A brief insight on the etiopathogenesis of oral lichen planus

Abstract

Oral Lichen Planus (OLP) is a relatively common, systemic, immune based disease. It usually, involves the oral mucosa, but other sites like the skin, genital mucosa, and scalp are also affected. In this auto-cytotoxic muco-cutaneous disease, the T lymphocytes trigger apoptosis of epithelial cells leading to chronic inflammation. OLP is mediated by both antigen specific and nonspecific pathways. Antigen presentation through basal keratinocytes and antigen-specific keratinocyte destruction by CD8+ cytotoxic T-cells are within the specific pathway spectrum. Whilst the nonspecific methods involve mast cell degeneration; leading to granular release and matrix metalloproteinase (MMP) activation. The process ultimately results in clustering of T cells in the upper layer of lamina propria, basal lamina disruption, T-cell inflow within the epithelium, along with apoptotic death of keratinocytes. The normal oral mucosa may be an immune privileged site and breach of the immune barrier could result in OLP and possibly other autoimmune oral mucosal diseases owing to deficient antigen-specific TGF-β1-mediated immunosuppression. However, many among these immuo pathologic mechanisms are still shroud in mystery.