Male-pattern baldness

Pattern hair loss is hair loss that primarily affects the top and front of the scalp. In male-pattern hair loss (MPHL), the hair loss often presents itself as a receding hairline, while in female-pattern hair loss (FPHL), it typically presents as a thinning of the hair. Pattern hair loss is hair loss that primarily affects the top and front of the scalp. In male-pattern hair loss (MPHL), the hair loss often presents itself as a receding hairline, while in female-pattern hair loss (FPHL), it typically presents as a thinning of the hair. Male pattern hair loss is believed to be due to a combination of genetics and the male hormone dihydrotestosterone. The cause in female pattern hair loss remains unclear. Management may include simply accepting the condition. Otherwise, treatments may include minoxidil, finasteride, or hair transplant surgery. Evidence for finasteride in women is poor and it may result in birth defects if taken during pregnancy. Pattern hair loss by the age of 50 affects about half of males and a quarter of females. It is the most common cause of hair loss. Classic male-pattern hair loss begins above the temples and vertex (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. Pattern hair loss is classified as a form of non-scarring hair loss. The Hamilton–Norwood scale has been developed to grade androgenic alopecia in males. Female-pattern hair loss more often causes diffuse thinning without hairline recession; similar to its male counterpart, female androgenic alopecia rarely leads to total hair loss. The Ludwig scale grades severity of female-pattern hair loss. KRT37 is the only keratin that is regulated by androgens. This sensitivity to androgens was acquired by Homo sapiens and is not shared with their great ape cousins. Although Winter et. al found that KRT37 is expressed in all the hair follices of chimpanzees, it was not detected in the head hair of modern humans. As androgens are known to grow hair on the body but decrease it on the scalp, this lack of scalp KRT37 may help explain the paradoxical nature of Androgenic alopecia as well as the fact that head hair anagen cycles are extremely long. Research indicates that the initial programming of pilosebaceous units of hair follicles begins in utero. The physiology is primarily androgenic, with dihydrotestosterone (DHT) being the major contributor at the dermal papillae. Men with premature androgenic alopecia tend to have lower than normal values of sex hormone-binding globulin (SHBG), follicle stimulating hormone (FSH), testosterone, and epitestosterone when compared to men without pattern hair loss. Although hair follicles were previously thought to be permanently gone in areas of complete hair loss, they are more likely dormant, as recent studies have shown the scalp contains the stem cell progenitor cells from which the follicles arose. Transgenic studies have shown that growth and dormancy of hair follicles are related to the activity of insulin-like growth factor (IGF) at the dermal papillae, which is affected by DHT. Androgens are important in male sexual development around birth and at puberty. They regulate sebaceous glands, apocrine hair growth, and libido. With increasing age, androgens stimulate hair growth on the face, but can suppress it at the temples and scalp vertex, a condition that has been referred to as the 'androgen paradox'.