The pilosebaceous unit (PSU) response to
androgen is variable. Certain population of PSU respond to
androgen in a distinctive pattern that results in sexual hair development in some, sebaceous gland development in others. Furthermore,
androgen excess is variably manifest in women as
hirsutism,
acne vulgaris,
seborrhea, or pattern
alopecia. Although sebaceous cells act as intracrine cells, activating pro-
hormones to potent
androgens that act within the sebocyte, hair follicle metabolism predominantly inactivates
testosterone.
Androgen action in the sexual hair follicle appears to be mediated by the dermal papilla and possibly, by inducing expression of a specific
keratin, hHa7, in the hair medulla. The data do not clearly support a relationship between idiopathic
hirsutism, the
hirsutism that occurs in the absence of
androgen excess, and variations in
androgen mechanism of action.
Androgens are prominent among the
hormones that modulate the
biological mechanism regulating the hair cycle. However, the basis for the variable pattern of PSU response to
androgen is unclear, as is the basis for the variable development of
hirsutism in response to
androgen excess and the incomplete reversal of
hirsutism by anti-
androgen treatment. Improved treatment of
hirsutism awaits improved understanding of the nature of the interaction between
androgens and other determinants of hair follicle biology.