlusion must be checked. Determine if the patient has a normal occlusion or a preexisting malocclusion before taking the patient to the operating room. In the case ofjaw malformations, such as a deep bite deformity, it may be impossible to use arch bars.

The prefabricated arch bar must be adjusted in shape and length according to the individual situation. The arch bar should not damage the gingiva. Firstly, the bar is adapted closely to the dental arch. It should be placed between the dental equator and the gingiva.

The hooks should be symmetrically positioned in the upper and lower jaw, because the symmetry is essential for right placing of the elastics. The bar should not extend past the most distal tooth or protrude into the gingiva.

One pitfall when using arch bars is the risk of contamination of blood-borne infection from patients. Passing the wires to secure the arch bar can.

Result in a puncture or tear in the surgeon’s glove and the possibility of disease transmission to the surgeon.

To fix the arch bar in place, a ligature is prepared in the premolar region of each side. The wire ends should not damage the surrounding soft tissues. After positioning the arch bar it is fixed with ligature using the wire twister. One end of the wire is above the arch bar and the other end below it. The wire is then cut with the cutter and its ends are turned away from the gingiva to prevent damage.

Mandibulomaxillary fixation can be used either intraoperatively to establish the correct occlusion or as part of postoperative management of the patient’s injury. Mandibulomaxillary fixation may be accomplished with wires or training elastics depending on the overall treatment plan for this patient. The wire loop is placed over the maxillary and mandibular lugs of the arch bar and the wire loop is tightened. Mandibulomaxillary fixation completed with wire fixation. At least three wires or elastics, a posterior wire loop in each side, and an anterior wire loop will provide stable fixation.

In cases of gross comminution, periodontal disease, or inadequate partial dentition (less than three occluding teeth per sextant), occlusal wafers or palatal splints are useful. These splints are fabricated after impressions have been taken. The gunning’s splint has been used to establish intermaxillary fixation for edentulous patients; this splint is essentially a denture base plate fabricated to the existingedentulous or partially edentulous ridgewith arch bars or suspension brackets. Dentures can also be secured to the jaws with bone screws before intermaxillary fixation is attempted.

Temporary mandibulomaxillary fixation during reduction serves to address the posterior height of the facial skeleton by utilizing the height of the ramus of the mandible, since the posterior maxillary buttress is not directly opened. Additional use of mandibulomaxillary fixation in the postoperative period for 2–4 weeks may be necessary depending on the fracture pattern and stability achievable in individual situations.

However, in many cases techniques of closed reduction alone led to complications including lack of midface projection and loss of vertical height. As a result, extended open reduction techniques were developed initially using wire and subsequently miniplate fixation of the maxillary buttress

System, along with concurrent treatment of associated fractures in order to avoid or minimize such complications.

As a general principle, all fractures should be exposed and reduced before plating.

Open reduction and internal fixation of midfacial fractures are usually accomplished via an intraoral sublabial approach with gingivobuccal incisions placed unilaterally or bilaterally, depending on the extent of fractures requiring subperiosteal exposure and reduction. This approach can be combined with various other methods including a transconjunctival approach to the orbital floor and rim, depending on fracture extent. Other approaches used to give access to the inferior, lower medial, and lateral aspects of the orbital cavity are subciliary, subtarsal, and infraorbital approaches.

Le Fort III fractures will often require an additional coronal approach for adequate exposure and reduction of the fracture. The coronal or bitemporal incision is also used to approach the anterior cranial vault, the forehead, and the upper and middle regions of the facial skeleton.

In some cases the glabellar approach can be used to expose nasoethmoidal fracture. It is particularly advantageous in elderly patients who have developed horizontal glabellar furrows. Facial fractures are often associated with lacerations. These existing soft-tissue injuries can be used to access directly the facial bones for management of the fractures.

The maxilla should be stabilized to the next highest stable facial structure, which varies with Le Fort fracture level. At the Le Fort I level, fixation is placed along the vertical buttresses of the maxilla at the piriform and zygomatic buttresses. The reconstruction sequence to reestablish midfacial pillars and dimensions begins with establishing the most reliable reference structures. This can be occlusion, an outside-to-inside or an up-to-down procedure as a first step. At higher Le Fort levels it may be necessary to use fixation to the nasalbones, the orbital rims, or the zygomaticofrontal sutures. The importance of achieving accurate three-dimensional reduction of the fractures along with accurate alignment of the occlusion prior to applying internal fixation cannot be overemphasized. Accurate reduction and titanium miniplate fixation of the fractured nasomaxillary and zygomaticomaxillary buttresses are key elements in stabilizing Le Fort I and II fractures. This should be accomplished after associated fractures are addressed, especially.

In patients with Le Fort II and III fractures, and the patient is placed in maxillomandibular fixation for occlusal alignment. Perioperative prophylactic antibiotics are prescribed in patients with midfacial fractures.

The introduction and acceptance of low profile titanium miniplates (1.5–2.0 mm screws) have improved the ability to stabilize the majorload-bearing midface buttresses. Even smaller microplates (1.0–1.3 mm screws) assist in stabilizing multiple comminuted segments in non-load-bearing regions after fixation of the major buttresses.

Complexity of fracture fixation is not only determined by fracture morphology, including the number of fracture lines, but also depends on the necessary approach, accessibility, visibility of the area of interest and the stability of the fracture reduction.

Every under- or overcontouring of the bony midface in primary fracture repair results very likely in unfavorable projection of the soft-tissue mask and this again results in an esthetic compromise. In addition, functional disorders may follow such as malocclusion or orbital dysfunction.

The number, size, and position of plates and screws might vary according to the biomechanical needs and individual fracture situation.

In cases of comminution with small fragments, surgical exposure may require these fragments be removed, resulting in a defect fracture. Immediate bone grafting has been advocated for the severely comminuted maxillary antrum. This treatment prevents prolapse of the facial soft tissue into the maxillary sinus and the facial deformation that results. Titanium mesh works well for this procedure. The use of plate fixation should be kept to the minimum required to achieve fracture stabilization. Multiple facial fractures should be treated as separate units.

Complications:
1. Infraorbital nerve paresthesia.
2. Enophthalmos.
3. Infection.
4. Exposed hardware.
5. Deviated septum.
6. Nasal obstruction.
7. Altered vision.
8. Nonunion.
9. Malunion or malocclusion.
10. Epiphora.
11. Foreign body reactions.
12. Scarring.
13. Sinusitis.

Some of it may not be readily apparent untilweeks or months after injury, but the potential for their occurrence should be in mind during evaluation and treatment of the patient. Perioperative and postoperative airway obstructions are unusual in cases of maxillary fracture alone. However, these conditions may occur in association with extubation while the patient is obtunded,with a septal hematoma or nasal packing, and with excessively edematous soft tissues that do not allow breathing through the nasal airways. Patients with intermaxillary fixation and complete dentition may have difficulty breathing during this time. Reintubation, opening nasopharyngeal airways, or merely removing the intermaxillary fixation may be effective. Uncorrected nasal septal fractures can lead to postoperative airway obstruction that remains afterall soft tissue swelling has resolved. Acute sinusitis can result from prolonged nasotracheal intubation. Acute or chronic sinusitis may also occur in the ethmoid, sphenoid, frontal, and maxillary sinuses because fractures may obliterate or obstruct the sinus ducts or ostia. Postoperative hemorrhage occurs if arterioles and veins are not ligated when lacerations are repaired, if inadequate bone reduction allows continued oozing of blood. Lacerations should be reexplored so that hemorrhage can be controlled. Hematomas should be drained. Oozing of blood from bone requires re-reduction or the use of bonewax. Hemorrhage from a major artery requires emergency tamponade; if the source cannot be identified, then arteriography and embolization are indicated. Aneurysms and pseudoaneurysms are complications of maxillofacial trauma but rarely occur as the result of isolated maxillary fractures.

They can also result in postoperative bleeding and are indications for angiography and embolization. Because of the proximity of the maxillato the orbits, complications associated with vision can occur. Blindness is rarely associated with midface fractures and is most often seen in fracture

Patterns involving the orbit, often with a more severe mechanism of injury. Immediate postoperative blindness can be a complication of the reduction of high Le Fort fractures (Le Fort III or fractures involving the orbits) and occurs because of increased intraorbital hemorrhage or pressure, a retinal artery spasm, retrobulbar hemorrhage, or the impingement of bone fragments on the optic nerve. An undiagnosed or inadequately treated orbital floor fracture (alone or in combination with a zygomatic omponent) can lead to enophthalmos and diplopia.The most obvious postoperative complication sare misplaced bone segments or fixation devices. These complications are readily identified by clinical examination (eg., Alocclusion) or postoperative radiographic examinations. A second surgical procedure will correct such complications. Other complications related to rigid internal fixation include palpability, infection, extrusion or exposure, translocation, stress shielding, cortical osteopenia, and nonunion. Nonunion of the fractured segments can occur as the result of inadequate blood supply, inaccurate position, movement of segments, infection, or nutritional deficiencies. 50 Infections may be caused by contaminated soft tissue lacerations or foreign bodies, hematomas, or odontogenic infections from previously diseased or fractured teeth. Infection round bone plates and screws can occur years after their placement. Malunion of maxillary fractures can obstruct the nasolacrimal ducts. This obstruction causes epiphora and may lead to episodes of dacryocystitis. Bone segments from fractured or improperly reduced maxillary fractures can also impinge on the infraorbital nerve, causing numbness of the distribution of the second division of the trigeminal nerve. Although the reduction and fixation of maxillary fractures may at times seem straightforward, the proximity of complicated anatomic structures and the consequences of inaccurate repair make it incumbent on the surgeon to follow sound surgical principles in the management of these fractures.

Fractures of the zygomatic complex. Classification, etiology, pathogenesis, diagnostics and treatment. Complications of the zygomatic fractures

The zygomatic bone occupies a prominent position in the facial skeleton. It plays a key role in determining facial width as well as acting as a major buttress of the midface. Its anterior projection forms the malar eminence and is often referred to as the malar bone. The zygoma has several important articulations in the midface. From a frontal view, the zygoma can be seen to articulate with 3 bones: medially by the maxilla, superiorly by the frontal bone, and posteriorly by the greater wing of the sphenoid bone within the orbit. From a lateral view, one clearly can see the temporal process of the zygoma join the zygomatic process of the temporal bone to form the zygomatic arch. The zygoma is the main buttress between the maxilla and the skull; but in spite of its sturdiness, its prominent location makes it prone to fracture. The mechanism of injury usually involves a blow to the side of the face from a fist, object, or secondary to motor vehicle accidents. Moderate force may result in minimally or nondisplaced fractures at the suture lines. More severe blows frequently result in inferior, medial, and posterior displacement of the zygoma. Comminuted fractures of the body with separation at the suture lines are most often the result of high-velocity motor vehicle accidents. In general, displaced fractures will involve the inferior orbital rim and orbital floor, the zygomaticofrontal suture, the zygomaticomaxillary buttress,and the zygomatic arch. Occasionally, however, a direct blow to the arch will result in an isolated depressed fracture of the arch only. Attached to the zygoma anteriorly are the zygomaticus minor and major muscles, as well as part of the orbicularis oculi muscle. Laterally, the masseter muscle from below attaches to the zygomatic arch and produces displacing forces on the zygoma. Lastly, the branches of the fifth and seventh cranial nerves lie within the bounds of the midface. Particularly, the temporal and zygomatic branches of the seventh nerve and the zygomaticotemporal and zygomaticofacial branches of the fifth nerve must be identified carefully upon surgical dissection of the area to prevent complications of paresis and paresthesias, respectively.

The integrity of the zygoma is critical in maintaining normal facial width and prominence of the cheek.

Fracture lines usually run through the infraorbital rim, involve the posterolateral orbit, and extend to the inferior orbital fissure. The fracture line then continues to the zygomatic sphenoid suture area and on to the frontozygomatic suture line. Most zygomatic complex fractures involve the orbit, making visual complications a frequent occurrence.

A modern classification of zygomatic fractures is based on CT scan data. CT provides information about facial structures, including both bone segmentation and displacement, allowing for complete repair of the fractures. This system divides fractures into low-energy, medium-energy, and high-energy injuries.

Low-energy zygoma fractures result in minimal or no displacement. These types of fractures often are seen at the zygomaticofrontal suture, and inherent stability usually obviates reduction.

Middle-energy zygoma fractures result in fractures of all buttresses, mild-to-moderate displacement, and comminution. Often, an eyelid and intraoral exposure is necessary for adequate reduction and fixation (Fig. 15.11).

Fig. 15.11. Buttresses of the midface

High-energy zygoma fractures frequently occur with Le Fort or panfacial fractures. The zygomatic fractures often extend through the glenoid fossa and permit extensive posterior dislocation of the arch and malar eminence. A coronal exposure, in addition to the oral and eyelid incisions, usually is necessary to properly reposition the malar eminence (Fig. 15.12).

Fig. 15.12. Le Fort classification of the midfacial fractures

Although isolated zygomatic complex fractures occur, fractures of this nature are usually associated with other facial skeletal and soft-tissue injury.

Initially, assessment of a zygomatic fracture in an emergent setting should be directed at prevention of life-threatening complications including major bleeding, airway compromise, aspiration, and identification of other fractures. Cervical spine injury should always be considered if the injury is the result of a high velocity event or if the patient has altered mental status. Intracranial, thoracic, extremity, and pelvic injuries require proper evaluation and management.

Once other more pressing injuries have been dealt with and the patient is stable, a thorough preoperative assessment of facial skeletal architecture can be performed. Symptoms include paresthesias in the distribution of the maxillary branch of the trigeminal nerve, trismus, diplopia, and flattening of the zygoma.

Signs classically include subconjunctival and periorbital hemorrhage (Fig. 15.13) and hypesthesias in the distribution of the maxillary branch of the trigeminal nerve. Flattening of the malar eminence, lateral canthal dystopia, and reduction in mandibular movement may be present. Ipsilateral epistaxis and buccal sulcus hematomas may occur. Reduced extraocular muscle function, diplopia, and enophthalmos can occur secondary to orbital floor fractures, resulting in entrapment of orbital contents.

Fig. 15.13. Le Fort III Fracture

A thorough ophthalmologic examination is required to evaluate and document ocular status. If a ruptured globe, retinal detachment, or traumatic optic neuropathy exists, treatment of these supersedes repair of a zygomatic fracture.

Radiographic evaluation of the fracture is mandatory and may include both plain films and a computed tomographic (CT) scan. Computed tomography imaging (CT scan) with three-dimensional reconstruction is most commonly used to confirm the presence of a fracture and optimize pre-surgical planning (fig. 15.14, 15.15). If physical findings and plain films are not suggestive of a zygomatic fracture, the evaluation may end here. However, if they do suggest fracture, a coronal and axial CT scan should be obtained. The CT scan will accurately reveal the extent of orbital involvement, as well as degree of displacement of the fractures. This study is vital for planning the operative approach.

Fig. 15.14. CT-3D of the midfacial fracture

Fig. 15.15. CT scans of the Le Fort III fractures

Surgical treatment

Historically, closed reduction was the method of choice for nearly all zygomatic fractures. Multiple methods were employed, but most involved simply exerting pressure underneath the malar eminence and popping the fragments back into alignment. Closed reductions yield unpredictable results with significant chance of relapse. It was also frequently associated with complications including persistent diplopia, orbital dystopia, malunion, and significant residual deformity.

If a zygomatic fracture (Fig. 15.16–15.19, 15.21) is displaced , an open reduction and rigid stabilization with mini- and microplates is used. The floor of the orbit is routinely explored and reconstructed, if needed, to restore orbital volume. The complications of an inadequately or unreduced zygomatic fracture are very difficult to correct secondarily and usually avoidable.

Fig. 15.16. Fractures of zygomatic complex

Fig. 15.17. CT scans of zygoma fracture

Fig. 15.18. Treatment of maxillary fracture by external devices

Fig. 15.19. Temporary immobilization in midfacial fractures

While 2-point fixation of zygomatic fractures may be used commonly, it often leaves an axis of rotation for the zygoma following an adequate reduction. Forces such as the masseter muscle often displace the zygoma postoperatively. Thus, making the diagnosis and then choosing the correct approach to establish 3-point fixation and ultimate stability is essential for obtaining a successful outcome. Since biomechanical properties are of primary importance underlying the treatment of zygoma fractures, a brief discussion is warranted. In terms of postoperative stability of a reduced zygoma fracture, 3-point fixation is undoubtedly best. However, at times, 2-point stabilization is perfectly adequate.

Rigid fixation with plates and screws restores 3-dimensional stability and allows for the least amount of motion between ends of fragments, the main cause of bone resorption and instability.

Presently, several types of microplating systems made of titanium and biodegradable materials are available to choose from when rigid fixation is needed for stabilization.

In many situations, resorbable plates and screws are adequate. Such situations may include the presence of primarily compressive forces of relapse and sturdy bone fragments that can be fixed in direct contact, since forces of relapse are absorbed by bone fragments and not the fixation system.

Arch fractures resulting in decreased mandibular motility can be dealt with via a gillies temporal approach or by a limberg hook, incerted via a small infrazygomatic incision. The temporal approach allows for surgical reduction of a depressed zygomatic arch while leaving a well-camouflaged scar within the hairline. Dissection exposes the deep temporalis fascia followed by creation of a plane between the fascia and temporalis muscle. The lateral eyebrow incision of the supraorbital approach allows for additional access to the frontozygomatic suture line. A supraperiosteal dissection plane allows for access to the arch. Both approaches provide safe and direct access to the zygomatic arch, since the seventh cranial nerve lies above the dissection planes.

An instrument such a zygomatic elevator or hook is placed beneath the arch. Once the instrument is properly positioned, the arch is elevated in a superolateral vector taking care to not use surrounding facial bones as a fulcrum. Proper placement of the instrument can be confirmed with palpation by the surgeon’s free hand placed within the intraoral, posterior buccal sulcus. A cracking sound is heard when the convexity of the arch is restored with full reduction. The surgeon should be cognizant of the normal flattening of the middle of the arch. A persistent protuberance will occur if care is not taken not to avoid fracture overcorrection. The wounds are closed, and the patient is advised to avoid direct contact to the area for several weeks (Fig. 15.20).

Fig. 15.20. Reposition of the zygoma by Limberg hook

Fig. 15.21. Surgical approaches to the  midfacial zone

Zygomatic complex fractures are usually repaired with open reduction and internal fixation. Plating systems are used to fixate the zygomaticomaxillary buttresses, zygomaticofrontal suture, and zygomatic arch. Osteotomies are indicated for fractures older than 1 month with onlay bone grafting for fractures present for 4 months or longer (Fig. 15.22; 15.23).

Fig. 15.22. Algorithm of the midfacial reconstruction

Fig. 15.23. Reconstruction of the zigomatic complex via coronal approach

Various approaches to zygomatic complex fractures include coronal, eyebrow, upper eyelid, transconjunctival and infraciliary lower eyelid, and maxillary vestibular approaches. The approach to the zygomatic complex is dictated by the degree of injury and need for exposure for open reduction and internal fixation. In most instances, 2 areas of internal fixation are necessary to provide rigidity and satisfactory malar contour and eminence. The frontozygomatic suture and maxillary buttresses are the usual fixation points, with plating of the inferior orbital rim when reconstruction of the orbital floor is necessary.

Fractures of the zygomatic complex frequently result in sensory disturbances in the infraorbital nerve distribution. These symptoms include dysesthesia of the skin of the nose, cheek, lower eyelid, upper lip, gingiva, and teeth of the affected side. These arise because fractures generally occur in the vicinity of the infraorbital foramen and canal.

Trismus is also a common finding (45 %), particularly after a fracture involving the zygomatic arch. It results from impingement upon the coronoid process of the mandible by a depressed zygomatic arch. This may indicate a need for elevation of the depressed arch, accurate reduction, and fixation. If new bone has formed in the space below the zygomatic arch and restricts the movement of the mandible, an intraoral approach for coronoidectomy may be required to permit mandibular movement.

Diplopia may occur after zygoma fractures for numerous reasons. These include, but are not limited to, hematoma, muscle injury, motor nerve injury to the extraocular muscles, entrapment of extraocular muscles, or damage to the fine connective tissue system. Diplopia that occurs after zygoma fractures not associated with significant orbital floor fractures and entrapment is usually transitory and is probably associated with hematomas.

A symptomatic diplopia associated with a positive forced duction test and CT evidence of entrapped muscle or soft tissue with no improvement over 1–2 weeks may be an indication for surgery. When diplopia is associated with enophthalmos, an improvement in vision can be predicted after correction of the enophthalmos. Diplopia associated with zygomatico-orbital fractures may persist longer, and young patients may recover more slowly than adults.

Enophthalmos

A frequency of this complication is 3–4 %. The displacement of orbital contents into an enlarged bony orbit with subsequent change to a more spherical orbital soft-tissue shape is thought to be the principal underlying mechanism behind the development of enophthalmos.

The most common causes of enophthalmos include the failure to properly reduce displaced zygoma fractures and malunited zygoma fractures. Blowout fractures of the orbit, especially those of the medial wall and those.

Of floor fractures behind the axis of the globe, and high-velocity comminuted fractures involving combinations of lateral wall, posterior floor, and medial wall fractures are other causes of enophthalmos. Other theories of possible causes of enophthalmos include fat atrophy, soft-tissue contracture, and fibrosis.

Before surgical correction of enophthalmos, examine the patient to assess visual function, extraocular eye movement, and the sensory function of the infraorbital nerve. Both thin coronal and axial slices on ct scans are helpful in determining the extent of orbital damage.

Infection

While an infrequent occurrence, infection is a problem that threatens all postoperative patients. Sinusitis has been found to be the most common type of infection seen in postoperative patients; preseptal cellulitis and dacryocystitis also can occur.

Complications with plates and/or screws

The usual cause is a palpable plate, although a pain syndrome may occur. More rarely, infections may occur. Very rarely, screws can fracture into bone and create problems for removal.

These problems may be limited by a broad availability of drill sizes for use in thin or dense bone.

Regeneration of the bone tissue bone tissue

Bone is a rather unique tissue with many functions. All bones have a mechanical function providing attachment to various muscle groups. In addition, is some parts of the body, bones provide a protective function to vital structures – skull (brain), ribs (lungs, heart) and pelvis (bladder, pelvic viscera). Some bones retain their haemotopoetic function in adults – vertebrae, iliac crests, proximal parts of femur and humerus. All bones serve as a reservoir of calcium and actively participate in calcium homeostasis of the body.

Macroscopically, bones are two types:

• Cortical (compact) bone. With a dense outer layer – the cortex.
• Cancellous (spongy or trabecular) bone. Present in the interior of mature bones. This structure resists compression.

Bone as a tissue consists of two main types:

• Primary bone tissue (non-lamellar bone). This bone is also known as “coarse fibred” or “woven” bone or immature bone. It is characterized by the presence of randomly oriented coarse collagen fibres clearly visible by polarization microscopy. Non-lamellar (woven) bone is seen in the bone of fetuses and young children. It is the osseus tissue first deposited on the cartilage matrix in endochondral ossification. It is also the first tissue to appear in the repair of bone (facture healing).
• Secondary bone (lamellar bone). This bone is also known as mature bone. It is characterized by the presence of collagen fibres arranged in parallel layers or sheets (lamellae) readily apparent when viewed by polarization microscopy. Lamellar bone is present in both structured types of adult bone, cortical (compact) bone and cancellous (spongy or trabecular) bone.

Bone is a very specialized type of connective tissue consisting of cells and an intercellular matrix.

There are three cell types:

• Osteoblasts – the bone forming cells, located on the surfaces of bone lying side by side like a simple cuboidal epithelium. These cells are responsible for the synthesis of organic components of the bone matrix. When active, they show high alkaline phosphatase activity.
• Osteocytes – the cells occupying the lacunae in the bone matrix. They possess long thin cytoplasmic processes – the filopodia locsted in thin cylindrical spaces or canals in the bone matrix – the canaliculi. Nutrients and oxygen pass between the blood vessels and distant osteocytes by the arrangement of the canaliculi. Osteocytes also break down the bone matrix by osteocytic osteolysis to release calcium for calcium homeostasis.
• Osteoclasts – the large, multi-nucleated cells formed by fusion of monocytes. They lie in shallow depressions on the bone surface called the howship’s lacunae.

The bone matrix is composed of:

• Organic matter. Consisting of type I collagen fibres embedded in the ground substance containing proteoglycans and glycoproteins. The collagen fibres are made up of bundles of fibrils to resist pulling forces.
• Inorganic matter. Made up of stiffening substances to resist bending and compression. The bone mineral is an analogue of crystals of calcium phosphate – hydroxyapatite a substance that can only be seen under electron microscopy. It is this association of hydroxyapatite with collagen fibres which is responsible for the hardness of bone.

There are two type of histogenesis of bone namely intra-membranous ossification and endochondral ossification.

Intra-membranous ossification – this occurs in flat bones such us the skull and clavicle. In this process, the bone is developed from a condensation of mesenchymal tissue – the ossification centre. This tissue differentiates directly into osteoblasts which synthesise osteoid which then undergoes calcification.

Endochondral ossification – this type histogenesis occurs in long bones and short bones. The primary ossificution centre appears in the middle of the long bone and produced chondrocytes. The chondrocytes then undergo hypertrophy and the cartilage matrix undergoes calcification. The chondrocytes are then invaded by primitive mesenchymal cells and blood vessels to differentiate into osteoblasts and blood-forming cells and bone marrow.

Bone has 3 basic types of constrictors:

• Osteogenesis, the synthesis of new bone by the cells of the graft or cells of host origin, is primary. Graft bone cells usually survive initial transplantation if properly handled and have been shown to synthesize a new bone. The cancellous bone, with its surface area, has a greater potential for forming a new bone than does the cortical bone.
• Osteinduction is a second way in which a bone graft may function as a source of osteogenesis. Osteoinduction is the recruitment of mesenchymal stem cells that differentiate into osteoblasts from the surrounding bed. The recruitment and differentiation of these cells are modulated by low-molecular-weight peptides such as the glycoprotein, bone morphogenetic protein. Bone morphogenetic protein is a hydrophobic, nonspecies-specific protein extracted from the diaphysis of the cortical bone, dentin, and various bone-forming tumors.
• Osteoconduction is a term referring to the three-dimensional process of growth of capillaries, perivascular tissue, and osteoprogenitor cells of the host into the graft. The graft functions as a trellis or scaffold for the ingrowths of a new host bone.

Phases of fracture healing:

1. Phase of inflammation.
2. Phase of osteogenic repair tissue.
3. Phase of remodeling.

Phase of inflammation. In this phase, also sometimes called the immediate reaction or the phase haematoma formation, bleeding occurring from the damaged bone ends adjacent soft tissue forms a haematoma between the bone fragments. This haematoma is essential for fracture healing to occur. The fibrin of the clot serves as a scaffold for fibrocellular invasion.

Phase of osteogenic repair tissue. The next phase consists of organization of the fracture haematoma. The haematoma becomes invaded by fibrovascular tissue replacing the clot laying down collagen fibres and matrix which later becomes mineralized to from the woven bone of provisional or primary callus.

In some cases, cartilage may form in the periphery of the callus.

There are two theories: osteoprogenitors cells and osteogenic induction.

Osteoprogenitors cells – repair tissue arises specialized cells with predetermined commitment to bone formation. Osteoprogenitor cells occur in close association with bone surface (cambial layer of periosteum) or with bone marrow.

Osteogenic induction – repair is due to activity of previously uncommitted fibroblasts (mesenchymal stem cells) which could develop the power of osteogenesis given the appropriate environmental stimulation by the phenomenon of osteogenic induction. There cells do not arise from the bone itself but from the adjacent surrounding soft tissue. Indeed, soft tissues play a key role in the healing of fractures. The fibroblasts in the soft tissue cannot be distinguished morphologically from osteoprogenitor cells of bone.

Phase of remodeling – once the fracture is bridged by bony callus of osteoid the newly formed bone must adapt to its new function. Remodeling occurs just as the process of replacement and repair goes on continuously in normal uninjured bone.

There is the modeling process occurring in the cortical bone which is quite different from that occurring in the cancellous bone. In remodeling the normal haversian system of osteons is developed from the initial less organized woven bone tissue. Remodeling is governed by wolff s law of functional adaptation of bone. The trabeculae realign themselves along directions of principal stress or strain to best protect them from bending. The end result is maximum structural support for minimum osseous structure.

In the cancellous bone, the cells are never very far away from the blood vessels. The whole process of bone apposition takes place on the surface of the trabeculae by the phenomenon of “creeping substitution”.

In compact bone, the presence of more deeply placed cells require the presence of haversian systems which must be replaced. Remodelling occurs in a more orderly sequence. First, the osteoclasts ream out a tunnel in the dead bone down which a blood vessel follows, bringing osteblasts which lay down the lamellar bone of a new osteon – osteoblastic “cutter head”.

Factors controlling fracture healing

Mobility. The amount of external callus formed is related to the amount of movement present, more mobility being associated with a larger amount of external callus producer. With such plating, the appearance of external callus reflects technical failure of fracture stabilization or fixation.

Cellular contact therapy. After two weeks, in the collars formed made no contact with each other, they undergo involution. It is the phenomenon limited in duration, is the primary callus response. With intact periosteum, the two collars readily establish contact. If the periosteum is disrupted, the two advancing collars may reach each other to from a purposeful bridge. Alternatively, if the developing collars are excessively separated by distraction of by interposition of soft tissue, cellular contact cannot occur and nonunion is produced. There is a subsequent stage in the process following the primary callus response – phase of external bridging callus with participation of induction mechanisms.

Mechanical influences. The “bioelectric phenomenon” described in 1957. It is whereby mechanical deformation of bone gave rise to electrical potential – “piezo-electric effect”. When a bone was fractured, the bone ends became more electronegative – associated with increased osteogenesis and advocated the non-invasive use of electromagnetic fields to promote fracture healing.

Humoral theory. Mechanical factors are not only stimulus in callus formation. Such factors cannot explain two points:

• The response to bridge fractures by external callus is not prolonged indefinitely.
• Continued mobility of the fracture does not cause continued callus response.

It is therefore postulates that there is a humoral inducing agent which plays a role in fracture healing – being present for only a limited period of time at the fracture site to induce osteogenesis.

At present, we are still unable to isolate the “wound hormone” that is released from the fracture ends. The exclusion of bone ends by silastic caps did not impair callus formation. The hormone is released most likely not from the injured bone itself but rather from the products of the primary response.

The humoral inducing agent is present only for a limited period of time at the fracture site to induce osteogenesis.

The formation of external callus can be considered to occur in two stages:

• An initial primary callus response, largely independent of environmental changes, arising from predetermined cells in bone tissue itself.
• A subsequent phase of bridging callus formation, the speed being dependent on the recruitment of cells from the surrounding tissues by the process of induction.

Medullary callus. It is distinguished from callus only by its location. Often cartilage formation is much less prominent in medullary callus. The second stage appears rather late in this healing process and the controlling factors involved appear to be quite different. Medullary callus is unaffected by effect of mechanical stability and often flourishes under these conditions.

Skeletal defects have been replaced by bony grafts for that 300 years. Autologous bone grafts remain the gold standard in bone transplantation. Autologous cancellous bone grafts contain hydroxyapatite and collagen as an osteoconductive scaffold while stromal cells have osteogenic potential.

Autograft:

• Healthy bone is harvested from the patient’s own body.

Advantage:

• No chance for rejection.
• Perfect biocompatibility, osteoinduction.
• Have stromal cells.

Disadvantage:

• Two surgeries are necessary.
• There is little “extra” bone to harvest.
• Works for small defect size in non-load bearing areas only.

One of the most challenging problems in surgery is the reconstruction of massive bone defects caused by resection of bone tumours, “gap nonunions” resulting from trauma and resection of genital pseudoarthroses. Options include the use of non-vascularised autologous bone transplant, free vascularised autologous bone transplant, allograft, bioceramics or prostheses. Non-vascularised autologous bone transplant are limited as to its availability in size, shape and amount and is therefore seldom used. Free vascularised autologous bone transplant is technically demanding and requires specialized expertise and facilities, incurring large costs and taking up long operating hours. Bioceramics is a simpler option but integration with the host bone is less ideal. A bigger disadvantage is that it is expensive. Allograft on the other hand is readily available, shows good osseo integration with the host bone and is relatively inexpensive. Allografts are therefore an attractive option provided they can be provided by a good tissue bank processing high quality bone allografts.

Allografts:

• Healthy bone is harvested from another source, either a donor or cadaver.

Advantage:

• Perfect biocompatibility, osteoinduction.

Disadvantage:

• Donors have little “extra” bone to harvest.
• Disease transmission is possible.
• High probability that the implant will be rejected.

Metals:

Advantage:

• Extremely high mechanical properties.
• Easily crafted and available in large quantities.
• Inert, thus no biological reaction to worry about.

Disadvantage:

• Poor implant-bone interface, leads to migration of failure.
• Mechanical attachment often destructive to patient.
• So strong they often erode surrounding “healthy” bone.
• Heavier than natural bone.

Ceramics:

Advantage:

• Extremely durable.
• Easily crafted and available in large quantities.
• Good implant-bone interface, osteoinduction.
• Many have similar chemical structure to actual bone.

Disadvantage:

• So durable they often erode surrounding healthy bone.
• Insufficient mechanical properties for load-bearing applications.

Chapter 16. Basics of craniomaxillofacial and plastic surgery

Surgical treatment of deformations of maxilla and mandibule

The term orthognathic surgery refers to the surgical alignment of the jaws to achieve a functional skeletal base occlusal relationship and an optimum soft tissue balance of the lower half of the face.

Whereas orthodontics is used to correct the position of the teeth relative to the dental arch, orthognathic surgery aims to correct the position of the jaws relative to the cranial base. It is uncommon for orthognathic surgery to be performed without concomitant orthodontic treatment, because the surgical movement of the jaws relies to a great extent on the alignment and position of the teeth.

The most important role of orthognathic surgery lies in the management of malocclusions that harbor a gross jaw discrepancy between the mandible and maxilla. Therefore, the dentofacial deformity that orthognathic surgery aims to correct is often described in terms of the jaw size and position as opposed to simply in terms of the dental malocclusion.

Orofacial development

Orofacial development is genetically predetermined, so discrepancies in the size, shape, and morphology of teeth and jaws will readily reflect the orofacial form and pattern of the parents. Occasionally dentofacial deformities such as cleft lip and palate may be the result of environmental insults to the developing embryo that occur during crucial stages or periods of gestation. Generally speaking, fewer than 10 % of a given population will have dento-facial deformities that may benefit significantly from orthognathic surgery.

Orthognathic surgery must be tailored to the growth pattern of each individual. Most important, it must consider the growth potential of the patient and target those regions where growth is undesirable.

There are two phases in which orthognathic surgery may be undertaken:

1. During the growth phase: This is considered interceptive surgery, whereby surgery is used to restrict unfavorable growth to minimize the degree of the subsequent dentofacial deformity. Unfavorable growth is defined as growth that is detrimental to the child’s health, psychosocial well-being, and development. Usually, but not always, a second surgical procedure is required at the end of the growth phase.
2. After growth has ceased: In adulthood, orthognathic surgery may be considered definitive surgery.

Controversy exists as to whether some deformities can be treated early and others only after growth is complete. For example, it is not uncommon for mandibular horizontal deficiency to be treated during early adolescence, while mandibul ar horizontal excess will not be treated until well after growth is complete.

• Maxillary anteroposterior deficiency: Inadequate growth of the maxilla in an anterior direction in combination with a Class III malocclusion.
• Vertical maxillary excess: Overgrowth of the maxillary alveolus in the inferior direction, creating excess display of the teeth and gingivae and often associated with an incompetent lip seal without mentalis muscle strain.
• Vertical maxillary deficiency: Vertically short maxilla resulting in an edentulous appearance and a short lower face, often combined with mandibular deep bite and a prominent chin.
• Alveolar cleft: Usually associated with maxillary constriction in the anteroposterior and transverse dimensions.

Common dentofacial deformities

In the classification of dentofacial deformities, it is preferable to describe the skeletal relationship rather than simply the dental relationships, because orthognathic surgery is fundamentally used to correct the underlying skeletal base discrepancies.

Maxillary deformities:

• Maxillary anteroposterior excess: Protrusive maxilla in which there is an overgrowth in an anterior horizontal direction.

Mandibular deformities:

• Mandibular anteroposterior excess (hyperplasia): Prognathism combined with Class III malocclusion (Fig. 16.1).
• Mandibular anteroposterior deficiency (hypoplasia): Deficient anterior growth of the mandible combined with Class II malocclusion.
• Mandibular asymmetry: Usually related to unbalanced excess or lack of growth on one side of the mandible, often the condylar process, but sometimes involving the ramus and body. Malocclusion may be present, depending on the compensatory growth in the maxilla that may have occurred. It appears clinically as a chin and mandibular midline shift (lower facial asymmetry) (Fig. 16.4).

Fig. 16.1. Macrogenia in the vertical dimension, exacerbated by Class III mandibular prognathism

Chin deformities

Chin deformities are often associated with other mandibular deformities:

• Macrogenia: Overgrowth of the chin in the vertical or anterior direction.
• Microgenia: Chin deficiency in the vertical and/or anterior direction (Fig. 16.2).

Fig. 16.2. Chin deficiency in both the verti­cal and horizontal dimensions, exacerbated by Class II mandibular deficiency

Combined maxillary and mandibular deformitie

Short-face syndrome (brachyfacial pattern): Deficient lower facial growth in the vertical dimension, resulting in low mandibular and occlusal plane angles. It is usually the result of Class II malocclusion combined with mandibular anteroposterior deficiency but sometimes is caused by Class II malocclusion combined with vertical maxillary deficiency.

Long-face syndrome (dolichofacial pattern): Excess lower facial height, usually associated with increased occlusal and mandibular plane angles. It is often the result of a combination of vertical maxillary excess and mandibular hypoplasia. Apertognathia: Anterior open bite, often associated with long-face syndrome or simply increased posterior facial height. Lower facial asymmetry: Usually caused by unbalanced aberrant growth in the mandible (e.g., condylar hyperplasia). Alteration in the maxillary cant will only arise if problem emerges during early facial growth, whereby compensatory growth of the maxilla will occur in relation to the aberrant mandibular growth pattern (Fig. 16.3).

• Correction of underlying skeletal jaw disharmony.
• Development of a functional occlusion in which the teeth are in the most ideal position to aid stability and esthetics.
• Formation of a surgical plan with the best esthetic result that does not compromise occlusal or skeletal stability.
• Development of an optimal balance among esthetics, function, and stability. Esthetics should not be sacrificed at the expense of function, and, in most instances, an improvement in function will bring about an improvement in esthetics.

Fig. 16.3. Long-face (dolichofacial) appear­ance with anterior open bite and incompetent lip seal

Fig. 16.4. Lower facial asymmetry in which the maxilla is also canted to the right

Patient evaluation and diagnosis

Patient concerns

Determine the patient’s feelings about the existing problems and his or her expectations for treatment results.

Clinical evaluation:

• Facial form (frontal and profile): Long, short, convex, concave, flat.
• Relationship of facial thirds (Fig. 16.5, 16.6): The face can be divided into equal thirds (only approximately), from the hairline to the eyebrows; from the eyebrows to the base of the nose; and from the base of the nose to the chin point. Facial proportionality can be assessed by comparing the middle and lower thirds of the face to determine where the face may be long or short.

Fig. 16.5. Facial proportions in a – profile and b – frontal views. The lower third of the face can be further subdivided into thirds from the base of the nose to the chin point

Fig. 16.6. Smile line, occlusal cant, and dental midlines in relation to the facial midlines

Relationship of soft tissues to dentition: Smile line, occlusal cant, and dental midlines versus soft tissues.

Vertical and horizontal radiographic measurements (Fig. 16.7, 16.8):

• Vertical dimensions: Essential to assessing vertical jaw dimensions in relation to the upper face which, in turn, will determine whether maxillary surgery or genioplasty is warranted.
• Horizontal angles: The horizontal lines that run through key radiographic landmarks are measured as angles with respect to the Frankfort horizontal line, which forms the main reference mark. High or low occlusal and mandibular plane angles will often determine whether maxillary surgery is warranted.
• Transverse dimensions: Important in determining whether segmental jaw surgery is required.
• Intra-arch dimensions: Important in determining if dental extractions will be required prior to presurgical orthodontics.

Fig. 16.7. Vertical measurements of facial height and proportion: (ADH) anterior dental height; (ULL) upper lip length; (LLL) lower lip length; (UF) upper facial height; (LF) lower facial height

Fig. 16.8. Horizontal plane angles: (CB) cranial base; (FH) Frankfort horizon­tal; (Pal) palatal plane; (Occ) occlusal plane angle; (MPA) mandibular plane angle. All angles are measured with respect to the FH plane, which is the main reference mark

Radiographic analysis

Cephalometric analysis: Lateral and anteroposterior cephalograms are used to undertake cephalometric analysis of the jaw positions and dimensions with respect to the upper face and cranial base. These measurements provide the reference base for determining whether the jaws are malpositioned, too large, or too small. The patient’s lips must be in repose and the teeth should be only lightly touching and in centric relation when the cephalogram is taken.

Panoramic radiograph: This is used to check for the position of the inferior alveolar canal and screen for gross pathology and impacted teeth.

Dental study casts:

• Accurate bite registration: Use of a facebow is indicated in two-jaw surgery.
• Two-jaw surgery requires duplicate casts.
• Trimmed or mounted casts should match the degree of discrepancy observed in the lateral cephalogram.

Other issues

Speech, audiometry (especially for cleft patients), psychological conditions, medical conditions (e.g., diabetes and bleeding disorders).

Sequence of treatment

1. Dental and periodontal treatment:

• Maintain as many of the teeth as possible.
• Stabilize the periodontium prior to orthodontic and surgical intervention.

2. Extractions:

• Facilitate orthodontics (e.g., premolar extractions).
• Facilitate subsequent surgery: Mandibular third molars must extracted 9 to 12 months prior to sagittal split osteotomy, or the lingual cortex will be weakened.

3. Presurgical orthodontics:

• Position the teeth over their respective basal bone.
• Align and level the teeth.
• Adjust for tooth size discrepancies.
• Correct rotated teeth.
• Ensure divergence of roots adjacent to surgical sites, especially with segmental maxillary osteotomies.
• Coordinate maxillary and mandibular arch widths: Correct transverse discrepancies without compromising stability and dental health, or further surgical options must be considered.

Different dentofacial patterns respond very differently to treatment:

• Brachyfacial (short-face) pattern: Flat mandibular plane in which growth tends to proceed horizontally. Best to use a nonextraction technique.
• Dolichofacial (long-face) pattern: Steep mandibular plane angle in which growth tends to proceed vertically. More likely to use an extraction technique.

Where skeletal form is unfavorable, dentoalveolar segments will compensate. Therefore, most of these dental compensations must be corrected prior to surgery, by positioning teeth in their ideal axial relationship to their respective skeletal bases.

4. Orthognathic surgery:

• Reposition the basal bone and/or dentoalveolar segments into more normal interrelationships.
• Provide the best functional and esthetic results and provide stability of the achieved results.
• Surgical preparation involves:
• Final STO tracing.
• Model surgery and construction of the surgical occlusal wafers.

5. Postsurgical orthodontics:

• Finalize tooth alignment and root parallelism.
• Ensure maximal interdigitation.
• Create ideal overbite and overjet.
• Ensure that centric occlusion is the same as centric relation.

It may take up to 10 months to fine tune the final occlusion while the bones and muscles continue to heal and adapt to the repositioning, depending on the accuracy of the preoperative setup of the occlusion.

Where rigid internal fixation is used, orthodontics can resume anywhere between 2 and 6 weeks postsurgery. The teeth and osseous segments can move very rapidly during the first few months postoperatively; therefore the orthodontist should initially examine the patient on a frequent basis (every 1 to 2 weeks) for adjustments so that rapid changes can be closely monitored. A good presurgical orthodontic setup will help to simplify the surgery, improve the stability and occlusion, and decrease the amount of postsurgical orthodontics required.

Mandibular surgery

Orthognathic surgical procedures of the mandible are classified according to the design of the osteotomy and the region where the surgery is undertaken: body or ramus. An osteotomy is a bone cut, whereas an ostectomy involves the removal of bone.

Classification

Ramus procedures:

• Condylotomy (subcondylar osteotomy).
• Condylectomy.
• Sagittal split ramus osteotomy.
• Vertical subsigmoid osteotomy.
• Inverted L-osteotomy.
• C or arcing osteotomy.

Body procedures:

• Anterior to mental foramen:
• Step osteotomy/ostectomy.
• Midline symphyseal osteotomy.
• Posterior to mental foramen:
• Y ostectomy.
• Rectangular ostectomy.
• Trapezoid ostectomy.
• Inverted V-ostectomy.

Subapical body procedures:

• Anterior:
• Kole osteotomy.
• Combined with midline symphyseal osteotomy.
• Posterior.
• Total.
• Mandibuloplasty.

Genioplasty:

• Genioplasty is described in detail in a later section.

Sagittal split ramus osteotomy

The techniques most commonly performed to move the mandible are the sagittal split ramus osteotomy and the vertical subsigmoid osteotomy. The vertical subsigmoid osteotomy only allows for setback of the mandible, while the sagittal split osteotomy allows anterior repositioning (advancement) and posterior repositioning (setback).

The sagittal split ramus osteotomy continues to be the most versatile and most commonly used technique of all mandibular osteotomies. The direct bone contact between the sliding fragments ensures stability and good healing between the bone segments in advancement, setback, and even rotational procedures.

Trauner and Obwegeser (1957)

They described a horizontal cut just above the mandibular foramen on the medial side of ramus, a vertical cut down the anterior border of the ramus, and an oblique cut made through the lateral cortex toward the angle of the jaw. It was a good technique for mandibular setback but provided poor bone contact with mandibular advancement. Aseptic necrosis of the angle of the mandible was a problem because of extensive stripping of the pterygomasseteric sling.

Dal Pont (1961)

Dal Pont modified the sagittal split by advancing the oblique cut toward the molar region and making the vertical cut through the lateral cortex. The main problem with setbacks was interference between the main retropositioned proximal fragment and the mastoid process, where occasional pressure on the facial nerve could occur as well.

Hunsuck (1968)

Hunsuck shortened the cut through the medial cortex of the ramus by extending it only as far as the mandibular foramen, which prevented the occasional shattering of the ramus in mandibular setbacks.

Bell and Schendel (1977) and Epker et al (1978). In this modification, in the anterior vertical cut, the whole of the lower border is sectioned through and through. The split is kept more laterally by directing fine osteotomes down the inner surface of the lateral cortex to produce easier splitting and greater protection for the inferior dental nerve. Blood supply to the ramus is preserved, because the need to strip the pterygomasseteric sling is eliminated.

Surgical procedures

Incision:

• Commence mucoperiosteal incision at the lateral crest of alveolus.
• Extend the incision up the anterior border of the ramus/ coronoid process and anteriorly along external oblique ridge as far forward as the first molar.

Dissection:

• Create subperiosteal exposure laterally over the body of the mandible to the lower border.
• Dissect medially just beyond the lingula and superiorly to expose the coronoid process.

Osteotomy (Fig. 16.9):

• Lingual cortex of ramus: Make the cut from the anterior border of the ramus, passing backward to just reach superiorly and posteriorly to the lingula.
• External oblique ridge: Make cuts down along the anterior border of the ramus, medial to the external oblique ridge, and then forward to about the second molar.
• Vertical cut: Cut the lateral cortex of the body down to and through the lower border of the mandible.

Fig. 16.9. Sagittal split ramus osteotomy: a – osteotomy sites for the sagittal split shown in grey; b – intraoperative view of the vertical cut in the buccal cortex

Split:

• Begin from the lower border of the vertical cut and then insert fine osteotomes along the alveolar cut to gently pry the two fragments apart.
• The neurovascular bundle must always lie on the medial side in the distal segment; if it does not, reposition it to that side.

Fixation options:

• Upper or lower border transosseous wires: Require a 4- to 6-week period of maxillomandibular fixation.
• Bicortical screws (Fig. 16.10): These are inserted transbuccally in a triangular or linear fashion via the trochar and cannula. The best biomechanical advantage is obtained with three screws placed in a triangular pattern. Disadvantages associated with this fixation technique include the requirement for a facial stab incision, the potential for direct damage to the teeth and inferior alveolar nerve, the torquing of condyles, and the difficulty in removing the fixation screws after healing.
• Monocortical plates and screws (Fig. 16.11): One or two plates may be used and placed transorally. It is much easier to remove hardware at a later date.
• Postoperative care.
• Drain tubes are optional and often unnecessary.
• If wire fixation is used, maxillomandibular fixation is required for 4 weeks.
• If screw fixation is used, maxillomandibular fixation is unnecessary, but training elastics are useful for a few weeks to help guide the occlusion.

Fig. 16.10. (grey shaded area) Exposed marrow space of a mandible that has three bicortical screws placed in a triangular pattern, which is been advanced with a sagittal split ramus osteotomy. One method of fixation of the sagittal split mandibular osteotomy

Fig. 16.11. Placement of miniplates and monocortical screws: a – the most common position of the plate is on the upper border of the osteotomy site, and at least two monocortical screws are placed on each side of the osteotomy; b – miniplates and monocortical screws are easy to place through the transoral approach

Limitations

Relapse is common in cases of:

• Anterior open bite: It is not appropriate to use sagittal split alone, particularly with short ramus height, in which case the inverted L-osteotomy is better suited. The sagittal split osteotomy may be used in conjunction with maxillary osteotomy.
• Mandibular asymmetry: Relapse is more likely to occur if there is rotational movement of the proximal fragment, particularly with setbacks. Rotational movements predispose to poor contact between the fragments; careful trimming minimizes angle flaring.
• Large advancements (more than 8 mm): Occasionally the sphenomanibular ligament prevents large advancements of the mandible and may need to be stripped off the lingula.
• In the presence of a thin or abnormal ramus structure, it is better to use an inverted L-, a C-, or an arcing osteotomy.
• The split is occasionally unpredictable.

Vertical subsigmoid (or ramus) osteotomy (Fig. 16.12)

Indications

Developed by Caldwell and Letterman in 1954, the vertical subsigmoid osteotomy has regained popularity in recent years because of the reduced potential for surgical trauma to the inferior alveolar nerve, particularly with mandibular setback procedures:

The procedure is mainly used for setback procedures and mandibular asymmetries.

It is not recommended for correction of anterior open bites.

It cannot be used for advancements.

It is used mainly for setback procedures when potential damage of the inferior dental nerve has to be minimized because of patient concerns.

• Maxillomandibular fixation is required for 6 weeks postoperatively.

Fig. 16.12. Vertical subsigmoid mandibular ramus osteotomy: a – osteotomy sites shown in red; b – intraoperative view of the proximal fragment of the ramus after the osteotomy and outward repositioning of the proximal segment using a periosteal elevator

Surgical procedures

Extraoral approach (unusual cases only):

• The easiest and safest method is to utilize the Risdon (submandibular) approach.
• Strip the whole lateral surface of the ramus of periosteum and masseter muscle.
• Reflect the medial pterygoid muscle insertion off the deep surface.
• Insert a Rayne subsigmoid retractor with fiber-optic light attachment.
• This approach has some disadvantages:
• External scar.
• Occasional damage to the mandibular branch of the facial nerve.

Transoral approach:

• This has become a more popular approach since the introduction of specially designed retractors, oscillating saws, fiber-optic illumination, irrigation, and suction.
• Submentovertex radiographs may occasionally help to assess the amount of outward flaring of the rami in order to establish feasibility of the transoral approach, because the more parallel the rami, the less direct vision is available to the surgical sites.

Make an extended third molar incision up the anterior border of ascending ramus and forward to the first molar, similar to the sagittal split osteotomy incision. Extensive muscle stripping from ramus may result in aseptic necrosis of the bone fragment and condylar sag. However, if inadequate muscle stripping occurs, there is an increased risk of relapse. Bell et al (1980) recommend that medial pterygoid muscle not be stripped off because it maintains the blood supply to the proximal fragment and helps keep condyle in place, although some (Welch 1989) believe this leads to greater relapse.

Begin the osteotomy halfway, first up and then down from the sigmoid notch to the angle, using an oscillating saw with a 120-degree blade angle. The depth of the cut should be no greater than 6 mm to avoid the risk of damage to medial tissues.

Identify the position of lingula by looking for a small bony thickening on the lateral surface of the ramus. Make a vertical bone cut a few millimeters posterior to this landmark; the cut should have a slight oblique angle anteroposteriorly. Set back the mandible so that the proximal fragment overlaps the distal fragment on the outer aspect. Lateral surface decortication may be required on the distal fragment to establish good bony contact and healing and on the proximal fragment to prevent deformity at the angle. Trimming of the angle from the proximal fragment may also be necessary to prevent flaring.

Transosseous fixation may or may not be used, although Epker and Wolford (1980) advocated wiring to ensure that the condyle is carefully seated in the fossa. Where setbacks are greater than 1 cm, a coronoidectomy may be necessary to prevent excessive tension on the temporalis muscle.

Establish maxillomandibular fixation, which remains for 6 weeks.

Genioplasty

The term genioplasty describes the numerous surgical techniques used to alter the size and morphology of the bony chin with concomitant changes in the surrounding soft tissues. Otherwise known as mentoplasty, chin surgery is commonly combined with other orthognathic surgical procedures. Although about 15 % of all dentofacial deformities primarily involve the chin, 85 % of the clinical changes associated with a maxillomandibular osteotomy and chin surgery are the result of the genioplasty. In other words, the genioplasty contributes more to the overall clinical changes in the facial appearance than does the movement of both jaws.

Historical review

In the past, most surgical chin procedures involved the use of alloplastic implants for augmentation. In 1942, Hofer described the osteotomy of the anterior lower border of the mandible via an extraoral submental incision. In 1957, Trauner and Obwegeser described the intraoral approach, or labial sulcus incision, to the osteotomy of the anterior mandibular lower border.

Applied anatomy

The chin is a region of the lower face that consists of bone and soft tissue elements. The bony chin is basically the mental protuberance, bounded by the mental tubercles superiorly, the mental foramina laterally, and the lower border of the anterior mandible interiorly. In chin surgery, the following are the most important structures:

• Mental nerves (foramen): Provide major sensory innervation of the chin.
• Mentalis muscles: Indirectly provide the major vertical support to the lower lip in addition to chin posture.
• Lingual muscle pedicle: Provides the major blood supply to the osteotomized segment of the chin and hence maintains viability of the bone and prevents resorption.
• Root apices of the mandibular incisors: Root apices must be identified and osteotomy cuts must be designed at least 5 mm below the apices.

Chin deformities

These may be esthetic (e.g., macrogenia) or functional (e.g., chin ptosis). Chin deformities may occur in isolation but are more commonly associated with other dentofacial deformities:

• Functional deformities (commonly iatrogenic):
• Chin ptosis.
• Lower lip incompetence.
• Esthetic deformities:
• Macrogenia (large chin):
• Vertical.
• Horizontal (anteroposterior).
• Combination of vertical and horizontal.
• Microgenia (small chin):
• Vertical.
• Horizontal (anteroposterior).
• Combination of vertical and horizontal.
• Asymmetry.

Transoral genioplasty procedures

Approach. Labial sulcus: Make an incision in the lip, 1 cm forward of the sulcus depth.

Dissection:

• Transect the mentalis muscle.
• Expose, isolate, and protect the mental nerves bilaterally.
• Maintain soft tissue attachment at the inferior border of the mandible.
• Horizontal osteotomy.
• Place the osteotomy at least 5 mm below the root apices of the mandibular incisors.
• There are numerous osteotomy designs:
• Horizontal osteotomy: most commonly used.
• Double horizontal osteotomy: for large advancements.
• Tenon and mortise osseous genioplasty.
• Sagittal osteotomy (Thompson, 1985).
• Horizontal-vertical step osteotomies.

Downfracture and repositioning:

• Always maintain an attached, broad-based lingual muscle pedicle to the osteotomized bony chin segment.
• By virtue of its simple anatomy and surgical versatility, the osteotomized chin may be repositioned in any of the three dimensions or directions: the horizontal, lateral, and vertical planes.

Fixation options:

• Transosseous wires.
• Bone plates and screws.
• Lag screws.

Closure:

• Restore mentalis muscle continuity.
• Close in two layers.
• Apply a light pressure dressing.
• Chin implants are placed in a subperiosteal pocket and often are not fixed by any means apart from the surrounding soft tissue pressure that holds them in place.

Genioplasty types Functional genioplasty. (Fig. 16.13)

First described by Michelet and Jacquet in 1973, it is used to correct abnormal mentalis muscle activity at an early age by surgically altering the underlying chin bone deformity:

• Indications:
• Vertical chin excess requiring vertical reduction genioplasty.
• Horizontal (anteroposterior) chin deficiency requiring advancement genioplasty.
• Timing: usually just after the eruption of the mandibular canines.

Augmentation genioplasty:

• Alloplastic onlay grafts: various materials, including hydroxyapatite.
• Biologic onlay grafting: allogeneic or autogenous bone (prone to resorption).
• Horizontal advancement osteotomy.
• Vertical downgraft osteotomy with interpositional graft.
• Lateral expansion: midline osteotomy with outward rotation of the genial segments.

Fig. 16.13. Various genioplasty procedures involving an osteotomy of the anterior mandible: a – advancement using a horizontal sliding osteotomy; b – setback using a horizontal sliding genioplasty; c – vertical augmentation using an interpositional graft. Fixation is not shown but can involve plates with monocortical screws or lag screws alone

Reduction genioplasty:

• Shave (osteoplasty) of the chin protuberance: high incidence of lower lip ptosis.
• Horizontal sliding osteotomy and setback.
• Vertical reduction osteotomy with wedge ostectomy (bone removal).
• Lateral reduction with midline ostectomy for broad-based chins.

Asymmetric genioplasty.

Asymmetric genioplasty is the vertical shift of the genial segment (propeller-type genioplasty).

Maxillary surgery

The maxilla may be moved as a whole or in segments in any combination of horizontal and vertical directions. This is achieved with a Le Fort I maxillary osteotomy that is approached by a circumvestibular incision in the labial sulcus. The Le Fort I osteotomy is still the most versatile technique for maxillary osteotomies and is the most widely used technique in orthognathic surgery involving the maxilla.

Cheever (1867).

As reported by Maloney et al in 1981, a Boston surgeon performed the first Le Fort I maxillary osteotomy for access to a nasopharyngeal tumor.

Cohn-Stock (1921).

He described the first anterior maxillary osteotomy to correct ananterior open bite.

Wassmund (1927).

Reported in his 1935 textbook, he performed a Le Fort I maxillary osteotomy to correct an anterior open bite. The maxilla was only partially sectioned from its bony attachments but not mobilized at the time of surgery. Maxillomandibular elastic traction was used postoperatively to close the open bite.

Axhausen (1934).

He was the first to advance a maxilla at the Le Fort I level that was incompletely mobilized at the time of operation; postoperative elastics were used.

Schuchardt (1942).

To prevent impairment of the vascular supply to the maxilla, a two-stage procedure was devised. The second stage involved separation of the maxilla at the pterygoid plates. Postoperatively, weights hung from an overhead traction device were used to advance the maxilla.

Gillies and Harrison (1950).

They performed the first Le Fort III osteotomy in 1941; the procedure was later made routine by Tessier in 1971.

Converse etal (1952).

They advanced the maxilla by means of a transverse palatal cut at the junction of the palatine and maxillary bones.

Bell (1969 to 1975).

Experiments on adult rhesus monkeys established the scientific basis for the safety of Le Fort I downfracture osteotomy with full mobilization under direct vision.

Obwegeser (1969).

He described a very high-level Le Fort I osteotomy whereby interpositional bone grafts were placed in the pterygoid plate region to aid stability in large advancements. Obwegeser also advocated the use of simultaneous Le Fort I and Le Fort III procedures.

Kufner (1970); Henderson and Jackson (1973).

These surgeons described various approaches to the Le Fort II osteotomy.

Bennett and Wolford (1985).

They developed the Le Fort I step osteotomy, which allowed bone cuts to be made parallel to the Frankfort horizontal plane.

Classification

Osteotomies of the maxilla may either be segmental, in which case only a segment of the dental arch is mobilized, or total, in which case the whole maxillary arch is mobilized.

Segmental maxillary surgery (Fig. 16.14):

• Single-tooth osteotomy.
• Corticotomy.
• Anterior segmental osteotomy:
• Wassmund (1935).
• Wunderer (1963).
• Epker and Wolford (1980).
• Posterior segmental osteotomy:
• Schuchardt (1959).
• Kufner (1971).
• Horseshoe osteotomy:
• Wolford and Epker (1975).

Fig. 16.14. Posterior segmental osteotomy and ostectomy: a – palatal view of the osteotomy and extraction of the first premolar; b – lateral view showing the extrac­tion of the premolar in order to move the posterior segment forward to improve the occlusal molar relationships; c – posterior maxillary osteotomy used to interi­orly reposition the posterior alveolar segment to close a posterior open bite; d – resultant gap above the segment that is usually bone grafted to enhance stability

Total maxillary surgery

There are many osteotomy techniques and designs that involve the movement of the whole maxillary arch in all three dimensions of space relative to the cranial base. They range from low-level Le Fort I osteotomies to subcranial Le Fort III osteotomies and everything between. The following is a list of some of the midfacial osteotomies involving the whole maxillary dental arch that have been described in the literature over the last half century:

Le Fort I osteotomy:

• Classic downfracture: Bell (1969 to 1975).
• Surgically assisted maxillary expansion: Buttress release.
• Quadrangular: Keller and Sather (1990; Fig. 16.15) Le Fort I osteotomy.
• Anterior Le Fort II osteotomy: (Fig. 16.16)
• Pyramidal Le Fort II osteotomy: Henderson and Jackson (1973; Fig. 16.17).
• Quadrangular Le Fort II osteotomy: Kufner (1971).

Le Fort III osteotomy (Fig. 16.18):

• Gillies (1940s).
• Tessier (1971).

Other midfacial osteotomies:

• Zygomatic osteotomies.
• Malar-maxillary osteotomy: Obwegeser (1969); malars attached as wings to maxilla (Fig. 16.19).

Bezrukov V. (1976) proposed method of surgical treatment of upper retrognathia with the modification of Le Fort osteotomia (Fig. 16.21). Malanchuk V. (1995) proposed method of surgical treatment of upper micro- and retrognathia which allows to remove retroposition of maxilla and narrow alveolar arch simultaneously during operation (Fig. 16.20).

Fig. 16.15. Quadrangular or high-level Le  Fort I osteotomy

Fig. 16.16. Anterior Le Fort II osteotomy. Technically, this is a segmental max­illary osteotomy involving only the anterior arch, but the procedure is included here as part of  the range of Le Fort II osteotomies

Fig. 16.17. Pyramidal Le Fort II osteotomy

Fig. 16.18. Le Fort III orbital floors osteotomy that involves the nasal bridge and anterior

Fig. 16.19. Malar-maxillary osteotomy, a variation of a high Le Fort I osteotomy in which the malar buttresses are attached as wings

Fig. 16.20. Scheme of osteotomia of maxilla by V. Malanchuk

Fig. 16.21. Scheme of osteotomia of maxilla by V. Bezrukov

Basic principles of segmental maxillary surgery

Surgical repositioning of small dentoalveolar segments is possible, provided that maximal palatal and labiobuccal mucoperiosteal attachments are maintained. The design of bone and soft tissue incisions should aim for the largest possible dento-osseous segment to preserve the greatest amount of soft tissue pedicle. Inadvertent injury to cementum in the midportion of a tooth frequently heals without problem. However, inadvertent apicectomy of teeth may initiate progressive pulpal necrosis and fibrous degeneration resulting in devitalization, despite pulpal and osseous revascularization.

Le Fort I maxillary osteotomy

The Le Fort I maxillary osteotomy is the most versatile and most commonly used orthognathic surgical procedure involving the maxilla and will therefore be described in more detail.

Bell et al (1969 to 1975) laid the biologic foundations for the safety of the Le Fort I downfracture osteotomy. Using 14 adult rhesus monkeys, they undertook microangiographic and histologic studies of healing at various time intervals after total maxillary osteotomy. They found only transient vascular ischemia, minimal osteonecrosis, and early osseous union.

Their results demonstrated:

• As long as the maxilla is pedicled to palatal mucosa and labiobuccal gingivae and mucosa, there are adequate nutrient pedicles required for Le Fort I downfracture and maxillary viability.
• Segmentalization, stretching of vascular pedicles, and transection of the descending palatine vessels have no discernible effect on revascularization or bone healing associated with Le Fort I osteotomies.

The work of Bell and colleagues permitted technical advances in total maxillary surgery, such as allowing full mobilization of the maxilla, hence reducing the risk of relapse, and permitting bone surgery under direct vision.

Surgical procedures (Fig. 16.22–16.27):

• Make a buccal incision a few millimeters beyond the sulcus, into the upper lip, extending from first molar to first molar. Previous palatal surgery may compromise palatal blood supply to the segmented maxilla, in which case vertical incisions and subperiosteal tunneling should be used instead.

Locate a Le Fort I – level osteotomy at least 5 mm above the apices of the:

• Straight-line osteotomies create a ramping effect, so that simple advancements also decrease the vertical height.
• The step osteotomy (Bennett and Wolford, 1985) allows horizontal bone cuts to be made parallel to Frankfort horizontal, permitting horizontal maxillary movements without altering vertical dimensions; hence, ramping effects are minimized:
• Anterior cuts: 4 to 5 mm
  above the canine apices
• Vertical cuts: zygomatic buttress region (excellent site for bone grafts)
• Posterior cuts: 4 to 5 mm above the molar apices Perform an osteotomy of the lateral nasal walls and nasal septum.

Fig. 16.22. Exposure of the right maxilla through an incision in the buccal sulcus a few millimeters beyond the attached gingiva: a – illustrated view; b – intraoperative view. Note the periosteal ele­vator inserted in the  lateral nasal wall

Fig. 16.23. Horizontal osteotomies made at the Le Fort I level. The osteotomies should be located at least 5 mm above the apices of the maxillary teeth, in particular the canine teeth, which have the longest roots. Note the  slight downward inclination of the bone cuts as they progress posteriorly

Fig. 16.24. Downfracture of the maxilla: a – separation of the maxilla from the midface; b – intraoperative view of the downfractured maxilla

Fig. 16.25. Downfracture of the maxilla using a large bone hook

Fig. 16.26. Use of Rowe disimpaction forceps to help downfracture and fully mobilize the maxilla from its attachments

Fig. 16.27. Miniplate and monocortical screw fixation of a Le Fort I osteotomy:
a – illustrated view; b – intraoperative view

Separate the pterygomaxillary junction:

• First advocated by Axhausen in 1934 by use of the curved osteotome.

Complications of unfavorable dysjunction in this region include:

• Excessive bleeding.
• Cranial nerve injury.
• Carotid artery injury.
• Unfavorable fracture.

Completely mobilize and trim the maxilla:

• Ensure that the maxilla can sit passively in the new position.
• Remove the pyramidal strut of bone surrounding the descending palatine arteries to allow posterior impaction (Johnson and Arnett, 1991).
• Carefully trim the lateral nasal walls and septum.

Provide fixation:

• Use 2-mm adaptational bone plates and monocortical screws to fix the maxilla in the desired position.
• Use two or four plates (Fig 16.28a), although two may be adequate for small movements.
• For advancements greater than 5 mm and downgrafts,stability and healing are greatly facilitated by interpositional bone grafts (Fig 16.28b), especially in the buttress region (placed under direct vision) and pterygomaxillary junction (placed blindly behind the maxilla).

Fig. 16.28. A gap of more than 4 to 5 mm in the osteotomy site requires i the repositioned maxilla an interpositional bone graft to fill the gap and thereby improve the stability

Surgical occlusal wafer/splint:

• In maxillomandibular surgery, two splints are required:
• The intermediate splint helps to guide the final position of the maxilla before it is fixed. The final splint guides the new position of the mandible.
• Wire the final splint to the maxillary teeth only if segmental maxillary surgery is performed.

Applications

With the establishment of the scientific basis for the various orthognathic surgical techniques, it has become possible to apply these procedures to the treatment of the numerous dento-facial deformities. As already mentioned, the most commonly used orthognathic surgical techniques are the Le Fort I down-fracture for the maxilla and the ramus osteotomy techniques for the mandible, in particular the sagittal split and the vertical sub-sigmoid osteotomies. This section will discuss the application of these most commonly used orthognathic surgical techniques for the management of the more common dentofacial deformities.

Common procedures

The most commonly performed orthognathic surgical procedures involve the movement of the jaws in any one or combination of the following directions relative to the cranial base.

Maxillary surgery:

• Vertical:
  • Superior repositioning (impaction).
  • Inferior repositioning (downgraft).
• Horizontal:
  • Anteroposterior (advancement).
  • Transverse (expansion).

Mandibular surgery:

• Horizontal (anteroposterior):
  • Advancement.
  • Setback.
• Vertical (autorotation): Vertical changes in the maxilla often give rise to the following vertical movements of the mandible without surgery in the mandible itself:
  • Clockwise: results in decreased chin projection.
  • Counterclockwise: results in greater chin projection.

Maxillary (Le Fort I downfracture) procedures

Maxillary impaction (superior repositioning)

Indications.

Vertical maxillary excess:

• With open bite.
• Without open bite.

Esthetics:

• Deformity mainly in the vertical facial balance (long-face [dolichofacial] pattern).
• Relatively long lower third of the face.
• Lip incompetence with excessive exposure of the teeth and gingivae.
• With open bite: excessive eversion and exposure of the lower lip at rest.
• Without open bite: excessive tooth display and narrow alar base of the nose.
• Profile:
  • Nasal prominence.
  • Marked interlabial distance.
  • Recessive chin, especially in patients with open bite.

Occlusion:

• Class II malocclusion.
• V-shaped maxillary arches.
• Open bite: maxillary crowding with posterior crossbites.
• Cephalometric features.
• Large lower facial height resulting from long posterior facial height Relative mandibular retrognathia and high mandibular plane angle.

Treatment planning:

• Ideal maxillary incisal exposure is 2 to 3 mm (Burstone, 1967) from stomion to incisal tip.
• With maxillary impaction, the upper lip moves 1 mm (20 %) for every 5 mm of superior repositioning of the anterior teeth.
• With maxillary impaction, the mandible rotates counterclockwise, which:
  • Shortens the lower face.
  • Makes the chin more prominent.

Surgical procedures:

• Vertical maxillary excess without open bite: One-piece maxillary osteotomy with careful trimming of bony interferences that may prevent the maxilla from seating passively in a superior position (e.g., pyramidal bony release around descending palatine artery).
• Vertical maxillary excess with open bite (see the section on open bite): Differential impaction of the maxilla, which may also require maxillormandibular surgery. Segmental maxillary surgery may be required to correct the transverse maxillary problem. Impaction of greater than 5 mm may require a horseshoe osteotomy to minimize the decrease in the nasal airway.

Maxillary downgraft (inferior repositioning)

Indications:

• Vertical maxillary deficiency: short-face (brachyfacial) pattern.
• Maxillary atrophy resulting from a prolonged edentulous state.

Esthetics:

• Poor incisal display even on smiling with the eversion of the lower lip.
• Diminutive anterior dentoalveolar height in both arches.
• Occlusion.
• Usually Class I but sometimes Class II malocclusion with dental crowding.
• Deep anterior overbite.
• Wide maxilla.

Cephalometric features:

• Negative incisal display with normal anteroposterior positioning of the maxilla.
• Square jaw with low, almost parallel, mandibular and occlusal plane angles.
• Prominent pogonion and labiomental fold.

Surgical procedures:

• Perform interpositional bone grafting for all downgrafting procedures. Bone grafting is essential because of the inherently high relapse rate of downgrafting.
• Aim for overcorrection with greater than 3 mm of incisal display.
• Maxillary downgrafting increases lower facial height and rotates the chin downward and backward as the occlusal and mandibular plane angles are increased.
• Position the maxilla slightly posteriorly to fit the occlusion if mandibular surgery is not planned.

Maxillary advancement Indications.

Anteroposterior maxillary deficiency (maxillary hypoplasia):

• Without cleft palate.
• With cleft palate.

Esthetics:

• The nasolabial angle is reduced.
• If the nasal bridge cannot be seen in profile because the eye (globe) protrudes beyond it, then the maxilla most likely needs an advancement at a higher level osteotomy.
• Maxillary incisal display is inadequate.
• The prominent everted lower lip is indicative of mandibular prognathism or maxillary hypoplasia.
• Nasal balance: Important preoperative measures include the nasal tip, nasolabial folds.

Occlusion:

• Class III malocclusion.
• Severe maxillary dental crowding.
• Constricted maxillary arch with posterior crossbites.

Velopharyngeal function:

Velopharyngeal function is of particular concern in cleft patients with short palates, because maxillary advancement may well accentuate velopharyngeal incompetence. If there is a strong risk of postoperative velopharyngeal incompetence, maxillomandibular surgery should be considered to minimize the amount of maxillary advancement required for esthetics and occlusion.

Surgical procedures:

• Place interpositional bone grafts within osteotomy gaps:
• For maxillary advancements greater than 5 mm.
• In difficult cleft cases.
• Use bone grafts:
• To accelerate bone healing between segments.
• To serve as physical stop for increased stability and to minimize relapse.
• Completely mobilize the maxilla until it can be passively placed in the desired anterior position.

Cleft lip and palate patients. Simultaneous maxillary expansion and grafting of alveolar clefts is readily achieved with properly designed soft tissue flaps.

• For patients with complete clefts, mobilize the greater and lesser segments of the maxilla independently; alternatively, bone graft the alveolar cleft defect at least 6 to 12 months before maxillary advancement if a single-piece maxillary osteotomy is required.
• Mobilization of the maxilla is difficult because of:
• The perpendicular plate of palatine bone.
• Scar tissue between the palate and nasal septum secondary to previous palatal surgery.
• The presence of a pharyngeal flap.
• Indications and features.
• Transverse maxillary deficiency (bilateral or unilateral), either isolated or with a Class III malocclusion.
• Narrow maxilla with dental crowding.
• Few facial or cephalometric features that are of any practical use for diagnosis.

Treatment planning:

• Children: They can be successfully treated with orthopedic rapid maxillary expansion.
• Adults:
  • For less than 5 mm of transverse deficiency, orthopedic expansion of maxilla is sufficient.
  • For greater than 5 mm of transverse deficiency or buccally inclined posterior teeth, a combined surgical-orthodontic expansion technique is used.

Combined surgical-orthodontic expansion. There are three surgical options:

Segmental posterior alveolar osteotomy, used for unilateral deficiencies.

Le Fort I downfracture with midline palatal split or horseshoe osteotomy.

Surgically assisted rapid maxillary expansion: Complete a Le Fort I osteotomy without the downfracture. Make a midline palatal split between the maxillary central incisors with a fine osteotome. Intraoperatively, activate an orthopedic expansion device that is bonded to the posterior maxillary teeth across the palate.

Mandibular (ramus osteotomy) procedures

Mandibular advancement

Deficiency in the anteroposterior direction:

• The chin and mandible are retruded.
• There is crowding in the mandibular anterior arch, with overangulated incisors and accentuated curve of Spee.
• This is corrected by mandibular advancement with ramus osteotomies, such as sagittal split ramus osteotomy Deficiency in the vertical dimension.
• The mandibular anterior dental height may be less than 40 mm.
• Sometimes the mandible appears clinically short but the actual problem is a deep overbite. This is best corrected by vertical lengthening of the chin by interpositional graft and augmentation.
• Deficient ramus height may be best treated with an inverted L-osteotomy and interpositional bone graft.
• Deficiency in the transverse dimension. This is corrected by body or symphyseal osteotomies or by subapical osteotomies to allow expansion of the arch.

Mandibular setback

Excess in the anteroposterior direction.

Mandibular prognathism is present and mandibular incisors are lingually inclined.

There is a Class III malocclusion with anterior and bilateral posterior crossbites:

• Presurgical orthodontics often worsens the appearance as teeth are uprighted over basal bone prior to surgery.
• This is usually treated with mandibular setback achieved via ramus osteotomies such as the sagittal split or vertical subsigmoid osteotomies.

Excess in the vertical dimension:

• Mandibular anterior dental height is increased.
• Reduction genioplasty is required.
• Excess in the transverse dimension.
• The mandibular dental arch is too wide in comparison to a normal maxillary arch.
• Arch width can be reduced by body and symphyseal ostectomies. Specific deformities.

Orthognathic surgery has a pivotal role in the management of the following common dentofadial deformities:

• Anterior open bite.
• Crossbite.
• Lower facial asymmetry.

Open bite

Clinical presentation.

In open bite, teeth in opposing jaws fail to contact each other.

Etiology:

• Anterior open bite: tongue thrust, thumb sucking, deficient eruption of anterior teeth and/or excessive eruption of the posterior teeth, skeletal base growth discrepancy (e.g., excessive posterior facial height, severe mandibular retrognathia, short ramus height, or long-face syndrome), condylar resorption: idiopathic, avascular necrosis.
• Posterior open bite: deficient eruption of posterior teeth, facial asymmetry that develops after growth is completed (e.g., condylar hyperplasia).

Classification:

• Dentoalveolar, skeletal base, combined dentoalveolar and skeletal base.

Management:

Management depends on the cause of the open bite:

• Discourage adverse habits such as thumbsucking or finger sucking with a variety of oral appliances, which will sometimes lead to spontaneous resolution of the open bite.
• Tongue thrust during swallowing will create forces large enough to result in open bite. The role of surgical reduction of the tongue as an adjunctive measure to the surgical-orthodontic management of anterior open bite is controversial. Assess the tongue size, morphology, and function in terms of:
• True macroglossia: excessively large tongue.
• Relative macroglossia: normal-sized tongue confined within a restricted oral space of relatively small dental arches.
• Functional macroglossia: excessive tongue activity.
• Segmental orthognathic surgery is especially useful in cases of infraeruption or supraeruption of the teeth; the dentoalve segment can be surgically repositioned anywhere in the vertical plane to close the open bite:
• Directly: Use an anterior subapical mandibular osteotomy with superior positioning to close an anterior open bite.
• Indirectly: Use a posterior maxillary osteotomy with impaction, which will bring the anterior segments together and close the anterior open bite.
• Total maxillomandibular orthognathic surgery can be used to surgically correct the problem of open bite caused by a skeletal base discrepancy:
• Mandibular body osteotomies and ostectomies are especially useful in the correction of a mandibular occlusal.
• Mandibular ramus osteotomies usually involve a counterclockwise rotation to close the open bite; this is often quite an unstable procedure with significant potential for relapse. The technique is mainly used for patients with mandibular retrognathia in whom maxillary surgery is also planned.
• Le Fort I maxillary osteotomy: Differential impaction of the whole maxilla yields a stable result and directly addresses the problem of increased posterior facial height. This is probably the most favored treatment option.

Crossbite

Clinical presentation

Crossbite is a reverse buccal overjet relationship of the teeth in opposing jaws:

• It may occur unilaterally or bilaterally.
• It can occur anteriorly or posteriorly.
• It is commonly related to a hypoplastic maxilla in patients with a Class III skeletal base malocclusion.
• It is also found in patients with lower facial asymmetry.

Etiology:

Crossbites are most frequently related to a transverse deficiency of the palatal vault or maxillary alveolar arch.

Treatment:

• Orthodontics: Tip or torque the teeth buccally. The results may be unstable if the transverse discrepancy is greater than 5 mm.
• Skeletal: Increase the width of the of the palate via:
• Palatal expansion devices during the growth phase.
• Surgically assisted rapid maxillary expansion: Use a combination of surgical relief of maxillary bony abutments and palatal expansion devices to rapidly open the midpalatine suture in a space of a few weeks.
• Segmental maxillary surgery: Make a midpalatal osteotomy at the time of the Le Fort I maxillary down-fracture to immediately expand the palate to the desired dimension in one step.
• Segmental posterior maxillary osteotomy may be used for unilateral deficiencies or crossbites.

Lower facial asymmetry

Clinical presentation

Lower facial asymmetry is usually related to unbalanced, aberrant growth of one side of the face; the aberrant growth often occurs in the condylar process of the mandible, but sometimes the ramus and body may be involved:

• Malocclusion may be present, depending on the compensatory growth in the maxilla.
• Alteration in the maxillary cant will only arise if the problem emerges during early periods of facial growth, whereby compensatory growth of the maxilla will occur in relation to the aberrant mandibular growth pattern.
• Clinical asymmetry results in a chin and mandibular midline shift (lower facial asymmetry) (Fig. 16.29).

Fig. 16.29. a – Lower facial asymmetry, b – corrected with maxillomandibular surgery and genioplasty

Etiology:

• Aberrant condylar growth:
  • Condylar hyperplasia.
  • Condylar hypoplasia.
  • Condylar aplasia.
  • Aberrant mandibular growth:
  • Hemimandibular elongation.
  • Hemimandibular hypertrophy/hyperplasia.
  • Hemifacial atrophy (Parry – Romberg syndrome).
  • Hemifacial microsomia (Goldenhar syndrome).
  • Hemifacial hypertrophy.
  • Traumatic deformities:
  • Condylar fractures.
  • Mandibular fractures (particularly of the ascending ramus).
  • Neoplastic and other diseases of the facial skeleton:
  • Neurofibromatosis (von Recklinghausen disease).
  • Bone neoplasms (eg, osteoma, osteosarcoma, or osteochondroma of the condyle).
  • Fibrous dysplasia.
  • Odontogenic tumors.
  • Large cystic lesions of bone (eg, odontogenic keratocyst).
  • Temporomandibular joint (TMJ) ankylosis (unilateral, arising during growth).

This section will discuss facial asymmetry caused by growth aberration rather than by disease, because orthognathic surgery does not address the disease process but only the consequences of the growth anomaly.

Clinical examination:

All normal individuals have a certain degree of facial asymmetry. Assess mainly the frontal view and start from the top, looking for obvious differences between left and right sides:

• Cranial vault (eg, plagiocephaly).
• Forehead: unilateral flattening or excess.
• Eyes: intercanthal and interpupillary levels.
• Malar prominences.
• Nose: level of alar bases.
• Lips: level of commissures.
• Chin point: deviation from midline.
• Dental midlines:
  • Maxillary occlusal cant.

Investigations:

• Serial photographs: over a period of time to establish whether asymmetry is progressive or static.
• Radiographs:
  • Diagnostic: use of cephalometric analysis on anteroposterior and lateral cephalograms as well as TMJ radiographs to determine the focal cause of the asymmetry (e.g., hyperplastic condyle).
• Radioisotope bone scans to determine sites of active bone growth.
• Three-dimensional computed tomographic scan reconstructions.
• Biopsy: when a disease process is suspected rather than just aberrant growth
• Treatment planning.
• Determine the side and site of the abnormal growth and where the compensatory growth has occurred.
• Eliminate all disease processes prior to undertaking any corrective surgery.
• Often the underlying skeletal abnormalities must be corrected before any soft tissue procedures. It sometimes may be necessary to undertake tissue expansion in deficient regions prior to the bony surgery.
• Aim not only to correct the site of aberrant growth but also to eliminate any compensatory growth that may have occurred.
• In growing children, functional appliance therapy is of immense value, particularly in those with mild lower facial asymmetry.

In patients with mild asymmetry, in the presence of a functional occlusion and unrestricted mandibular movements, orthognathic surgery is best confined to a camouflage genioplasty.

In the presence of a maxillary occlusal cant, make an esthetic judgment, based on incisal display, as to whether to impact the maxilla on the excess side or downgraft the maxilla on the deficient side, regardless of where the aberrant or compensatory growth lies.

Timing of corrective surgery:

• Early surgery (during the growth phase):
  • It will stimulate development of a functional occlusion through the creation of a proper interocclusal relationship at an early age.
  • It will stimulate soft tissue development on the affected side.
  • Early esthetic and functional improvement has a positive psychologic effect on both the parents and the child.
• Delayed surgery (after growth is completed):
  • It avoids possible untoward effects of early surgery on subsequent facial growth.
  • It avoids the difficulty in predicting final facial form that arises if early surgery is planned.
  • It provides a more predictably stable result with less likelihood of multiple procedures.

Distraction osteogenesis

Distraction osteogenesis (DO) is a technique in which new bone is created through physical stretching of a developing callus between two bony ends that have been osteotomized or fractured. As the two bony fragments are gradually separated (distracted), the resulting gap is filled with an expanding callus that eventually develops into new bone (osteogenesis). DO has been touted as an alternative to conventional osteotomies.

Historical review

The first report of bone lengthening by gradual distraction was published in 1905 in the orthopedic literature (Codivilla, 1905), but it was many decades before the concept attracted the attention of llizarov, a Russian orthopedic surgeon. Ilizarov is credited as the pioneer in the development of DO, especially in the treatment of limb deformities. It was not until the 1970s, however, that the idea of using the DO technique in the jaws emerged with animal studies (Snyder et al, 1973; Michel)) and Miotti, 1977).

Tairov U. (1982) proposed the surgicaly-orthopedic method of distraction of mid-face zone.

After another hiatus of more than a decade, McCarthy and coworkers (1992) published a report of the first clinical application of DO for the management of congenitally hypoplastic mandibles in children. The publication brought to light the possibility of treating very young children with severe and disfiguring facial deformities without the need for conventional osteotomies. As interest in DO gradually gathered momentum during the 1990s, bold predictions were made that DO would eventually replace all conventional osteotomies, even in adult patients.

Surgical procedures

• Select the site of the osteotomy.

Make an incomplete bone cut through the cortex only. Fix the distraction apparatus across the osteotomy site with bone plates and screws.

Complete the osteotomy and ensure that free and unobstructed movement of the bone fragments on both sides of the osteotomy is possible.

To allow time for the initial callus to develop, do not commence distraction by a screw-type apparatus until 5 to 7 days following the osteotomy.

Thereafter, have the patient activate the screw device twice daily to achieve a distraction (callus-lengthening) rate of 1 mm per day until the desired length is achieved. Leave the distraction apparatus fixed in place for a further 2 to 3 months until the distracted callus has fully mineralized into new bone before removing the device.

Clinical applications

The fundamental fuel that drives the interest in the distraction technique is the concept of new bone growth, which in itself is a startling medical breakthrough. DO has been applied to the following situations.

Mandibular lengthening

Mandibular lengthening was the first application for DO, and presently myriad devices, both intraoral and extraoral, are available on the market. Despite the obvious advantages of the intraoral devices, the external devices are making a slow comeback, because the complex three-dimensional vectors of distraction required to lengthen a hypoplastic mandible cannot be adequately addressed with the simpler intraoral devices.

Mandibular widening at the symphysis

Symphyseal widening can be used in combination with ramus-body distraction devices to lengthen and widen the mandibular arch at the same time. Some researchers have raised the concern that widening of the mandibular arch may torque the condyles and result in TMJ pain and dysfunction. Clinical experience has so far failed to show any significant detrimental effects of DO on the TMJs.

Alveolar augmentation

Distraction techniques are also gaining popularity for the augmentation of alveolar ridges both in width and height to facilitate the placement of dental implants. Distraction is an alternative to the conventional onlay bone grafts and sandwich or visor osteotomies used in the past.

Palatal expansion

Palatal expansion using orthodontic appliances is a well-known technique that has been utilized for many decades. The introduction of surgically assisted rapid maxillary expansion has enabled palatal expansion to be undertaken in adult (nongrowing) patients. Palatal expansion techniques were the earliest form of DO, which predated the pioneering mandibular lengthening devices of the early 1990s.

Midfacial distraction

Midfacial distraction devices such as the RED system and Modular Internal Distraction system (Stryker) are designed to advance the midface at various levels, from low Le Fort I to high Le Fort III and beyond to fronto-orbital levels. As with the mandibular devices, attempts to make the midfacial devices almost fully implantable beneath the skin have met with the problem of uniplanar directional control. To address the three-dimensional vector requirements, the RED system, which has a fully adjustable external frame, permits multidirectional vectors of advancement of the midface; in particular the maxilla. The biggest drawback is the unsightly head frame.

Mandibular resection and distraction

Mandibular resections are also amenable to the technique of DO. The technique involves the creation of a transporter segment of bone that is osteotomized a few millimeters from the edge of the resection margin and distracted across the resection defect with an expanded callus following behind it.

Advantages

DO has a number of essential advantages compared with conventional osteotomy techniques:

• It eliminates the need for bone harvesting from remote donor sites.
• It allows gradual expansion of the surrounding soft tissue envelope.
• It may provide better stability than conventional osteotomies (yet to be proven).
• A much greater degree of bone lengthening can be attained.
• Surgical morbidity is lower.
• Operating time is reduced.

Disadvantages

The biggest disadvantage of DO is the distraction device itself:

Expensive hardware is required.

The metallic hardware protruding through the mouth, face, scalp, or neck is unsightly and uncomfortable.

Exposed hardware will draw unwanted attention.

There may be an increased potential for ascending infection via exposed hardware into the osteotomy site (not yet proven).

External devices result in pin-tract scarring of the skin.

A high level of patient compliance is required in terms of daily screw activation and meticulous hygiene.

The vector of lengthening (distraction) is difficult to control because of the three-dimensional nature of the maxillofacial skeleton. Mandibular distraction often results in anterior open bites unless due diligence is taken in the proper positioning of the device.

A second surgery is required to remove the device at the completion of treatment.

Complications

The evolution of surgical techniques and instrumentation and the introduction of new technology (e.g., miniature bone plates and screws and bone substitutes) have contributed to the improved safety and predictability of orthognathic surgery. Complications associated with orthognathic surgery can be divided into several categories.

Preoperative complications

• Poor communication:
  • Surgeon.
  • Orthodontist.
  • Patient: unrealistic expectations.
• Incorrect diagnosis:
  • Insufficient clinical data.
  • Lip and mandibular posturing.
  • Errors in radiographic measurements.
• Unsatisfactory laboratory work:
  • Incorrect bite registration.
  • Poor-quality surgical wafers or splints.
• Poor patient preparation:
  • Unsatisfactory presurgical orthodontics.
  • Inadequate medical history and examination.
  • Poor workup of medically compromised patients (including psychiatric patients).

Intraoperative complications:

• Hemorrhage:
  • Poor surgical technique.
  • Awkward anatomy.
• Nerve injury:
  • Neuropraxia.
  • Axonotmesis.
  • Neurotmesis.
• Unfavorable osteotomy:
  • Poor design.
  • Poor surgical technique.
• Jaw malpositioning:
  • Soft tissue interferences.
  • Bony interferences.
  • Poorly constructed surgical splints.
  • Improper seating of condyles.
  • Inadequate surgical reference markings.
• Fixation problems (especially with bicortical screws):
  • Direct injuries to tooth roots.
  • Direct injuries to the inferior alveolar nerve.
  • Excessive torque on condyles.

Postoperative complications

Acute phase (less than 2 weeks):
• Wound dehiscence.
• Hemorrhage:
• Reactionary.
• Secondary.
• Infection.

Chronic phase (more than 3 months):
• Relapse:
• Relapse is the propensity for the jaws to revert back to their original, preoperative position after surgery.
• Magnitude of movement: Any single jaw movement greater than 8 to 10 mm is potentially likely to relapse.
• Direction of movement: Maxillary downgrafts and counterclockwise rotation of the mandible are inherently unstable.
• Type of fixation: Rigid fixation with plates and screws is more stable than wire fixation because of three-dimensional control of fragments.
• Latent growth (age of patient): Class III mandibular setbacks in growing adolescents are highly likely to relapse.
• Condylar resorption: Patients with Class II skeletal relationships, steep mandibular plane angles, and preexisting TMJ symptoms are most likely to suffer condylar resorption following mandibular advancement procedures.
• Neurologic dysfunction:
• Persistent paresthesia or anesthesia lasting more than 6 months.
• Dysesthesia.
• Poor esthetics:
• Lip imbalance.
• Nasal base problems: excessive alar width, upturned tip, or nasal asymme try caused by an unsupported anesthetic tube that buckles the nasal septum.
• Soft tissue of the chin-throat angle.
• Poor bone healing:
• Delayed union.
• Nonunion.
• Inadequate fixation:
• Loose.
• Annoying.
• Exposure and infection.
• Unhappy patient:
• Poor esthetic result.
• Unrealistic expectations.
• Psychiatric issues:
• Depression.
• Dysmo rphobia.

Prevention and management

Prevention of most complications can be achieved through proper preoperative preparation and planning. Good presurgical orthodontic alignment of the teeth will help simplify the surgery and therefore minimize the likelihood of complications. Identifying problems before they occur eliminates the unwelcome surprises that often lead to unnecessary delays and a protracted course of treatment. Communication among the surgeon, the orthodontist, and the patient should be nurtured and maintained at all times to effectively produce a treatment plan that satisfies all parties concerned.

Response to a problem is a matter of the training, experience, attitude, and approach of the individual clinicians concerned. Maxillomandibular (two-jaw) surgery with rigid fixation and appropriate bone grafting are often effective measures that help to reduce the likelihood of relapse. Problems tend to arise when clinicians fail to recognize the merits and limitations of each of the treatment options, such as trying to close an anterior open bite with a mandibular osteotomy alone. A broad-minded attitude and sensible approach to problem solving are indispensable traits every surgeon must acquire during the protracted course of surgical treatment

Facial reconstructive surgery. Skin grafts and flaps. Principles and techniques for local plastics

Few procedures are more challenging than the surgical repair of patients with craniomaxillofacial deformities and defects. They are the end results of the trauma, cancer, infection, or congenital anomalies. These defects may involve both bone and overlying soft tissue. No matter how subtle a deformity is, it will more than likely be quite obvious when involving the cranio – maxillofacial region.

Regardless of the etiology, surgeons must direct their repair toward the correction of the aesthetic defect with the restoration of function.

When treating patients who have undergone tumor resection or suffered severe facial trauma, both the surgeon and the patient must understand that the patient most likely will never function or appear as they did prior to their trauma or tumor surgery. The difficult task for the craniomaxillofacial surgeon is not the surgical correction of the deformity, but the basic understanding of the deformity’s nature.

As with all patient interviews and examinations, the information obtained during the initial assessment will be the first insight into the patient’s general health and mental readiness regarding their surgical treatment. This information should be clearly recorded and readily accessible to all those involved in the patient’s treatment. At this point, the surgeon’s feelings toward the accuracy and reliability of the history and information obtained should be stated. Was the patient or informant confused, cooperative, and was there a language barrier? Psychosocial problems that may pose potential problems regarding the surgery and its final outcome should be identified early in the patient interview if possible. In the adolescent and adult patient, the surgeon should try to identify who is the driving force regarding the chief complaint (i.e., the patient, family members, or friends). This information will again reflect the psychosocial status of the patient and family and should be noted because missed signals at this point may cause problems for the treating surgeon when patients enter treatment with unrealistic or misconceived expectations.

A variety of medical conditions are commonly associated with craniomaxillofacial deformations and defects. In planning for the surgical correction of craniomaxillofacial deformities, medical risk factors that contraindicate general anesthesia and surgical reconstruction must be identified.

Clinical assessment of facial defects from the esthetic point of view is a rather complicated process.

Dating back to ancient civilizations, many attempts have been made to establish a set of standards for facial beauty. Mathematicians have also attempted to calculate and quantify facial measurements to distinguish what is beautiful and what is not, but these calculations can be complex and difficult to interpret. However, it was Leonardo da Vinci who felt that anatomic relationships were more valuable than absolute numerical values. His studies furnished important data upon which many modern concepts of facial beauty are based. He divided the face into equal thirds and noted that these divisions should be relatively equal and symmetric. Therefore, the clinical examination should begin with the general assessment of symmetry and deformity in the frontal and profile views.

In the study of facial harmony, symmetry is one of the most obvious yet most critical concepts to appreciate. The aesthetic face requires reasonable symmetry. When planning a surgical procedure (either reconstructive or cosmetic), the surgeon must have symmetry as a primary goal.

Balance among different aesthetic units of the face also plays a very important role in creating facial harmony. The facial units that should be systematically studied preoperatively include the forehead, nose, eyes, malar prominences, lips, chin, and mandibular angles.

Over the past 50 years the development and application of several different flaps has led to reliable reconstruction of facial defects. Most defects can be reconstructed immediately, leading to better restoration of form and function with early rehabilitation.

Commonly there is a wide range of options for repairing a given defect, including healing by secondary intention, primary closure, placement of a skin graft, or mobilization of local or regional tissue. Compared to skin grafts, local flaps often produce superior functional and esthetic results.

When deciding which option to use, there should be a progression from simple to complex treatments. Consideration should be given to primary closure or the use of skin grafts first, followed by local, then regional, and finally distant pedicled or microsurgical free tissue transfer. Flaps require additional incisions and tissue movement, which increase the risks of postoperative bleeding, hematoma, pain, and infection. Confirmation of tumorfree margins should be done prior to flap reconstruction if a malignant lesion has been excised.

Some defects are amenable to closure with a single flap, but others require a combination of flaps for optimal results. An advantage of using multiple flaps is that they can be harvested from separate esthetic units. This decreases the size of the secondary defect and may allow placement of scars between esthetic units, thus improving scar camouflage leading to better cosmesis. Often, separated repair of individual facial subunits with separate flaps provides a better cosmetic result than if a single flap is used to reconstruct the entire defect.

Skin grafts

A skin graft may be defined as an intact piece of the skin that has been completely separated from its donor site attachment and is transferred to a different recipient site.

At this site, it reestablishes a new blood supply. A full-thickness skin graft is an intact piece consisting of the entire epidermis, complete thickness of dermis, with no connection to subcutaneous fat. A split-thickness skin graft consists of the entire thickness of epidermis, a varying thickness of dermis, and no connection to the underlying subcutaneous fat. Composite grafts consist of intact skin, both epidermis and dermis, with an additional component such as fat or cartilage directly attached.

Full-thickness grafts offer several advantages over split-thickness grafts. Full-thickness grafts have less tendency to contract, their cosmetic appearance is generally better and improves with time; they are more durable, there is a better chance for texture and thickness match. At the same time grafting creates a defect of a donor site that must be repaired, graft failure, there is a chance of unfavorable appearance, contracture along free margins, as well as potential surgical complications at two sites. A clean, well-vascularized recipient bed is also necessary for full-thickness grafts.

Survival of transplanted skin is primarily dependent upon reestablishing blood supply to ischemic tissue. The phases of graft vascularisation are: plasma imbibition, inosculation, and capillary ingrowth. The phase of serum imbibition occurs during the first 24 to 48 h after skin graft transplantation. During this time, the graft survives by taking up nutrients from the wound exudate.

The phases of inosculation and capillary ingrowth are characterized by the host endothelial buds’ “hooking up” to existing arterioles and venules present within the graft. These vascular buds grow through the fibrin layer. Thus the graft is revascularized from ingrowth of new vessels from the margin and base of the recipient bed. Actual blood flow is on 5 to 7 day after an operation. The speed at which vascularization occurs depends primarily on the vascularity of the donor site and on graft thickness.

Full-thickness skin grafting is a useful technique for resurfacing and reconstructing various surgical defects. Selection of a full-thickness graft to resurface a defect depends on various factors. Local factors to be considered are defect size, location, lack of adequate adjacent tissue, and mobility. Tissue quality factors such as injured tissue, underlying medical disease, adjacent hair-bearing skin, and heavy smoking may all adversely affect local tissue transfer. Irradiated skin typically is also of poor quality with compromised vasculature. In certain anatomic areas, grafts may provide a better cosmetic result than flaps. Sites frequently used for full-thickness grafts include the distal nose, ear, lower eyelid, and inner canthus.

A variety of donor areas exist for free skin grafts. It is necessary to match the qualities of the donor skin and the surrounding recipient area. Texture, color, and actinic damage vary from donor site to recipient site and should be matched if at all possible. Most full-thickness grafts are harvested from the preauricular skin, postauricular skin, supraclavicular and clavicular areas, neck, and inner upper arm areas. The groin, hypothenar area, and wrist are less frequently used.

It is important to measure and size the graft correctly. This should include the depth of the defect. A template is ideal to ensure exact sizing. An imprint of the defect is made, cut out along the blood-tinged paper, and placed over the donor area for marking.

Removal of the donor graft is performed with standard surgical technique. After the graft is incised, a tip of the graft is grasped, and with sharp and blunt dissection the graft is removed. Next, hemostasis is obtained and the donor site is repaired with a layered closure. Sometimes a local skin flap or split-thickness graft is required to close the donor defect. Defatting the graft requires meticulous technique, patience, sharp scissors, and adequate lighting. The graft should be frequently moistened with saline to prevent desiccation. Once the fat is removed, the dermis may be thinned as to sculpt the graft thickness to match the surrounding defect thickness. If the graft is placed at the same time of tumor or scar removal, little donor site preparation is required. Absolute hemostasis must be obtained and any devitalized tissue should be removed. Once the recipient bed is prepared, the moistened graft is placed over the bed. The graft is aligned into position. All wrinkles or folds should be straightened. The graft is then trimmed and tailored to the defect. The graft edges must proximate the recipient bed margin exactly. If not, a suboptimal result will occur.

Precise suturing technique is required for full-thickness grafts. Initially “tacking” interrupted sutures may be placed to hold the graft in position at key anchoring points. Then, interrupted or simple running sutures may complete graft placement. The sutures may be placed directly into the graft margin as a tacking suture or a few millimeters away from the graft edge. The graft must be secured and protected from the outside environment. The dressing should prevent shearing forces from disturbing the graft and firmly hold the graft against the recipient bed to reduce the potential for hematoma and seroma formation. The graft is immediately covered with a thin layer of antibiotic ointment followed by a nonstick contact layer. Sterile cotton balls are moistened in saline or Betadine and placed over the contact layer.

Specific instructions for postoperative care should be reviewed with each patient. Removal of a dressing is done in 5 to 7 days. Grafts take time to mature. Thus, the initial cosmetic appearance may be discolored and have contour irregularity. Reviewing the graft’s color and contour and the future expectations of the patient is essential. Initially grafts may be pink, reddish blue, or dusky. Darker colors may indicate superficial epidermal and dermal loss. However, the deeper papillary and reticular dermis may be viable. Full-thickness loss of graft may be indicated by necrotic black tissue.

Placement of a graft immediately after soft-tissue surgery may not be possible if exposed bone or cartilage is present. The intact undisturbed perichondrium or periosteum must be in place to supply vascularity to the graft. If an exposed cartilage or bone exists, one may delay grafting until sufficient granulation tissue covers the exposed cartilage or bony surface. This may take 2 weeks or longer, depending upon the size of the exposed surface.

Complications

Bleeding is a postoperative complication that must be evaluated immediately. If active bleeding exists, the graft should be taken off and hemostasis accomplished. This may require suture, spot electrodesiccation, pressure, liquid thrombin. Milia and cyst formation are frequently seen and are treated with simple incision and drainage. Graft hypertrophy is managed with massage and intralesional steroids. Contour irregularity may be improved with spot dermabrasion of the graft and the immediate surrounding area. Pigmentation, scaling, and erythema may be concealed with cosmetics. Graft contraction may be improved with massage or if marked may require revision and placement of a second graft.

Flap surgery

Flaps differ from grafts in that they maintain their blood supply as they are moved. The pedicle connects the flap to the surrounding tissue; it is also called the base of the flap. Abundant dermal and subdermal plexus allow for predictable elevation of random cutaneous flaps. A cutaneous flap may also have its arterial supply based on a dominant artery in the subcutaneous layer. Survival of the flap is dependent upon blood flow across the flap. Placement and size of the base must take into account local arterial blood flow into the flap as well as venous and lymphatic drainage.

Because local flaps provide their own blood supply, they are particularly useful in patients with compromised recipient sites such as those that have been irradiated.

The recovery of sensory nerve function in facial flaps is dependent on the intimacy of contact between the flap and the recipient bed and on the viability of the type of restoration.

Classification

There are many methods described for classifying cutaneous flaps: by the arrangement of their blood supply, their configuration, location, tissue content, and method of transferring the flap.

By location, flaps may be classified as local, distant, or free flaps. Local flaps imply use of tissue adjacent to the defect (from the same or an adjacent cosmetic unit). A great advantage of local tissue transfer is that the tissue closely resembles the missing skin in color and texture. These flaps can be rotated, advanced, or transposed into a tissue defect. Regional tissue can also be recruited to repair facial defects. Distant flaps are harvested from different parts of the body. Because the skin of the flap is transposed over intervening skin of one or more cosmetic units, these flaps are executed in two or more stages. After a local blood supply is developed in the flap, the pedicle is severed and returned to its initial site. Free flaps represent a combination of characteristics between flaps and grafts. They are excised at a distant site along with a major artery and completely severed from the skin as in harvesting a graft. The free skin is then sewn into the primary defect anastomosing the artery to a major artery in the surrounding skin. The transplanted skin thus carries its own blood supply analogous to flaps.

Flaps may also be classified according to their blood supply. These include random pattern, axial pattern, and pedicle flaps. Axial pattern flaps are based on a major artery, that is oriented longitudinally along the flap axis. Their advantage is that of a more secure blood supply. This allows the sur geon to harvest larger flaps with smaller width/length ratios. Random pattern flaps are supplied by the dermal and subdermal plexus alone and are not based on any specific artery. They are most successful in richly vascularized regions, particularly the head and neck, or when small flaps are performed in other areas. Because of the lack of a defined blood supply, there are restrictions on the size of the flap and on the width/length ratios considered safe for optimum flap survival. Pedicle flaps are supplied by large named arteries that supply the skin paddle through muscular perforating vessels.

Flaps are often referred to by their geometric configuration. Examples of these flaps include bilobed, rhombic, and Z-plasty (Fig. 16.30).

Fig. 16.30. Z-plasty by Limberg

The layers of tissue contained within the flap can also be used to classify a flap. Cutaneous flap refers to those flaps that contain the skin only. When other layers are incorporated into the flap they are classified accordingly. Examples include myocutaneous and fasciocutanous flaps.

A final classification is based on the type of flap movement. Advancement flaps are mobilized along a linear axis toward the defect and are slid in a linear fashion from adjacent skin into the primary defect. Rotation flaps are slid in an arcuate manner into the surgical defect. Although most flaps are moved by a combination of rotation and advancement into the defect, the major mechanism of tissue transfer is used to classify a given flap. Transposition flaps are cut, elevated, and rotated over an incomplete bridge of skin into the defect. Interposition flaps differ from transposition flaps in that the incomplete bridge of adjacent skin is also elevated and mobilized. An example of an interposition flap is a Z-plasty. Interpolated flaps are those flaps that are mobilized either over or beneath a complete bridge of intact skin via a pedicle. These flaps often require a secondary surgery for pedicle division. The first stage moves tissue into the primary defect, with the relatively bulky pedicle spanning over normal skin. In 3 to 4 weeks, an adequate local blood supply develops in the flap tip, and the pedicle is severed and discarded or replaced to its original position. Microvascular free tissue transfer from a different part of the body relies on reanastomosis of the vascular pedicle.

There are many options for reconstructing facial defects. Often the optimal method is not readily apparent. A stepwise approach can be helpful in selecting and designing a flap. The characteristics of the defect and adjacent tissue must be analyzed. These include color, elasticity, and texture of the missing tissue. The defect size, depth, and location are evaluated as well as the availability and characteristics of adjacent or regional tissue. It is important to determine the mobility of adjacent structures and to identify those anatomic landmarks that must not be distorted. The orientation of the RSTLs and esthetic units should by analyzed closely.

Potential flap designs should be drawn on the skin surface being careful to avoid those designs that obliterate or distort anatomic landmarks. The final location of the resultant scar should be anticipated by previsualizing suture lines and choosing flaps that place the lines in normal creases.

The secondary defect that is created as the tissue is transferred into the primary defect must be able to be closed easily. When designing a flap, it is important to avoid secondary deformities that distort important facial landmarks or affect function. Avoid obliterating critical anatomic lines that are essential for normal function and appearance.

Proper surgical technique involves gentle handling of the tissue by grasping the skin margins with skin hooks or fine-toothed tissue forceps. Avoid traumatizing the vascular supply by twisting or kinking the base of the flap. Deep sutures minimize tension on the flap and eliminate dead space. Excessive tension on the flap may decrease blood flow and cause flap necrosis.

Usage of different flap types for facial reconstruction

Advancement flaps are sliding flaps. They have a linear configuration and are advanced into the defect along a single vector. They limit wound tension to a single vector with minimal perpendicular tension. These flaps can be single or double. For random pattern advancement flaps, an adequate pedicle must be maintained to ensure the blood supply to the distal flap tip. In general, a 3:1 length/width ratio is considered safe. In areas of rich vascular supply, such as the helix of the ear or nasal dorsum, 4:1 length/width ratios are safely achieved.

Advancement flaps are created by parallel incisions approximately with the width of the defect. Once designed and cut, the flap is undermined in a mid-subcutaneous fatty plane. Enough fat must be maintained to protect the blood supply and fill the defect but not so much as to create a bulky appearance. Standing cutaneous deformities (“dog ears”) are usually created and are managed with excision. Advancement flaps are most useful in areas of good tissue extensibility and elasticity and the resulting incision lines can be hidden in natural creases. These include the cheek, preauricular region, lips, and chin. They are also indicated in areas of pronounced linear skin tension lines or cosmetic borders. They are often helpful in reconstructing defects involving the forehead, helical rim, lips, and cheek The forehead, nasal dorsum, and helix of the ear represent such sites.

Intraoral uses of advancement flaps include covering oroantral fistulas and alveolar clefts. A disadvantage of buccal advancement flaps is the decrease in vestibular sulcus depth.

The rotation flap is also a sliding flap that is pulled into the position across the primary defect. They have a curvilinear configuration so the design of a rotation flap is slightly more complex than that of an advancement flap. As with all random pattern flaps, survival of a rotation flap depends in part on the adequacy of its pedicle. Another important consideration, however, is that the degree of force of the secondary motion is inversely proportional to the flap/defect size ratio. For these two reasons, rotation flaps tend to be large, particularly around free margins. In areas of lesser tissue extensibility they must also be cut large, such as on the forehead, scalp, or dorsal hands. These flaps are usually random in their vascularity but may be axial. The flap/defect size ratio should be 3:1 or 4:1 to ensure adequate blood supply across the pedicle and to limit stresses due to secondary motion.

The flap should be cut and undermined. The undermining is carried beyond the base of the flap and around the edges of the flap and the primary defect for 1 to 2 cm. The key suture is placed through the center of the leading edge of the flap and is anchored into the far edge of the primary defect, thus pulling the flap across the defect and closing.

Rotation flaps are most useful in areas with arcuate cosmetic borders or arcing skin tension lines. These include the lateral forehead/temple regions, cheeks, upper lip, and chin (Fig. 16.31). They are most easily employed in more elastic skin as they are pulling-type flaps. However, they are also useful in regions with very inelastic, nonextensible skin such as the scalp, nasal dorsum, and dorsal hands. To reconstruct a scalp defects one or more rotation flaps can be used. Because of the relative inelasticity of the scalp tissue, these flaps must be large relative to the size of the defect.

Fig. 16.31. Rotation flap

Transposition flaps are conceptually the most difficult of this group to design and execute. These flaps are rotated and advanced over adjacent skin to close a defect. However, these efficient flaps offer a number of advantages to the surgeon performing facial repair. Transposition flaps are small compared to advancement and rotation flaps, generally equaling the size of the defect. They are usually designed so that one border of the flap is also a border of the defect. These flaps are advantageous in areas where it is desired to transfer the tension away from closure of the primary defect and into the repair of the secondary defect. They are pushed rather than pulled into the defect, which allows them to drape into place. They are ideal for use around free margins such as nasal alar rims and lower eyelids. The example of transposition flap is a traditional rhombic flap. The rhombic flap is a precise geometric flap that is useful for many defects of the face. The traditional rhombic (“Limberg”) flap is designed with 60 and 120° angles and equal-length sides. The angle of the leading edge of the rhombic flap is approximately 120° but may vary.

Interpolation Flaps. Interpolation flaps contain a pedicle that must pass over or under intact intervening tissue. A disadvantage of these types of flaps is that for those passing over bridging skin, the pedicle must be detached during a second surgical procedure. Occasionally it is possible to perform a single-stage procedure by deepithelializing the pedicle and passing it under the intervening skin. Advantages of interpolation flaps include their excellent vascularity, and also their skin color and texture match.

The forehead flap (median and paramedian) is a commonly used interpolation flap used for large nasal defects. The nasolabial flap is useful for reconstructing defects involving the oral cavity and those involving the lower third of the nose. It can be used as an interpolation flap with either a single or staged technique. The lip-switch flap (Abbe) can be taken from either lip, but it is most commonly switched from the lower to the upper lip. This flap can be used to reconstruct as much as one-third of the upper lip. The labial artery supplies the flap and should be maintained with a small cuff of subcutaneous tissue and muscle surrounding the vascular pedicle. The pedicle is divided after approximately 2 to 3 weeks.

For large facial defects, local flaps may not provide sufficient tissue to adequately restore the missing tissue. In these cases consideration should be given to using a regional flap.

Regional flaps are defined as those that are located near a defect but are not in the immediate proximity. They are frequently harvested from the neck, chest, or axilla and can provide coverage of large surface areas on the face. Selection of a specific regional flap depends on the size and location of the defect and also on the properties of the flap. Advantages of regional flaps include the large amount of soft tissue and skin available. Disadvantages of these types of flaps include poor color and texture match, excessive bulkiness of the flap, and donor site morbidity.

Alternatively distant flaps can be used. The most frequently used technique is a tubed pedicle flap or Filatov’s graft. In this flap the sides of the pedicle are sutured together to create a tube, with the entire surface covered by skin. The tube pedicle was developed by Vladimir Petrovich Filatov in Odessa, between 1916 and 1917. A tube pedicle is a flap of skin sewn down its long edges, with one end left attached to the site of origin, the other is attached to the site to be grafted.

The procedure begins with the lifting of a long, large flap of skin by making a roughly “U” shaped incision. The rounded end of the flap is cut to shape to fit the area to be repaired. The long edges of the skin flap are stitched together to form a tube to prevent drying out and infection of the raw side of the skin flap. The shaped end of the tube is then attached to the site to be repaired whilst the other end of the tube remains attached to its site of origin. After a number of weeks, the tube is cut near the area to be repaired leaving enough skin on the graft site to shape and model. The remainder of the tube can once again be opened and returned to its original position. On occasion, multiple tubes might be taken to rebuild substantial parts of the face or body.

Tissue must be taken from distant parts of the body in stages. For example a tube might be taken from the stomach area and attached to the wrist. After a number of weeks the tube would be disconnected from the stomach, the arm raised and the loose end of the tube attached to the site on the face to be repaired. Once again after a number of weeks the tube is disconnected from the wrist and this loose end of the tube is attached to another part of the face. Only then can the tube be opened and modelled to the face. Any mature tubed flap, in comparison with other sophisticated flaps, is suitable for the meticulous detailed modelling that is particularly important in face reconstruction.

Many things must be considered to ensure a functionally and cosmetically successful flap surgery. Cosmetic units and borders, skin tension lines, blood and lymphatic flow, tissue elasticity, and local anatomy all play roles in the final appearance of a flap along with technical execution.

One should always consider several flaps when planning any closure, working through the advantages and disadvantages of each. Variations in local anatomy, defect size and depth, available tissue, prior surgeries, and patient factors such as smoking or diabetes may impact the appropriateness of a given flap in a given patient. The proper respect for the complexity of flap surgery and associated risks must be maintained. Technical skills must be supported by knowledge of the basic science relative to skin anatomy and physiology, wound healing, and complications. Factors particular to the individual patient must be considered for each procedure. Only then can we satisfy the requirements of qualified flap surgeons as demanded by our patients and peers.

Complications of the flap surgery

Postoperative complications can be minimized with careful preoperative planning of flap design and by early recognition of problems.

A medical history can be used to identify patients with risk factors involving small vessels. These risk factors include smoking, diabetes, hypertension, previous radiation, and pre-existing scars. Flap survival depends on early recognition of flap compromise. Ischemia is defined as an inadequacy of perfusion in providing tissue needs. Signs of arterial ischemia include a pale and cool flap that does not blanch with pressure and typically does not bleed with a pinprick. Flaps are somewhat ischemic initially because the original tissue perfusion has been compromised by flap elevation. Most tissue can survive on 10 % of its average blood flow.

Whether the flap will undergo necrosis depends on patient-related and surgery-related factors that influence the risk of necrosis in facial flaps. Smoking is associated with an increased risk of flap failure. Patients should be advised to quit smoking during the perioperative period.

Hyperbaric oxygen (HBO) has been shown to be beneficial in improving the vascularity of marginal tissues.

Prophylactic HBO therapy in cutaneous flap surgery in the irradiated tissue bed may be particularly helpful to combat the hypoxia and hypocellularity. Tissue oxygenation is an important factor in prevention of wound infection and is closely related to blood supply. Infections involving local flaps may result in flap failure or poor cosmetic outcome secondary to wound dehiscence and scarring.

Reconstruction of lips

The lips are multifunctional folds of skin, mucosa, and muscle which consist of many small cosmetic subunits and naturally occurring landmarks. The upper lip is composed of three cutaneous subunits and the upper vermilion. The two lateral cutaneous subunits of the upper lip are bounded superiorly by the nose, laterally by the nasolabial folds, and medially by the philtral crests.

There are two philtral columns along the midline of the upper lip. Between the philtral columns, a philtral groove or dimple should be present. The philtrum is the central cutaneous subunit of the upper lip. Just inferior to the philtral groove should lie the symmetric Cupid’s bow that follows the vermilion border of the upper lip in the midline. The sole cutaneous component of the lower lip is bounded laterally by the inferior extension of the nasolabial fold and inferiorly by the labiomental crease. The lateral commissure at the angles of the mouth separates the upper and lower lips. Both the right and left commissures should be symmetric in repose.

Because there are no bony or cartilaginous supporting structures, the lips are capable of a wide range of motion and a multitude of functions. A competent oral aperture contributes to proper deglutition, verbal and nonverbal communication, oral continence, and maintenance of a stable intraoral milieu. Thus, it is extremely important to consider functional integrity as well as the aesthetic outcome when planning reconstruction of defects involving the lip and perioral tissue. The lips should be examined from the facial and profile view where symmetry and balance are important. Obvious deformities such as clefts, scars, lesions, and asymmetric regions should be documented.

The favorable lines of closure lie within the relaxed skin tension lines, which are created by the cutaneous tension from the underlying facial musculature. In the perioral region, these lines are usually perpendicular to the vermilion-cutaneous junction. If possible, optimal cosmetic results are obtained by placing the incisions along the boundaries of the cosmetic units.

The reconstructive modality of choice for repair of defects involving the lips and perioral tissue will largely depend on the location, size, and depth of the wound. Partial-thickness wounds may heal by second intention, close primarily, or need local flaps. Occasionally, skin grafting can be used for reconstruction of superficial perioral wounds. Reconstruction of full-thickness (into the oral cavity) defects usually requires more extensive tissue rearrangement such as wedge repair, switch flaps, or full-thickness local flaps.

Before undertaking any reconstructive procedure, one should clearly delineate and mark the cosmetic units and favorable lines of closure prior to local anesthesia. Reconstruction of perioral defects requires a multilayered approach, carefully approximating the mucosal, submucosal, muscular, and subcutaneous tissues, followed by realignment and eversion of the vermilion border and cutaneous tissue.

Most of the partial-thickness wounds are repaired with local flaps, while second intention wound healing and skin grafting are less commonly used. Because the lips have no bony attachment, the free margin of the lip may be unfavorably displaced during normal scar contracture, resulting in an incompetent oral aperture.

Skin grafts in the perioral region have a greater tendency to heal with a convex contour than elsewhere, and thus they are rarely used for lip repair. However, in certain defects, if the size and location of the wound are unfavorable for flap reconstruction it requires skin grafting to minimize functional and cosmetic distortion of the lip. Local skin flaps provide the most useful and diverse approach to achieving optimal cosmetic results in lips reconstruction.

Large defects on the cutaneous portion of the lips are reconstructed with a more complex variation of the advancement flap. Complex advancement flaps require extensive undermining to release the redundant tissue of the lateral lip and cheek. A releasing incision is commonly made at the lateral aspect of the defect, along the vermilion-cutaneous junction. Because of the lateral tissue availability, there is usually only minimal displacement of the philtrum.

Rotation flaps are rarely used to repair the defects of the perioral tissue because it is difficult to place the incisions within the normal relaxed skin tension lines.

Transposition flaps are extremely useful in mobilizing local tissue on many areas of the face, especially the nose. Depending upon the size and location of the wound, the transposition flap can be inferiorly or superiorly based to harvest excess tissue from the nasolabial fold.

Complex wounds which involve several cosmetic subunits may require a combination of surgical techniques for adequate reconstruction.

Full-thickness wounds of the lips and perioral tissue extend through the mucosa into the oral cavity. Usually, full-thickness lip defects of the upper lip which are less than one-third of the vermilion length (1.5 to 2 cm) can be closed primarily in a wedgelike fashion. Various modifications of the wedge closure may be helpful to achieve optimal functional and cosmetic results. Full-thickness defects greater than one-third of the vermilion length usually require more extensive tissue rearrangement. The Abbe flap is a fullthickness, lip-switch flap which is pedicled on the labial artery. These flaps are created by incising a wedge of tissue from the lip opposite the defect and rotating the full-thickness flap on its vascular pedicle into the defect. Once collateral circulation has been established (approximately 2 to 3 weeks), the pedicle is transected and the vermilion is carefully realigned.

For defects greater than one-half of the vermilion length, recruitment of large amounts of local tissue may require unilateral or bilateral cheiloplasty followed by medial advancement of the cheek tissue.

Immediately following wound repair, an antibiotic ointment is applied to the incision and the wound is covered with a simple pressure dressing. It is extremely important to stress that the patient should minimize use of his or her lips, including chewing, talking, laughing, smiling, or frowning. Liquids and small bites of soft foods are highly recommended postoperatively. The cutaneous sutures are usually removed at 5 to 7 days postoperalively. Prophylactic antibiotics are routinely used after reconstruction.

Reconstruction of the nasal defects

The nose is a respiratory and olfactory organ made up of skin and muscle overlying a skeleton of bone and cartilage which is lined with mucosa. Its midline position is best examined in the frontal view, and its anterior projection from the profile view. The nose is examined in relation to the forehead, orbital rims, eyes, maxilla, lips, and chin. Examination of the nose should include inspection from the lateral, frontal, and submental vertex views, as well as a complete intranasal examination. The proximal third of the nose is supported by the paired nasal bones. The skin of the upper nose is usually elastic and easily undermined. The underlying bony rigidity resists distortion and contributes to the successful outcome of many skin flaps on the upper nose. The middle third is supported by the upper lateral nasal cartilages. The distal third is supported by the lower lateral cartilages medially and the sesamoid cartilages and dermis laterally.

The nasal septum provides support for both aesthetics and function by separating the bony and cartilaginous vault of the nose. The nasal septum also aids airflow and supports the tip and columella. The mobile portion of the nose includes the membranous septum, columella, and lobule, which contains the tip and alae. Each alar cartilage is shaped like a wishbone, with the apex supporting one side of the nasal tip. The nasal cartilages are highly mobile and do not resist distortion well.

Although nasal reconstruction is an ancient art, the complexities of nasal anatomy and physiology continue to make the repair of nasal defects one of the most challenging aspects of reconstructive surgery.

There are no simple guidelines to nasal reconstruction, although a number of approaches to management, reconstructive algorithms, and classifications of nasal defects have been proposed. However, one reasonable approach to the repair of soft-tissue defects is to consider more conservative options first. Superficial wounds and wounds in certain anatomic areas may heal naturally with excellent cosmetic results, and direct primary closure often works well on the upper nose. Full-thickness skin graft repair often works well for nasal defects with an adequate subcutaneous bed, although the skin color and texture match may be poor. In general, local skin flaps offer a superior color and texture match for nasal skin and are the repairs of choice for deep nasal defects. Penetrating defects may require reconstruction of the nasal lining and provision of structural support.

Full-thickness skin grafts usually offer a better color and texture match than the best split-thickness graft and have less tendency to contract. They may be used to repair superficial nasal defects, either immediately or following a period of secondary intention during which the wound will contract and granulation tissue will begin to fill deep defects, possibly enhancing graft viability.

Composite grafts, which consist of skin and other structures and include combinations of skin and fat, skin and perichondrium, and skin and cartilage, may be used to repair deep defects of the lower nose, columella, and alar free margin. The auricular helix, conchal bowl, and lobe are the most common donor sites, and the donor defect can be closed in a variety of ways.

Free cartilage grafts can be used to provide structural support for skin flaps and are most commonly harvested from the nasal septum, conchal bowl, auricular rim, and occasionally from costal cartilage. Cartilage grafts can be placed within nasolabial or forehead flaps, or a composite graft of skin, perichondrium, and cartilage may be used. Free cartilage grafts require highly vascular tissue beds to ensure their survival.

A large number of skin flaps have been described for the repair of nasal defects. The majority are harvested in the upper nose, adjacent cheek, nasolabial fold, and the forehead. Surgical undermining is relatively simple on the upper nose and becomes increasingly more difficult toward the nasal tip. Undermining is usually performed below the muscles of the upper nose and above the perichondrium or periosteum in order to prevent vascular injury (Fig. 16.32; 16.33).

Fig. 16.32. Nasal reconstruction by rotation flap (a, b, c, d)

Partial or total nasal prostheses may be of value in both cosmetic and functional rehabilitation. Severe trauma and extensive nasal tumors may be treated by total rhinectomy and the permanent use of a prosthetic nose. Alternatively, a prosthesis can be used if delayed reconstruction is planned. An accurate color match is essential and requires the services of an expert prosthetist. Patients must be able to clean and apply the prosthesis, which may be retained in place by a combination of adhesives and appliances such as those used for spectacles or dentures.

Major nasal defects can involve the loss of any combination of skin, mucosa, and structural support; each of the lost nasal structures needs to be replaced, Any such repair is likely to be followed by flap contraction due to granulation of the undersurface of the flap. Defects of nasal mucosa or structural support must be repaired prior to replacing the missing skin. Reconstruction of the nasal lining may involve split- or full-thickness skin grafts. Free mucosal grafts harvested from the buccal mucosa can be also used. A nasolabial or reverse nasolabial flap can be used to replace lost nasal lining with cheek skin. Pivoted mucosal flaps can be raised from intranasal donor sites (vestibule, vault, and septum). These flaps are thin and yet provide highly vascular beds for free bone or cartilage grafts.

Reconstruction of missing nasal bone or cartilage is required to support skin flaps, maintain a normal nasal shape, and prevent nasal collapse. Support can be provided in a number of ways. A skin-cartilage composite graft together with a cutaneous flap can be used. Cartilage grafts may be placed within folded nasolabial flaps in the reconstruction of the nasal ala. Alternatively, cartilage or bone grafts can be buried beneath the tips of planned nasolabial or forehead flaps, and sometime later they are transferred to the nasal defect as an integral part of the flap. Sculpted bone or cartilage grafts can be assembled on a highly vascular, pivoted septal mucosal flap and covered with a thin forehead flap Cartilage grafts can be inserted into skin flaps as a secondary procedure after the flaps have been allowed to establish a local blood supply, although the results may be inferior to the primary placement of the cartilage. Structural support of the upper nose and dorsum can be provided by skeletal rib or iliac crest cantilever bone grafts anchored to the nasal process of the frontal bone and covered with a forehead flap.

Esthetic surgery of the face

Modern society raises conditions to our appearance. Word “beauty” is becoming synonymous of success, sexuality and healthy. A beauty person have more chances in professional, social and biological realization. That is why every year necessity in plastic surgery procedures increases between individuals.

Esthetic face surgery is aimed to achieve harmony of the face appearance, elimination of pathological aging changes of the soft and hard tissues.

Ecological environment, harmful habits, insolation, bad dietary, genetic predisposal and stresses are factors that cause premature aging.

The first feature of aging process in the skin and subdermal layer is the decreasing of the concentration of hyaluronic acid, ptosis of tissues and decreased tone of the skin.

From 25 years of age the reduction of the quantity of hyaluronic acid in the skin and subdermal layer begins.

Aging changes in face appearance: wrinkles, fat herniation eyelids, rounding the eyes, skeletonizing orbits, deep nasolabial folds, Crown’s feet, thinning lips, hanging nose tip, ptosis of skin and fat, squaring of the face, platysma banding, dropping mouth corners.

Facial rejuvenation procedures:

• injection techniques (botulinum toxin injections, fillers, biorevitalization);
• blepharoplasty;
• browlift;
• extended SMAS facelift and neck lift.

Injections of botulinotoxin are used for eliminating mimic wrinkles of forehead, glabella region, lateral orbital region (Crown’s feet), nose, upper lip, corners of the mouth. Clostridium botulinum was first identified in 1897, in Belgium, by Professor Emile van Ermengem who was investigating fatal cases of food poisoning following the consumption of macerated ham.

During the Word War II research continued into this potent neurotoxin as a possible agent (“agent X”) for biological warfare. Dr Alan Scott performed first clinical tests of usage of botulinum toxin A on humans for treatment of strabismus in 1978. Then, botulinum toxin A was used for treatment of blepharospasm, hemifacial spasm, cervical distonia and its rejuvenating effect was also noticed.

Botulinum toxin induces paralysis by blocking the release of acetylcholine at the skeletal neuromuscular junction, thereby inhibiting the transmission of nerve impulses across the synaptic junction to the motor end plate.

Standart zones of botulinum toxin injections for wrinkles treatment: glabellas’ region, horizontal wrinkles of the forehead, Crow’s feet, mouth corners, platysma banding, “turkey” neck bundles.

Fig. 16.34. Points of botulinum toxin injections:
1 – forehead horizontal wrinkles; 2, 3 – glabella region; 4 – periorbital region (Crow’s feet); 5 – oblique wrinkles of the nose; 6 – for dropping mouth corners

Injection techniques are also used for filling wrinkles and flattening the surface of the skin. This method is called contour plastics, it also used for augmentation of lips, malar eminences, and correction of tissue loss. For these purposes are used resorbable materials, such as collagen, hyaluronic acid, agarose, fat, and permanent materials – silicone, acrylamide gel, tephlon and others. Preference is given to resorbable materials. Typical zones of usage are glabellas vertical wrinkles, nasolabial folds, horizontal wrinkles of the forehead, dropping mouth corners, periorbital region (Crow’s feet) and others.

Standard surgical procedures for face rejuvenation are blepharoplasty, browlift, facelifting (Fig. 16.35).

Fig. 16.35. Surgical procedures for face rejuvenation:
1 – upper blepharoplasty – scar hides into upper palpebral crease; making it almost invisible; 2 – zones of herniated fat removal; 3 – lower blepharoplasty – scar lies under lashes, it becomes invisible after few months; 4 – lines of tissue tension during facelifting procedure; 5 – cosmetic incision line used for facelifting procedure

Method of blepharoplasty is based on excision of excess of skin and removal of herniated fat of the lower and upper eyelids (Fig. 16. 36). It is the most frequently performed cosmetic surgical procedure.

Fig. 16.36. Method of the upper (a, b) and lower (c, d, e) blepharoplasty y Kruchinskiy

Endoscopic browlift allows raising brows and forehead using only small incisions hidden on the hearbearing zone of the head.

After endoscopic forehead periosteum transsection and detaching of the depressor muscles 10–12 suspension sutures are placed for fixation of the forehead on its new position.

Facelifting procedures (Fig. 16.37) – extended SMAS facelift and neck lift. Incision of the skin performed in temporal hierbearing region, descends in the preauricular area & then hides in the postauricular area. Subcutaneus undermining performed to the vertical line drawn through the lateral corner of the eye. Malar fat pad and cheek fat are pushed upward and backward by several sutures, fixed to temporal fascia and fascia parotideamassetterica. The superficial muscle aponeurose system of the face (SMAS) has to be pushed upwards and backwards, excess of fascia parotideamassetterica is excised and refixed by sutures. Then excess of the skin is removed and cosmetic sutures are applied on skin edges.

Fig. 16.37. Scheme of the facelift by the method of Rauer – Michelson

Microsurgery of the maxilla-facial area

Microsurgery – the highest level of surgical technique. This technique involves the use of special equipment and facilities and opens up entirely new opportunities in every field of surgery. This line of surgery involves the use of intraoperative magnification (surgical microscope), as well as microinstruments for surgical interventions on the very small structures of organism.

The main areas of microsurgery, the following:

1. Emergency operations – replantation of lost limbs.
2. Damage to peripheral nerves of different origin.
3. Tendon suture.
4. Surgery on the face, including allotransplantation large tissue fragments with the restoration of the innervation and blood supply (“face transplant”). This kind of operation was firs presented by Professor Bernard Devauchelle in 2005 (Fig. 16.38–16.41).
5. Transplant tissue complexes with the restoration of blood supply.

Fig. 16.38. Patient with traumatic disfigurement of the face (dog bite) defect of nose, right chic, lips, chin

Fig. 16.39. Scheme of tissue block including oral and nasal mucosa, nose cartilages, mimic muscles, skin of the lips, nose, cheek and chin, nutritive arteries, veins, motor and sensitive nerves

Fig.16.40. Allotransplant was taken accordingly to preoperative planning

Fig. 16.41. Patient’s face appearance with microsurgical allotransplantation of the face after 4 years

Microsurgery techniques allow the transfer of tissues for reconstruction from one area of the body to the other. A wider range of donor sites is available, very large flaps can be transferred, and a multiplicity of tissues can be included in the flap for an optimal functional reconstruction. Microsurgical tissue block transplantation is more effective procedure than free tissue grafting in cases when recipient zone is compromised – irradiated in oncologic patients, cicatricated after inflammatory processes or burn injury.

The development of microsurgical free tissue transfer resulted in a dramatic evolution in head and neck reconstruction, allowing for a significant increase in the available choices of anatomic and functional rehabilitation. The first surgical microscope was built by Dr. Carl Nylen, a Swedish otolaryngologist who used it for the first time in 1921. In the late 1950s and early 1960s Jacobson and Suarez performed successful anastomosis of carotid arteries in dogs and rabbits with a 100 % patency rate. When Jacobson presented the outcome of his research at a national meeting, a leading surgeon at a prestigious institution stated in front of the audience, “This is very nice work, but it is simply ridiculous to bring a microscope into the operating room.” During the 1960s microsurgery was promoted by neurosurgeons and plastic surgeons with encouraging results. In 1973, there was established the first department of microsurgery in Moscow, Research Institution for Clinic and Experimental Surgery under Ministry of Health. Similar clinics have been organized in Leningrad, Kiev and Tbilisi. In 1975 Taylor and colleagues described the free fibula flap, while Hidalgo applied the technique for mandibular reconstruction in 1989. In 1981 Yang developed the radial forearm flap, while Soutar and colleagues popularized the technique for intraoral reconstruction with and without the addition of a portion of the radius in the mid-1980s. In 1978 Taylor described the transfer of the iliac crest as an osteomyocutaneous flap based on the blood supply from the circumflex artery and vein. Free flaps became popular in the head and neck region due to the ability to transfer vascularized bone and soft tissue in one stage at the time of the resection, with predictable high success rates.

The microsurgery instruments require the following specifications. Their weight must not exceed 15 to 20 g. They must be at least 10 cm long so that they lie loosely in the hand. The closing pressure of some instruments such as forceps or scissors should lie between 50 and 60 g. Tremor increases with higher closing pressure. The vascular clamps must exert an evenly distributed pressure over the whole length of the jaw of the clamp. The jaws must lie parallel with each other. Microscissors should have an opening of less than 4 mm. They can be either straight or curved, but it is imperative that they cut tissue in a clean fashion in order to reduce the risk of a thrombosis in a vascular anastomosis or the formation of a neuroma in a crushed nerve. A magnification of 10 is usually enough for anastomosis. During surgical interventions surgeons needed support for hands and special work places (chair), as part of the operation lasting many hours. Therefore, there exists the need for more comfort for the body during surgery.

Prior to undertaking a microsurgical procedure skills should be learned in the laboratory on experimental animals. The laboratory should include an operating microscope, microinstruments, and animals for practice. Several manuals exist for the graded exercises necessary for acquiring microsurgical skills. Before presuming to do this surgery in the operating room, surgeon patency rate in the laboratory should exceed 99 per cent in 1-mm vessels, such as rat femoral vessels.

During transplantation composite flap with the resumption of blood supply may be different options for applying microvascular anastomoses. In head and neck surgery both end-to-end and end-to-side anastomoses are used for the artery and vein. Suitable recipient vessels, such as superior thyroid or facial vessels, are dissected. The venous anastomosis is done before the arterial anastomosis, and the clamps are released simultaneously after completion of both. The donor and recipient arteries are prepared by carefully dissecting the adventitial layers. For end-to-end anastomosis, the vessels are placed in a clamp approximator, gently dilated, and irrigated with heparin solution (Fig. 16.42).

Fig. 16.42. A technique of microsurgery suturing (a, b, c, d, e)

The suture (usually 9–0) is passed at a distance from the margin of the vessel similar to that of the thickness of the wall. It is recommended to apply a counterforce while passing the needle through the vessel by holding the forceps open inside the lumen instead of grasping the vessel wall which may damage the edge of the vascular structure. After the suture has passed through both ends of the vessel, a small “tail” of 2 to 3 mm is left in order that the knot can be performed while seeing the suture end within the field of the surgical microscope.

After the first suture is placed the second suture is usually placed 180° from the first. The third suture is placed in between the first and the second, and two more interrupted sutures are placed on the same side. After finishing one side the vascular clamps are turned to expose the other side of the anastomosis. The sutures should always be at the same distance as the edges of the vessel as well as the same distance between each one of the sutures.

When the vascular anastomosis cannot be performed “end-to-end” due to very significant differences in the diameter of the lumen, an “end-to-side” anastomosis is a viable alternative. An oval excision of the wall of the large-diameter artery is performed, and the sutures are executed in a similar fashion as explained in the end-to-end anastomosis. After the anterior sutures are placed, the clamp is turned over, and the posterior sutures are placed. The clamps are released and a patency test is performed. For end-to-end anastomosis, an opening equal to the diameter of the smaller vessel is made in the larger vessel. The arteriotomy should be made by resecting a small lenticular piece of the arterial wall; the venotomy may be made as a simple slit. The initial sutures are placed 180° apart at the “heel and toe.” The two walls are then completed. A mattress suture facilitates eversion of the vein. The patient is anticoagulated with a single bolus of heparin prior to clamping and maintained on low molecular weight dextran thereafter for the first postoperative week.

The benefits of a free flap should be weighed against the risks of a prolonged operative procedure and the greater risk of flap failure from anastomotic thrombosis.

The probability of thrombosis depends on the quality of the vascular suture, hemodynamic disorders in the area of the anastomosis due to the turbulent blood flow, vascular spasm, the maximum linear rate of blood flow, the ratio of blood coagulation and anticoagulation system. In this possibility of anastomoses evaluated clinically, visualy, instrumentally and using angiography. Anesthetic maintenance of microsurgical operations has a number of features, because sometimes they can last up to 46.5 hours. In this case, the patient should be immobilized, and the anesthesia occur with a stable blood pressure. Output from anesthesia should proceed without vascular spasm, which is important to ensure consistency created anastomosises, as well as for high-quality restoration of circulation in the transferred tissues.

If you need to ensure reinervation of tissues one could used stapling nerve or transplantation of fragments of nerve fibers. At the same time one should try to identify the bundles of functions: sensory and motor. Suture of the nerve may impose without dividing into groups of beams, split into groups of beams and divided into separate beams. Neurorrhaphy is the act of nerve suturing for both direct and gap repairs (Fig. 16.43). The trigeminal nerve is repaired using epineurial sutures. Generally, an 8–0 monofilament nonresorbable nylon suture is chosen since a resorbable material would invoke inflammation and disturb the area of anticipated neural healing. At least two sutures are used per anastomosis site to prevent rotation, but not more than three or four sutures should be used per anastomosis.

Fig. 16.43. Direct epineurial neurorrhaphy

The first suture is placed on the medial side of the anastomosis since it is more difficult to access. The epineurium is pierced with the needle of 0.5 to 1.0 mm from the edge of the nerve. The second suture is placed 180° from the first suture, and then an assessment is made regarding the need for more sutures. When neurorrhaphy is not possible without tension and a nerve gap exists, an interpositional graft must be considered for indirect neurorrhaphy. The options for autogenous nerve grafting include but are not limited to the sural nerve, the greater auricular nerve, and possibly the medial antebrachial cutaneous nerve.

The sural nerve is the preferred nerve for grafting since it most appropriately matches the nerve diameter and the fascicular number and pattern of the trigeminal nerve. Sural grafts up to 20 cm in length are possible, and patients tolerate the donor site deficit well. The greater auricular nerve is a poor choice for trigeminal repair. Patients are generally not amenable to sacrificing one facial region for another. Additionally, the small diameter of the nerve makes it useful only when used as a cable graft. The sole advantage of a greater auricular graft over a sural graft is in situations when it can be harvested via the same incision for another procedure, such as the repair of an extraoral mandibular fracture or management of pathology. The basic premise with graft repair is that the graft supplies the Schwann cells and growth factors necessary to support and encourage axonal sprouting through the graft toward the target site.

As for the structure of flaps, using for transferring (transplants), they are divided into skin-fat, skin-fascial, skin-muscle, muscle, skin and bone, etc. In this composite flap is used to restore lost functions or replace tissue defects. But the main purpose of this type of surgery is often the restore of body tissue defect with the resumption of its inherent function.

Undoubtedly the main advantage of transplantation using microsurgical technique is to restore blood flow in free transferred tissues. This process has several stages: A period of acute disorders (ischemia during transplantation, a decrease in sources of blood, the axial reorientation of the vessels, hypotension) the formation of vascular connections and the final adjustment. To succeed in this type of transplantation is necessary to ensure adequate arterial blood flow along with adequate venous outflow, a reliable contact between the graft and recipient bed, immobilization of the segment, to prevent compression of the vascular pedicle graft (vein, artery).

It is suggested a large number of different flaps for transplantation, which are used for different purposes and have different anatomical features. Thoracodorsal flap proposed by G. Maxwell (1976), incorporates the subscapular artery, the envelope of the scapular (D = 1.5–3 mm, length 8–14 cm), 2 accompanying veins, the thoraco-dorsal nerve. In this case, there are different versions allowing the flap to include in the graft: skin, muscle and bone fragments. Its advantages are the following: accessibility, ease of harvesting, large sizes – up to 43 × 16 cm, long pedicle, large caliber vessels and a slight lack of features, the ability to use a fragment of rib. The disadvantage is cosmetic defect.

Parascapulery (lower shoulder) skin-fascial flap (size – up to 15 × 30 cm) incorporates skin Parascapulery artery, the envelope of the scapular (length 4–14 cm) and a concomitant vein. Its advantages are the following: a long pedicle, large diameter feeder vessels, small thickness, which is convenient for oral and maxillofacial surgery. The external skin-fascial thoracal flap includes thoracodorsal artery (D = 2.3 mm, length 10 cm), the accompanying vein and cutaneous branch of the second intercostal nerve. This graft is characterized by up to 19 × 14 cm, small thickness, the possibility of reinnervation, the long vascular pedicle, a large defect in the vessels. Costal flap proposed R. Danice (1975) incorporates a rear intercostal neurovascular bundle and fragment edges. Deltoid flap was first proposed in 1984 I. Franklin. The flap includes a pair posterior branch of the artery, a vein of the same name and the lateral cutaneous nerve of the arm. It is characterized by a fairly large volume, large diameter vessels and the opportunity of reinervation.

The radial forearm flap is perhaps the most commonly used soft tissue microvascular flap for intraoral and oropharyngeal defects. It has gained wide acceptance because of its reliability, adaptability, ease of harvest, and the thin pliable nature of the flap. The arterial blood supply of the radial forearm fasciocutaneous flap is based on perforators of the radial artery. The venous drainage of the radial forearm flap occurs through the interconnecting superficial (cephalic vein) and deep (venae comitantes) systems. The free radial forearm fasciocutaneous flap is extremely useful in head and neck reconstruction. The flap’s reliability, adaptability, ease of harvest, and the similar character of the thin pliable skin to the lining tissues of the oral cavity make its use commonplace in modern maxillofacial reconstruction.

The fibula is ideal for large bony defects since it offers up to 25 cm of vascularized cortical bone (Fig. 16.44). The blood supply to the fibula is delivered through perforators originating in the peroneal artery which is usually between 2 and 4 mm in diameter. The venae comitantes provide the venous drainage; these are paired vessels that run along the artery. The free fibula flap can be raised with or without a skin paddle but the skin paddle had a poor prognosis. A significant limitation of the free fibula flap is the common presence of peripheral vascular disease in the lower extremities.

Fig. 16.44. Elevation of free fibula flap after the osteotomy (adapted from Serafin D)

The blood supply to the osteomyocutaneous iliac crest flap is based on the deep circumflex iliac artery and vein. This artery takes origin from the external iliac artery or femoral artery in the region of the inguinal canal. It courses a distance of about 5 to 7 cm between its origin and the anterior superior iliac spine, following thereon the inner aspect of the iliac crest. The iliac crest provides a significant segment of the bone that may reach 4 cm in height and 11 cm in length. The dimensions of the flap may allow for a reconstruction of a hemimandibulectomy or anterior mandibular defect. There are some significant advantages to the iliac crest free flap: the amount of bone available for potential reconstruction with osseointegrated implants; and the availability of a thin and broad muscle that can be left to heal by secondary epithelization intraorally. In most cases the inner aspect of the iliac crest is sufficient to reconstruct a mandibular defect, having the advantages of a less deforming defect and avoiding the lateral dissection of the gluteus medius muscles. The disadvantage of the flap is the relatively short vascular pedicle and the potential for herniation of the abdominal contents.

The rectus abdominis free flap has been used mostly for base of skull reconstruction and tongue reconstruction. It is based on two vascular pedicles: the deep superior epigastric vessels; and the deep inferior epigastric vessels, which are branches of the external iliac artery. The deep inferior epigastric vessels have a larger diameter and a longer vascular pedicle which makes them the preferred choice for anastomosis to the recipient vessels with very high reliability and success.

Other flaps have been used for oropharyngeal reconstruction, including free omentum for oral lining, gracilis muscle free flaps with the anterior obturator nerve for facial reanimation, and lateral thigh or lateral arm free flaps for pharyngeal reconstruction. Even free temporoparietal fascial flaps have been used based on the superficial temporal vessels for intraoral lining or combined with the overlying skin or underlying bone. In the treatment of ankylosis of temporomandibular joint an autograft of foot bones is used for arthroplasty.

The flaps described in the current chapter are the most commonly used in head and neck reconstruction. The ability to transfer vascularized tissues allows for a significant varietyof options.