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Oral Pathology

Oral ulcérations Marjorie A. Woods* / Abdel R. Mohammad** / James E. Turner*** / Harry H. Mincer***^

Ukerafions are common occurrences In the mouih. Causes include physical n-auma, ra- diation, chemical injury, und imcrohial infection (bacterial, viral, and fungal). Some ulcérations, such as recurrent aphlhous stomaiitis, Behçet's .^yndronie, and , are of uncertain etiology, whereas others (eg, , peniphigoid) are apparently of immunologie origin. Malignant neoplasms also may present as uleera- tions. Beeause fhe natural history and Irealmenf varies with ihe diagnosis, the practi- tioner should become faniiliar wiih ihe clinieal appearance of the various types of ulcér- ations so that appropriate treatment can be insliluted. (Quintessence Int 1990;2i:14I-15L)

Introduction etiology, clinical appearance, pertinent histologie fea- tures, and treatment of some of tbe more common An ulcer is an area of discontinuity of an epithelial oral ulcers. surface. Ulcers frequently occur in tbe and vary greatly in terms of etiology, signs and symptoms, prog- nosis, and treatment. Common causes of oral ulcers Ulcers caused by physical injury include physical or ehemical injury, infectious neopla- sia, and abnormalities of tbe immune system, partic- Traumatic ulcers ularly autoimmune disorders. The cause of most oral The most common ulcer of the oral cavity is caused nleers may be easily determined by history and chnical by some form of physical injury and is referred to as presentation, and many of these lesions can be satis- a traumatic ulcer. The initial injury is a laceration, factorily treated by a variety of conservative protocols. , or thermal burn that develops into a typical Some ulcers, by contrast, require , culture, or nonspecific ulcer. Most traumatic ulcers are self-in- other laboratory procedures for definitive diagnosis flicted injuries such as intentional or unintentional and institution of an appropriate, specific treatment bites of the mucosa or toothbrusb injuries. Unfortu- regimen. The purpose of this paper is to discuss the nately, some ulcers are caused by trauma inflieted by clinicians during tbe course of treatment. Inadequately controlled hand or rotary instruments, overextended impression trays with rough borders, sharp provision- al crowns, or improper placement of aspiration de- vices can lead to oral wounds. A unique iatrogenic oral ulcer is the "cotton roll injury," which oeeurs * Assistant Professor, Department of Biologic and Diagnostic when drying results in adherence of a cotton roll to Sciences, University of Tennessee, College of , 875 Union Avenue, Memphis, Tennessee 38163. , and retnoval of the roll tears the ** Professor, Department of Pathoiogy, University of Irbid, PO attaehed mucosa. Box 1975, Irbid, Jordan. Other common oral traumatic ulcers are those as- *** Professor and Chairman, Department of Biologic and Diag- nostic Sciences, University of Tennessee, College of Dentistry, sociated wiih complete or partial prostheses, com- 875 Union Avenue, Memphis, Tennessee 38163. monly known as denture ulcers. Ulcers occurring at "*' Professor and Director, Division of Oral Pathology, Depart- the flange of an applicance are usually due to over- ment of Biologic and Diagnostic Sciences, University of Ten- extension or a rough surface, while those occurring nessee, College of Dentistry, 42 North Dunlap, Room 516, Memphis, Tennessee 3S163. beneath tbe denture base, particularly those on the

Quintessence Internationai Volume 21. Number 2/1990 141 Oral Pathology

Fig 1 A regular or irteguiar erythematous border encir- Fig 2 Aspirin burn involving a localized area in whicti the cles the yeilow-white eschar covering the base ot a trau- aspirin tablet has been held ih contact with the mucosa. matic ulcer.

crest of the alveolar ridge, may be caused by either asis is a common complication of radiation mucositis, improper occlu.sion, a rough surface, or a poor fit. and, in concert with radiation injury, xerostomia, atid Regardless of the cause of traumatic ulcers, they are nutritional deficit, conspires to cause diffuse tender- most often oval, shallow, and less than 1 cm in greatest ness and chronic ulcération. Usually, mucositis re- diameter, A regular or irregular erythematous border gresses at the termination of therapy, but unfortu- encircles the yellow-white eschar covering the base of nately, in some cases, xerostomia persists indefinitely the ulcer {Fig 1). Healing of the ulcer requires com- and complicates healing and maintenance of optimal pletion of epithelial migration over a bed of vascular oral hygiene, A regimen of topical fluoride applica- and fibrous connective tissitc. Generally, healing of the tion, chlorhexidine rinses, and artifical sahva is the typical traumatic ulcer is completed in 10 to 14 days. cornerstone of care for these patients. Ulcers resulting Since traumatic ulcers are often small and minimally from radiotherapy are often managed in the .same way painful, treatment may not be required. Larger, pain- as traumatic ulcers with local applications of emol- ful ulcers may be managed successfully with topical lients, antiseptics, saline rinses, and topical anes- anesthetics, antimicrobials and corticosteroids. Rare- thetics. ly, recalcitrant ulcers, especially those lying over bone, may require surgical incision of the ulcer margin and debridement of the ulcer base to enhance wound heal- Ulcers caused by chemical injury ing. The "aspirin burn" is an example of ulcération cattsed by a local application of a chemical. The lesion de- velops within hours and involves a localized area in Radiation mucos it is which aspirin tablets are held in contact with the tnu- Physical injtiry of cells of the oral mucosa occurs dur- cosa (Fig 2). The covering pseudomembrane is irreg- ing radiotherapy of malignant tumors of the head and ularly .shaped and resembles other lesions caused by neck and almost always results in mucositis, which is application of phenol, silver tiitrate, or other caustic commonly accompanied by ulcération. The extent of agents to oral tissues. Occasionally, dental impressiott injury varies according to dose, portal of the beam, materials, moitthwashes, or ingredients of tooth- and age and health of the patient. The first reaction pastes, such as sodium lauryl sulfate and flavoritigs, appears during the second week of a 5- or 6-week can be etiologic factors in oral ulcérations,' fractionated dose. The response begins as a diffuse Ingestion of many chernicals can cause oral ulcér- erythema, which is followed by desquamation of ep- ation. Organic mercury causes ulccration by a cyto- ithelium and ulccration. Xerostomia is often profound toxic effect on oral mucosa, while others, such as ben- and predisposes tissues to traumatic ulcers, Candidi- zene, caitse marrow depression, which allows ulcers to

142 Quintessence International Volume 2t, Number 2/1990 Oral Pathology

develop. In contrast to ulcers caused by local appli- cation of cytotoxic drugs, ulcers that arise in patients with concomitant marrow depression commonly lack the marginal erythematous zone. Drugs used to treat cancer or arthritis or to prevent rejection of trans- plants may also cause uleerations. Most of these drugs cause injury hy a direct toxic effect on oral tissues by producing an allergic response or both. Side effects of drugs used to treat systemic diseases include xerostomia, anemia, nutritional deficits, leu- kopenia, or other conditions that reduce host re- sponse, thereby predisposing tissues to ulcération. Furthermore, some drugs have a propensity for en- hancing or amhfying latent disease that shows mini- Fig 3 In ANUG, the involved gingiva bieeds easiiy, and the tip of the necrotic papilla appears to be punched out mal expression. For example, allopurinol has been and covered with a yellow or yellow-white pseudomem- shown to increase the severity of ulcération associated brane. with erosive .- Many of these ulcers are secondarily infeeted by opportimistic bacteria, fungi, protozoa, or viruses and may require a specific anti- biotie or chemo therapeutic regimen. are portant role in the pathogenesis of the disease. Can- often helpful in affording symptomatic relief to pa- crum oris, a particularly severe form of fusospiroche- tients with ulcers secondary to chemotherapy These tal disease, is most commonly seen in malnourished mouthwashes usually contain some combination of individuals in the third worid countries,'' This condi- sahne, hydrogen peroxide, topieal anesthetics, anti- tion often involves perforation of oral tissues and may biotics, sodium hicarbonate, and a lubricant, such as terminate in death. Kaopectate, Some investigators stress prevention as The treatment of acute or ehronic neerotizing ul- an effective means of controlhng the oral cytotoxic cerative includes debridement of the necrotic effects of chemo therapeutic regimens. Preventive areas and superficial scaling of hard and soft deposits methods include correction of existing oral disease on adjacent teeth. Effervescent mouthwashes like hy- and occlusal disharmony, oral hygiene instruction, drogen peroxide and systemic treatment with anti- and smoothing rough areas or overextended flanges biotics, particularly penicillin or metronidazole, are of removable prostheses.^ effective adjuncts.'

Syphilis Ulcers caused by bacterial infections The mouth may he affected by any of the three stages Acute and chronic neerotizing ulcerative gingivitis of . The primary lesion, or ehancre, presents Acute necrotizing uicerative gingivitis (ANUG) most as a firm nodule on the hp, , or that commonly affects young adults and begins suddenly breaks down to form an indurated ulcer with raised as a necrotizing lesion involving interdental papillae. margins. The lesion is not painful and heals in a few Characteristically, the involved gingiva bleeds easily week with no sear. At this stage, serology is negative, and the tip of the neerotic papilla appears to be but the organism ( Treponema palliduin ) can be iden- "punched out" and covered with a yellow or yellow- tified hy darkfleld examination of a smear of the le- white pseudomembrane (Fig 3). Pain, fever, malaise, sion. fetid breath, and lymphadenopathy characterize the The oral lesions of secondary syphilis are highly clinical features of ANUG. The disease often follows contagious and may present months after the primary a chronic course (CNUG) with subsequent develop- stage as well-defined, gray, sloughing ulcers. These are ment of periodontitis. Spirochetes and fusobacteria classically linear ("snail-track ulcers'") or circular are major etioiogic factors of ANLJG, but the path- ("mucous patches") but may be any shape. At this ogenesis of the disease is not entirely clear. According stage, serology is positive and there are associated sys- to many investigators, nonspecific stress plays an im- temic features such as fever, malaise, generalized

Quintessence Internationai Volume 21, Number 2/1990 143 Oral Pathology

lymphadenopathy, and a macular skin rash. Tertiary tent in nerve-cell bodies until reactivation occurs, at syphilis is now rare because of successful treatment which point the infectious virions travel to mucosal with antibiotics during the early stages of the disease. or cutaneous via peripheral sensory nerves The tertiary stage may show extensive white hyper- to produce the recurrent lesion. The mechanism of keralolic lesions, especially of the tongtie (syphilitic reactivation is also not clear but may involve such ), or gummatous necrosis (gummas) of the diverse stimuli as stress, trauma to mucosa or skin, body of the longue. Gummas may also involve the upper respiratory tract infections, or exposure to ul- or the or result in perforation ofthe traviolet light. The immune system is also apparently palate. involved, because immunosuppressed patients, espe- cially those with defects of cell-mediated immunity, tend to have more frequent and more severe recurren! HSV infections. Ulcers caused by viral infections Ihe standard laboratory method for confirming viral injections HSV infection is isolafion of ihe virus in tissue culture. Herpes simplex viruses (HSV-f and HSV-2) commonly Combining culture and immunologie detection meth- cause infection and have been isolated from many vi.s- ods has resulted in more rapid identification of HSV ceral and mucocutaneous sites. The clinieal manifes- Cytologie specimens using Papanicolaou stain can tations and course of HSV infections are determined demonstrate typical herpes virus changes in epithelial by the anatomic sites involved and the age and im- cells. Unfortunately, all laboratory techniques may be mune status of the hosl.^ negative during the ulcerative stage of the disease. Both viral subtypes can infect either orofacial or Treatment of primary and recurrent lesions usually genital tissues; the lesions in these sites are clinically requires supportive therapy only. In immunosup- indistinguishable. Herpes simplex virus type 1 most pressed patients, topical, intravenous, or oral treal- commonly causes oral lesions, while type 2 usually ment with acyclovir lessens the severity and duration affects genital tissues. The patient with primary oral of primary and recurrent herpes. In immunologically herpes (primary herpetic gingivostoniatitis) lacks HSV competent patients, topical acyclovir has shown var- serum antibodies during the acute phase. Children be- iable results.^ tween the ages of 1 and 3 are usually affected, and the infection is often characterized by systemic signs and symptoms such as fever, malaise, ptyalism, dysphagia, Herpes zoster and iyinphadenopathy. The mucosal lesions may not Herpes zoster infection is caused by the varicella-zos- be apparent for 24 to 48 hours but then develop rap- ter virus, which also causes in children. idly. The initial oral lesion is often a non-necrotizing The zoster eruption () represents a reactiva- marginal gingivitis, which is followed by development tion ofthe virus, which has been dormant in the pos- of vesicles that involve the masticatory and nonmas- terior root ganghon of a sensory nerve, a mechanism ticatory mucosa. The fragile vesicles soon rupture and analogous to that with recurrent herpes simplex in- leave shaiiow irregular ulcers that typically heal with- fections. Herpes zoster usually strikes middle-aged or out scarring in 10 to 14 days. In many patients, how- elderly adults. When the trigeminal nerve is involved, ever, primary HSV infection is so mild that it goes the mouth and facial skin are affected. The onset of unnoticed. the lesions is preceded by pain in the affected area. If The lesions of recurrent herpes type ] infections are the oral structures are involved, the pain may be severe morphologically identical to those of the primary dis- enough to be mistaken for . The character- ease, but recurrent herpes usually affects adults, has istic pain of herpes roster is a result of acute inflam- a shorter duration, involves a smaller area and runs mation in the nerve ganglion. Rarely, it may cause a milder course. Although any oral site may he in- permanent damage resulting in post-herpetic neural- volved in recurrent herpes, keratinized tissues, espe- gia. The initial visible event is an erythematous rash cially the lower , are more commonly affected. followed after a few days by vesicles that rupture, crust over, and then begin to heal. The pathogenesis of recurrent herpes simplex is not entirely understood. A popular concept is that during Ulcers similar to those of herpes simplex are seen primary herpetic gingivostomatiîis, the virus migrates in the mouth but they are always unilateral and limited to the trigeminal ganglia. There the virus remains la- to the distribution of the affected division of the tri-

144 Quintessence International Volume 21, Number 2/1990 Oral Pathology

geminal nerve. Severe erythema along the route of the nerve may be associated with the ulcers. Either skin lesions or oral ulcers heal in 2 to 4 weeks, but occa- sional scarring results. Herpes zoster infections are particularly severe in a «i inamnnocompromiscd patients, especially children re- ceiving chemotherapeutic regimens for eancer, Acyclo- vir appears to be useful in treating these patients.**

Coxsackie virus infections More than 30 types of Coxsackie virus cause infections in humans, and two of these feature oral ulcérations," Fjg4 Ulcers, caused by a Coxsackje virus infection, af- Hand, foot, and mouth disease (Coxsackie A, type 4) fecting the posterior area of ttie . and (Coxsackie A, type 16) present with small, scattered oral ulcers that are preceded by a tran- sient, rarely notieed vesicular stage. The lesions are characteristically limited to the posterior aspects of the mouth, especially the posterior , soft palate (Fig 4), and . They may coalesce to form larger or the patient has au inadequate immune response, ulcers. Candida spp can be seen in smears or biopsy material, In contrast to herpes simplex infections, oral but confirrnation of the diagnosis and speciation of Coxsackie virus infections usually cause no gingivitis the fungi requires the growth of the organism on ap- and little systemic upset or lymphadenopathy. In propriate culture media. hand, foot, and mouth disease, which is not related In all eases of , predisposing factors must to hoof and mouth disease of cattle, there are also be considered. These include ill-fitting dentures and lesions of the hands and soles of the feet, Coxsackie inadequate vertical dimension. In dentulous patients infections often occur in minor epidemics among and in persistent cases involving edentulous patients, schoolchildren. They are usually self-limitmg diseases systemic factors must also be considered. Immuno- with a duration of 7 to 10 days, deficiency disorders such as acquired immunodefi- ciency syndrome and rare hereditary immune defi- ciencies are often characterized by intraetable muco- Epstein-Barr virus infection eutaneous candidiasis," Candidiasis often occurs in The Epstein-Barr virus, classified as a herpes group patients receiving immunosuppressive drugs for the virus, is the etiologic factor of infectious mono- treatment of cancer or autoimmune disease, or to pre- nucleosis (glandular fever). Patients with rnononu- vent transplanted organ rejection. Patients with dia- cleosis often present with palatal petechiae. sore betes mellitus also appear to have increased suscep- throat, lymphadenitis, and severe nonspecific oral ul- tibility to Candida infectioti. More commonly, candi- cération. diasis occurs in patients during or following treatment of infectious disease with broad spectrum antibiotics. In this situation, the antibiotic suppresses the normal Ulcers caused by fungal infections flora and allows Candida spp to prohferate. Among the clinical forms of candidiasis presenting as oral ul- Candidiasis (candido.sis. motùliasis. thrush) cers are acute pseudomembranous candidiasis, acute atrophie candidiasis, and chronic atrophie candidi- Candidiasis is the most common fungal infection in- asis. volving the oral cavity and shows a variety of clinical presentations, including ulcération,"* The usual caus- Acute pseudomembranous candidiasis, often re- ative organism, Candida albieans, is present in the oral ferred to as "thrush," usually follows antibiotic ther- flora in about 40% of individuals without signs and apy. Any age group may be affected, and clinically the symptoms of candidiasis. This fungus, however, is ca- lesion is characterized by the presence of a soft, white pable of causing infection when the oral flora is altered pseudomembrane involving any site in the oral cavity.

Quintessence i Vp[|imp 91 Numhar 2/1990 145 Oral Pathology

Fig 5 Acute pseudoniembranous candidiasis is charac- Fig 6 Minor aphthous ulcers are round, 0.5 to 1.0 cm in terized by the presence of a soft, white pseudomembrane diameter, and bave a gray base and an erythematous bor- that can be easiiy removed and leaves a raw, bieeding der. surlaee.

The pseudomembrane is easily removed and leaves a treatment of angular cbelitis caused by Candida spp, raw, bleeding surface (Fig 5). and nystatin suspension is an efficacious treatment for Acute atrophie candidiasis may follow acute pseu- acute pseudomcmbranous candidiasis. domembranous candidiasis. Some cases arise de novo and many are the sequelae of long-term antibiotic therapy. The affected oral tissues are erythematous, and this form of candidiasis is consistently painful. Ulcers caused by recurrent aphthous Chronic atrophie candidiasis is rarely painful, and Recurrent apblbous stomatitis (RAS) is a eommon patients are often unaware that the lesion exists. Many disease of the oral mucosa that affects approximately patients with chronic atrophie candidiasis in the form 20% of the population in the United States.'- It is of "denture sore mouth" may also have angular cheil- characterized by recurring oral ulcers that usually he- itis or perleche. This condition often begins bilaterally gin in adolescence. Three clinical patterns of ulcéra- at the lip commissures as areas of wrinkling or ma- tion are recognized; minor aphthous ulcers, major ceration that subsequently become deep fissures. The aphthous ulcers, and herpetiform ulcers. fissures do not involve the mucosal surface but spread Eighty percent of patients with RAS have the minor obliquely from the commissure to involve tbe skin. form. The ulcers are characteristically round, 0.5 to Although angular often occurs in patients 1.0 cm in diameter, with a gray base and an erythem- wiih complete removable dentures that lack proper atous border (Fig 6). They occur in crops of one to vertical dimension, it may also appear in dentulous five lesions and usually affect the nonkeratinized sur- patients who have vitamin B-complex deficiency, es- faces of the buccal mucosa, hps. floor of mouth, and pecially riboflavin deficiency. ventral surface of the tongue. They may be associated Treatment of ulcerative forms of eandidiasis in- with much pain and discomfort. They usually recur volves assessment and ehmination, if possible, of any every 1 to 4 months, although the interval may varj' predisposing factors. Tbe most appropriate treatment with each occurrence. The ulcers heal in 7 to 10 days for ulcerative forms of is topical an- without scarring. tifungal therapy such as nystatin, ketoconizole, or Major apbthous ulcers represent about 10% of cases chlortrimazole. Nystatin is preferred because it lacks and manifest as round, ovoid, or irregular ulcers of associated side effects. Several preparations of nystatin variable size, often more than 1 cm in diameter. They are available, including suspensions, trocbes, suppos- also involve nonkeratinized mueosa, especially the sofl itories, and creams. Effective treatment of chronic palate, tonsils, and the fauces. Because they may per- conditions may require use of a combination of prep- sist for weeks or even months, and may develop raised, arations. Nystatin cream is particularly effective for rolled margins, they often must be differentiated from

146 Quintessence International Voiump i-'r 2/1990 Oral Pathology

malignant ulcers by biopsy. Major aphthoits lesions have similar mucosal lesions affecting the , cause moderate to severe pain and result in scarring, genitals, or eyes, and also lesions of the joints, skin, Herpetiform ulcers account for the final 10% of kidneys, or nervous system. This is called Behçet's patients with . These patients may syndrome, a severe systetnic disorder eharacterized by present with crops of as many as 100 stnall ulcers that widespread immune complex vasculitis, probably of clinically resemble those seen in herpes simplex itifec- autoimmune origin. Behçet's syndrome is common in tions, Herpetiform itlcers differ from minor and major Japan and the Middle East but is rarely seen in North aphthae; they occur predominantly in females, and the America, Treatment often requires the prolonged use usual age of onset is later, in the third decade. The of systcmie eorticosteroids. ulcers are tiny (1 to 4 mm) and poorly defined with a gray base. Although any site may be affected, they occur most often on the ventral tongue and floor of Ulcers caused by erythema multiforme y: the mouth. In some cases, the lesions coalesce to pro- Erythema multiforme is an acute disorder that may t: duce large ragged areas of shallow ulcération. Periods occur at any age but usually affects young males. Skin of recurrence vary, and healing takes place in 7 to 10 or mucous membrane may be involved either inde- days, usually without scarring. pendently or together. The majority of cases affect There are a number of recognizable predisposing mucous membrane and without skin involvement. factors that are relevant to the diagnosis and man- The typical skin lesions are múltiple round erythem- agement of RAS, In particular, 10% to 15% of pa- atous macules showing a central papule, vesicle, or ik tients with RAS may have sérologie evidence of a de- area of eyanosis or necrosis. The configuration pro- •sx fieiency of iron, fohc acid, or vitamin B,, that may be duces the so-called target lesions. Target lesions sel- dietary in origin. Occasionally an underlying gastroin- dom appear on mucous membranes. Oral lesions testinal disorder may be present, and 3% of these pa- usually show an abrupt onset of macules, vesicles, or tients have been shown to have ccliac disease or bullae that rapidly deteriorate into painful ulcers, Crohn's disease,'' Other predisposing factors include pseudomembranes, or crusts, Stevens-Johnson syn- menstruation, mental stress, and mild mucosal trauma drome, a particularly severe form of erythema multi- ¡m such as from toothbrushing or abrasive foods. There forme, is aeeompanied by severe constitutional symp- fuii is also a peculiar relationship with cigarette smoking, toms and in addition to lip, oral, and skin lesions alw (¿ in that some older individuals who give up the habit involves the conjunctiva, tirethra, and gastrointestinal ^ develop aphthous ulcers for the first time. Diagnosis tract. j'¿ is nearly always made on the basis of history and The lesions usually heal in about 2 weeks without Jl,. ciinical features, but in some cases a biopsy may be scarring. Treatment is symptomatic and supportive. required. Topical anesthetic or corticosterold elixir may be help- ,[ij. No treatment regimen is uniformly satisfactory, but ful in improving patient comfort. In severe eases, op- j¿( the disease may be controlled by elimination of pre- timal treatment may require the use of systemic cor- j- disposing factors, prevention of secondary infection, ticosteroids. ,,. and promotion of healing. Sources of trauma should •^ be avoided, and possible deficiency states excluded by Ulcers caused by pemphigus ¿ careful history, examination, and appropriate labo- j ratory tests. The treatment of choice is topical stc- Pemphigus is an uncommon but serious dermatologie -,, roids. Ointments or emollients (such as triamcinolone disease that, in about 50% of cases, affeets the mouth J in Orábase (Colgate-Hoyt) are useful for single, ac- first but eventually shows generalized skin , I cessible ulcers. Use of chlorhexidine , involvement. It is histologically characterized by intra- commencing at the onset of ulcération and continuing epithelial bulla formation in which the cells of the f three or four times a day until healing is complete, prickle cell layer lose their intercellular connections '', often relieves the pain and may accelerate healing by (acantholysis) thereby producing a split within the epithelium. Evidence indicates that pemphigus is an I 2 or 3 days."* autoimmune disease in which autoantibodies are di- rected against antigens in the intercellular spaces of 0 Ulcers caused by Behçet's syndrome epithelial cells. Direet immnnofiuoreseence identifies antibodies to the intercellular substance in up to 80% K Some patients with apparent aphthous stomatitis may

Quintessence int Niimhsr 2/1990 147 Oral Pathology

which the epithehum is separated from the to form a spaee filled with inflammatory exú- date and often blood,'^ Direct immunolluorescence shows antibodies to the epithelial in approximately 50% of cases. There are two main types of ; benign mucous membrane pem- phigoid and bullous pemphigoid. Benign mucous membrane pemphigoid is mainly a disease of oral, ocular, and genital mucosa, although contiguous skin is also sometimes involved. Females more than 60 years of age are most frequently affected. Most eases start on the soft palate with hullae thai rapidly break down to form large, well-defined, shal- Fig 7 Orai lesions resuiting Irom pemphigus usualiy pres- low ulcers. These heal slowly, often with marked sear ent as persistent, painful erosions with ragged outiines and erythematous bases. formation, giving rise to the disease's alternative name of cicatricial pemphigoid. The attached gingiva is often involved by widespread erosions giving a red, of eases. The intercellular substance is the primary site raw appearanee called "." This of involvement as substantiated by electron micros- may also be a feature of erosive hchen planus. copy, which shows that dissolution of intercellular ce- The oral vesicles and bullae have a full thickness of ment substances is the initial event. Immunofluoresc- epithehal roof and are thus stronger and more likely ence studies show both immunoglobulin (especially to be seen intact than those of pemphigus. They ap- igG) and complement (especially C"3) localized inter- pear as blood-filled or clear lesions occurring at any cellularly in the epithelium of patients with active dis- site but most frequently involving the soft palate, gin- ease. In addition, the patient's serum contains anti- giva, or tongue. Although the mouth alone may be bodies in titers directly proportional to the severity of involved for months or even years, some patients sub- the di.sease. These antibodies react in intercellular sequently develop eye lesions that may heal with scar- spaces when tested against skin of a normal individual ring and cause blindness. or the patient's uninvolved skin. Bullous pemphigoid is another form of pemphigoid There are several types of pemphigus, but pemphi- that is primarily a skin disorder; the mouth is affected gus vulgaris is most frequently encountered. Pemphi- in only about 20% of cases and rarely before skin gus occurs sometimes in children'' but the majority lesions develop. The oral lesions, clinically and his- of affected individuals are between 40 and 70 years of tologically, are similar to those of benign mucous age. Males are affected more commonly than females membrane pemphigoid. A presumptive diagnosis of are. pemphigus or pemphigoid can often be made on the The oral lesions rarely present as vesicles but rather basis of the clinical history and appearance, but it as persistent, painful erosions with ragged outhnes must be confirmed by a biopsy showing the charac- and an erythematous base (Fig 7). They may oecur at teristic histologie findings. For the pathologist to carry any site but usually affect the lips, , and lateral out immunofluorescence techniques, fresh tissue for borders of the tongue and gingiva. Gentle stroking of frozen sections or specimens preserved in a special the mucosa or skin may induce a bulla, a phenomenon medium must be submitted to the laboratory Previous known as Nikolsky"s sign. The skin lesions consist of arrangement with the laboratory is helpful, and spec- multiple vesicles or bullae that rapidly break down to imens should be taken from a recent and preferably produce large denuded areas from whieh fluid loss ean intaet lesion in an area of uninvolved skin or mucosa. be severe. Secondary infection is common, and with- These diseases cannot be cured but can be ade- out appropriate treatment mortality is high. quately controlled by steroids. Conditions showing only a few lesions can be managed by the use of topical corticosteroid elixirs, ointments, or emollients, hut Ulcers caused by pemphigoid more massive involvement of skin or mucous mem- Pemphigoid is an uncommon dermatologie disease brane requires vigorous treatment with systemic cor- characterized by subepithehal bulla formation in ticosteroids.

148 Quintessence Internationai Volume 21. Oral Pathology

Fig 8 Desquamative gingivitis is a condition characterized Fig 9 Tiie erosive form of licfien pianus. by intense erythema and desquamation of the altaehed gin- giva.

Ulcers caused by desquamative gingivitis than 40 years of age. Women are affected almost twice as often as men are. The buccai mucosa is the most Desquamavite gingivitis is not a specific disease entity, commonly involved oral site, followed in incidence by but is rather a condition characterized by intense er- the tongue, lips, gingiva, palate, and fioor of the ythema and desquamation ofthe attached gingiva (Fig mouth. Bilateral distribution is common. Skin lesions, 8). Since the histologie and immunologie features in which can develop concomilantly with or independ- many cases are so similar to benign mucous membrane ently of oral lesions, occur in approximately 28% of pemphigoid, some investigators beheve desquamative cases and are particuiariy likely to affect the flexor gingivitis is often a variant of mucous membrane pem- surface of the extremities. phigoid that is limited to attached gingiva," Clinically, there are three major forms of oral hchen The patient usually complains of pain from minor planus; reticular, hypertrophie, and erosive. The ero- trauma as well as during brushing or flossing. Rub- sive form (Fig 9) is mosi common, but various forms bing the gingiva may lead to desquamation of a large may appear simultaneously. The reticular (annular) area of tissue or formation of a blood-filled bulla. The form shows fine, slightly raised, white or violaceous condition has a decided predilection for postmeno- threadlike lesions that intersect or from ringlike pat- pausal women but is not limited to this group. A va- terns. This configuration forms the clinical entity riety of diseases may present clinically with similar known as Wickham's striae. The hypertrophie form is lesions; these include erosive lichen planus, allergic characterized by homogeneous white plaques, often stomatitis, and bullous pemphigoid. showing a peripheral reticular patlern. Erosive lichen The most effective therapy for desquamative gingiv- planus shows erylhema, shallow ulcers, pseudoinem- itis appears to be corticosteroids in the form of emol- brane formation, and occasionally vesicles and bullae. lients, elixirs, or gels. Some investigators prefer lo fab- Lichen planus is often asymptomatic or the patient ricate a custom tray for holding the steroid in optimal may experience burning, thickening, or a tightening contact with the tissues.'^ Dapsone has also been sensation ofthe affected areas. Severe symptoms only shown to be effective in some cases.'^ occur with the erosive form. The cause of lichen planus is unknown. It is inter- esting to note that exacerbations often follow an ep- Uicers caused by lichen pianus isode of mental stress. Fortunately, in most cases the Lichen planus is a chronic disease of the skin and condition becomes stable and many complete remis- mucous membrane that is characterized by the devel- sions occur. On the other hand, squamous cell carci- opment of papules, plaques, erosions, or any combi- has been reported to arise rarely in hchen plan- nation of these lesions.'" It is essentially a disease of us.-' However, according to some authors, the rela- tionship is simply coincidental.'- adults; the majority of cases occur in individuals more

Quintessence lnt"rnnti'-"'ñi "nhimp ^^ 149 Oral Pathology

Fig 10 frequently presents as Fig 11 Necrotizmg sialometaplasia is an uncommon le- an ulcer, sion of unknown etiology. The probable cause is ischemia.

Treatment, if required, generally consists of locally therapy. Chemotherapy, to date, has yielded disap- applied analgesics in combination with topical corti- pointing results. costeroids. Systemic corticosteroid therapy has been shown to be effective in alleviating the symptotns of Ulcers of unknown etiology severe cases. Necrotizing sialometaplasia is an uncommon lesion, particularly affecting men and almost invariably oc- Ulcers caused by malignant neoplasms curring on the hard palate (Fig 11), The probable Any malignant neoplasm of the orai cavity rnay ul- cause ts ischemia. According to some reports, the con- cerate during the course of the disease, Squamous cell dition is most common among alcoholics and heavy carcinoma, the most comtnon of oral cancers, fre- smokers,-' quently presents as an ulcer (Fig 10), While the.se le- Clinically, the lesion has a sudden onset and the sions may arise in any area ofthe oral cavity, the lateral ulcération may be preceded by a feeling of fullness cr border of the tongue is most comtnonly involved, fol- swelling. The ulcer is considerably deeper and larger lowed in succession by the fioor of the mouth, man- than the typical oral ulcer. dibuiar gingiva, buccal mucosa, and retrornolar-tri- The clinical and microscopic features of necrotizing g one-ton sillar area. These anatomic sites, while eom- sialometaplasia greatly resemble squamous cell car- posing only 25% of the total surface area of the oral cinoma and care must be taken not to misdiagnose mucosa, account for 80% of ¡ntraoral squarnous cell the lesion. The condition is not particularly painful carcinomas. Typically, these lesions affect patients be- and is considered to be a self-limiting entity in which tween the ages of 50 and 65, Men are affected more healing is by secondary intention. Debridement ofthe commonly than are women; whites are affected more necrotic tissue is recommended, often than are blacks. Snmmary In comparison to other oral ulcers, .squamous cell carcinomas are rnore apt to have a longer duration, Oral ulcérations are common clinical entities, and the are more likely to be painless, and tend to have an practioner should be knowledgable about the various irregular outHne, Also, the margins are often raised, types. Effective management of these conditions is an indurated, and show red or white foci. integral part of dentistry. Small squamous cell carcinomas of the oral cavity in rnost cases can be controlled by either surgery or References radiation or both. Advanced lesions, by contrast, t, Rubrigtit we, et al: Oral slough caused by dentifrice detergents show a high incidence of local recurrence or distant and aggravated by drugs wilh antisialic activity. / Am Dmi metastasis even after extensive surgical or radiation Assoc 1978;97:2] 5-230.

150 Quintessence International Volume 21, Numher ?/1990 Oral Pathology

2. Chau NY, et al: Allopunnol-amplified lichenoid reactions of 13. Bernstein ML, McDonald JS: Oral lesions in Crohn's disease. the oral miicosa. Oral Surg Oral Med Oral Puiliol 1984;58:397- Oral Surg Oral Med Oral Pallio! 197K:46:234-245. 400. 14. Addy M, Tapper-Jones L, Seal M: Trial of ¡islringent and an- 3. DePaola LG, et al: Prosthodontic considerations for patients tibacterial niouthwashes in the management of recurrent undergoing cancer chemotherapy. J Am Dem A.^soe aphthous ulcération. Br Dem J 1974; 135:452-455. 1983;107:48-5l. 15. Mincer HH, Sebelius CL, Turner JE: Juvenile pemphigus vul- 4. Grinin JM, et al: Noma. Report of two cases. Oral Surg Oral garis. Orat Surg Oral Med Oral Paflwl 1975:40:257-260. Med Oral Pa!liol 19S3:56:605-607. 16. Silverman S, et al: Oral mucous membrane pemphigoid. Oral 5. Lekovic V, et al: The efTect of nietronidazole on human peri- Surg Ond Med Oral Pathol 1980:61:233-237. odontal disease. J Periodomot 1983:54:476-480. 17. Peng T, Nisengard RJ, Levine MJ: Gingival basement mem- 6. Corey L, Spear PG: Infections wiih herpes sirnplex viruses. 1. brane antigens in desquamativc lesions oï the gingiva. Ond Suig ¡V EngI J Med 1986:314:686-691; 1986;314:749-757. Oral Med Oral Palhol 1986;61 :;S4-589. 7. Fiddian AP, et al: Successful treatment of witK 18. Atifdemorte TB, Devile; RL, Parel SM: Modified topical steroid topical acyclovir. Br Med J (Clin Res) 19S3;6(suppl):4H7. therapy for the treatment of oral mucous membrane pemphi- 8. Shep DH, Dandhker PS, Meyers JD: Treatment of varicella goid. Oral Surg Oral Med Oral PaiimI 1985:59:256-260. zosier virus infection in severely immunocompromised patients: 19. Nisengard RJ, Rogers RS: The treatment of desquamativc gin- a randomized comparison of Acyclovir and Vidarabine. N EngI gival lesions. J Periadomol 1987;58:167-172. /MPJ I9S6;314:208-212. 20. Silverman S, Griffith M: Studies on oral lichen planus. II. Oral 9. Nolte WA (ed): Oral Microbiology wi!ti Basic Microbiolagv and Surg Ora! Med Oral Polhol 1974:37:705-710. immunotogy. ed 4. St Louis, CV Mosby Co, 1984, p 446. 21. Silverman S, Gorsky M, Lozada-Nur F: A piespective follow- 10. Epstein JB, Pearsall NN. Truelove EL: Oral candidiasis: effects up study of 570 patients with oral lichen planus: persistance, of antifungal therapy upon clinical signs, symptoms, salivary remission and malignant association. Oral Surg Oral Med Oral antibody and mucosal adherence of . Oral Surg Palhol 1985:60:30-34. Oral Med Oral Parhol 1981:51:32-36. 22. Eisenberg E, KrutchkoffD: Letter to the ediior Ond Surg Oral 11. Silvennan S, et al: Oral findings in people with or at high risk Med Oral Palhol 1986:61:582. for AIDS: a sludy of 375 homosexual males. / Am Dem Assire 23. Abrams AM. Melrose RJ, Hcwell FV: Necrotizing sialometa- 1986;li2:187-193. plasia. A disease simulating malignancy. Cancer 1973;32:130- 12. Antoon JW, Miller RL: Aphthous ulcers -- a review of the 135. D literature on etiology, pathogenesis. diagnosis and treatment. J Am Dem Assoc 1980:101:803-808.

Quintessence Symposium in Esthetic Dentistry March 30-31, 1990, Madrid, Spain ESTHETICS IN THE 90s

speakers Ronaid E. Goldstein, DDS, USA Richard J. Simonsen, DDS, USA Program Chair and Coordinator: Jaime A. Gil, DDS, Albia Clínica Dentai Edifioio Aihia i-13°, S. Vicente 8 48001 Bilbao, Spain

Quintessence International V/nhirrjft Ç>-\. Ntjmüer 2/1990 151