Immunopathogenesis of oral lichen planus and recurrent aphthous stomatitis.
Oral mucosal bullous/desquamative/ulcerative diseases involve immunopathological mechanisms that account for loss of adhesion between contiguous keratinocytes or to structures within the basal lamina. Some are antibody mediated, in which specific adhesion molecules of the desmosome, hemidesmosome, and basement membrane become antigenic targets. Oral lichen planus and recurrent apthous ulcers, although manifesting disparate clinical appearances and natural history, share immunopathological features that involve T cell-mediated immunity. Although the antigens, haptens, or autoantigens are not usually apparent, current research poses the hypothesis that both of these common oral mucosal diseases are a delayed-type hypersensitivity or cell-mediated response to an antigenic stimulus residing within the epithelium. This article reviews the research evidence for this hypothesis.
Eversole
L R
LR
UCLA School of Dentistry, Los Angeles, CA 90095, USA.
D000906:Antibodies / Q000276:immunology; D000941:Antigens / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D001485:Basement Membrane / Q000276:immunology / Q000473:pathology; D001768:Blister / Q000276:immunology; D002448:Cell Adhesion / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000276:immunology; D018865:Dental Research; D003896:Desmosomes / Q000276:immunology; D004848:Epithelium / Q000276:immunology; D006241:Haptens / Q000276:immunology; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007111:Immunity, Cellular / Q000276:immunology; D015603:Keratinocytes / Q000276:immunology / Q000473:pathology; D017676:Lichen Planus, Oral / Q000276:immunology*; D019226:Oral Ulcer / Q000276:immunology; D012008:Recurrence; D013281:Stomatitis, Aphthous / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D000906:Antibodies; D000941:Antigens; D001324:Autoantigens; D015815:Cell Adhesion Molecules; D006241:Haptens