Abstract
A case of cutaneous graft versus host disease (GvHD) presenting as fibrosing alopecia in a pattern distribution (FAPD) is discussed, possibly providing a mechanistic model for a better understanding of the pathogenic events underlying cicatricial pattern hair loss. The implication of a follicular inflammation and fibrosis associated with patterned hair loss has emerged from several independent studies. Eventually, Zinkernagel and Trüeb reported a peculiar type of cicatricial pattern hair loss with histopathological features consistent with lichen planopilaris (LPP) associated with androgenetic alopecia (AGA). With regard to its pathogenesis, LPP is regarded to constitute a T-cell-mediated autoimmune reaction. An as yet unknown antigenic stimulus from the malfunctioning hair follicle may initiate a lichenoid tissue reaction that triggers apoptosis of the follicular epithelial cells in the susceptible individual. GvHD is a complication following allogeneic tissue transplantation and is induced and maintained by immunocompetent cells from the donor tissue that particularly attack epithelia of fast-proliferating tissues in the recipient. Due to its analogies with lichen planus, GvHD constitutes a valid immunologic model for lichen planus, LPP and ultimately FAPD. Specifically, the presentation of GvHD of the scalp combines features of AGA and of LPP, as originally proposed in earlier observations on permanent alopecia after bone marrow transplantation.