Pathophysiology of MPB (Male Pattern Baldness)

Provided Courtesy of: Richard Lee, MD

MPB or alopecia androgenetica is caused by progressive miniaturization of the hair follicles on the scalp; not a destruction on the involved hair follicles. So, it’s not a loss in the number of hairs. MPB is a loss in the quality of the hair.

The gene or genes responsible for MPB have not yet been positively identified, but the hereditary pattern is considered to be an autosomal dominant with variable penetrance, which is a complicated way to say that MPB can be inherited from the mother or the father (or both). There are also arguments that the trait demonstrates not a single gene abnormality, but rather a polygenic inheritance. A predisposition inherited from an affected mother may be of greater importance than that inherited from an affected father because affected women carry more predisposing genes and therefore transmit more of them to their offspring. In any one individual, we can never predict the incidence, extent or pattern of MPB.

In the quail-chick model, there are differences in the embryonic origin of the dermis of the fronto-parietal scalp compared to the occipital scalp. Dermis of the frontoparietal scalp is derived from the neural crest, whereas dermis of the occipital/temporal scalp is derived from the mesoderm. This difference in the origin of the skin of the scalp may explain why the back and sides of the head are not affected in MPB.

After the third decade (maybe even in the second decade), the incidence of MPB parallels the decade, i.e. 30% of men in their thirties will have MPB, 40% of men in their forties will have MPB, etc. The incidence seems to peak at about age 65. The basic etiologic factors in MPB are presumed to be the same as in FPB, although the clinical presentation is different. Women with FPB have diffuse thinning with greater involvement of the frontal area, but without recession of the frontal hairline. In contrast, men with MPB commonly show bitemporal recession and vertex hair loss, which may progress to an absolute baldness in the affected areas.

Hair growth (and loss) due to the influence of androgens requires formation of an androgen-androgen receptor complex, which then binds to the androgen-response element DNA-binding site. This, in turn, causes transcription of certain proteins in the nucleus of the cells and results in a change in the phenotypical appearance of the hair.

Androgens are 19-carbon steroid structures normally produced by both the adrenals and the gonads. It’s the 17-hydroxy group that is responsible for the highest affinity to androgen receptor binding. So, testosterone, dihydrotestosterone (DHT) and androstenediol are the most potent. Since androgens begin to be produced by the body during puberty, MPB can be apparent as a teenager.

As you can see from this diagram, the precursors of testosterone are easily converted to testosterone, just as testosterone can be converted into dihydrotestosterone by the action of 5 alpha reductase or into an estrogen by the action of an aromatase.

Balding scalp shows a decreased amount of aromatase as compared to areas of non-balding scalp. Women with FPB have six times more aromatase in the frontal scalp than do men with MPB, which may explain why women with FPB have a milder expression of pattern balding and usually retain their frontal hairlines. The biochemical events that result in MPB are very complicated and are not completely understood. There is evidence for more than one form of androgen receptor protein. Other hormones may also be important to the balding process.