Ethiopatogenic Hypotheses in Lichen Planus

Lichen planus is a mucocutaneous inflammatory dermatosis characterized by a papular rash; the disease is self-limited, has several clinical subtypes and follows a chronic or subacute clinical course. This article presents some etiological hypotheses: stress, genetic predisposition, systemic diseases, viral infections, materials used in dentistry. Also, medicines or contact allergens can cause lichenoid reactions, which are the main differential diagnosis. Autoimmune hypothesis can be supported by the association with other autoimmune diseases, such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosus, myasthenia gravis. This disease seems to be mediated through an antigenic mechanism of cytotoxic T lymphocyte activation, and production of proinflammatory cytokines, cascade of events that causes apoptosis of basal keratinocytes. A good understanding of the pathogenesis, clinical presentation and early diagnosis of lichen planus is critical in determining the appropriate therapeutic management. This present article aims to present and discuss the various etiopathogenetic concepts of lichen planus.