Male and female pattern hair loss (MPHL and FPHL; common balding) is an androgen-dependent hereditary disorder. More is known about the condition in men than in women. The frequency and severity increase with age in both sexes, and at least 80% of Caucasian men show evidence of MPHL by age 70. A smaller percentage of women eventually express the trait. This pattern of hair loss is so common that in most cases it should be thought of as a physical trait rather than a disease.
Pathogenesis
Both genes and hormones are implicated in the pathophysiology of this hair disorder, and inheritance is almost certainly polygenic, with genetic input from either or both parents. Women with FPHL are less likely than men to have a strong family history of the disorder.
The androgen hormones testosterone and dihydrotestosterone (DHT) each have selective roles at puberty. Testosterone is associated with increased muscle mass, growth of the phallus and scrotum, voice change, sex drive, and the presence of terminal pubic and axillary hair fibers. The hormone DHT is associated with temporal scalp hair recession, acne, growth of the prostate gland, and the development of terminal hairs in the beard region, external ears, nostrils, and on the limbs.
The expression of male androgenetic alopecia is particularly related to DHT. Testosterone is converted to DHT by the enzyme 5α-reductase, of which there are two isoenzymes, type I and type II. Type I 5α-reductase is present predominantly in sebaceous glands and the liver, whereas type II 5α-reductase dominates in scalp, beard and chest hair follicles, as well as in the liver and the prostate gland. The genetic absence of type II 5α-reductase prevents development of male androgenetic alopecia.
Using a variety of techniques, investigators have localized androgen-metabolizing enzymes to various regions of the hair follicle. In scalp biopsy specimens taken from men with androgenetic alopecia, 5α-reductase activity and DHT levels are increased compared to non-balding scalp skin. DHT is implicated in the appearance of miniaturized hair follicles and hair fibers, and decreased levels in both the skin and the blood have been associated with a reversal of miniaturization. Other enzymes involved in androgen metabolism (in addition to 5α-reductase) have also been found in the human scalp hair follicle and may play a role in pathogenesis.
In women, a similar pathophysiology is postulated: namely, androgens causing follicle miniaturization and production of smaller, miniaturized hair shafts. Women, however, may develop their balding patterns during or after puberty, in the perimenopausal period and during menopause. Women who develop balding shortly after puberty commonly have a positive family history for pattern baldness in both male and female family members. Women who develop pattern alopecia in the perimenopausal and menopausal periods may be developing hair loss not only because of a genetic predisposition but also because of alterations in androgen metabolism at the level of the hair follicle as well as systemic hormonal changes.
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