Male Pattern Baldness Dallas

Male Pattern Hair Loss

Androgenetic Alopecia (male pattern baldness)

Androgenetic alopecia (AGA) is also known as male pattern baldness and is the most common cause of hair loss. Approximately 50% of men are affected by the age of 50 and 20 to 53% of women are affected by the age of 50. Although the condition is benign, the psycho-social ramifications to AGA can be significant, and the majority of this website is dedicated to understanding the clinical features of AGA as well as medical and surgical treatments to improve AGA.

Genetics Factors regarding Male Pattern Baldness.

The old wives’ tale that one’s mother’s father should be evaluated for hair loss as indicative of the likelihood that an individual will go bald is incorrect. In reality, the genetic factors that lead to baldness are polygenic and can be inherited from either parent. The gene frequency is most common in Caucasians with a lower frequency in Africans and even lower in Ameridians, Asians, and Inuits. Although it is recognized today that AGA is derived from multiple genes, the exact genes that contribute to AGA are at this time not yet known. Perhaps the Human Genome Project will help discover which genes may play an important role in AGA.

Hormonal Factors regarding Male Pattern Baldness

A major determinant of AGA concerns androgen metabolism, more specifically the enzymes 5-alpha reductase and aromatase as well as androgen receptor proteins. 5-alpha reductase isoenzymes, type I and II, convert testosterone (T) to dihydrotestosterone (DHT). Type I enzyme is found in sebaceous glands, epidermal and follicular keratinocytes, dermal papilla cells, and sweat glands. Type II enzyme is located in the outer root sheath of the scalp hair follicles as well as in the epididymis, vas deferens, seminal vesicles, prostate, and fetal genital skin. Both Type I and Type II 5-alpha reductase enzymes contribute to AGA. Both isoenzymes are increased in the frontal balding follicles compared with the non-balding follicles in the back of the head. DHT levels are also increased in the balding scalp compared with the non-balding scalp. Further women have 3 to 3.5 times less 5-alpha reductase Type I and II than men, which probably accounts for why female AGA is less severe in most cases than with male AGA. Interestingly, individuals born without 5-alph reductase Type II do not develop AGA.

Aromatase is an enzyme that is part of the normal androgen metabolism that may have protective effects on AGA. Aromatase converts T into estradiol and estrone and thereby results in less conversion of T into DHT. Aromatase is found in much higher levels in female scalps with 6 times in the frontal scalp and 4 times in the occipital scalp than in men. This may explain why women who suffer from AGA may still be able to preserve their frontal hairline.

Androgen receptor proteins (ARP) are found in the outer root sheaths and in the dermal papilla fibroblasts of the scalp follicles. ARPs are found to be 30% higher in the frontal balding scalp than in the non-balding occipital follicles. ARPs are found to be 40% lower in women than in men. ARPs are responsible for the signal transduction in the hair follicle that promotes the conversion of a thick terminal hair into a miniaturized vellus hair. Interestingly, ARPs have the opposite effect in the beard and mustache, promoting thicker follicles in these areas at puberty.

Clinical Features regarding Male Pattern Baldness

Thinning of the hair can begin as early as the age of 12 and as late as 45. Typically, AGA occurs early in most cases between the ages of 15 and 25 with lifetime progression. Most oftentimes, the clinical course is a gradual one with periodic episodes of increased telogen loss. Maximum pattern is usually attained by one’s forties with ongoing thinning throughout the remainder of one’s life.

Hair loss is non-scarring with preservation of follicular ostia. The first change that is evident is loss of hair along the fronto-temporal angle, which is seen in 96% of mature Caucasian men even in those who do not progress to substantive AGA. The Norwood-Hamilton grading scale defines the patterns of ongoing hair loss and are reviewed in a separate section of this website.

One of the hallmarks of AGA is the conversion of thick terminal hairs into vellus and vellus-like hairs. This process of miniaturization in which hairs that were once thick become quite thin (0.03 mm in diameter) and very short relative to the previously thick terminal hairs increases the see-through effect and lack of visual density in AGA. These vellus hairs are then lost over time to reveal naked scalp. In addition, in AGA the normal 90% anagen to 10% telogen ratio is changed over to 80% anagen and 20% telogen. Although there is no increase in telogen, the shortening of the anagen phase leads to an increase in telogen hairs. The terminal to vellus ratio is normally 7:1 with a shift to 2:1 in AGA.