Oral Lichen Planus

Same text but with different contextual interpretation.

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Sugarman PB, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002;13:350-365.	Lodi G, et al. Current controversies in oral lichen planus: Report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;1:40-51.	Roopashree MR, et al. Pathogenesis of oral lichen planus – a review. J Oral Pathol Med 2010;39:729-734.
The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. The role of autoimmunity in disease pathogenesis is supported by many autoimmune features of OLP, including disease chronicity, adult onset, female predilection, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in OLP patients, and the presence of auto-cytotoxic T-cell clones in lichen planus lesions (Sugerman et al., 1992, 1993, 2000b). We suggest that keratinocytes express lichen planus antigen but only at the lesion site, i.e., the clinical distribution of lichen planus lesions is determined by the distribution of the lichen planus antigen. Hence, an early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Subsequently, intra-epithelial CD8+ cytotoxic T-cells recognize the lichen planus antigen associated with MHC class I on lesional keratinocytes and trigger keratinocyte apoptosis.	LP has a well-defined clinical distribution and there is a clear demarcation between lesional and nonlesional tissue. A possible explanation for this pattern of presentation is that keratinocytes express the LP antigen, but only at the lesion site. In other words, the clinical distribution of lichen planus is determined by the distribution of the antigen. Hence, an early event in LP lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent. Following altered keratinocyte antigen expression, antigen-specific CD41 and CD81 T cells may be either (1) on routine surveillance in the epithelium and encounter the keratinocyte antigen by chance (‘‘chance encounter’’ hypothesis) or (2) attracted to the epithelium by keratinocyte-derived chemokines (‘‘directed migration’’ hypothesis). The ‘‘chance encounter’’ hypothesis is supported by findings of CD81 T cells in normal human epidermis141,142 and basal cell degeneration in the absence of a dense inflammatory infiltrate in LP lesions.143 Conversely, the ‘‘directed migration’’ hypothesis is supported by findings of constitutive chemokine receptor expression by naı¨ve T cells144 and a dermal T-cell infiltrate prior to the appearance of intraepithelial lymphocytes and epithelial damage in LP lesions.145 In this context, keratinocyte antigen expression6chemokine production are primary events in oral LP lesion formation, followed by keratinocyte apoptosis triggered by antigen-specific CD81 cytotoxic T cells (Fig 1).	The lichen planus antigen is unknown, although the antigen may be a self-peptide, thus defining lichen planus as a true autoimmune disease. An early event in lichen planus lesion formation may be keratinocyte antigen expression or unmasking at the future lesion site induced by systemic drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), bacterial or viral infection, or an unidentified agent (3).