Female pattern baldness is a quite common, non-scarring form of hair loss that may be observed in all ages, but most notably in postmenopausal women. This condition typically manifests as a diffuse reduction of hair density over the frontal and vertex regions. The occipital and parietal areas may also be involved.
The pathophysiology of female pattern baldness has not yet been completely elucidated, and the exact mechanism remains elusive. Still, there is ample evidence that etiology is multifactorial. In other words, female pattern hair loss arises as a result of the interplay of hormonal, genetic and environmental factors.
The pathologic hallmark of patterned hair loss (both male and female) is a decline in the propensity of hair follicles to produce hair. The duration of anagen (active growth phase of a hair follicle) becomes shorter and that of telogen (the resting phase of a hair follicle) lengthens. Although the period for which the telogen club hair is contained within the follicle remains the same, the reentry of the hair into anagen is postponed.
Hair follicles then undergo a regressive process known as miniaturization, which eventually leads to their deletion. A principal histologic feature is an increased proportion of small vellus-like follicles, frequently coupled with a mild to moderate chronic inflammatory infiltrate around the follicular infundibulum. This is the part of the follicle that extends from the epidermis to the orifice of the sebaceous gland duct.
Follicular miniaturization is generally regarded as a gradual process that occurs over the course of several hair cycles. This has yet to be proved to occur in properly designed longitudinal studies, as there is some evidence that miniaturization occurs rapidly, possibly even within a single hair cycle.
Myriad studies have shown that women with hair loss are more likely to exhibit elevated levels of androgens or demonstrate other signs of androgen excess, in comparison with women without hair loss. Nevertheless, in almost all studies, a variable proportion of women with female pattern baldness do not show any clinical or biochemical signs of androgen excess.
This indicates that female pattern hair loss, unlike male pattern baldness, may evolve even in the absence of androgen stimulation. To further complicate the problem, some women with androgen insensitivity due to alpha reductase deficiency present with patterned scalp alopecia. Another recent questionnaire-based study demonstrated that androgen therapy can even improve female pattern hair loss in some individuals.
A genetic predisposition is thus thought to be necessary for this condition. In fact, a polygenic mode of inheritance for female pattern hair loss has been well established. The implicated genes may determine the age of hair loss onset, pattern, progression, as well as the severity of the problem. The androgen receptor/ectodysplasin A2 receptor locus found on the X-chromosome has been found to predispose to female pattern baldness.
Clearly, age also plays a pivotal role in this condition. Cross-sectional data points to declining hair density in the female population around the age of 30 years, with a concomitant decrease in mean hair diameter. Hair thinning in women who show female pattern hair loss often extends to areas not typical of androgenetic alopecia, such as the occipital and parietal scalp. This lends further credence to the hypothesis that there are androgen-independent mechanisms underlying female pattern baldness.
In addition, female pattern hair loss can be both precipitated and exacerbated by certain factors that cause telogen effluvium (a type of diffuse hair loss). These include certain medications, weight loss, stress, as well as hormonal therapies with proandrogenic effects. Other proposed factors include hypothyroidism and hyperprolactinemia.