Pattern Balding

Androgenetic alopecia, androgenic alopecia, or pattern baldness, has been a part of the human race for as long as we have historical records. Evolutionary evidence suggests androgenetic alopecia has been around longer than the modern human race. Our nearest non-human primate relatives, orangutans and gorillas can also develop androgenetic alopecia. Androgenetic alopecia is a very common form of hair loss and could be described as part of our general genetic phenotype. People who do not develop androgenetic alopecia are in the minority. We could even say these non-bald people are the deviants from the norm!

Medicine has long recognized androgenetic alopecia as an inherited systemic disease associated with sexual development. Ancient Greek doctors realized that male pattern baldness can develop in men of any age after puberty. They recorded that young boys castrated before puberty did not develop androgenetic alopecia regardless of their genetic family history. However, boys castrated during or after puberty could develop androgenetic alopecia. We now know that the reason for their observations is that castration prepuberty stops hair follicles from being exposed to androgens made by the gonads during adolescence. Castration after puberty is too late. Once hair follicles have been exposed to androgens they are fated to become androgen sensitive and androgenetic alopecia can develop.

Onset of Androgenetic Alopecia

Androgenetic alopecia affects between 50 and 80% of Caucasian men. For some the alopecia can begin in their teen years. A rule of thumb is for men in their thirties, 30% have androgenetic alopecia. For men in their forties, 40% have alopecia and so on until about 80% of men are affected when 80 or more years old. African and Asian men have a lower frequency of andorgenetic alopecia, perhaps about half the rate of Caucasian men.

Despite its standard name of “male pattern baldness” androgenetic alopecia is also the most common form of hair loss in women. Hair loss is first observed in women in their late twenties to early forties, somewhat later in age than first onset in men. Unlike men, the frequency of women affected does not continue to increase with increasing age. After the fifth decade of life the numbers of women with androgenetic alopecia does not increase. Androgenetic alopecia has been suggested to be present in the general female population at a rate anywhere between 20 to 40%. It is perhaps one of the best kept secrets that female androgenetic alopecia is so common.

Development of Androgenetic Alopecia

Androgenetic alopecia develops as a gradual reduction of scalp hair follicle size, and reduced time in the anagen active growth phase, leading to more hair follicles in the telogen resting stage of the hair cycle. In men, the hair loss is typically limited to the top of the head and can involve thinning and/or receding hair lines. In women the presentation is usually different with just diffuse thinning over the top of the head and sometimes thinning over the entire scalp. Where there is a limit to the hair loss, such that there are still sizable areas of normal hair growth on the scalp, the individual is usually suitable for a hair transplant. If however, the hair loss affects the scalp extensively, there may not be enough normal hair follicles left to transplant and get a good result.

The gradual changes that occur in the androgenetic alopecia affected scalp skin is the same whether describing male of female baldness. Androgenetic alopecia does not develop in all hair follicles at the same time. Some are more quickly affected than others. When looking at a punch biopsy under the microscope neighboring hair follicles can be seen to be variably affected. Some will be normal healthy terminal hairs with an average diameter of 0.06mm, others will be miniaturized vellus hair follicles with an average diameter of 0.03mm. So, one parameter of androgenetic alopecia is a decrease in the density of terminal hairs and an increase in the vellus hair count. Hairs in an intermediate state between terminal and vellus hairs will also be observed.

Shortening of the growth cycle

Over time the terminal scalp hair follicles undergo progressively shorter and shorter cycles involving reduced anagen growth periods. This applies regardless of whether the hair follicles are terminal, intermediate, or vellus hairs. Although periods of anagen are reduced catagen and telogen time periods remain the same. The net effect is that androgenetic alopecia is characterized by a gradual increase in the number of resting telogen hair follicles present at any one time. In unaffected scalp the percentage of hair follicles in telogen is up to 10%. In the early stages of androgenetic alopecia affected scalp the number of telogen stage hair follicles can be up to 20% of the total. As androgenetic alopecia progresses the total number of hair follicles can be reduced as the hair follicles are irreversibly destroyed.

In androgenetic alopecia the terminal hair follicles reduce size both in length and diameter. The hair bulb moves upwards in the dermis yielding a small vellus hair follicle. These vellus hair follicles can be affected by fibrosis. Beneath the miniaturized vellus hair follicle a fibrous tract, known as a streamer or follicular stela, can be observed marking the terminal hair follicle bulb’s original position to the base of the current vellus hair dermal papilla. Eventually the hair follicles may disappear altogether. This is not unusual in men although a complete loss of hair follicle in women is relatively rare.