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AT-A-GLANCE
Lichen planus is an idiopathic T cell–mediated process without a clear autoantigen.
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The worldwide prevalence of lichen planus is approximately 1%.
The lesions are well-marginated, flat-topped, red-violet polygonal papules.
The distribution is symmetrical and grouped lesions affect the flexural aspects of the arms and legs.
Variants are based on configuration, morphology of lesion, and site of involvement.
Histology shows basal keratinocyte damage with a lymphocyte-rich interface reaction.
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Lichen planus (Greek leichen, “tree moss”; Latin planus, “flat”) is a common inflammatory condition that can affect any ectodermal-derived tissue. Both Hebra and Erasmus Wilson described a similar inflammatory papulosquamous eruption, lichen ruber and lichen planus, respectively, which likely represented the same entity.1 Weyl and Wickham elaborated upon the morphology of lichen planus, and Gougerot and Burnier described disease involvement of mucosal sites.2-4 Although no single feature of lichen planus is a sine qua non, classic lichen planus is typified clinically by “the four Ps”—(1) purple, (2) polygonal, (3) pruritic, and (4) papules—and histologically by a brisk lymphocytic interface reaction.
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The pathogenesis of lichen planus is unknown. Many contributing factors are implicated and include infectious, immune, metabolic, and genetic causes. It is evident that specific immunologic mechanisms control the development of lichen planus. T cell–mediated pathologic alterations involving proinflammatory and counterregulatory mechanisms function in the pathogenesis of lichen planus. No consistent alterations in immunoglobulins have been shown in lichen planus, and humoral immunity most likely is a secondary response in immunopathogenesis. Cell-mediated immunity, on the other hand, plays a major role in lichen planus. One consistent feature of lichen planus is CD4-positive T-helper (CD4-Th) cells in the dermis despite disease chronicity and CD8-positive T-cytotoxic (CD8-Tc) cells in close proximity to damaged basal keratinocytes.5 Based on these observations and insights from other lichenoid tissue reactions (LTRs), such as graft-versus-host-disease (GVHD), modern theories encompass three major stages: antigen recognition, lymphocyte activation, and keratinocyte apoptosis. A fourth stage, resolution, is a new and emerging facet of the disease to further understand the pathogenesis of lichen planus.
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The CD8-Tc cell is the effector cell of lichen planus; however, the initial antigen recognition and CD8-Tc stimulation may be driven by the initial interaction between the CD4-Th cell with the Langerhans cell (LC). The targeted antigen(s) and trigger(s) for lichen planus remains unknown. However, in other similar diseases, such as lichenoid GVHD, the target antigens are alloantigens. In oral disease, a lichen planus–specific antigen associated with major histocompatibility complex (MHC) class I on keratinocytes has been reported.6 It is unknown if this antigen is unique to oral lichen planus and if this antigen is an autoreactive peptide or an exogenous antigen. Circulating antibodies have also been identified in multiple studies without a clear target antigen.7,8 A small but significant population of CD ...