Lichen planopilaris (LPP), a follicular form of lichen planus, is a rare inflammatory lymphocyte mediated disorder. Although the physiopathology is unclear, an autoimmune etiology is generally accepted. Women are affected more than men, and the typical age of onset is between 40 and 60 years. LLP is a primary cicatricial alopecia whose diagnosis is supported in the early stage by both clinical and histopathological findings. Within the margins of the expanding areas of perifollicular violaceous erythema and acuminate keratotic plugs, the histology can show the lichenoid perifollicular inflammation. LPP can be subdivided into 3 variants: classic LPP, frontal fibrosing alopecia (FFA), and Lassueur Graham-Little Piccardi syndrome. With the exception of FFA, the hairless patches of the scalp can be unique or can occur in multiples and can present with a reticular pattern or as large areas of scarring. This condition can have major psychological consequences for the affected patients. The therapeutic management often is quite challenging, as relapses are common after local or systemic treatments. Further research is needed on the pathogenesis, and randomized controlled trials of treatment with scientific evaluation of the results are necessary to appreciate the proposed treatment.

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Folliculitis decalvans (FD) is a chronic inflammatory disease of unknown aetiology. Although Staphylococcus aureus, frequently found on lesional skin, is thought to play a causal role, the importance of its involvement remains controversial. To examine the role of S aureus, we compared superficial and subepidermal microbiota in 20 FD patients who had S aureus on lesional skin and in 20 healthy controls using culture techniques and genomic identification, before and after an anti‐staphylococcal treatment; we also screened for S aureus virulence factors. When present on lesional skin, S aureus colonized non‐lesional and subepidermal skin in 80% of cases. These data imply a break in the epidermal barrier integrity and that an abnormal non‐lesional skin microbiota persists in FD. S aureus had no superantigenic toxin in 31% of cases and no toxin specificity. Clinical improvement obtained in most cases upon treatment was associated with the disappearance of S aureus in all studied areas, with an incomplete restoration of normal microbiota and a significant increase in negative bacterial samples. This persistent unbalanced, subepidermal microbiota may act as a reservoir of abnormal flora and explain the chronicity of FD, suggesting new avenues of research to restore normal microbiota.

This pilot study provides the first evidence of the presence of bacterial biofilms in the infra infundibular part of human scalp hair follicles. These biofilms were detected both in FD patients and controls, suggesting their ubiquity as a commensal biofilm with a possible pathogenic shift in FD.