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SINGLE ULCERS
The document discusses various types of single ulcers that can occur in the oral mucosa. The most common type is a traumatic ulcer, which is usually caused by mechanical, chemical, thermal or self-inflicted trauma. Traumatic ulcers present as tender lesions that vary in size and shape and can persist for weeks. Differential diagnoses include carcinomatous and recurrent aphthous ulcers. Other single ulcers discussed include eosinophilic ulcers of the tongue, histoplasmosis, blastomycosis, mucormycosis, and syphilitic ulcers. Diagnosis involves biopsy and cultures. Treatment depends on the specific condition but may include topical steroids, antifungal agents
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SINGLE ULCERS
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- 3. SINGLE ULCERS YA SM I N M O I D I N 2 0 0 8 B ATC H A L A Z H A R D E N TA L C O L L E G E THODUPUZHA
- 4. INTRODUCTION The mostcommon cause of single ulcers on the oral mucosa is trauma
- 5. TYPES Traumatic ulcer Eosinophilic ulcer of tongue Histoplasmosis Blastomycosis Mucormycosis Syphilitic ulcer
- 6. TRAUMATIC ULCER Mostcommon oral mucosal ulcer Types of trauma Mechanical Chemical Thermal Radiation Self-inflicted Iatrogenic
- 7. CLINICAL FEATURES Tenderness or pain in the area of lesion Sites : tongue, lips, mucobuccal fold, gingiva and palate Persist for few days or lasts for weeks Vary in size and shape Borders are raised and reddish Bases are yellowish necrotic surface Frequently, a painful regional lymphadenitis occur as a result of contamination of ulcer by oral flora
- 8. DIFFERENTIAL DIAGNOSIS Carcinomatous ulcer Recurrent aphthous ulcerations MANAGEMENT Removal of traumatic factor Most traumatic ulcer become painless within 3 to 4 days After the injury producing agent has been eliminated, most heal with 10 days
- 9. Less seriousvarieties, treat with triamicinolone acetonide with emolient before bed time and after meals usually relieves the pain and hastens the healing Orabase protects the denuded CT from continued contamination by oral liquids and cortisone component tend to arrest the inflammatory cycle Persistent ulcers are surgically excised
- 10. EOSINOPHILIC ULCER OFTONGUE ETIOLOGYAND PATHOGENESIS Inflicting crush injury on tongue-most common site Deep and penetrating
- 11. RIGA-FEDE DISEASE Lesion seen on ventral tongue Infants Cause- tongue rasping against newly erupted primary incisors
- 12. CLINICAL MANIFESTATIONS Bimodal age distribution 1st group- in 1st 2 years of life-lesion associated with erupting primary dentition 2nd group – adults – 5th and 6th decades
- 13. ORAL FINDINGS Children – anterior ventral or dorsal tongue associated with erupting mandibular or maxillary incisors Adults – posterior and lateral aspect of tongue Ulcer – not painful & persist for months History of trauma
- 14. Appear cleanlypunched out, with surrounding erythema & whiteness Size – 0.5cm Surrounding tissue is indurated 5 % - multifocal and recurrences are not uncommon In some cases , lesions are ulcerated , mushroom- shaped , polypoid mass on the lateral tongue
- 15. DIFFERENTIAL DIAGNOSIS Recurrent aphthous ulcers Squamous cell carcinoma T-cell lymphomas
- 16. LABORATORY FINDINGS Biopsy is needed to make diagnosis MANAGEMENT Intralesional steroid injections Wound debridement Use of nightguard on lower incisor – reduce nighttime trauma
- 17. HISTOPLASMOSIS ETIOLOGY ANDPATHOGENESIS Caused by fungus Histoplasma capsulatum Infection results from inhaling dust contaminated with droppings, from infected birds or bats
- 18. CLINICAL MANIFESTATIONS The expression of the disease depends on the quantity of spores inhaled, the immune status of the host and the strains of the organism Asymptomatic and mild flulike illness for 1 to 2 weeks The inhaled spores are ingested by macrophages within 24 to 48 hours and specific T lymphocyte immunity develops in 2 to 3 weeks
- 19. TYPES Acutehistoplasmosis Self –limited pulmonary infection Acute symptoms are fever, headache, myalgia, nonproductive cough, anorexia Patient is ill for 2 weeks Calcification of hilar lymph nodes
- 20. Chronic histoplasmosis Primarily affects the lungs Affects older, emphysematous, white men or immunosuppressed patients Patients typically exhibit cough, weight loss, fever, dyspnoea, chest pain, hemoptysis, weakness and fatigue
- 21. Disseminated histoplasmosis Less common It is characterized by progressive spread of the infection to extrapulmonary sites It occurs in older, debilitated, immunosuppressed patients and patients with AIDS Tissues that affect include: spleen , adrenal glands, liver, lymph nodes, GIT, CNS, kidneys and oral mucosa
- 22. Common sites– tongue, palate, buccal mucosa It appears as a solitary, painful ulceration of several weeks duration Some lesions appear erythematous or white with an irregular surface Ulcerated lesions have firm, rolled margins
- 23. ORAL FINDINGS Oral lesion begin as an area of erythema , becomes papule & forms Painful , granulomatous –appearing ulcer Cervical lymph nodes are enlarged and firm Patients with HIV has an ulcer with border, seen on gingiva , palate , tongue indurated
- 24. DIFFERENTIAL DIAGNOSIS Traumatic ulcerative granuloma Squamous cell carcinoma Lymphoma
- 25. LABORATORY FINDINGS Biopsy – stained with PAS OR methanamine silver – reveal presence of fungi MANAGEMENT Immunocompromised patients -IV amphotericin B AIDS – itraconazole & maintenance therapy Immunocompetent – itraconazole or ketoconazole for 6 to 12 months
- 26. BLASTOMYCOSIS ETIOLOGY ANDPATHOGENESIS Caused by Blastomyces dermatitidis Infection results from inhalation and is found in agricultural and construction workers
- 27. CLINICAL MANIFESTATIONS It is acquired by inhalation of spores , particularly after rain The spores reach the alveoli of lungs, where they begin to grow as yeasts The infection is halted and contained in the lungs The sites of dissemination include skin, bone, prostate, meninges, oropharyngeal mucosa and abdominal organs
- 28. Types Acuteblastomycosis Resembles pneumonia, characterised by high fever, chest pain, malaise, night sweats and productive cough with mucopurulent sputum Rarely, the infection may precipitate life-threatening adult respiratory distress syndrome
- 29. Chronic blastomycosis More common Characterisezd by low grade fever, night sweats, weight loss and productive cough Chest radiographs shows diffuse infiltrates or pulmonary or hilar masses Calcification is not typically present Lesion begins as erythematous nodules that enlarge , becoming verrucous or ulcerated
- 30. ORAL FINDINGS It may result from either extrapulmonary dissemination or local inoculation with the organism Lesions have an irregular, erythematous or white intact surface Appear as ulcerations with irregular rolled borders and varying degree of pain
- 31. LABORATORY FINDINGS Diagnosis by biopsy and culture demonstrates presence of multinucleated yeast cells with dark cytoplasm & colorless cell walls with characteristic of B.dematitidis TREATMENT Disseminated or progressive – ketoconazole , fluconazole , itraconazole for mild to moderate Amphotericin B – sever disease
- 32. MUCORMYCOSIS ZYGOMYCOSIS/ PHYCOMYCOSIS ETIOLOGY AND PATHOGENESIS Caused by saprophytic fungi Occurs in soil or as a mold on decaying food Fungus is nonpathogenic
- 33. CLINICAL MANIFESTATIONS Rhinocerebral zygomycosis Patient experiences nasal obstruction, bloody nasal discharge, facial pain or headache, facial swelling or cellulitis and visual disturbances with concurrent proptosis With progression of disease into the cranial vault, blindness, lethargy and seizures may develop followed by death
- 34. If maxillarysinus is involved, the initial presentation may seen as intraoral swelling of maxillary alveolar process & palate If the condition is untreated, palatal ulceration, appears as black and necrotic and massive destruction
- 35. ORAL FINDINGS Ulceration of the palate Lesion is large & deep, causing denudation of underlying bone Other sites- gingiva, lip , alveolar ridge Initial manifestation confused with dental pain or bacterial maxillary sinusitis caused by maxillary sinus invasion of
- 36. LABORATORY FINDINGS Biopsy is split into culture & histopathology Histopathologic findings- necrosis & nonseptate hyphae Necrosis & occlusion of vessels is present
- 37. MANAGEMENT Combinationof surgical debridement of the infected area Amphotericin B for 3 months Observed for renal toxicity Posaconazole , antifungal agent is used for patients unable to tolerate toxicity of amphotericin
- 38. SYPHILITIC ULCER Syphilisis a sexually transmitted disease , caused by Treponema pallidum CHANCRE Seen in genital region Other sites- lips , tongue, palate, tonsillar regions In initial stage- papule seen which subsequently erodes Typical syphilitic ulcer is punched-out, non tender, indurated and associated with yellowish discharge
- 39. Associated nodesare firm & non tender on palpation Self-limiting & last for 2 weeks Heal with minimum scar formation MUCOUS PATCHES Appears after a latency period of 6 months Patient complains of fever, headache, bodyache & sore throat Cutaneous maculopapular lymphadenopathy rashes associated with
- 40. Oral lesionsare characterised by appearance of oval red macules (palate) or papules (buccal mucosa & commissures) and mucous patches Mucous patches are seen as raised erosive areas covered by a grayish white pseudomembraneous and surrpunded by an erythematous halo Measure about 1 cm in diameter Small lesions join together to give rise to snail track ulcers severe & generalised form – lues maligna, also termed ulceronodular disease
- 41. Oral mucosareveals shallow crater like ulcers Common sites – palate , buccal mucosa, tongue, lower lip, and gingiva GUMMA It is a highly destructive lesion It occurs 8 to 10 years after initial infection Common sites – hard palate , tongue
- 42. MANAGEMENT Parenteralpencillin G Allergic to pencillin, treated with doxycycline , tetracycline , erythromycin