For example, when the genetics of FFA are examined using one method and the genetics of LPP are evaluated in a different way, an important opportunity is missed to understand the similarities and differences between these conditions.

Importantly, directions for future research must investigate the genetic and pathogenic mechanisms of LPP, FFA, and LPP/FFA overlap in tandem because this is the only way that we will truly begin to appreciate how these conditions are similar and where they diverge.

Abbreviations: 5ARI ( 5α-reductase inhibitor), α-MSH ( α-melanocyte-stimulating hormone), AA ( alopecia areata), AGA ( androgenetic alopecia), CRH ( corticotropin-releasing hormone), eHFSC ( epithelial hair follicle stem cell), EMT ( epithelial‒mesenchymal transition), FFA ( frontal fibrosing alopecia), HF ( hair follicle), IP ( immune privilege), K ( keratin), KC ( keratinocyte), LPP ( lichen planopilaris), MAC ( macrophage), MHC ( major histocompatibility complex), PCA ( primary cicatricial alopecia), PCP ( personal care product), PPAR-γ ( peroxisome proliferator–activated receptor-γ), SC ( stem cell), SP ( substance P) As particularly promising translational research avenues toward direly needed progress in the management of these disfiguring, deeply distressful cicatricial alopecia variants, we advocate to focus on the development of bulge IP and epithelial SC protectants such as, for example, topically effective, HF‒penetrating and immunoinhibitory preparations that contain tacrolimus, peroxisome proliferator–activated receptor-γ, and/or CB1 agonists.

We propose that LPP and FFA share a common initial pathobiology, which then bifurcates into two distinct clinical phenotypes, with macrophages possibly playing a key role in phenotype determination. In this paper, we synthesize recent progress in LPP and FFA pathobiology research, integrate our limited current understanding of the roles that genetic, hormonal, environmental, and other factors may play, and define major open questions. This induces both apoptosis and pathological epithelial‒mesenchymal transition in epithelial SCs, thus depletes the bulge, causes fibrosis, and ultimately abrogates the HFs’ capacity to regenerate. These model epithelial stem cell (SC) diseases are thought to result from a CD8 + T-cell‒dominated immune attack on the hair follicle (HF) SC niche (bulge) after the latter has lost its immune privilege (IP) for as yet unknown reasons. Lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) are primary, lymphocytic cicatricial hair loss disorders.

Approach to alopecia ppt