Androgenetic alopecia in polycystic ovary syndrome: a cutaneous marker of systemic metabo-inflammatory and endocrine dysfunction
Abstract
Polycystic ovary syndrome (PCOS) is a multifaceted endocrine-metabolic disorder in which androgenetic alopecia (AGA) serves as a prominent clinical marker of profound systemic dysregulation, extending beyond simple hyperandrogenism. This condition imposes a significant psychosocial burden on affected women, yet its complete pathophysiology remains incompletely understood, leading to therapeutic plateaus. This review advances the central hypothesis that alopecia in PCOS results from a synergistic failure of local follicular metabolic signaling and genetic predisposition. This framework posits that the hair follicle in susceptible individuals is a site of intrinsic vulnerability where systemic insults, principally insulin resistance and chronic low-grade inflammation, converge with specific gene polymorphisms. This local pathology both amplifies and is amplified by systemic hyperandrogenism, rendering androgen action a necessary but insufficient component of the complete pathophysiological cascade. This integrated perspective recontextualizes the roles of insulin, inflammatory mediators, and genetic variants as direct effectors of follicular distress, not merely as upstream triggers of androgen excess. We critically synthesize the evidence supporting this model, examining the intricate intersections of systemic hormone bioavailability, local androgen conversion, follicular bioenergetics, and genetic susceptibility. Furthermore, we provide an evidence-based, mechanistically…
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