Lichen planus and lichenoid drug-induced eruption: a histological and immunohistochemical study

Introduction Lichenoid drug eruption (LDE) shares similar features with lichen planus (LP), that could reflect the same pathogenesis. In LP, an autoimmune attack is accepted and cytotoxic T-lymphocytes (CD8+) predominate, especially in late lesions. Apoptosis of keratinocytes may be mediated by CD8+ T and NK cells in two distinct ways: by the release of cytotoxic molecules such as perforin and granzyme B or by the Fas/FasL system. The immunological mechanisms involved in LDE are not yet fully established. Objectives Investigate immunohistological features in LP and LDE to add clues to better understand their pathogenesis. Material and methods Twenty-two patients fulfilled all clinical, laboratory, histopathological, and follow-up features of lichen planus (n = 16) and lichenoid drug eruption (n = 6). Classic histological features favoring LP or LDE were evaluated by two observers. HAM56, MAC387, UCHL-1, OPD4, CD8, Granzyme B, Perforin, and ICAM-1 antibodies were used to decorate the immune infiltrate. Results were analyzed through Pearson correlation, Students t-test, and linear discriminant analysis. Results A higher number of necrotic keratinocytes as well as plasma cells and eosinophils within inflammatory cells were associated with LDE diagnosis. Only in LDE, a correlation was found between the number of T and CD8+ cells and between the number of granzyme B+ cells and apoptotic keratinocytes. Conclusion Our findings suggest a more important role of CD8+ granzyme B-containing cells in LDE group, being its synthesis associated with more intense apoptosis. So, LP and LDE may have a somewhat distinct pathogenesis.