There is specific impact of steroid hormones in both sexes. Testosterone/estrogen ratio in males and females gives reason for differences in skin thickness and texture. Male epidermis for example is 20% thicker than female epidermis, being able to bind a larger amount of moisture, and containing more collagen in all ages, thus, making male skin more dense and vigorous [1].

Androgens stimulate sebum production. Therefore, due to higher androgen levels male seborrheic glands produce more sebum leading to fatty glow and coarser pores of the skin [2]. Consequently, acne, acneiform eruptions, and blemishes are more common in seborrheic areas (face, back, upper thorax, shoulders) (Figure 1). Due to androgen triggered follicular hyperkeratosis sebum is “trapped” within the follicle forming primary acne lesions (comedones). Comedones act as ideal breeding ground for habitual microbacteria like several cocci, propionibacterium acnes, and certain malassessia species, making them proliferate above physiological amounts. Hence, these microbacteria metabolize only a certain amount of sebum “leaving behind” free fatty acids. These “corrode” the follicular epithelium, and invading surrounding tissue they lead to irritation and immuno-chemical reactions. Chemotaxis causes “invasion” of granulocytes, inflammation, and development of secondary acne lesions (papules, pustules, nodes, and cysts). Severe manifestations may also involve sweat glands leading to hidradenitis or cause fistulae and gum boils in axillary, inguinal, or perineal locations. Early treatment of acne lesions aims at limitation of long-term sequels.

Figure 1: Acne papulopustulosa (source: Derma, Graz).

Wet shaving is an additional risk factor for male facial skin, causing dryness, irritation, redness, and exfoliation, as well as cutting damage caused by the razor blade followed by bleeding and scar formation. Decades back, male skin care consisted of washing and shaving only, since the beginning of the 21^st century it has changed a lot. Today, skin care products particularly designed for male skin have revolutionized the market. A great variety of cosmeceuticals, aligned to the individual skin type, is now used by the young generation.

In general, water contact exhausts lipids from epidermal skin layers. Frequent water contact disturbing the barrier function of the skin, leads to dryness and eczema reactions. Moreover, testosterone has proven negative effect on the barrier function, making male skin particularly more sensitive than female skin [3]. Regular application of skin care products can reduce vulnerability of the skin and eczema probability by supplying the skin with lipids and moisture.

On one hand, male skin regenerates more quickly than female skin due to testosterone controlled higher cellular turnover, on the other hand wound healing turns out to occur more slow than in females, due to higher testosterone levels [4].

In females hyperandrogenism causes characteristic changes of the skin and impacts on hair growth, resulting in fatty skin and hair by increased sebum production (seborrhea), acne, hirsutism, androgenetic alopecia, as when all together, they can be summarized under the term SAHA-syndrome and hyperpigmentation in skin folds, referred to as acanthosis nigricans. Severity may vary, but exclusion of polycystic ovary syndrome should be accomplished [5].

There is a lack of evidence-based literature on the context of testosterone and skin aging [6]. Sparse trials have shown that there is no specific difference in skin aging processes in both sexes. Presumably, males tend to develop a larger number of seborrheic keratosis and females preferably solar lentigines [7]. UV-exposure and Fitzpatrickskin- type are predispositions for developing wrinkles and rhytides in both sexes [8]. Males may develop melanomas more easily than women [9,10].

Hair follicles develop during the first trimester of fetal development. At that time the whole skin except palms and soles, lips and semimucosal areas is covered with fine lanugo hair follicles. Each hair follicle is “loaded” with an individual genetic code, telling when during the lifespan, where on the skin, due to which trigger a hair will grow or fall out. Androgens play an important role in androgenic hair loss, even if androgen levels are within normal ranges, as androgen sensitivity of the hair follicles varies individually due to genetic determination.

Androgenetic alopecia male type

Di-hydro-testosterone DHT, synthesised by the activity of the enzyme 5-α-reductase is the most important metabolite of testosterone concerning hair growth and hair loss. Whereas DHT is responsible for hair loss in certain areas of the scalp, it represents the main trigger for hair growth in androgen sensitive areas in (elderly) males (Figure 2), and hirsute females. On the scalp hair follicles miniaturize according to the androgensensitivity of the individual, thus, leading to the clinical appearance of androgenetic alopecia presenting a receding frontal hairline as well as vertex and total balding [11]. Severity of androgen dependent balding can be scored according to the Norwood-Hamilton scale [12] (Figure 3). The transformation of testosterone into DHT can be reduced by finasteride, a 5-α-reductase inhibitor. Finasteride is used successfully in the prevention and treatment of androgenetic alopecia [13].

Figure 2: Norwood-Hamilton Score for male type androgenetic alopecia.

Figure 3: Variable androgen sensitivity in certain body areas: hair-loss vs. hairgrowth (source: Derma, Graz).

Androgen induced hair loss has an individual impact on psychosomatic status and quality of life has been evaluated in a multinational telephone survey: more than 60% of over 1.500 individuals reported negative impact of hair loss on their self-confidence, 21% showed depressive symptoms [14].

Androgenetic alopecia female type

DHT plays an inferior role in hormonal hair loss in women, androgen metabolites like dihydro-epi-androsterone DHEA and androstendione are more important in female androgenetic alopecia, causing a certain phenotype gradually developing sparse hair in parietal areas, scored according to the Ludwig scale (Figure 4). A ndrogentic female hair loss is most likely retaining the frontal hairline [15].

Figure 4: Ludwig score for female type androgenetic alopecia.

Antiandrogens like Cyproterone-Acetate (CPA) may reduce hormonal hair loss in females. Finasteride should not be used for the treatment of AGA in premenopausal women, as male fetus´ may feminize, whereas several studies have shown that finasteride is able to stop further hair loss in post-menopausal females [16,17].

The amount of hair growth in certain body areas differs according to culture and ethnicity. Thus, the differentiation between androgeninduced Hair growth in hirsute women has to be differentiated from increased vellus hair growth in females with mediterranean or indogenic background. Hirsutim defines a male phenotype pattern of hair growth in females, 5% of all women are affected (Figure 5 and 6).

Figure 5: Hirsutism: androgen-induced hair growth (source: Kopera).

Figure 6: Undesired hair growth in androgen-sensitive area (source: Derma, Graz).

From internal-medical view hirsutism may have various reasons: ovary and adrenal tumors are rare, congenital adrenal hyperplasia is even more so, insulin-resistance-syndrome, Mb. Cushing and Polycystic Ovary Syndrome (PCOS), representing the most common endocrine disorder in 5% to 10% of all females. More than 70% of hirsute women feature PCOS – occurring also in females with normal menstrual cycle.

Hirsute females must not necessarily show increased Testosterone levels, but there may be a “masked” hyperandrogenism. It is a very sophisticated mechanism that is controlled by increased LH/FSH-ratio, increased GnRH-excretion and the insulin metabolism in females with PCOS. Nevertheless, in severe cases elevated androgen levels lead to manifest hyperandrogenism. Moreover, the LH-synergistic effect of insulin on theca-cells in the ovaries also attributes to increased androgen production. On the other hand, it inhibits SHBG production, which should bind testosterone, thus, leading to elevated free testosterone levels [18].

Hirsutism may cause negative impact on psychosocial health and behaviour [19] (Figure 7). In order to achieve optimal results, management of hirsute females requires optimal interdisciplinary care, combining endocrinologic, dermatologic, gynecologic, and aesthetic know how for the application of individual treatment options like antiandrogens, insulin sensitizers, and light-assisted hair reduction.

Figure 7: Psychosocial comorbididy and hirsutism.