Androgenic alopecia (also known as androgenetic alopecia, alopecia androgenetica, or male pattern baldness) is hair loss that occurs due to an underlying susceptibility of hair follicles to androgenic miniaturization. It is the most common cause of hair loss and will affect up to 70% of men and 40% of women at some point in their lifetimes. Men typically present with hairline recession at the temples and vertex balding, while women normally thin diffusely over the top of their scalps.[1][2][3] Both genetic and environmental factors play a role, and many etiologies remain unknown.

Classic androgenic hair loss in males begins above the temples and vertex, or calvaria, of the scalp. As it progresses, a rim of hair at the sides and rear of the head remains. This has been referred to as a 'Hippocratic wreath', and rarely progresses to complete baldness.[4] The Hamilton-Norwood scale has been developed to grade androgenic alopecia in males.

Female androgenic alopecia is known colloquially as "female pattern baldness", although its characteristics can also occur in males. It more often causes diffuse thinning without hairline recession; and, like its male counterpart, rarely leads to total hair loss.[5] The Ludwig scale grades severity of androgenic alopecia in females.

Animal models of androgenic alopecia occur naturally and have been developed in transgenic mice;[6]chimpanzees (Pan troglodytes); bald uakaris (Cacajao rubicundus); and stump-tailed macaques (Macaca speciosa and M. arctoides). Of these, macaques have demonstrated the greatest incidence and most prominent degrees of hair loss.[7][8]

Research indicates that the initial programming of pilosebaceous units begins in utero.[9] The physiology is primarily androgenic, with dihydrotestosterone (DHT) the major contributor at the dermal papillae. Below-normal values of sex hormone-binding globulin , follicle-stimulating hormone , testosterone, and epitestosterone are present in men with premature androgenic alopecia compared to normal controls.[10] Although follicles were previously thought permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitors from which the follicles arose.[11]

Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor at the dermal papillae, which is affected by DHT.[12]Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age,[13] androgens stimulate hair growth on the face, but suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.[14]

These observations have led to study at the level of the mesenchymal dermal papillae.[15][16]Types 1 and 2 5 reductase enzymes are present at pilosebaceous units in papillae of individual hair follicles.[17] They catalyze formation of the androgens testosterone and DHT, which in turn regulate hair growth.[14] Androgens have different effects at different follicles: they stimulate IGF-1 at facial hair, leading to growth, but stimulate TGF 1, TGF 2, dickkopf1, and IL-6 at the scalp, leading to catagenic miniaturization.[14] Hair follicles in anaphase express four different caspases. Tumor necrosis factor inhibits elongation of hair follicles in vitro with abnormal morphology and cell death in the bulb matrix.[18]

Studies of serum levels of IGF-1 show it to be increased with vertex balding.[19][20] Earlier work looking at in vitro administration of IGF had no effect on hair follicles when insulin was present, but when absent, caused follicle growth. The effects on hair of IGF-I were found to be greater than IGF-II.[21] Later work also showed IGF-1 signalling controls the hair growth cycle and differentiation of hair shafts,[12] possibly having an anti-apoptotic effect during the catagen phase.[22]In situ hybridization in adult human skin has shown morphogenic and mitogenic actions of IGF-1.[23] Mutations of the gene encoding IGF-1 result in shortened and morphologically bizarre hair growth and alopecia.[24] IGF-1 is modulated by IGF binding protein, which is produced in the dermal papilla.[25]

DHT inhibits IGF-1 at the dermal papillae.[26] Extracellular histones inhibit hair shaft elongation and promote regression of hair follicles by decreasing IGF and alkaline phosphatase in transgenic mice.[27] Silencing P-cadherin, a hair follicle protein at adherens junctions, decreases IGF-1, and increases TGF beta 2, although neutralizing TGF decreased catagenesis caused by loss of cadherin, suggesting additional molecular targets for therapy. P-cadherin mutants have short, sparse hair.[28]

At the occipital scalp, androgens enhance inducible nitric oxide synthase (iNOS), which catalyzes production of nitric oxide from L-arginine.[14] The induction of iNOS usually occurs in an oxidative environment, where the high levels of nitric oxide produced interact with superoxide, leading to peroxynitrite formation and cell toxicity. iNOS has been suggested to play a role in host immunity by participating in antimicrobial and antitumor activities as part of the oxidative burst[29] of macrophages.[30] The gene coding for nitric oxide synthase is on human chromosome 17.[31]

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