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Tahani Abualteen
Oral Ulceration
Definition: Ulcer = localized defect in the surface epithelium exposing the underlying connective tissue base leading to inflammation Most common lesion of the oral mucosa May be a manifestation of many disease entities (local and general disorders) Erosion = superficial ulcer (partial loss of epithelial thickness not exposing the connective tissue base) Causes of oral ulceration: Infective (viral, bacterial, fungal) Traumatic (mechanical, chemical, thermal, factitious injury, radiation, eosinophilic ulcer "traumatic granuloma") Idiopathic (recurrent aphthous stomatitis "major, minor, herpetiform") Neoplastic (SCC, other malignant neoplasms) Associated with systemic diseases (GIT diseases, hematological diseases, Behcets disease, HIV infection) Associated with dermatologic diseases (lichen planus, chronic discoid lupus erythematosus, vesiculobullous diseases) ** All these should be kept in mind as differential diagnoses for ulcers Traumatic Ulceration: 1- Mechanical Ulceration: o Three criteria for diagnosis: Define a cause of trauma (e.g. sharp cusps, biting, outstanding teeth, ill-fitting appliances) Cause must fit size, shape and location of ulcer On removal of the cause, ulcer must show signs of healing within 10 days o Mechanical ulcers don't usually present a problem in clinical diagnosis o Problems in diagnosis arise with chronic traumatic ulcers o Chronic Traumatic Ulcers Present for several weeks Present as deep crater-like lesions with rolled everted margins and Induration on palpation (due to surrounding fibrosis) Differentiation of chronic traumatic ulcers from a neoplastic ulcer may be difficult o When is biopsy indicated? If we remove the cause and the presumed chronic traumatic ulcer does NOT show signs of healing within a period of 10-14 days
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o Etiology of RAS: Most likely immune mediated (there is increasing evidence that damaging immune responses are involved) A number of Co factors (local and general factors) may play a contributory role in a proportion of cases Pathogenesis of RAS: Epithelial destruction is most likely the result of T-cell mediated cytotoxicity Epithelial antigen(s) which are responsible for triggering the immune response leading to the Cytotoxic damage remain unknown However, it is suggested that immune mediated damage may be due to cross-reactivity between streptococcal protein antigens and epithelial plasma membrane proteins ** Cross-reactivity between bacterial and epithelial heat shock proteins (HSP) has been demonstrated ** In susceptible individuals, the host's immune response to streptococcal antigens may also damage the oral epithelium T cell mediated cytotoxicity: CD4 + T cells predominate in the pre-ulcerative phase CD8+ Cytotoxic T cells predominate ulcerative phase CD4 + T cells predominate in the healing phase Hereditary predisposition 45% of patients have family history Mode and pattern of inheritance hasn't been established Trauma May precipitate and influence the site of some ulcers Doesn't play an essential role in the etiology of RAS Emotional stress Precipitating factor Unlikely to be the direct cause of ulceration Stress may be associated with pernicious habits, such as: check biting, which may precipitate and influence the pattern of ulceration
Associated factors: -
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o Histopathology of RAS: In the pre-ulcerative stage, there is infiltration of the lamina propria by lymphocytes Small number of lymphocytes also infiltrate the epithelium As the ulcerative stage approaches, there's increased infiltration of the tissues by lymphocytes (especially the epithelium) associated with damage to epithelial cells leading eventually to their death and the formation of an ulcer In the healing phase, the number of lymphocytes decreases ** The fluctuations in lymphocytic infiltration throughout the ulcerative cycle suggests that immune mechanisms are involved in the pathogenesis of RAS ** As the ulcerative phase begins, the population of T lymphocytes capable of inducing Cytotoxic effects (CD8+) in epithelial cells increases within the epithelial infiltrate ** Current evidence suggests that RAS is due to immune-mediated Cytotoxic damage to oral epithelial cells through the activity of T lymphocytes o Diagnosis: Clinical features (site, number, history of recurrence, family history) Histopathological features (non-specific to RAS)
Behcet's disease (syndrome): o Characterized by RAS and at least 2 of the following: Genital ulcers Eye lesions Skin lesions Positive Pathergy test (rapid acute inflammation of skin in response to minor trauma) ** Cutaneous Pathergy test = development of sterile papule of the skin 1 day after injection of saline
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