Oral Ulcerative Disease TRAUMATIC ULCERS Because of the constam motion of the masticatory mucosa over the teeth and the introduction of hard objects into the oral cavity,traumatic ulcers are frequent.Generally.traumatic ulcers are the consequence of mechanical injury resulting from inadvertent biting of the mucosa.from imritation caused by fractured amalgam restorations of prostheses,or from sharp objects introduced imo the mouth.Ulcerations may also occur as a consequence of thermal or chemical burns. Sympcomatically,the most outstanding feature of traumatie ukers is pain.Discomfort usually follows 24 to 48 hour after insult to the tissue.The patient can often identify a specifie event or object associmed with the trauma although,in the case of faulty restoeations.a specific event may be absent.The clinical appearance of traumatic uleers is similar to that of aphthous ukers.The ulcer is usually ovoid and has a yellowish-white necrotic center surrounded by a broad erythematous border.In the case of mechanical trauma.the lesion usually conforms in area and linearity to the source of the traumn.Hence.any ulerathion that appears to be linear is usually the result of trauma. The diagnosis of traumatie ulcer is based c the history or on the identification of a specific source of irritation.Once the souree of imitarion is eliminated.traumatic ukers heal in approximately 10 to 14days.Treatment of traumatie uleers is aimed at maintaining cleanliness by frequent rinsing with saline or hydrogen peroxide in water.palliation with anesthetie ointments and elimination of the source of irritation APHTHOUS STOMATITIS Recurrem aphthous ulcerations.frequently referred to as canker sores,are among the most common lesions of the mouth.Their recurrent patter and associated discomfort make them extremely bothersome and,at times,debilitating to patients.Aphthous stomatitis may occur as occasional single ulcerations or may be manifested as a never-kending continuum of severe ulcerative lessons. The prevalence of aphthous stomatitis depends largely on the population studied.Although an overall prevalence of 20%has been reported.individuais in middle and upper middle class economic groups appear to be most frequently affected.An incidence of aphthous stomatitis of 66%was noted among professional students.as compared with only%in an indigent population. There appears to be a slight predilection for females.Seasonal peaks have also been noted in wimer and spring. The etiology of aphthous stomatitis has been scrutinized for some time and as yet is not completely resolved.It seems that a specific cause for the condition is idemifiable in about 30%of cases.A suspected infectious cause was originally attributed t0 herpes simplex virus (HSV). However.mumerous atterpts to isolate HSV from aphthous ulcerations have failed to demonstrate its presence.In addition,no anti-HSV antibodies could be demonstrated in patients with aphthous stommtics.Furthermore.the relatively high frequency of HSV infection in parients of low cconomic status is incompatible with the demographic pattern of the discase. The observation that exacerbations of aphthos stomatitis in women may correlate with the menstrual cyele has led to speculation that there may be a hormonal bases for the disease. However.the nearly equ distributhion of aphthous stomatitis inmen and women argues against this possibelit. 16
Oral Ulcerative Disease TRAUMATIC ULCERS Because of the constant motion of the masticatory mucosa over the teeth and the introduction of hard objects into the oral cavity, traumatic ulcers are frequent. Generally, traumatic ulcers are the consequence of mechanical injury resulting from inadvertent biting of the mucosa. from irritation caused by fractured amalgam restorations ofprostheses, or front sharp objects introduced into the mouth. Ulcerations may also occur as a consequence ofthermal or chemical burns. Symptomatically, the most outstanding feature of traumatic ulcers is pain. Discomfort usually follows 24 to 48 hour after insult to the tissue. The patient can often identify a specific event or object associated with the trauma although, in the case of faulty restorations, a specific etent may be absent. The clinical appearance of traumatic ulcers is similar to that of aphthous ulcers. The ulcer is usually ovoid and has a yellowish-white necrotic center surrounded by a broad ery4hernatorrs border. In the case of mechanical trauma, the lesion usually conforms in area and linearity to the source of the trauma. Hence, any ulcerathion that appears to be linear is usually the result of trauma. The diagnosis of traumatic ulcer is based on the history or on the identification of a specific source of irritation. Once the source of initation is eliminated. traumatic ulcers heal in approximately 10 to l4days. Treatment of traumatic ulcers is aimed at maintaining cleanliness by frequent rinsing with saline or hydrogen peroxide in wateq palliation with anesthetic ointments and elimination of the source of irritation. APHTIIOUS STOMATITIS Recurrent aphthous ulcerations, frequently referred to as canker sores, are among the most common lesions of the mouth. Their recurrent pattern and associated discomfort make them extremely bothersome and. at times, debilitating to patients. Aphthous stomatitis may occur as occasional single ulcerations or may be rnanifested as a never-kending continuum of severe ulcerative lesions. The prevalence of aphthoustomatitis depends iargely on the population studied. Although an overall prevalence of 20o/o has been reported, individuals in middle and upper middle class economic groups appear to be most frequently affected. An incidence of aphthous stomatitis of 66Yowas noted among professional students, as compared with only 5Yoin an indigent population. There appears to be a slight predilection for lbmales. Seasonal peaks have also been noted in winter and spring. The etiology of aphthous stomatitis has been scrutinized for some time and as yet is not completely resolved. It seems that a specific cause for the condition is identifiable in about 30'A of cases. A suspected infectious cause was originally attributed to herpes simplex virus (HSV). However, numerous attempts to isolate HSV from aphthous ulcerations have failed to detnonstrate its presence. In addition, no anti-HSV antibodies could be dernonstrated in patients with aphthous stomatits. Fufthermore, the relatively high frequency of HSV infection in patients of low economic status is incompatible with the demographic pattern of the disease. The observation that exacerbations of aphthous stomatitis in women may correlate with the menstrual cycle has led to speculation that there may be a hormonal bases for the disease. Howeveq the nearly equal distributhion of aphl.hous stomatitis in men and women argues against this oossibiliw. i96
Most likely.multiple factors can initiste aphthoxus stomatitis.A number of workers have suggested and emorional cause for the disease.The finding of a comelation berween stress and severity of the disease.as well as its demographic distrinuticn.suppors a psychogenic cause. Animal srudies have demonstraed aphthous stomalitis-like lesions following artificially induced stress. A variety of other cooditions have also been identified as causative of true sphthous or aphthous-like lesions.These include deficienis of vitarin B12.folate,zinc,and imn.cyelic neropenia hurtan immunodeficiency virs(HIV)infection,ngrarulocytoses,Croln's disease, and food allergies. The pmthophysiologic basis of aphthous stomatitis seems to be clarer.Evidenxce naw suggests an auntoimmune mechanism for the tissue destruction noted in apathous lesions.The histologic appearance of aphthous lesions is one of norspecific uiceration preceded by a lymphocytic infinrate.The latter isestivfa sell-mediated immune response. In vitro measurements of cell-mediated immunity(CMD,using lymphocytes from patients with aphthous somatitis,also support an antaimmune mechanism fo the pathophysiology of the discase. Lymphncyte proliferatinriblastogenasis)in respanse to an antigen correlstes with cell-mediated immumnity Lehner aliowed peripheral blood lymphocytes from patients with active aphthous stomatitis to react with allogeneic fetal tissue hamogenates and measured the amount of lympbocytic proliferalion.Lymphocytes from patients with no history of sphthous stomaritis or patienls in remission. A roie for CMI in aphthous stomatitis is alsa suggested by the ability of lymphocytes from parients with aphthous stomaitis to mediaie the cytalysis of oral mucosal cell.Dolby found that ymphocytes from patients withcive aphthous lesions were ahle to lyse gingival tang cells. 5 This work has boen confirmed by Togers and collengues,who found thal whereas lymphocytes from paents who were free of dissase did not effectively lyse oral epithelial tanget cells. lymphocytes from patents with those of Lefrer,sugpest that an immune mechanism is peohobly active in the initiation of the destructive phose of aphthous stamatitis. 5 Clinically.aphthaus stomatitis is characteriged by the recun of oral ulcerntiors.Tbe f ulcer stage is usually preceded by a 2.to 3-day pericd in which the patient nates a vague feeling of discomfort.The only clinical finding at this time may be an area uf erythema.This is sou followed by the appearance of a deep ulcerative lesion.The lesion is usually ovoid,has seme depth,a yellowish-white recrotic base.and a surroumding zone of erythemna in a ring Rarely do ksions exced I cm in diameter.Most comnmanty,aphtho.s esions are fourd on the buccal,labial. f or alvealar muccas or on the ventral surface of the tongue.It is uncommon for nphthous stomatitis to irvoive heavily kermtinized areas such as the hard palate or attached gingive.The mijor symptom associsted with aphthous stomatitis is pain of such severity that eating and speaking patterns may be significantly altered.Because it is relatively common for patients to develop edematous anlargement of the tissue surrounding the ulcer,trauma to the lesion may accur inadverently.Cienerally,lksions last a maximum of 7 to 14 days,although they are clinically most e painfui during the early phases of the disease. The diagrosis of aphthous stamstitis is hased on the clinical appearance and course o the lesion and recurrent histey.It is sually difficul to establish a specific stressful incident related to the appeararce of lesions,although there may be some correlation with the menstrual cycle. 197
t 1 j 1 S f n IVIost likely. muttiple factors can initiate aphthous stomatitis' A number of workers have sgggested and emotional cause for the ciis'ease. The finding of a correlation betlveen stress and severity of the disease, as well as its demographic distribution, supports a psychogenic cause' Animal studies have demonstrated aphthoLrs stomatitis-like lesions following ar-tificially induced SITESS. A variety of other conditions have also been identified as causative of true aphthous or aphthous-like lesions. These include deficielcies of vitamin 812, folate' zinc' and iron' cyclic neutropenia, human immunodeficiency virus(HlV) infection, agranulocytoses' Crohn's disease' and food allergies. The pathophysiologic basis of aphthous stomatitis seems to be clearer' Evidence now suggests an autolmmune mechanism for the tissue destruction noted in aphthous lesions' The histologic appearance of aphthous lesiotrs is one of nonspecific ulceration preceded by a lymphocytic infiltrate. The latter is suggestive of a sell-mediated immune response' In vitro measurements of cell-mediated immunity(cMl), using lymphocytes from patients with aphthous stomatitis, also support an antoimmune mechanism for the pathophysiology of the disease. Lymphocyteproliferation(blastogenesis)inresponsetoanantigencorrelateswith cell-mediated immunity. Lehner allowed peripheral blood lymphocytes from patients with active aphthous stomatitis to react with allogeneir: fetal tissue homogenates and measured the amount of lymphocytic proliferation. Lymphocytes from patients with no history of aphthous stomatitis or patients in remission. A role for cMI in aphthous stomatitirs is also suggested by the ability of lymphocytes from patients with aphthous stomatitis to mediatie the cytolysis of oral mucosal cells' Dolby found that lymphocl.tes from patients with active aphthous lesions rvere able to lyse gingival target cells' This work has been confirmed by Togers and colleagues, who found that, whereas lymphocytes from patents who were free of disease did not effectively lyse oral epithelial target cells' lymphocyes from patients with those of [,efner, suggest that an immune mechanism is probably active in the initiation of the destructive phase of aphthous stomatitis' Clinically, aphthous stomatitis is characterized by the recurrence ol oral ulcerations' The ulcer stage is usually preceded by a2-to 3-day period in which the patient notes a vague feeling of discomfort. The only clinical finding at this time may be an area of erythema' This is soon followed by the appearance of a deep ulcerative lesion. The lesion is usually ovoid' has some depth, a yetlowish-white necrotic base, and a surrounding zone of erythema in a ring' Rarely do lesions exceed 1 cm in diameter. Most conrmonly, aphthous lesions are found on the buccal' labial' or alveolar mucoas or on the ventral surface of the tongue. It is uncommon for aphthous stomatitis to involve heavily keratinized areas such as the hard palate or attached gingive. The major symptom associated with aphthous stomatitis is pain of such severity that eating and speaking patterns may be significantly altered. Because it is relatively common for patients to develop edematous enlargement of the tissue surrounding the ulcer, trauma to the lesion may occur inadverlently. Generally, lesions last a malimum of 7 to 14 days, although they are clinically most painful during the early phases of the diseeLse' The diagnosis of aphthoustomatitis is based on the clinical appearance and course of the lesion and recurrent history. It is usually difficult to establish a specific stressful incident related to the appearance of lesions, although there may be some correlation with the menstrual cycle' )I f I. S v ). i l t97
Aphbous lesions must be differentiated from traumatic es.acute herpetic gingivitis allergy. and erythema multiforme as well as ulreratinns csused by systemic disease or conditions descrihed above. The differentistion hetween aphthous lesions and thruma is hased on the history and the relatinnship of the sion ta a source of irritation.Esserially,there is no clinical or histologic difference between aphthous and traumatic ulerations,although any linearity in ucleratioh suggests a traumalie cause Acute HSV infction may present as ulcerntive lesians after vesices have ruptured.This is a concurrent phenomenca,usually involving a number of areas in crop-like fashion.Patients with HSV infection may have experienced constitutional symptoms.These lesions tend to occur in a younger,nonsocioecnomically restricted age group with simultaneous gingival invalvemert.Allengic lesions tend to be more diffuse than aphthous lesions and although erythematous are us.ally nonulcerative.Erythema multiferme may present with sume ulcerntion, especially afer rupture of bullae.However.these lesions are nonrecurrent and are more diffuse than aphthous lesions.It may be difficult to differentiate ulcerations caused by systemie diseases from aphthous stomatitis.Tne major difference lies in the lack of recurrence and delayed healing time.Any uleer that fails to heal in 14 days should undergo biapsy. Aithough aphthous uleers heal spontanecusly 10 to 14 days after onset.they are extremety painful.The goal of therapy should be to reduce infammation,minimize pain and discomfort in affected areas,and speed healing.Currently,no medicatians meet all three goais.A wide runge of tremments have been suggested,including amibiotics.immunomodulators,antimicrobial mouthrirses.and dietary supplements.However,topical seroids remain the mainstay for the treatment of aphthous stomatitis in which a spocifie etiology has not been identified.These are dispensed either as an ointment (triameinolene acetonide in Orabase)or as n cream (triamcinolone ercam)It has been suggesied that the aintment form is nnt as effective as the cream,because the certicoseroid may be inhibited by the bulk of the ointment.If the cream is used,Orahase ointment can be placed over it ti help maintain it in position.IN peesctibing triaminolone.i is impcant to infom the patient to dry the ulcer befoe applicarion and then to use the drug tid or qid.Some systemic disass such as hypertensicn.proclude the use of corticosteroids.Corticsteroids may also be ndministered by inicction of small amounts of the drug (0.1ml)into the lesion.The dissdvantages of this form of tremtment are its relianee on professicnal application and the limitation in casage. 98
Aphthous lesions must be differentiated from traumatic ulcers, acute herpetic gingivitis, allergy, and ery.thema multiforme as well as ulcerations caused by systemic disease or conditions described above. The differentiation between aphthous lesions and thruma is based on the history and the relationship of the lesion to a source of irritation. Essentially, there is no clinical or histologic clifference between aphthous ald traumatic ulcerations, although any linearitv in ucleratioh suggests atraumatic cause. Acute HSV infection may present as ulcerative lesions after Vesicles have ruptured. This is a concurrent phenomenon, usually involving a number of areas in crop-like fashion. patients with HSV infection may have experienced constitutional symptoms. These lesions tend to occur in a younget nonsocioeconomically restricted age group with simultaneous gingival involvement. Allergic lesions tend to be rnore diffuse than aphthous lesions and aithough erythematous are usually nonulcerative. Erythema multiforme may present with some ulceration, especially after rupture of bullae. However, these lesions are nonrecurrent and are more diffuse than aphthous lesions. It may be difficult to differentiate ulcerations caused by systemic diseases from aphthous stomatitis. The major difference lies in the lack of recurrence and delayed healing time. Any ulcer that fails to heal in 14 days should undergo biopsy' Although aphthous ulcers heal spontaneously 10 to i4 days after onset, they are extremely painful. The goal of therapy should be to reduce inflamrnation, minimize pain and discomforl in affected areas, and speed healing. Cunently, no medications meet all three goals' A wide range of treatments have been suggested, including antibiotics, immunomodulators, antimicrobial mouthrinses, and dietary supplements. However, topical steroids remain the mainstay for the treatnrenr of aphthous stomatitis in which a spec;ific etiology has not been identified. These are dispensed either as an ointment (triamcinolone acetonide in Orabase) or as a cream (triamcinolone cream). It has been suggesred that the ointment form is not as effective as the cream' because the corticosteroid may be inhibited by the bulk of the ointment. If the cream is used, Orabase ointment can be placed over it ti help maintain it in position. IN prescribing triamcinolone, it is impotant to inform the patient to dry the ulcer befor appliczrtion and then to use the drug tid or qid- Some systemic diseases, such as hypertension, preclude the use of corticosteroids. Corticosteroids may also be administered by injection of small amounts of the drug (0.lml) into the lesion' The disadvantages of this form of treatment are its reliance on professional application and the limitation in dosage. 198