There was overall preserved follicular architecture without obvious areas of follicular dropout but with hypoplastic (atrophic) appearance of the sebaceous glands in all specimens. The atrophy varied from volumetric decrease in the number and size of the sebaceous lobules (Fig. 2A) to remnants of undifferentiated epithelial strands (mantle-like structures) (Fig. 2B). The average follicular density was 17.6 follicles with an average vellus number of 11.1. The terminal follicles were unaffected by perifollicular lamellar fibrosis or lichenoid/interface lymphohistiocytic infiltrate. No compound follicular structures (eye- or goggle-like structures) were found. The vellus follicles in all but 1 specimen showed lichenoid lymphohistiocytic infiltrate (Fig. 3A) with prominent histiocytic component in 1 case (Fig. 3B) and eosinophils in 2 other cases (Fig. 3C). The infiltrate was organized in layered (surrounding the circumference of the follicle) or patchy (unilateral) collections in approximation to the other root sheath. There was no perifollicular fibrosis around the vellus follicles. In all but 1 specimen, the stroma appeared “busy” by the presence of scattered fibrohistiocytes (Fig. 4), mast cells, and eosinophils. A skin-colored papule of the occipital scalp in 1 patient was biopsied and showed interface dermatitis without follicular involvement.
The atrophy of the sebaceous glands is a well-known histologic feature of scarring alopecias. Although no data exist for FFA, research has shown that peroxisome proliferator-activated receptor (PPAR) gamma (a transcription factor that is critical for the healthy pilosebaceous unit and its lipid metabolism and peroxisome biogenesis) is significantly decreased in expression in lichen planopilaris.15
The busy stroma cannot be considered a specific finding because scalp biopsies from black patients may show increased stromal cellularity including melanophages. However, in the setting of our series, it is curious for 2 reasons: our specimens originate from 5 white patients and 1 Asian patient with early FFA and no skin atrophy. It, therefore, can be assumed that the stroma is involved early in the pathogenesis. In fact, one study that used Snail-1 immunohistochemistry has shown that there is rational to suspect epithelial–mesenchymal transition in the areas of fibrosis in FFA.16 Transition of the epithelial stem cells into mesenchymal cells of fibroblast phenotype is currently a favored mechanism implicated in the pathogenesis of FFA.17
In conclusion, lymphohistiocytic inflammation of the vellus follicles and atrophy of the sebaceous glands in scalp biopsies of the hairline are a clue to the diagnosis of early FFA even in the absence of the classic perifollicular lichenoid inflammation and concentric fibrosis. Future prospective histologic studies are necessary to confirm this observation. Retrospective studies are not useful because this pattern may have been misdiagnosed as androgenetic alopecia because of the absence of classic features for lymphocytic scarring alopecia and the abundance of vellus follicles.
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