Patterned hair loss, the most common type of hair loss affecting men an women, is characterized by a process of progressive hair miniaturization whereby large, pigmented terminal hairs are replaced by fine, colorless vellus hairs (1,2). In men, this condition preferentially affects hair on the superior and anterior temporal areas of the scalp, whereas in woman it more commonly presents in a diffuse pattern in the crown, with or without sparing of the frontal fringe (3,4).

In unaffected scalp, hair has a normal, healthy life cycle of anagen phase of two to six years, catagen phase of two to three weeks, telogen phase of two to three months (5). The key point in patterned hair loss is progressive shortening of anagen phase. Since there is less time to grow, hairs become shorter and finer, to the point where individuals appear to be bald, despite the continuing existence of large numbers of fine vellus hairs (6,7)

Androgens play a central role in this process of miniaturization, hence the reason both male pattern hair loss (MPHL) and female pattern hair loss (FPHL) are collectively referred to as androgenic or androgenetic alopecia. MPHL appears to result from a combination of hyperandrogenism, an androgen-dependent genetic predisposition to androgen sensitivity and an androgen-independent genetic predisposition to androgen sensitivity. (8).

The influence of androgens in FPHL is not pronounced as in MPHL. Certainly, women with clinical hyperandrogenism- identified by the development of acne, hirsutism, and oligomenorrhea- frequently develop a pattern of hair loss similar to what is seen in males, with deep bitemporal recession and vertex thinning. Similarly, those with androgen-producing tumors develop male pattern of thinning. However, the majority of women with FPHL show no clinical signs of hyperandrogenism and have normal testosterone and dehydroepiandrosterone sulfate (DHEA-S) levels (33,35).

Explanations for the more limited androgen role in females have focused on the enzyme aromatase, which has a scalp concentration fivefold higher in females than in males. Aromatase catalyzes the conversion of testosterone and androstenedione to the estrogens, estradiol, and estrone, respectively (16). It has been proposed that these estrogens modulate hair loss by increasing the levels of sex hormone binding globulin (SHBG), a serum protein that binds androgens, and in doing so decreases the amount of bioavailable hormone. This theory is congruent with the studies demonstrating an inverse correlation between sex hormone binding globulin levels and the degree of hair loss in women (36)

In addition, aromatase may blunt the impact of androgens by decreasing tissue levels of DHT, via the metabolism of androstenedione, a precursor hormone to DHT (37). Lending support to the important role of aromatase is the finding that women treated with aromatase inhibitors experience FPHL as a side effect (21).

The incidence of female pattern hair loss (FPHL) is more difficult to establish than in men and its diagnosis is more challenging. This is because of less obvious patterns of hair loss than in men and because of the frequency with which other type of hair loss occurs. In brief, it is “the great mimicker” and should be included in the differential diagnosis of diffuse hair loss in any woman. (6).

Three frequently occurring patterns of hair loss have been described in women:

Hamilton examined 214 women in his study and found at least Type II MPB in 79% of them after puberty. He noted, however, that the bi-temporal recessions seen in Type II tended to be less prominent in women than in men and was likely to go unnoticed until their late twenties. Type IV MPB occurred in 25% of women by the age of 50 years and 50% had Type IV by the age 60 years. Type IV was defined as consisting of (i) deep fronto- temporal recessions extending more than 3 cm posterior to a coronal plane between the external auditory meatus and (ii) some mid-frontal hairline hair loss. (7)

A “centrifugal pattern” of hair loss first discussed by Ludwig (8): it consisted of hair loss over the caudal scalp. In contrast to Hamilton, he emphasized the essentially intact frontal fringe in these individuals. This type of hair loss arbitrarily divided in to three degrees of severity as shown in Fig. 2B2-4b. Postmenopausal women shoved an increased tendency to a more male pattern of hair loss.

A “Christmas tree” pattern first described by Olsen (9) (Fig. 2B2-5a and b). She noted that women with hair loss did not necessarily present with diffuse hair loss over the entire vaultal scalp, but instead may have increasing hair loss toward the frontal scalp “with encroachment on and sometimes breach of the frontal hair line”.loss.

1- Such women also frequently have or may eventually develop decreased hair density in temporal, parietal, and occipital areas that are normally used as donor areas for transplanting. Therefore, they may or may not be acceptable candidates for transplanting (11).

2- Many of these women develop small (2 to 5 mm) oval irregular shaped areas of total alopecia that are scattered within the areas of diffuse thinning. Such areas can be punched out and then sutured or transplanted with a mixture of two-to three FU (11).

3- In women, there appears to be two main peaks of onset of pattern hair loss: the third and fifth decades. Those having earlier onsets tend to develop more severe degrees of hair loss and this should be borne in mind when a decision is made about treating women in their late teens or twenties (6)

4- Norwood also believes that androgen-dependent MPB is a different disease than FPHL. In his study he found that FPHL begins in the late twenties and peaks after 50 year of age when testosterone levels are falling, suggesting that it is not an androgen dependent. Birch et al. also have written that evidence exists for FPHL being either androgen dependent or androgen independent in different individuals. They summarized their view of the condition as follows: “Female pattern hair loss and it is possible that both androgen-dependent and androgen- independent mechanisms contribute to the phenomenon” (16).

Before we start medical treatment, it’s very important that the patient is well informed about the course of this progressive-genetic hair loss/miniaturization, the length and frequency of the medical treatments; otherwise patients generally quit few months after the start of therapy mentioning that the therapy he/se has given was not effective and even might blame physician to be a trades man to sell therapies to the patients.

The best way to prevent misunderstandings and future problems regarding the effectiveness of the therapies that you have advised is thorough information. So how I do it;

We can assume the scalp like a tank filled with water with a hole on the bottom. Tank represents the scalp and the water in it represents the existing hairs. I tell my patients that, there exists a hole on the bottom of their tanks coming genetically where there is no way to close and continue telling that this hole’s size may vary accordingly to genetic tendency and their stress levels -which clears why the hair fall tends to peak time to time- and continue to tell that, their tanks will leak all the time and best treatment to keep and increase the water level is keep adding water from outside. I also resemble the medical treatments like a fuel that we put in to our car’s tank where we need regular refueling. After this point they most likely understand that there is no miracle treatment which will cure their problem when applied few times and convince to have these treatments regularly.

Here is the exact way how I describe & simplify the treatment options for my patients. I group the treatments under three main headings:

SECTION-A:

–Male & Female Pattern Hair Loss, Chapter 2; Hair Transplantation 5th Edition by Walter Unger

SECTION-B:

-My personal contribution which briefs about The Explanation Strategy of Female Pattern Hair Loss Course & Medical Therapy Options Classification to the patients.