Pathogenesis of androgenetic alopecia

Abstract

The pathogenesis of androgenetic alopecia (AGA) is a complex interplay of genetic, hormonal, and environmental factors. In scalp follicles of susceptible individuals, androgens promote miniaturization of hair and shorten hair growth in the anagen stage, ultimately leading to AGA. The major circulating androgen, testosterone, is converted to the more potent androgen dihydrotestosterone by the enzyme 5α-reductase (5αR). Androgen receptors (ARs) and 5αR are significantly more in balding scalp hair follicles than those from nonbalding follicles. Genetic predisposition plays a crucial role in AGA. Various genetic loci including AR gene and the ectodysplasin A2 receptor (EDA2R) (AR/EDA2R locus in Xq11-q12) have been strongly implicated. The basic pathology of AGA is progressive miniaturization of the terminal hair follicles and eventual conversion of terminal hair to vellus hair. The duration of the anagen phase diminishes progressively with each cycle, while the length of telogen phase remains constant or may be prolonged. This eventually results in a reduction of the anagen to telogen ratio. With each successive shortening of hair cycle, the length of each hair shaft is reduced, and it becomes too short for the growing hair to attain even the minimum length required to reach the skin surface, resulting in an empty follicular pore. Hair follicle miniaturization leads to conversion of terminal hairs into secondary vellus hairs. Although many mechanisms have been proposed, the actual mechanism of hair miniaturization has not yet been fully elucidated. This article attempts to collate the existing information regarding the pathogenesis of AGA.