Menopause is defined as the last menses, recognized after 12 months of amenorrhea that is not associated with a pathologic cause. On average, the age of onset of the menopause is 50 years, but it may vary among women, ranging from 45 up to 56 years of age (1, 2).

The menopause is a result of a transition from full ovarian function to a complete lack of ovarian estrogen biosynthesis. It is now apparent, that estrogens have additional, important and diverse functions (3). Undoubtedly, decrease in estrogens synthesis leads to climacteric changes, which hinder life of woman and worsen the quality of life. Typical menopausal symptoms comprise hot flushes, sweating, insomnia and vaginal dryness or urinary frequency. Up to 75% of menopausal women experience one or more of such symptoms. Postmenopausal disturbances are observed in the cardiac system (progressive coronary heart disease, increased blood pressure), in a loss of bone mineral density or as metabolic changes (worsening lipid profile, altered body fat distribution with central obesity, altered glucose and insulin balance) (4, 5).

A number of studies have shown that estrogens have many important, beneficial and protective roles in the skin physiology. An impact of estrogens on human skin is recognized as changes that are observed in post-menopausal women, with a number of studies documenting differences seen following the menopause. Many women report a sudden onset of skin aging several months after climacteric symptoms begin (6).

The menopause leads to skin aging, which becomes thinner with a loss of collagen content, decreased elasticity and increased wrinkling (3). The decline in estrogen, which occurs during the menopause, reduces the mitotic activity in the epidermal basal layers as well as modyfing epidermal lipid synthesis, causing xerosis (7). There are fewer blood vessels and their walls are often damaged, resulting in easier occurance of skin extravasations. Further, unpleasant symptoms, include numerous teleangiectases, roughness, sallowness, sagging and pigment alternations (8).

Aging associated with climacteric hormonal changes also affects some hair characteristics and is responsible for decreased hair coverage in middle-aged women (9). With menopause, the hair distribution of the female body starts to change, but some changes can occur both in a distribution and in a structure of hair. Age related decrease in hair copper and calcium concentration is observed in perimenopausal women (2, 10, 11). The optical fibre diameter analysis reveals that diameters of hair in the frontal and parietal scalp are lower in postmenopausal women, but there is no change in the occipital hair diameter (12).

The hair follicles are often affected in menopausal women, and indeed, hair represents a specific receptor structure expressing declines related to fluctuations in circulating levels of sex steroids (9). As it is was mentioned above, one of the major changes during menopause is the virtual cessation of ovarian estrogen production. The major source of estrogen after the menopause is from conversion of adrenal androgen to estrogen by the enzyme aromatase in the peripheral tissues (12). There is an evidence that an estrogen receptor pathway within the dermal papilla regulates the telogen-anagen transition of the hair follicle (13). In humans, estrogens reduce the rate of hair growth, but prolong the duration of growing phase of hair cycle growth and probably shorten its resting phase (14, 15). Estradiol has also been noted to induce aromatase activity in human scalp follicles and it is the possible one mechanism by which it may exert own biological activity (12). While it has been recognized, that estrogens stay important modulators of hair growth, the details of molecular regulatory pathways have not been well characterized. In contrast, the role of androgens on hair growth has dominated the field of hair biology and they are the most important among sex hormones, that regulates hair growth (16). Androgens can lead to the conversion of fine vellus hairs to terminal hairs in pubic and axillary areas, but they cause the opposite hair conversion on the scalp (17). In postmenopausal women, testosterone levels decrease compared to young women, although the residual ovarian synthesis after the menopause appears to contribute to a higher proportion of circulating testosterone, relative to estrogens. This may be due to higher LH levels and their effect on ovarian stromal steroidogenesis. As there is a free available to cells and SHBG (sex hormone binding globulin) bounded – testosterone, in the postmenopausal period, estrogens dependant SHBG levels decline and may account for higher bioavailability of testosterone (18). The increase in androgen to estrogen ratio may cause some changes in hair distribution seen during menopause. Hair loss occurs for example in axillary and pubic areas, whereas some women also start to lose hair on the scalp and androgenic alopecia or frontal fibrosing alopecia should be considered. It is observed that, the frequency of all-over thinning and frontal hair loss increases with age of women, whereas hair loss at the temples do not increase with age (19, 20). In contrast, some women may also experience an increase in facial hair (2, 7, 17).

As the role of androgens in perimenopausal alopecia has not been clearly established, the most preferred term for female androgenetic alopecia is currently female pattern hair loss (FPHL). It much better describes diffuse hair loss patterns in women with uncertain relationship between androgens and this entity (7, 21). The term FPHL distinguishes from male pattern of hair loss described by James Hamilton, which features the fronto-temporal recession and hair loss over the vertex while the occipital scalp is preserved (17, 22, 23). A studies supporting a notion of nonandrogen pathways involved in FPHL show, that sebum secretion, a marker of end-organ androgen response, is not elevated in perimenopausal women (12). It is rather suggested, that the FPHL occurs in genetically predisposed women due to androgens (16, 24, 25). Summarizing, neither the androgen-dependent nature nor the genetic basis of the FPHL has been clearly established (26).

Typically, hair in FPHL is fine textured and the pull test is negative, but some visibility occurs on the scalp and increases spacing between hair on the vertex compared with the occiput (12, 27). There is a diffuse reduction in hair density over the crown and frontal scalp with relative sparing of the anterior hair line, leaving there 2-3 cm of frontal hair zone (7, 17, 21, 24, 28). Women who present with a reduction in hair density, frequently exhibit thinning and widening of the area of hair loss on the central part of the scalp, which when it includes a breach of the frontal hairline is described as Christmas tree pattern, the one observed in the majority of women with FPHL (17, 29).

The clinical evaluation and definition of the FPHL has traditionally relied on the Ludwig scale, which divides the severity of hair density reduction over the crown into three grades. Further estimation of hair loss, was developed as Savin density scale, which classifies FPHL into 8 stages of increasing crown balding, in addition to a special subcategory to detect frontal anterior recession. The simplification of Savin’s scale, which assesses the degree of hair loss using the midline part, was created by Sinclair as five-point visual analogue scale (21, 23, 29, 30).