Maxillofacial and neck benign tumours

Maxillofacial and neck benign tumours.

Premalignant diseases of mucous membrane of oral cavity and lips.

Trauma of jaw facial arena  

Surgical Therapy

Closed Reduction of Dentate Patients

Erich arch bars

• Initially, use a bar of sufficient length to accommodate the maxillary and mandibular arches from first molar to contralateral first molar.

• Next, use 24-gauge stainless steel circumdental wires at the first bicuspid positions, one on each side of the arch to secure the arch bar.

• At this point, tightly place circumdental wires along the greater segment of the fracture. The greater segment is the fracture segment; that is the most tooth-bearing segment.

• Loosely place circumdental wires along the lesser segment of the fracture. The lesser segment is the fracture segment that bears the least amount of teeth.

• Then tightly place circumdental wires along the opposing arch.

• Place the patient into his or her preinjury occlusion. With the patient held into occlusion, tighten the looser segment circumdental wires. This prevents arch bar placement from interfering with proper occlusion.

• Place interarch 25-gauge stainless steel box wires along the molar/premolar region and the premolar/canine region bilaterally.
  
  

Mandibular fracture. Interarch elastics may be used for maxillomandibular fixation. They also may be used loosely for guidance during postoperative care.

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Mandibular fracture. Interarch elastics may be used for maxillomandibular fixation. They also may be used loosely for guidance during postoperative care.

• Placement of arch bars can be difficult when dentition is poor, the fracture is unstable and comminuted, and dentoalveolar fractures are present.

Bridle wire

·         Bridle wire is used for temporary stabilization of a fractured segment. This provides some patient comfort by minimizing mobility of the fracture segments.

Mandibular fracture. Patient presents with occlusal step off between right mandibular central and lateral incisors.

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Mandibular fracture. Patient presents with occlusal step off between right mandibular central and lateral incisors.

·         Manually reduce the segments with the use of local anesthesia.

·         Loop two teeth (if available) with 24-gauge wire anterior and posterior to the fracture segment. The closest stable teeth can be used if the adjacent dentition is poor or missing.

·         Tighten the wire in a clockwise fashion while manually reducing the segments.

Mandibular fracture. View of occlusal step off.

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Mandibular fracture. View of occlusal step off.

Mandibular fracture. Bridle wire used to decrease mobility and provide patient comfort.

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Mandibular fracture. Bridle wire used to decrease mobility and provide patient comfort.

Ivy loops

• Ivy loops are used for intermaxillary fixation when full dentition is present in good condition and the fracture is displaced minimally.

• Construct a loop in the middle of a 24-gauge wire.

• Pass the loose ends of the wire interproximal to two stable teeth.

• Loop the wire ends around the mesial and distal sides of the teeth.

• Pass the distal wire under or through the loop and then tighten it to the mesial wire in an apical direction.

• Accomplish the same procedure on the opposite arch directly opposing the first wire.

• The loops need to be short enough to allow for an interarch wire to be tightened.

• Pass a 25-gauge interarch wire through the two opposing loops and tighten it in a clockwise fashion.

• At least one ivy loop on each side is necessary.

A variety of wiring techniques (eg, Essig wire, continuous-loop [Stout] wiring) besides those mentioned above has been used for closed reduction and intermaxillary fixation.

Closed Reduction of Partially Edentulous Patients

If a patient is partially dentate, the existing partial denture can be used for intermaxillary fixation. The partial dentures can be secured to either jaw using circummandibular or circumzygomatic wiring techniques. If the patient has no existing partial denture, acrylic blocks also can be fabricated with an incorporated arch bar and secured with circummandibular or circumzygomatic wires.

Closed Reduction of Edentulous Patients

• If dentures are available, they can be secured with circummandibular wires, circumzygomatic wires, or palatal screws.⁴²

• Dentures also can be fabricated with incorporated arch bars as well as a space in the anterior for feeding (Gunning splint). They are secured in the same fashion with circummandibular wires, circumzygomatic wires, or palatal screws.

• Biphasic pin fixation (external pin fixation or Joe Hall Morris appliance) also is used for edentulous patients. Its indications for use are as follows:

1.     In edentulous patients with a discontinuity defect because of either severe trauma or resection

2.     In severely comminuted fractures

3.     When intermaxillary or rigid fixation cannot be used

• Biphasic pin fixation using two pins on both the proximal and distal fragments: Use a transbuccal trocar approach to place two bicortical screws on either side of the fracture. Secure a series of locking plates and bars to the 4 or more pins and then construct a self-curing acrylic secondary splint.

Open Reduction

Wire osteosynthesis

This is rarely used for definitive fixation since the advent of rigid fixation.⁵⁴ However, it may be useful for help in alignment of fractured segments prior to rigid fixation.

• This can be placed either by an intraoral or extraoral route. The wire should be a prestretched soft stainless steel.

• A straight wire can be used across the fracture site. This is placed so the direction of pull of the wire is perpendicular to the fracture site. This can be placed as a monocortical or bicortical wire.

• A figure-of-8 wire can provide increased strength at the superior and inferior borders compared to the straight wire.

Intraoral approach

• Advantages over the extraoral approach are that it is quicker to perform, results io extraoral scar and no damage to the facial nerve, and can be performed under local anesthesia.⁵⁵

• Complication rates and infection rates appear to be similar between the intraoral and extraoral approaches when large numbers of patients are studied.

• Symphysis and parasymphysis fractures can be accessed through a genioplasty-type incision. Identification of the mental neurovascular bundle is important to preserve its integrity.⁵⁶

• Body, angle, and ramus fractures can be accessed through a vestibular incision that may extend onto the external oblique ridge as high as the mandibular occlusal plane. Extending the incision higher predisposes the buccal fat pad to prolapsing onto the surgical field. The entire surface of the ramus and the subcondylar region can be exposed by stripping the buccinator and temporal tendon with a notched ramus retractor and periosteal elevator. Bauer retractors placed in the sigmoid and antegonial notch can help in gaining access to the subcondylar and ramus regions.

Submandibular approach

• The submandibular approach often is referred to as the Risdon approach since he first described it in 1934.⁵⁷

• Make the skin incision approximately 2 cm below the angle of the mandible in a natural skin crease.⁵⁸

• Dissect the subcutaneous fat and superficial cervical fasciae to reach the platysma muscle.

• Sharply dissect the platysma to reach the superficial layer of the deep cervical fascia. The marginal mandibular nerve runs just deep to this layer.⁵⁹

• Carry dissection to bone through the deep cervical fascia with the aid of a nerve stimulator. Carry the dissection down to the level of the pterygomasseteric sling.

• Sharply divide the sling to expose the bone.
  
  

Mandibular fracture. Intraoperative view demonstrating fixation of mandibular segments.

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Mandibular fracture. Intraoperative view demonstrating fixation of mandibular segments.

Mandibular fracture. Left lateral view.

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Mandibular fracture. Left lateral view.

Mandibular fracture. Right lateral view.

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Mandibular fracture. Right lateral view.

Mandibular fracture. Open reduction rigid internal fixation of left mandibular body fracture.

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Mandibular fracture. Open reduction rigid internal fixation of left mandibular body fracture.

Mandibular fracture. Postoperative radiograph demonstrating reduction and fixation.

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Mandibular fracture. Postoperative radiograph demonstrating reduction and fixation.

Retromandibular approach

• Hinds first described this approach in 1958.^60,61

• Make the incision approximately 0.5 cm below the lobe of the ear and continue it inferiorly 3-3.5 cm. Place it just behind the posterior border of the mandible; it may extend below the level of the mandibular angle.

• Carry the dissection through the scant platysma, superficial musculoaponeurotic layer (SMAS), and parotid capsule.
  
  

Retromandibular approach to right mandibular condylar fracture.

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Retromandibular approach to right mandibular condylar fracture.

• The marginal mandibular branch and the cervical branch of the facial nerve may be encountered.⁶²

• The retromandibular vein runs vertically in this region and commonly is exposed. This vein rarely requires ligation unless it has been transected inadvertently.

• Carry out sharp incision through the pterygomasseteric sling.

• Strip the muscle off the lateral surface of the mandible superiorly, which gives access to the ramus and subcondylar region of the mandible.
  
  

Intraoperative view. Fixation of right mandibular condyle fracture.

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Intraoperative view. Fixation of right mandibular condyle fracture.

Preauricular approach

• This approach is excellent for exposure to the temporomandibular joint.⁶³

• Make the incision sharply in the preauricular folds, approximately 2.5-3.5 cm in length as described by Thoma⁶⁴ and Rowe.⁶⁵

• Take care not to extend the incision inferiorly, since it may encounter the facial nerve as it enters the posterior border of the parotid gland.

• Carry the incision and dissection along the perichondrium of the tragal cartilage. Some surgeons advocate making the incision through the tragus.

• The temporal fascia is encountered along the superior portion of the incision. Take care to be sure one is deep to the superficial temporal fascia or the temporoparietal fascia.

• Make an incision through the superficial (outer) layer of the temporalis fascia beginning from the root of the zygomatic arch just in front of the tragus anterosuperiorly toward the upper corner of the retracted flap.

• Insert the sharp end of a periosteal elevator in the fascial incision, deep to the superficial layer of temporalis fascia, and sweep it back and forth.

• Once the periosteal elevator dissection is approximately 1 cm below the arch, sharply release the intervening tissue posteriorly along the plane of the initial incision.

• Retract the entire flap anteriorly, exposing the joint capsule. Fracture location dictates whether the capsule is opened.

Intraoperative Details

Concomitant dentoalveolar injuries should be evaluated and treated concurrently with treatment of mandibular fractures. Teeth in the line of fracture should be evaluated and if necessary, extracted. Whether teeth in the line of mandibular fractures are associated with increased morbidity is a controversial subject. Neal, Wagner, and Alpert⁶⁶ reported that there was no statistical difference whether teeth in the line of fracture were removed or retained when examining 257 fractures with teeth in the line of fracture (molars, premolars, anteriors). Amaratunga⁶⁷ looked at 191 patients with 226 fractures and used the following criteria for removal of teeth in the line of fracture:

• Excessive mobility

• Root exposure due to distraction of the fracture

• Tooth fracture with pulp exposure

• Caries with pulp exposure

Fractures were treated with maxillomandibular fixation (MMF) for 4 weeks or open reduction. He found that 13.7% of teeth removed in the line of fracture had complications and that 16.1% of teeth retained in the line of fracture had complications. He concluded that there was no significant difference between the number of complications in the teeth removed and teeth retained groups, which indicates that noninfected teeth in the line of fracture can be preserved when antibiotics are used. After a review of the literature, Shetty and Freymiller⁶⁸ made the following recommendations concerning teeth in the line of mandibular fracture:

• Intact teeth in the fracture line should be left if they show no evidence of severe loosening or inflammatory change.

• Impacted molars, especially full bony impactions, should be left in place to provide a larger repositioning surface. Exceptions are partially erupted molars with pericoronitis or those associated with a follicular cyst.
  
  

Left mandibular angle fracture involving tooth #17. Right mandibular body fracture.

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Left mandibular angle fracture involving tooth #17. Right mandibular body fracture.

Tooth #17 was extracted. A superior border plate was placed at the left mandibular angle. An inferior border plate was placed for the right mandibular body fracture.

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Tooth #17 was extracted. A superior border plate was placed at the left mandibular angle. An inferior border plate was placed for the right mandibular body fracture.

• Teeth that prevent reduction of fractures should be removed.

• Teeth with crown fractures may be retained provided emergency endodontics is performed.

• Teeth with fractured roots must be removed.
  
  

Right mandibular body fracture. Left mandibular angle fracture going through tooth #17.

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Right mandibular body fracture. Left mandibular angle fracture going through tooth #17.

Right mandibular body and left mandibular angle fractures status post fixation. Tooth #17 was extracted.

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Right mandibular body and left mandibular angle fractures status post fixation. Tooth #17 was extracted.

• Teeth with exposed root apices tend to develop pulpal or periodontal complications.

• Teeth that appear nonvital at time of injury should be treated conservatively due to potential for recovery.

• Perform primary extraction when there is extensive periodontal damage.

• Timing of the fracture is important; less complications occur when reduction and adequate fixation is instituted as soon as possible.

Complications

Delayed union and nonunion

• Delayed union and nonunion occur in approximately 3% of fractures.

• Delayed union is a temporary condition in which adequate reduction and immobilization eventually produce bony union.

• Nonunion indicates a lack of bony healing between the segments that persists indefinitely without evidence of bone healing unless surgical treatment is undertaken to repair the fracture.

• Nonunion is characterized by pain and abnormal mobility following treatment.

• Radiographs demonstrate no evidence of healing and in later stages show rounding off of the bone ends.

• The most likely cause for delayed union and nonunion is poor reduction and immobilization.

• Infection is often an underlying cause. Carefully assess teeth in the line of fractures for possible extraction or they may be a nidus for infection.

• Decreased blood supply can lead to a delay in healing. Excessive stripping of the periosteum, especially in comminuted and edentulous fractures, can lead to delayed healing.

• Alcoholics have been shown to have an increased incidence of delayed union and nonunion. These patients usually are at increased likelihood to sustain a mandibular fracture. Whether metabolic and vitamin deficiencies, poor compliance with intermaxillary fixation, poor bone quality, impaired local blood supply, or, most likely, a combination of the above reasons is the cause for an increased incidence of nonunion and delayed union is unknown.

Infection

• In some studies, particularly those without antibiotics, infection may occur in more than 50% of patients.

• Systemic factors include alcoholism, immunocompromise, and lack of antibiotic coverage.
  
  

Mandibular fracture. Patient with poorly controlled type 1 diabetes with left open, complete, moderately displaced mandibular angle fracture between teeth #17 and #18.

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Mandibular fracture. Patient with poorly controlled type 1 diabetes with left open, complete, moderately displaced mandibular angle fracture between teeth #17 and #18.

• Local factors include poor reduction and fixation, fractured teeth in the line of fracture, and comminuted fractures.

• Most infections are mixed iature, with alpha-hemolytic streptococci and Bacteroides organisms found most commonly.

• When infection is present it must be managed with debridement of sequestra, drainage, and antibiotic therapy. Apply rigid internal fixation with or without intermaxillary fixation across the fracture site. If a gap is present between the bone ends, a bone graft may be necessary.
  
  

Mandibular fracture. Patient with poorly controlled type 1 diabetes with left open, complete, moderately displaced mandibular angle fracture between teeth #17 and #18.

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Mandibular fracture. Patient with poorly controlled type 1 diabetes with left open, complete, moderately displaced mandibular angle fracture between teeth #17 and #18.

Mandibular fracture. Treated initially with a superior border plate and an inferior border plate as well as extraction of tooth #17.

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Mandibular fracture. Treated initially with a superior border plate and an inferior border plate as well as extraction of tooth #17.

Mandibular fracture. Patient returns with infected nonunion of left mandibular angle and loose hardware. The superior border plate was removed. Tooth #18 was extracted. The patient was treated with intravenous and oral antibiotics.

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Mandibular fracture. Patient returns with infected nonunion of left mandibular angle and loose hardware. The superior border plate was removed. Tooth #18 was extracted. The patient was treated with intravenous and oral antibiotics.

Mandibular fracture. Rigid fixation with an 8-hole plate. Two holes in the center are used to span the fracture site.

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Mandibular fracture. Rigid fixation with an 8-hole plate. Two holes in the center are used to span the fracture site.

Mandibular fracture. Patient lost to follow-up at local county jail presents with infected nonunion of mandibular symphysis.

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Mandibular fracture. Patient lost to follow-up at local county jail presents with infected nonunion of mandibular symphysis.

Malunion

• Malunion is defined as improper alignment of the healed bony segments. Not all malunions are clinically significant.

• When a dentate portion is involved in the malunion, a malocclusion can result.

• These malocclusions may be treated with orthodontics or osteotomies after complete bony union

Ankylosis

• Ankylosis is a rare complication of mandibular fractures.

• It is most likely to occur in children and is associated with intracapsular fractures and immobilization of the mandible.

• Ankylosis is believed to occur secondary to intra-articular hemorrhage, leading to abnormal fibrosis and ultimately ankylosis.

• Ankylosis may result in disturbed growth and underdevelopment of the affected side in children. The use of only short periods of intermaxillary fixation in children can help reduce the occurrence of this complication.

Nerve injury

• The inferior alveolar nerve and its branches are the most commonly injured nerves. The prominent sign of inferior alveolar nerve deficit is numbness or other sensory changes in the lower lip and chin.

• Damage to the marginal mandibular branch of the facial nerve is rare. More commonly, nerve damage caused by trauma in the region of the condyle, ramus, and angle of the mandible and by lacerations along its course is seen.

• Most of the sensory and motor functions of these nerves improve and return to normal with time.

 

Both benign and malignant tumors are found in the maxillary-facial regio.

Benign tumors divide into: osteogenic (osteoma, osteoid osteoma, osteoblastoclastoma), unosteogenic and unodontogenic (hemangioma, hemangioendothelioma, fibroma, neurofibroma, myxoma, chondroma),

odontogenic (adamantinoma, odontoma, odontogenic fibroma) and also considerable group of tumors-like formations (fibrous dysplasia, odontogenic cysts, eosinophilic granuloma etc).

There are next kinds of hemangiomas: simple, cavernous, racemous, combine, mixed and systemic angiomatosis. Capillary, racemous and cavernous hemanhiomas are found in clinic most often.

Capillary hemangioma is smooth, pink-red and cyanotic regio of tissue, which consists from the glome of capillaries and arterioles, which are interwoven between selves.

Racemous tumor consists from wide and sinuous arterial vessels. Arterial hemangioma alwais pulsate.

Cavernous hemangioma consists from group of large cavities, which are covered by epithelium and filled up by blood.

Treatment: small hemangiomas are treated by electrocoagulation, radial therapy, hotiing by trichloracetic acid. Large capillary hemangiomas are treated by help the surgery methods or different methods of sclerosing therapy (chonin-urethane mixture, 95% wine spirit).

Osteoblastoclastoma is found in maxilla, and has both central (17%) and peripheric (48% – gigantocytous epulid) placing. As a role, women are ill by osteoblastoclastoma. Tumor is situated on upper jaw in the regio of molars, on lower jaw in the regio of premolars.

Clinic: patient’s complaints depend on localizsation and stage of development of tumors. Sometime patient complains of a periodic inflammatory process in the tumor’s regio, which is completed by development of fistula with purulent discharge. Teeth, which are situated in the tumor’s regio, get loose. Peripheric osteoblastoclastoma is characterized by appearance of pale pink tumor on a gingiva. It’s base is wide, in contrast to usual epulid, several teeth, which are mobile in diffrent degree.

Clinic of central osteoblastoclastoma. It is difficult to determine the beginning of development of central osteoblastoclastoma, because the desease develop slowly and imperceptibly. Only some patients complain of a pain in a tumors regio. General state is not broken. Then central tumors become apparent as a bulge of jaw, the color of mucous coat isn’t changed. Regional lymphonodus isn’t increased. If inflammatory process join, clinic picture change sharply. When inflammatory appearance calm down, tumors with tistulous channel remain on the face or on the gingiva.

Diagnosis. Puncture. It is possible to receive the fluid of different color from brown to light-yellow, sometime – blood and never – cholesterin.

Roentgenography. There are a lot of cavities on roentgenogramm, which are divided by osteal septas, jaw is fusiformly thicken. Roots of teeth, which are situated in the cavity of cyst, are resorpted on 1/3 of their value.

Treatment is surgical: scraping of tumor or the resection of jaw if the tumor is big. Treatment of peripheric osteoblastoclastomas consists in resection of alveolar process.

Prognosis: as a rule, osteoblastoclastomas isn’t transform in the malignant tumor, but it is possible their recidivation or degeneration in cancer.

Adamantinoma. Term “adamantinoma” of jaws is a group of tumours, which have epithelial origin. Mainly women from 20 to 40 years old are situated in the regio of angle of the lower jaw.

Pathogenesis of adamantinoma is connected narrowly with question about the origin of epithelial tissue.

Clinic. Patients complain of unsymmetry of the face. There are possible to elucidate from anamnesis, that aching pain disturbed by patients during long time, occurrences of periostitis appeared in the regio of tumor periodically, fistulas with purulent discharge.

Objectively: inflation of lower jaw is defined on early stages, palpatory tumor is smooth, uneven, it’s consistence is hard. Skin’s color isn’t changed, skin is touch in fold. Then appear symptoms of cyst: regio of parchmental cruch, fluctuation, skin become thin, mucous membrane isn’t changed.

Roentgenography: roentgenographic picture of adamantinoma consists with cavities of different transparences.

Treatment is surgical.

Median cysts and fistulas of neck is situated in median line between incisure of thyroid cartilage and hyoid bone. They proceed without symptoms. Patients complain of presence of second chin, if it is fistula they complain of constant mucopurulent discharge.

Diagnosis is determined on the basis of anamnesis, exposure of epithelial calls, leucocytes, individual crystals of cholesterin in punctate.

Lateral cysts of the neck develop from ectoped residue of the branchial apparatus. As a rule, they show in youthful age. Localization of lateral cysts is typical – on the front border of the sternocleidomastoid muscle in it’s upper one third or in the retro fosse.

Palpatory their consistence is hardly-elastic, the color of skin over them isn’t changed, cyst isn’t united with bone.

Clinic. Painless tumor define in the regio of upper one third of sternocleidomastoid muscle or in the retro fosse.

Puncture of bone supplement diagnosis; liquid mucous punctate with epithelial cells, crystals of cholesterin, lymphocytes and erythrocytes is defined.

Treatment is surgical. Extirpation of median and lateral cysts and fistulas is begun from their filling by methylene blue.

Prognosis is favourable.

Mixed tumors of parotid gland consists near 50% among another tumors of parotid glands. It consists from epithelial, mixoid, chondroid structures and sometime from osseous tissue.

Clinic. Patients complain of unsymmetry of the parotid and mandibular regio, sometime pain. Palpatory tumor is painless, has round or oblong form, smooth or uneven surface, hardly-elastic consistence. Skin isn’t changed. If it is recidivation, the surgical treatmnt are supplemented with radiotherapy.

 

Cysts

 

General features

Learning objectives

You should:

•   know the types of cyst that can occur

•   the origins of the different types of cyst.

A cyst is a pathological cavity, not formed by the accu­mulation of pus, with fluid or semi-fluid contents.

Cyst growth

Several mechanisms are described for cyst growth, including:

•   epithelial proliferation

•   internal hydraulic pressure

•   bone resorption.

Classification of cysts

Cysts can be classified on the basis of

• location
— jaw

—maxillary antrum

—soft tissues of face and neck

• cell type

—epithelial

—epithelial

• pathogenesis

—developmental

—inflammatory.

Box 9 lists the cysts found in the orofacial region using these groups.

Other cysts

Cysts associated with the maxillary antrum

•   stsas mucosal cyst h the maxillary antrum

•   Postoperative maxillary cyst (surgical ciliated cyst of
tive maxillar_y

Cysts of the soft tissues of the mouth, face and neck

•   Dermoid and epidermoid cysts

•   Lymphoepithelial (branchial cleft) cyst

•   Thyroglossal duct cyst

•   Cysts of the salivary glands: mucous extravasation
cyst, mucous retention cyst, ranula.

Classification of cysts of the orofacial region

Based on the World Health Organization 1992 classification.

Epithelial cysts

Developmental odontogenic cysts

odontogenic       cysts

Dentigerous cyst (follicular cyst)

Eruption cyst

Lateral periodontal cyst

Gingival cyst of adults

Glandular odontogenic cyst (sialo-odontogenic)

h,Glandular   odontogenic cyst(s

Radicular cyst (apical and lateral) Radicular cyst Residual cyst

Non-odontogenic cysts

Nasopalatine cyst Nasopalatine cyst

Non-epithelial cysts {not true cysts) Solitary bone cyst Aneurysmal bone cyst

 

Odontogenic cysts

Odontogenic cysts are lined with epithelium derived from the following tooth development structures:

•   rests of Malassez: radicular cyst, residual cyst

•   reduced enamel epithelium: dentigerous cyst,
erous cyst,

•   Remnants of the dental lamina: odontogenic
keratocyst, lateral periodontal cyst, gingival cyst of
adult, glandular odontogenic cyst

•   Unclassified: paradental cyst.

Examination

Learning objectives

You should;

•   know the clinical signs and symptoms of cysts

•   understand the radiological appearance of cysts and the
features that need to be noted.

General clinical features

Cysts may be detected because of clinical symptoms or signs (Table 10). Occasionally an asymptomatic cyst may be discovered on a radiograph taken for another purpose. Symptoms may include:

•   swelling (Fig. 123)

•   displacement or loosening of teeth

•   pain (if infected).

The most important clinical sign is expansion of bone. In some instances, this may result in an eggshell-like layer of periosteal new bone overlying the cyst (Fig. 124). This can break on palpation, giving rise to the clinical sign of ‘eggshell cracking’. If the cyst lies within soft tissue or has perforated the overlying bone, then the sign of fluc-tuance may be elicited by palpating with fingertips on each side of the swelling in two positions at right angles to each other.

If a cyst becomes infected, the clinical presentation may be that of an abscess, the underlying cystic lesion only becoming apparent on radiographic examina­tion.

 

 

Fig. 123 Photograph showing buccal swelling caused by residual cyst in maxilla.

Radiological examination: general principles

As a basic principle, radiological examination should commence with intra-oral films of the affected region; for small cystic lesions, intra-oral films may be all that is needed for diagnosis, while for all cysts the fine detail of intra-oral radiography will help to clarify the relation­ship between lesion and teeth. For larger lesions, more extensive radiography is appropriate. Selection of films should take account of the value of having two views with differing perspectives (preferably at right angles to each other; Fig. 124).

Maxilla. Suitable views are:

•   periapicals and oblique occlusals

•   panoramic radiograph or lateral oblique

•   occipitomental (OM)

•   true lateral (anterior maxilla)

Mandible. Suitable views are:

•   periapicals and true occlusals

•   panoramic radiograph or lateral oblique

•   postero-anterior (PA) of mandible.

Computed tomography (CT) may be useful in planning surgery of large cysts, particularly in the posterior maxilla.

Radiological signs

Classically, cysts appear as well-defined round or ovoid radiolucencies, surrounded by a well-defined margin.

Margins. Peripheral cortication (radio-opaque mar­gin) is usual except in solitary bone cysts. ‘Scalloped’ margins are seen in larger lesions, particularly kerato-cysts. Infection of a cyst tends to cause loss of the well-defined margin.

Shape. Most cysts grow by hydrostatic mechanisms, resulting in the round shape. Odontogenic keratocysts and solitary bone cysts do not grow in this manner and have a tendency to grow through the medullary bone rather than to expand the jaw.

An odonlogenic keratocyst of the left mandible: A. Part of a panoramic radiograph showing expansion at the lower border of the mandible. B. Part of a postero-anterior radiograph of the same lesion.

 

Locularity. True locularity (multiple cavities) is seen occasionally in odontogenic keratocysts. However, larger cysts of most types may have a multilocular appearance because of ridges in the bony wall.

Effects upon adjacent structures. Where a lesion abuts another structure, such as a tooth or the inferior dental canal, it may cause displacement. Roots of teeth may be resorbed. When a cyst reaches a certain size, the cortex of the bone often becomes thinned and expanded. In posterior maxillary lesions the antral floor may be raised. Perforation of the cortical plates may be recog­nised as a localised area of greater radiolucency overly­ing the lesion.

Effect on unerupted teeth. Unerupted teeth may become enveloped by any cyst, a feature which may lead to erroneous diagnosis as a dentigerous cyst.

 

Specific cysts

Radicular cyst

Radiology

A well-defined, round or ovoid radiolucency is associated with the root apex or, less commonly in the lateral posi­tion, of a heavily restored or grossly carious tooth. A corti­cated margin is continuous with the lamina dura of the root of the affected tooth. The appearances are similar to those of an apical granuloma, but lesions with a diameter exceeding 10 mm are more likely to be cystic (Fig. 125).

Pathology

The cyst lumen is lined by a layer of simple squamous epithelium of variable thickness, which may display areas of discontinuity where it is replaced by granula­tion tissue. Arcades and strands of epithelium may extend into the cyst capsule, which is composed of gran­ulation tissue infiltrated by a mixture of acute and chronic inflammatory cells. This infiltrate reduces in intensity as the more peripheral areas of the cyst capsule are approached, where mature fibrous tissue replaces the granulation tissue.

Several features associated with inflammatory odon­togenic cysts may be present in the cyst lumen, lining and capsule: cholesterol clefts, foamy macrophages, haemosiderin and Rushton’s bodies

 

A radicular cyst related to the retained root of a first mandibular premolar. The corticated margin of the cyst is continuous with the lamina dura on either side of the root.

 

Photomicrograph of a radicular cyst.

Residual cyst

Radiology

The residual cyst has a well-defined, round/ovoid radiolucency in an edentulous area.                                            Occasionally
flecks of calcification may be seen.

Pathology

The lining and capsule are similar to the radicular cyst; however, both appear more mature, with the former lacking the arcades and strands of epithelium extending into the capsule.

Odontogenic keratocyst

Radiology

There is a well-defined radiolucency in odontogenic ker-atocysts, often with densely corticated margins. The shape margins may be ‘scalloped’ in shape. Occasionally, there is a multilocular appearance. Expansion typically limited, with a propensity to grow along the medullary cavity (Fig. 127).

Pathology

The cyst is lined by a continuous layer of stratified squa-mous epithelium of even thickness (5-10 cells) the surface of which is corrugated. The basal cell layer is well defined, being composed of cuboidal or columnar cells that display palisading. This epithelium is most com­monly parakeratinising, although orthokeratosis may be observed. The lumen of the cyst is filled with shed squames. The cyst capsule is composed of rather delicate fibrous tissue and is, classically, free from inflammation (Fig. 128). However, should the cyst become infected then an inflammatory infiltrate may be seen and the character­istic features of the epithelial lining will be lost.

The presence of daughter cysts within the capsule is a well-recognised finding, particularly in those odonto­genic keratocysts arising as a component of the basal cell naevus syndrome.

Dentigerous cyst

Radiology

In dentigerous cysts, there is a pericoronal radiolucency greater than 3-4 mm in width

 

that is suggestive of cyst

 

Odontogenic keratocyst. The lesion is very well defined with a corticated margin. The wisdom tooth appears displaced, as does the inferior dental canal, visible at the inferior and posterior aspects of the cyst. The shape is not round or ovoid, but rather irregular with a separate locule below the crown of the wisdom tooth.

formation in a dental follicle. The well-defined, corticated radiolucency is associated with the crown of an unerupted tooth. Classically the associated crown of the tooth lies centrally within the cyst, but lateral types occur (Fig. 129).

Pathology

The defining feature of a dentigerous cyst is the site of attachment of the cyst to the involved tooth. This must be at the level of the amelocemental junction. The lining of the cyst is composed of a thin layer of epithelium, either cuboidal or squamous iature, some 2-5 cells thick (Fig. 130). This lining is of even thickness and may

 

 

Photomicrograph of a keratocyst

A dentigerous cyst associated with the lower left third molar. The radiolucency is located pericoronally. Note that both the tooth and inferior dental canal appear to have been displaced interiorly by the lesion.

 

 

Photomicrograph of a dentigerous cyst.

include mucous cells along with focal areas of keratini-sation of the superficial epithelial cells. The cyst capsule is, classically, free from inflammation. However, in com­mon with the odontogenic keratocyst, the normal fea­tures of the epithelial lining may be distorted when an inflammatory infiltrate is present.

Eruption cyst

Radiology

The extra-bony position of the eruption cyst means that the only radiological sign is likely to be a soft tissue mass.

Pathology

An eruption cyst is basically a dentigerous cyst in soft tissue over an erupting tooth. The histological features are similar to those of the dentigerous cyst, though reduced enamel epithelium is often seen.

Gingival cysts

Gingival cysts are commonly found ieonates but are rarely encountered after 3 months of age. Many appear to undergo spontaneous resolution. White keratinous nodules are seen on the gingivae and these are referred to as Bonn’s nodules or Epstein’s pearls. Gingival cysts arise from the dental lamina and histologically are ker­atin containing. Many open into the oral cavity forming clefts from which the keratin exudes. Gingival cysts are lined by stratified squamous parakeratotic epithelium. Ieonates and infants, the cysts are typically between 2 and 5 mm in diameter. They do not involve bone and no treatment is required.

Gingival cysts of adults are much less common and are found mainly in the buccal gingivae in the mandibu-lar premolar-canine region. The cyst typically presents as a solitary soft blue swelling within the attached gin­givae, seldom larger than 5 mm in diameter. Gingival cysts of adults are lined by a thin cuboidal or flattened epithelium resembling dental follicle. They do not extend into bone although they may rest in a shallow depression in the cortex. They are usually removed by excision biopsy for diagnosis.

Nasopalatine cyst

Radiology

The nasopalatine cyst appears as a well-defined, round radiolucency in the midline of the anterior maxilla (Fig. 131). Sometimes it appears to be ‘heart-shaped’ because of superimposition of the anterior nasal spine. Radiological assessment should include examination of the lamina dura of the central incisors (to exclude a radicular cyst) and assessment of size (the nasopalatine foramen may reach a width of as much as 10 mm).

Pathology

The cyst is lined by a layer of pseudostratified ciliated columnar epithelium and/or stratified squamous epithelium. The capsule of the cyst is fibrous and may include the incisive canal neurovascular bundle

 

Nasopalatine cyst. This small example could easily be mistaken for a radicular cyst, but the presence of the lamina dura of the incisors indicates that this is not the case.

Nasolabial cyst

Radiology

As the nasolabial cyst is a soft tissue lesion, radiography may reveal nothing. However, radiography will be per­formed to exclude other causes of the swelling. ‘Bowing’ inwards of the anterolateral margin of the nasal cavity has been recorded as a feature. Ultrasound examination would be an appropriate investigation.

Pathology

The nasolabial cyst is lined by non-ciliated pseudostrat-ified columnar epithelium, which is often rich in mucous cells.

Solitary bone cyst

Radiology

The solitary bone cyst appears as a well-defined but non-corticated radiolucency. Typically, it has little effect on adjacent structures and ‘arches’ up between the roots of teeth (Fig. 132). The inferior dental canal may not be displaced, but the cortical margins of the canal may be lost where it overlies the lesion. Expansion is rare.

Pathology

The cyst is lined by fibrovascular tissue that often includes haemosiderin and multinucleate giant cells.

Aneurysmal bone cyst

Radiology

The aneurysmal bone cyst typically presents as a fairly well-defined radiolucency. Sometimes it has a multilocular

Solitary bone cyst. There is a large radiolucency in the body of the mandible that arches up between the roots of the teeth, which appear otherwise unaffected. The lower border cortex is very thin. The inferior dental canal is not displaced but appears to stop abruptly at the posterior end of the lesion appearance because of the occurrence of internal bony septa and opacification. Marked expansion is a feature.

Radiology

The predominant feature of an aneurysmal bone cyst is the presence of blood-filled spaces of variable size lying in a stroma rich in fibroblasts, multinucleate giant cells and haemosiderin. Deposits of osteoid are also seen.

Surgical management of cysts

Surgical management of cysts generally implies enucle-ation, but occasionally marsupialisation is the technique of choice. Some small radicular cysts do not require surgery and regress once the root canal of the associated tooth has been effectively cleaned and filled. Antibiotic therapy may be required if a cyst has become infected. Aspiration of fluid from a pathological cavity may be helpful in confirming the presence of cyst rather than maxillary sinus (air) or tumour (solid). Biochemical analysis of the aspirate indicating protein content of less than 40 g/1 and cytology showing parakeratinised squames suggests an odontogenic keratocyst.

Enucleation

Enucleation of a cyst involves the removal of the whole cyst, including the epithelial and capsular layers from the bony walls of the cavity. This permits histopatholog-ical examination and ensures that no pathological tissue remains. A large mucoperiosteal flap, usually buccal, is raised to ensure that closure will be over adjacent sound tissues and not the bony cavity. Primary closure is nearly always undertaken unless the cyst is very infected, in which case this may be delayed and the cav­ity initially dressed with Bismuth Iodoform Paraffin Paste (BIPP) on ribbon gauze.

Enucleation of a nasopalatine cyst will require the raising of a palatal flap to provide surgical access and cyst removal. This inevitably damages the nasopalatine nerves and vessels and results in a small area of paraes-thesia, which usually does not cause concern to the patient.

Marsupialisation

Marsupialisation is a simple operation that may be per­formed under local anaesthesia in which a window is cut and removed from the cyst lining. This allows decompression of the cyst, which then slowly heals by bone deposition in the base of the cavity. However, this technique permits histopathological examination of only a small and possibly non-representative sample of tissue. Primary closure is not undertaken but rather the cyst lining is sutured to the oral mucosa to keep the cav­ity open (Fig. 133). The cavity must be filled with a dressing such as BIPP, which must be frequently replaced, to prevent food debris trapping during the many months the cavity may take to heal. Alternatively, an extension may be added to a denture to protect the cavity, which becomes reduced in size as the cavity heals. Marsupialisation is advocated when the cyst is so large that jaw fracture is the likely outcome of enucle-ation, although enucleation and simultaneous bone grafting may be preferable. The technique may also be useful if there are associated structures, such as the infe­rior alveolar nerve, maxillary antrum or nose, that are at risk of damage during enucleation. Similarly, marsupi­alisation of an eruption cyst will allow the eruption of a tooth without it being damaged by enucleation.

Surgical management of particular cysts

Radicular cysts

Large radicular cysts, or small ones that do not resolve following conventional endodontic treatment, require enucleation and surgical endodontic management to seal the root canal of the associated tooth.

Access for apical surgery is gained via a three-sided or a semi-lunar mucoperiosteal flap

The latter

Enucleation of a radicular cyst. A. A three-sided incision. B. A semi-lunar incision to gain access to a radicular cyst associated with a maxillary lateral incisor. C. Oblique sectioning of the apical root to permit good access to seal the root canal with amalgam

Keratocyst

High recurrence rates are reported (up to 60%) because of technical difficulty in removing all of the cyst lining, including projections into cancellous bone. Enucleation must be thorough. Some advocate irrigating the cyst cavity with chemical fixatives to cause necrosis of any remaining remnants, and others suggest excision to include a bone margin about the cyst. Annual radio-graphic review is recommended.

Eruption cysts

Reassurance of the parents is usually the only manage­ment required as these cysts frequently fenestrate spon­taneously and require no surgical intervention. Occasionally, however, they may require marsupialisa-tion to expose the tooth.

Solitary bone cyst

These bone cysts are often incidental findings on radio­graphs. Aspiration may reveal clear fluid or air indicat­ing that no further intervention is necessary.

Aneurysmal bone cyst

These cysts benefit from curretage. However, they may be associated with a second pathological lesion such as a vascular malformation which may lead to profound haemorrhage. Patients with this cyst need to be man­aged in hospital.

Premalignancy and malignancy

Premalignant conditions and lesions

Premalignant conditions

Premalignant conditions are a group of disorders associ­ated with a small increased risk of developing oral carci­noma. The common link is thought to be epithelial atrophy, which may confer greater susceptibility to carcinogens. Atrophic epithelium has altered cell turn over rates and is likely to be more permeable. Patients with premalignant conditions should be advised to eliminate tobacco use and to limit alcohol intake, as these are risk factors for developing oral cancer.

Submucous fibrosis

Oral submucous fibrosis is related to using paan, which is a leaf quid containing areca nut. Many types exist, includ­ing fresh products consumed in the Indian subcontinent and southeast Asia as well as packed proprietary prod­ucts. Tobacco, slaked lime, spices and other ingredients may be added; in southeast Asia, areca nuts are often chewed fresh. The mucosa and teeth become stained orange-brown because the paan is held in the mouth for long periods. The affected mucosa becomes pale in colour and feels firm on palpation (Fig. 151). Fibrous bands may develop in the buccal mucosa and a pale, constricting fibrosis typically involves the palate. Mouth opening becomes restricted and swallowing may be difficult. The risk of developing oral carcinoma has been estimated at around 5%, although the risk of submucous fibrosis itself cannot be separated from the risks posed by carcinogenic substances in paan. In biopsy material, a subepithelial band of fine fibrillary collagen is seen in the lamina pro-pria and the oral epithelium can be reduced to only a few cell layers in thickness. Keratinisation and chronic inflam­mation may be present in some cases. Where areas of erythroplasia and leukoplakia are present, biopsies may show epithelial dysplasia or even carcinoma.

 

Submucous fibrosis showing tethering bands involving the buccal mucosa.

 

Atrophic lichen planus

Links between lichen planus and oral cancer have been debated. Some evidence links atrophic variants of oral lichen planus, characterised by red areas of mucosal thinning and erosions, with an increased tendency to develop oral cancer. There are no proven associations between oral non-erosive lichen planus or cutaneous lichen planus and malignant transformation. Also a type of epithelial dysplasia known as lichenoid dysplasia, in which there is resemblance both clinically and micro­scopically to lichen planus, has been described. Other forms of lichenoid mucositis, such as lichenoid reaction and discoid lupus erythematosus, may additionally be confused with lichen planus. Tobacco use should be dis­couraged in lichen planus. sufferers.

Sideropenic dysphagia

A number of conditions can result in difficulty in swal­lowing. The association of primary iron-deficiency anaemia and difficulty in swallowing because of forma­tion of a postcricoid fold (oesophageal web) is known as the Patterson-Kelly-Brown or Plummer-Vinson syn­drome. Chronic iron deficiency results in generalised mucosal atrophy as iron is an essential growth require­ment for the oral epithelium. Carcinoma may develop in the oesophagus and less commonly in the oral cavity.

Genetic disorders

The rare disorders tylosis and dyskeratosis congenita

predispose to the development of leukoplakia and oral cancer.

Prematignant lesions

Premalignant lesions of the oral mucosa are areas of morphologically altered tissue in which cancer can arise. Various terms have been used to describe these lesions arid diagnosis is often made by exclusion. Many lesions do not progress to cancer and some even regress. It is probable that a proportion of lesions diagnosed as premalignant are actually reactive, and for this reason the term ‘potentially premalignant’ is often used when considering leukoplakia and erythroplakia.

Leukoplakia

Various definitions of leukoplakia have been proposed but it is essentially a predominantly white lesion that cannot be characterised as any other definable lesion. Leukoplakia is a clinical diagnosis and has a variable histology.

•   Homogeneous leukoplakias are plaque-like lesions with a uniform smooth or wrinkled surface; there is
less risk of malignant transformation.

•   Non-homogeneous leukoplakias tend to be less circumscribed and show a greater range of
appearances. Verrucous leukoplakia has a warty appearance and rrucous leukoplakia has
interspersed red areas. Heaping up of keratin, nodularity and ulceration may be present. The risk of
malignant transformation is greater ion- homogeneous leukoplakia.

The diagnosis can only be made after careful clinical examination with representative mucosal biopsy, as these procedures are essential for exclusion of other defined disorders. A semantic problem exists in that diagnosis by exclusion may ‘lump’ more than one dis­ease together and depends on which diseases are recog­nised as ‘definable.’ The prevalence of leukoplakia varies from 0.2 to 4% and the risk factors are tobacco, alcohol and possibly candidal infection.

The risk of malignant transformation is difficult to estimate in any individual case. Lesions in the floor of mouth and ventral tongue, and those showing evidence of epithelial dysplasia or carcinoma in situ, are at high risk (Fig. 152). Paradoxically, the risk of malignant trans­formation is greater ion-smokers than in smokers. Leukoplakia is very rare ion-smokers. The regression of leukoplakia in smokers following cessation suggests that a proportion of lesions are reactive, whereas leuko­plakia ion-smokers more often represents a local cel­lular genetic change that tends to be progressive. However, there is evidence to suggest that smoking ces­sation in leukoplakia reduces risk, and an appropriate intervention is advised.

 

Other terms for leukoplakia

A variety of terms have been employed to describe potentially premalignant lesions

 

 

Leukoplakia of the floor of the mouth. An area of early malignant transformation is seen at the right margin of the lesion.

 

Sublingual keratosis. This term is applied to leuko-plakia affecting the floor of mouth and ventral tongue. One reported series described a malignant transforma­tion in over 30% but this has not been confirmed by later studies. The term is not generally favoured because of lack of evidence supporting it as a distinct entity.

Candidal leukoplakia. Chronic hyperplastic candidia-sis results in a firm warty or specked plaque that cannot be scraped off. It occurs most commonly on the dorsal tongue and buccal mucosa behind the angle of the mouth. Staining with periodic acid-Schiff’s base (PAS) shows pseudohyphae of Candida species growing into the keratin layer, where they are typically associated with a neutrophil inflammatory infiltrate. There is marked epithelial hyperplasia with formation of elon­gated and blunted rete processes. Elimination of predis­posing factors such as smoking, poor denture hygiene and haematinic deficiency, combined with systemic antifungal therapy, may cause resolution of the white plaque. Malignant potential exists but is now accepted as being low. The presence of microscopic dysplasia in this lesion causes concern.

Syphilitic leukoplakia. This is not relevant to contem­porary practice but carried a high risk of malignant transformation when it was prevalent. It was a compli­cation of tertiary syphilis and tended to affect the dor-sum of the tongue.

Erythroplakia

Erythroplakia has been defined as a bright-red velvety change on the oral mucosa that cannot be characterised as any other definable lesion. There is a high risk of trans­formation. Histopathologically, erythroplakia tends to show dysplasia, often in a distinctive pattern with drop-shaped rete processes, marked nuclear and cellular pleo-morphism and minimal keratinisation. Carcinoma in situ is often seen also.

 

 

Pathology and genetics

Learning objectives

You Should:

•   know the features of epithelial dysplasia

•   understand what is meant by carcinoma in situ

•   know the management of premalignancies.

Epithelial dysplasia and carcinoma in situ

The term dysplasia is used in a variety of contexts in pathology and means literally ‘abnormal growth’. In the context of oral potentially premalignant lesions, it refers to a combination of cytological changes and distur­bances of cellular arrangements seen during the process of malignant transformation. Epithelial dysplasia is graded by oral and maxillofacial pathologists into mild, moderate and severe grades. The term carcinoma in situ is applied when abnormalities involve the entire thick­ness of the epithelium, though severe dysplasia is often described as amounting to carcinoma in situ where only a thin keratinising layer is present. The histopath-ological features recognised in dysplasia are given in Table 12.

Grading of dysplasia

Studies on histopathological grading show poor kappa agreement between even specialist pathologists. This problem arises because of lack of scientific evidence for weighting the various features of dysplasia. For exam­ple drop-shaped rete processes are generally accepted as a sinister feature, whereas increased mitotic rate may be seen in reactive processes. Both inter- and intraobserver variabilities between pathologists are high and the bio­logical behaviour of the lesion does not always correlate

 

with its grading. Problems may also arise because of non-representative sampling at the time of biopsy. Although histopathological grading is intrinsically unreliable, the presence of dysplasia in a suspicious lesion remains the best predictive indicator of malignant change.

Tumour suppressor genes and oncogenes

The process of malignant transformation is the result of accumulation of genetic damage. There may be genomic instability or stepwise accumulation of genetic events (Fig. 153). The latter process is thought to operate in most oral cancers and studies have demonstrated muta­tions, methylation, or loss of various tumour suppressor genes (e.g. p53, pl6, p21, retinoblastoma) in oral cancers. Loss of function of a tumour suppressor gene confers a selective growth advantage on the cell, resulting in an expanded population in which further genetic abnor­malities are thought to arise. Abnormal oncogene activ­ity may increase cell proliferation rates and drive malignant progression. Dysplasia is likely to represent a histopathological change owing to genetic alterations, and research may lead to a better understanding of potentially premalignant lesions.

Management of potentially premalignant lypremaligna

Clinical risk factors for malignant change include tobacco habit, high alcohol intake and possibly poor diet. Clinical factors that must also be taken into account are:

•   female gender

•   extensive or spreading lesions

•   lesions in the floor of mouth/ventral tongue,
retromolar area or pillar of fauces

red, speckled, verrucous or nodular appearance

 

 

 

The multistage hypothesis related to oral cancer.

Most important is the presence of dysplasia or carci­noma in situ. Management should include:

•   clear information and explanation of the significance
of the lesion to the patient

•   intervention to stop tobacco habit and limit alcohol
interve

•   treat anaemia and candidal infection if present

•   surgical or laser excision or drug treatment may be
ionordrugtrea

•   regular review and observation: investigation if signs
of cancer present.

Referral to a specialist centre is usually advisable for patients presenting with white or red mucosal patches, or other suspicious lesions. Biopsy is normally required for diagnosis and to determine whether epithelial dys­plasia is present. Some patients may be followed up in plasiais pre sent.Somepatients_m

Oral cancers

Learning objectives

You should:

• know the epidemiology and types of oral cancers

us

know the clinical and pathological features of squamous cell carcinoma

• understand the management of squamous ceil carcinoma

including its grading.

Most oral cancers do not arise in a clinically recognised premalignant lesion and are diagnosed as primary can­cerous lesions. They are typically painless, unless infected or advanced, and often cause no symptoms. For this reason, the need to conduct a careful systematic examination for every patient cannot be stressed too much. Extra-oral examination should include both visual inspection of the face and neck and palpation of the neck (see Ch. 1). The patient’s head should be tilted forwards and the lymph nodes in the neck palpated in relaxed tissue. A routine technique should be adopted, perhaps starting with the submental nodes and then moving to more posterior node groups. The oral mucosa and oropharynx should be examined carefully. The tongue should be protruded to detect lateral deviation and then relaxed and lifted to allow examination of its ventral surface and the floor of mouth. Correct position­ing and the use of good illumination and mirrors are important factors. When oral cancer is detected, prompt referral is essential. The importance of attending at the hospital should be stressed, without provoking undue anxiety. Until a biopsy result is available, definitive diagnosis should be avoided. Any ulcer that fails to heal within a 3-week period should be regarded as suspi­cious and the patient should be referred to a specialist.

Epidemiology

Global incidence and trends

The global incidence of oral cancer has been estimated at over 350 000 new cases per year. Of these over 30 000 occur in the USA and just under 3000 occur in the UK. There is marked geographical variation in distribution, with the highest incidence in the Indian subcontinent and southeast Asia, because of the particular use of paan and tobacco. Oral and oropharyngeal cancer ranks in the top ten in prevalence tables. The incidence of oral cancer is rising and more cases are seen in younger age groups. The male to female ratio of around 2.5:1 is also changing, with an increasing oral cancer incidence in women, particularly involving the tongue.

Morbidity and mortality

Overall 5-year survival for oral cancer is around 50% but depends very much on the stage at initial diagnosis and clinical factors. Squamous cell carcinoma of the lip has a better prognosis than intra-oral carcinoma. In general, prognosis is worse when tumours arise in the more pos­terior parts of the oral cavity and oropharynx than in the anterior area. Midline carcinomas in the floor of mouth and ventral tongue may, however, spread to both sides of the neck. Staging is a system used to describe the degree of spread or tumour Toad’ and the most widely used TNM (tumour, lymph node, metastases) system is described in Tables 13 and 14. Survival at 5 years for TNM stage I oral carcinoma is around 80%, whereas sur­vival is reduced to 15% for stage IV. Morbidity refers to the reduction in function, both physical and psycholog­ical. Again, morbidity tends to relate to stage, as large tumours may require removal of a large amount of tis­sue or radical radiotherapy. Hospital re-admission is fre­quent during treatment and in many cases rumours prove refractory to all forms of therapy. Quality of life can be assessed and is an important measure of morbid­ity. Good dental health is a significant factor.

 

 

 

 

 

 

 

 

 

 

 

Types of oral cancer

Squamous cell carcinoma accounts for around 95% of all oral cancers. It arises from the epithelial lining of the oral cavity. It is described in detail in the next section.

A number of other forms of malignant disease also arise in the oral cavity.

Minor salivary gland cancers. These tend to occur in the palate and upper lip and they present as rubbery nodules, sometimes ulcerated and painful. They are described in Chapter 12.

Malignant melanoma. This typically occurs in the palatal and gingival mucosa. A spreading brown-pig-mented patch or a raised ulcerated nodule, surrounded by pigmented mucosa, may be seen (Fig. 154). Prognosis is grave iodular malignant melanoma.

Malignant lymphoma. Extranodal lymphoma arises principally in the oropharynx in the area of Waldeyer’s ring. Nodular infiltration of the mucosa is seen and lymph nodes in the neck may become involved.

Generalised gingival enlargement caused by acute leukaemia.

Leukaemia. Leukaemia may present with oral signs such as persistent gingival haemorrhage and oral ulcer-ation. Acute myeloid leukaemia and childhood leukaemia may cause gingival enlargement because of direct infiltration of leukaemic cells.

Fig. 154 A malignant melanoma involving the palate.

Metastatic deposits. Metastasis from primary cancers in the kidney, gastrointestinal tract, lung, breast, prostate and other sites occur in the oral cavity. Often they present as gingival nodules or as destructive bone lesions. Metastatic lesions in bone are usually radiolu-cent, but prostate and some breast metastases appear as radio-opacities in bone.

Rare neoplasms. Soft tissue and bone tumours can arise in the oral cavity. Odontogenic malignant tumours are known but are very rare.

Squamous cell carcinoma

Aetiology

Smoking

Cigarette smoking is the most important aetiological factor for intra-oral cancer in the Western world. Risk increases with cumulative dose, which is measured in ‘pack-years’. There are no safe levels. The risk is greatest when combined with high alcohol intake. It is believed that carcinogens in tobacco smoke accumulate in the floor of mouth, accounting for the increased risk of squamous carcinoma at that site.

Paan and other tobacco use

Paan, also known as betel quid, is used throughout the Indian subcontinent. Leaf of the betel piper vine is used to form a rolled-up quid, into which areca nut is placed. Areca is thought to contain alkaloid carcinogenic pre­cursors. In addition, tobacco, spices and slaked lime may be added. The quid is held in the oral cavity for a considerable time and is habit forming. Buccal and labial cancers are commonly associated with paan use. Other tobacco habits exist, including smearing tobacco paste into the mouth and reverse bidi smoking, which has been linked to palatal cancer. In recent times, areca nut has become popular in southeast Asia.

Alcohol

Alcohol is an important cofactor when combined with smoking but may not be a risk factor in its own right. It may increase epithelial permeability, allowing greater access of carcinogenic substances to the basal cells.

Ultraviolet light

Ultraviolet B is an important factor in lip cancer. Fair-skinned races in tropical latitudes are particularly at risk from sunlight. Protection, using measures such as sun block and wearing a wide-brimmed hat, is advocated where there is high risk.

Diet

Evidence is accumulating that a poor diet with low antioxidant action (deficient in fresh vegetable content) is an important contributory factor.

Clinical features

The lip

Although the lip is the most common site for oral cancer, intra-oral cases are detected more often by dentists. The lower lip is almost exclusively affected, often to one side of the midline (Fig. 156). Shallow ulceration, crusting or thickening are typical presentations. Spread to the sub-mental nodes tends to be slow; if detected early, this can­cer has the best prognosis.

Intra-oral surfaces

The floor of the mouth, ventral tongue and lateral ante­rior tongue are most commonly involved. All too fre­quently, the tumour is symptomless and reaches an advanced stage before detection. The classical descrip­tion is of a hard, fixed ulcer, with raised rolled margins and a necrotic base (Fig. 157). It is vital to remember that squamous carcinomas may also present as white or red mucosal patches, fleshy polyps, punched-out ulcers, indurated plaques or by tethering mucosa. The tongue may become fixed to the floor of mouth, making it diffi­cult for the patient to raise it. Alternatively, the tongue

 

A squamous cell carcinoma of the lower lip

 

 

 

A squamous cell carcinoma of the floor of mouth showing the raised rolled borders. The lesion was painless and the patient presented requesting new dentures.

 

may deviate to the side of an oropharyngeal tumour on protrusion (Fig. 158). Sometimes patients present with nodal metastasis from an occult primary lesion in the oropharynx.

Squamous cell carcinoma also arises on the gingivae, alveolar ridge, buccal mucosa and palate, albeit less commonly. Bone invasion is an early feature of carci­noma arising in mucoperiosteum.

Head and neck

Dentists should also be aware of extra-oral cancers. Basal cell carcinoma is not uncommon on the facial skin. Squamous cell carcinoma arises in the maxillary sinus (Ch. 6), nasopharynx and larynx. Persistent hoarse voice can be a presenting sign of laryngeal cancer and should trigger referral to an otolaryngologist.

Pathology

Histopathological features

Microscopically, squamous cell carcinoma comprises sheets of squamous epithelial cells supported by a fibrous stroma containing the tumour vasculature. The

 

 Tongue deviation on thrusting the tongue outwards. The patient had a large carcinoma in the oropharynx, which had tethered the tongue on the left side squamous cells can be recognised by their tendency to form flattened layers held together by prominent intra-cellular bridges (desmosomes). Often, individual cells undergo keratinisation and the most conspicuous fea­ture is the formation of keratin pearls or whorls (Fig. 159). The vast majority of tumours are moderately dif­ferentiated, though examples of well-differentiated and poorly differentiated carcinomas occur. Increased mitotic activity is seen and often bizarre mitotic figures are present. Nuclear and cellular pleomorphism and nuclear hyperchromatism are typical features. Necrosis is present in some cases and is usually associated with poor prognosis. A key feature is invasion of the adjacent tissues by detachment and movement of the carcinoma cells. Invasion may be on a cohesive front or a diffuse non-cohesive front. Carcinoma spreads along anatomi­cal planes. It may spread along nerves, vascular chan­nels or into the sarcolemmal sheaths of muscle fibres. A chronic inflammatory response is usually seen at the invasive front.

When an incisional biopsy is undertaken on clinically suspicious mucosal lesions, it is important to include the margin of the ulcer. The biopsy must be of sufficient depth and crush damage must be avoided. Failure to sample appropriately may lead to misdiagnosis.

Bone invasion

In addition to local spread into soft tissues, oral squa­mous cell carcinoma can spread into adjacent bone. At first the periosteum acts as a barrier but cortical resorp-tion can lead to entry of the carcinoma cells to marrow spaces and bone destruction. Radiographs show irregu­lar bone destruction and teeth may be displaced or resorbed. Computed tomography (CT), magnetic reso­nance imaging (MRI) and particularly positron emission tomography (PET) scanning can help to determine the extent of bone and soft tissue spread (Fig. 160).

 

 

 

 

A squamous cell carcinoma showing keratin pearls and cellular pleomorphism

Bone invasion by oral squamous cell carcinoma.

Metastasis

Carcinoma spreads to regional lymph nodes via the lymphatics. The primary site is important: lip cancers spread to the submental nodes, whereas intra-oral tumours are more likely to spread to the cervical nodes (see Fig. 1, p. 4). Involved lymph nodes become first pal­pable and then fixed and hard. With increasing tumour deposition, nodes may become matted together or even cystic as a result of central necrosis. Tumours in the anterior floor of the mouth may metastasise to both sides of the neck.

Distant metastasis is a relatively late event but spread may occur to the lungs, brain, viscera and bone. Chest radiography, isotopic bone scans and CT or MRI may be used to detect distant metastasis.

Grading and staging

Histological grading: prognostic features

Histological grading :pr o gnostic features seen in the microscope that can be related to the biological behav­iour of the tumour. The degree of differentiation is not a particularly good indicator of prognosis. Pattern of invasion is more important; tumours that invade tissue on a non-cohesive front (single cells or narrow strands) have a worse prognosis than those that invade on a broad front. Basaloid and anaplastic tumours have a very poor prognosis. Perineural and vascular invasion are also indicators of poor prognosis. As yet, no molecu­lar markers are in routine use.

Staging: TNM classification

Clinical and pathological staging refers to determina­tion of the extent of tumour size and spread. The patient is examined carefully and imaging is used to aid in the detection of involved neck nodes. The TNM (Tables 13 and 14), system is widely used. Pathological staging (pTNM) is undertaken on surgically resectioned speci­mens and is more accurate.

Imaging of oral squamous cell carcinoma

The role of imaging in oral cancer management includes:

•   identifying rumour size and anatomical extent

•   detection of regional nodes (staging)

•   post-treatment follow-up.

Plain radiographs obviously have a very limited role to play in assessment and management of oral squamous cell carcinoma. Advanced lesions on the floor of the mouth may cause gross bone destruction in the adjacent mandible, but detection of early bony involvement has poor sensitivity. Radioisotope bone scans are used to detect such early bone destruction. These bone scans, particularly in combination with CT, lead to good diag­nostic sensitivity in detection of bone involvement.

Imaging of oral squamous cell carcinoma relies upon cross-sectional techniques (i.e. CT or MRI). Thin slice (3-5 mm) CT sections are usually performed through the oral region and neck. Intravenous iodinated contrast is given and the scans are repeated, because neoplastic lesions of the floor of mouth and tongue base tend to enhance, which improves the delineation betweeor­mal and abnormal tissues. Contrast also highlights ves­sels, allowing them to be more easily distinguished from nodes.

When examining images of submandibular and jugulo-digastric nodes of the internal jugular chain, those nodes with a diameter exceeding 1.5 cm are abnor­mal; in other parts of the neck 1 cm is the maximum size of normal nodes. A low-density centre may be seen in nodes containing tumour, although this finding is also seen in inflammation. Neoplastic (and inflammatory) nodes frequently show ring enhancement following contrast injection. Imaging contributes to the clinical staging process not least because it shows nodes (retropharyngeal) beyond the scope of clinical examina­tion.

Treatment

Surgery

Radical surgery is used to remove biopsy-proven pri­mary oral cancers. It is first necessary to undertake a full hospital examination. This often includes examination of the upper aerodigestive tract under general anaesthe­sia to exclude second primary lesions. Other tests are used to exclude distant metastases. Informed patient consent and support are vital.

The surgical operation aims to remove the carcinoma, with a 2 cm margin of normal tissue beyond the clinical

edge of the tumour where possible. When the carcinoma involves bone then part of the mandible or maxilla must also be rerrtoved. Reconstruction is required to maintain function after excision of all but the smallest lesions. This may be accomplished using local flaps or distant pedicled or microvascular free flaps. The latter may include bone as well as soft tissues. A large variety of flaps are available and this simultaneous resection and reconstruction has revolutionised the surgical manage­ment of patients with oral cancer. The emphasis is now on improving the quality of the functional and aesthetic result. The reconstruction may involve the use of osseointegrated implants (Ch. 5).

A selective (removing lymph nodes at certain levels) or radical (removing nodes at all levels) neck dissection may be needed because of possible lymph node involve­ment. Neck dissection results in some morbidity and modern surgical techniques aim to minimise loss of function.

Radiotherapy

External beam (teletherapy) and implanted radioactive seeds or needles (plesiotherapy) can be used to treat oral cancer. Radiotherapy can also be used as an adjuvant therapy, combined with surgery. Acute mucositis occurs during treatment. Later complications include:

osteoradionecrosis pathological fracture dry mouth radiation scar chronic ulceration.

A very rare late complication is the induction of neo­plasms such as osteosarcoma.

Role of the dentist in prevention, detection and treatment

Learning objectives

You should:

•   understand how the general dental practitioner can
educate patients in prevention of oral cancer

•   be aware of the need to look for and follow up suspicious
lesions

•   understand postoperative dental care for patients with oral

cancer.

Prevention

Spending a few moments with a patient discussing giv­ing up smoking is known as an anti-smoking intervention

It has been shown that such interventions are most effec­tive when undertaken by health-care professionals and are a cost-effective method of prevention.

Early diagnosis and screening

Careful history taking and examination are essential for identification of suspicious oral mucosal lesions. Palpation of neck nodes and systematic examination of the oral mucosa should be routine practice. Use of tolo-nium blue as a screening test in primary care is not sup­ported by robust evidence and it may generate false-positive results.

Referral

Delay should be avoided when a suspicious mucosal lesion is detected. Telephone referral to hospital with a confidential, detailed, follow-up letter to the specialist is a good option when cancer is suspected. It is important to avoid undue alarm to the patient and use of the word ‘cancer’ should be avoided.

Dental care prior to radiotherapy

The dentist is an important clinician in the multidiscipli-nary team managing oral cancer. Preventive advice and completion of treatment to render the patient dentally fit are vital. Teeth with a poor prognosis may be extracted to avoid later problems with osteoradionecrosis and dental sepsis when radiotherapy is to be given to the jaws.

Post-treatment care

Once the acute mucositis associated with radiotherapy has subsided, patients may experience dry mouth, bone pain and increased caries rates. Surgical patients may require specialised restorative care and reconstruction. Recurrence or a second primary lesion is always possi­ble and it is important to undertake regular review both to reassure and to detect any mucosal changes at the earliest opportunity. Maintenance of dental health is also important; radiotherapy is a high risk factor for caries and 6-monthly bitewing radiographs are recommended.