Vulvar lichen sclerosus (LS) represents a benign chronic inflammatory skin lesion that carries a risk for development of vulvar squamous cell carcinoma (SCC). We aimed at determining whether premalignant changes in vulvar LS, a multifactorial disease, presenting a welter of evidence implicating the immune system in its pathogenesis, could be identified by analysing the Langerhans¿ cells (LCs), the primary cell responsible for antigen recognition and presentation.
The relationship existing between inflammation and cancer due to chronic infection, and demonstrated in many solid tumors, led us to study LCs in eight cases of vulvar LS, which showed an evolution to carcinoma of the vulva and in ten cases of unchanged vulvar LS in matched patients by immunohistochemistry for antibodies CD1a and S100. We did not find a statistically significantly different number of LCs counted either in S100 stained specimens, nor in CD1a stained specimens of LS epithelium in unchanged or evolving cases. The data emerging in our study do not support the hypothesis that the variation in the number of LCs may be related to the development of SCC in late stage LS cases.
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