The Role of Inflammation and Immunity in the Pathogenesis of Androgenetic Alopecia
December 2011 | Volume 10 | Issue 12 | Original Article | 1404 | Copyright © 2011
Background: Female pattern hair loss affects many women; its pathogenetic basis has been held to be similar to men with common baldness.
Objective: The objective of this study was to determine the role of immunity and inflammation in androgenetic alopecia in women and modulate therapy according to inflammatory and immunoreactant profiles.
Materials and Methods: 52 women with androgenetic alopecia (AA) underwent scalp biopsies for routine light microscopic assessment and direct immunofluroescent studies. In 18 patients, serologic assessment for antibodies to androgen receptor, estrogen receptor and cytokeratin 15 was conducted.
Results: A lymphocytic folliculitis targeting the bulge epithelium was observed in many cases. Thirty-three of 52 female patients had significant deposits of IgM within the epidermal basement membrane zone typically accompanied by components of complement activation. The severity of changes light microscopically were more apparent in the positive immunoreactant group. Biopsies from men with androgenetic alopecia showed a similar pattern of inflammation and immunoreactant deposition. Serologic assessment for antibodies to androgen receptor, estrogen receptor or cytokeratin 15 were negative. Combined modality therapy with minocycline and topical steroids along with red light produced consistent good results in the positive immunoreactant group compared to the negative immunoreactant group.
Conclusion: A lymphocytic microfolliculitis targeting the bulge epithelium along with deposits of epithelial basement membrane zone immunoreactants are frequent findings in androgenetic alopecia and could point toward an immunologically driven trigger. Cases showing a positive immunoreactant profile respond well to combined modality therapy compared to those with a negative result.
J Drugs Dermatol. 2011;10(12):1404-1411.
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Androgenetic alopecia (AGA) in women or female-pattern hair loss (FPHL) affects a significant percentage of women with increased prevalence with aging; over 70 percent of patients in the seventh decade of life experience significant hair loss.1 It is characterized by a gradual onset of nonscarring alopecia. The pathogenetic basis has been held to be similar to that proposed for male pattern hair loss (MPHL) with a higher incidence among those with a positive history for AGA. Diffuse central thinning or Ludwig type, frontal accentuation or Olsen type and frontotemporal recession/vertex loss or male pattern/Hamilton type represent the AGA clinical variants.2-4
Hair loss in AGA reflects a shortening of the anagen phase eventuating into a hair that recapitulates a vellus hair resulting in a progressive reduction of the terminal-to-vellus hair ratio. These small, light-colored short hairs are typically found on the glabrous skin and do not normally represent a component of the follicular composition of the scalp.2-4
Although FPHL has not been studied in the same detail, the follicular pathology and, in essence, pathophysiology is thought to be the same as in men, particularly the role of hyperandrogenism. Despite these findings, anti-androgen therapy is not as efficacious in the treatment of FPHL; conversely, not all men respond to anti-androgen therapy.5-7 One of the authors (CMM) noticed that immunoglobulin deposition within the epidermal basement membrane zone was a finding in AGA, although initially when she encountered this finding the immunoreactant profile was held to be indicative of a lupus-like diathesis and not part of the expected immunoreactant profile in AGA. Interestingly, similar findings of complement and immunoglobulin immunoreactant deposition within the epidermal