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The condition male pattern baldness is common, estimated to be present in 50% of white males by 50 years of age. It is characterized by the loss of hair from the scalp in a defined pattern and, although there are no serious direct health consequences, the loss of scalp hair can be distressing. Understanding male pattern baldness might also reveal some fundamental secrets of biology.

Hair follicles on the scalp seem to be pre-programmed to undergo a transformation from the normal long growing phases and short resting phases to cycles of long rest and short growth periods. This process is coupled with progressive miniaturization of the follicle.

Unusual postulated causes have ranged from an old idea that baldness was the result of wearing hats and depriving the scalp of sunlight and air, to more recent suggestions of skull expansion [1]. However, the factors that determine male pattern baldness appear to be genetic predisposition coupled with the presence of sufficient circulating androgens. Evidence in support of androgenic influence comes from the fact that eunuch’s do not go bald. For this reason male pattern baldness is also known as androgenetic alopecia.

The mystery, and the potential for fundamental biological discovery, is why front hair should vanish, while that at the back of the head should flourish. Presumably genetic predisposition alters expression of key genes in a regionally specific manner to cause patterned hair loss. But what genes are involved and how are they affected?

Prime candidates for baldness are genes encoding enzymes and receptors involved in sex steroid metabolism. Key enzymes include 5a-reductase that converts testosterone (T) to the more active dihydrotestosterone (DHT) and aromatase that converts estrogen to T. Both T and DHT to exert their effect by binding to the androgen receptor (AR), a member of the steroid-thyroid hormone nuclear receptor superfamily. In balding scalp there are observed high levels of T, DHT and AR.

Références

[1] Taylor P.J., “Big head? Bald head! Skull expansion: alternative model for the primary mechanism of AGA”, Medical Hypotheses, 72, 2009, 23-28.

[2] Ellis J.A., Stebbing M., Harrap S.B., “Polymorphism of the androgen receptor gene is associated with male pattern baldness”, J. Invest. Dermat., 116, 2001, 452-455.

[3] Kuster W., Happle R., “The inheritance of common baldness: two B or not two B?”, J. Am. Acad. Dermatol., 11, 1984, 921-926.

[4] Hillmer A.M., Brockschmidt F.F., Hanneken S., Eigelshoven S., Steffens M., Flaquer A., Herms S., Becker T., Kortum A.K., Nyholt D.R. (Zhao Z.Z., Montgomery G.W., Martin N.G., Muhleisen T.W., Alblas M.A., Moebus S., Jockel K.H., Brocker-Preuss M., Erbel R., Reinartz R., Betz R.C., Cichon S., Propping P., Baur M.P., Wienker T.F., Kruse R., Nothen M.M., “Susceptibility variants for male-pattern baldness on chromosome 20p11”, Nature Genetics, 40, 2008, 1279-1281 et Richards J.B., Yuan X., Geller F., Waterworth D., Bataille V., Glass D., Song K., Waeber G., Vollenweider P., Aben K.K.H., Kiemeney L.A., Walters B., Soranzo N., Thorsteinsdottir U., Kong A., Rafnar T., Deloukas P., Sulem P., Stefansson H., Stefansson K., Spector T.D., Mooser V., “Male-pattern baldness susceptibility locus at 20p11”, Nature Genetics, 40, 2008, 1282-1284.