Abstract
Oral mucosal inflammation evolves in response to microbial pathogens and non-infectious antigens which activate humoral and cell-mediated immunologic processes. Most of these disease processes invoke a leukocyte response culminating in cellular infiltration of the submucosa and, to some degree, transmigration into the epithelium itself. Calprotectin, a leukocyte-derived dimeric protein complex that has potent antibacterial and antifungal effects, has recently been identified in skin and mucosal keratinocytes implying that epithelium may biochemically contribute to the overall mechanism of host defense. In this study, the upregulation of calprotectin as assessed immunohistochemically is pursued for oral diseases of immunopathologic, fungal and viral origin. In lichen planus, candidiasis, herpes virus stomatitis, and oral hairy leukoplakia, calprotectin was found to be expressed to a significantly higher level than in normal control mucosal samples.
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