Androgenetic alopecia

   Androgenetic alopecia, also known as pattern alopecia, is an extremely common disorder affecting both men and women. The incidence of androgenetic alopecia is statistically considered to be greater in males than females but some evidence suggests that the apparent differences of androgenetic alopecia may be a reflection of different expression in males and females. Androgenetic alopecia is a genetically determined disorder and is increasingly through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients with androgenetic alopecia have a lessened in the terminal-to-vellus hair ratio, normally about 4:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical patterned distribution of hair loss.

   In androgenetic alopecia, studies have demonstrated a self-renewal of the hair follicle via keratinocyte stem cells positioned at the area of the bulge of the hair follicle. In addition, a series of studies using mice has indicated that interfollicular keratinocyte stem cells could generate de novo hair follicles in adult mouse skin. These regenerated hair follicles cycled through stages of telogen to anagen. However, these changes between bulge and epidermal keratinocytes have not been seen yet in human studies. The onset of androgenetic alopecia is advancing by continuous degrees. Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline. For the most part, the evolution of baldness progresses according to the Norwood/Hamilton classification of frontal and vertex thinning. Women with androgenetic alopecia usually present with diffuse thinning on the crown. Bitemporal recession does occur in women but usually to a lesser degree than in men. Usually, women maintain a frontal hairline.

    In both males and females with androgenetic alopecia, the transition from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs in the involved areas is gradual. As the androgenetic alopecia progresses, the anagen phase shortens with the telogen phase remaining constant. As a result, more hairs are in the telogen phase, and the patient may notice an increase in hair shedding. The end result can be an area of total denudation. This area varies from patient to patient and is usually most marked at the vertex.

   Women with androgenetic alopecia generally lose hair diffusely over the crown. This produces a gradual thinning of the hair rather than an area of marked baldness. The part is widest anteriorly. The frontal hairline is often preserved in women with this disorder, whereas men note a gradual recession of the frontal hairline early in the process. Androgenetic alopecia is a genetically determined condition. In 2008, 95 families were studied genetically, and the locus with strongest evidence for linkage to androgenetic alopecia was the 3q26 site on the X chromosome. In addition, an association between androgenetic alopecia and chromosome 20pll and the androgen-receptor gene has been reported.

   Androgen is necessary for progression of androgenetic alopecia, as it is not found in males castrated prior to puberty. The progression of androgenetic alopecia is stopped if postpubertal males are castrated. Androgenetic alopecia is postulated to be a dominantly inherited disorder with variable penetrance and expression. However, it may be of polygenic inheritance. It has been noted that follicles from balding areas of persons with androgenetic alopecia are able to produce terminal hairs when implanted into immunodeficient mice.This suggests that systemic or external factors may play a role in androgenetic alopecia. Interestingly, female androgenetic alopecia has been reported in a patient with complete androgen insensitivity syndrome. This suggests that factors other than direct androgen action contribute to patterned hair loss or androgenetic alopecia.