Parameter |
Change |
Gender differences |
Impact of Sex hormones |
| Wrinkles |
Develop and become more pronounced with age |
No established gender differences. |
Wrinkling may be related to reduced stimulation of collagen and glycosaminoglycan synthesis by estrogen. |
| Skin thickness |
Becomes thinner with age in both sexes (atrophy).
Epidermal thickness decreases 6.4% per decade [67].
Dermal thickness decreases 20% by old age [68]. |
Skin of adult men is thicker then that of women [62].
Skin thickness decreases faster in older women than in older men [67]. |
Much of the decrease in skin thickness is thought to result from collagen changes in the dermis (see below) |
| Collagen (dermis) |
Fibers more disorganized; balance between synthesis and degradation shifts toward greater degradation [70].
Collagen matrix degrades and fibroblasts collapse [71,72] |
See above. |
Androgens promote thicker skin and higher collagen production in murine models [91,92]
DHEA declines result in lower procollagen synthesis and more collagen degradation [73,74].
DHEA is the principal source of estrogen synthesis in postmenopausal women. Estrogen supplementation in postmenopausal women increases skin collagen content [78,168] |
| Elastin (dermis) |
Fibers degrade; skin less elastic |
Alterations more pronounced in older women [68].
In the first 5 years following menopause, facial skin elasticity declines 1.5% per year [83,84]. |
Women who received HRT in the first 5 years following menopause exhibited no significant change in skin elasticity [83,84]. |
| Skin barrier function |
Baseline barrier function (as measured by TEWL) unchanged [100,101].
Once compromised, barrier integrity takes longer to be restored [101-103] |
No established gender differences [104] |
Androgens reduce skin barrier function and estrogens increase it [64,105,106] |
| Skin moisture and water holding capacity |
Reduced water content of stratum corneum [108].
Reduced water-holding capacity of the dermis due to declines in glycosaminoglycans and hyaluronic acid [109]. |
No established gender differences. |
Estrogens increase skin moisture and water-holding capacity [110] by increasing levels of hyaluronic acids [112,169] and glycosaminoglycans [113] |
| Sweating and thermoregulation |
Impaired with advancing age [117-119]. |
Men sweat to a greater degree than women in similar situations [114,115].
Elevated temperature thresholds for sweating and reduced sweat response more pronounced in older women than in men [119]. |
Sweat glands express 5α-reductase (which converts androgens to DHT) and the androgen receptor through which DHT exerts its action. |
| Sebum production |
Gradual decrease in women. |
In men, sebum levels change minimally from puberty until about age 80.
In women, sebum secretion decreases gradually from menopause through age 80, after which no appreciable change occurs [124]. |
Sebocytes regulate the effect of androgens in the skin.
DHEA enhances sebum production in both sexes [75], but not through direct action on sebocytes [128]
Testosterone promotes DHT synthesis in sebocytes and stimulates sebum production [126].
In older women, estrogen supplementation suppresses sebum production; progesterone overcomes this effect [87].
Sebum production is affected by the interplay of growth factors (IGF-1), estrogen, progesterone and androgens (DHEA) [127,128]. |
| Hair growth |
Androgenetic alopecia usually begins around age 30 in genetically susceptible men and women. |
Male-pattern baldness is more common and severe can start as early as late adolescence.
Female-pattern baldness is less common and usually milder. |
Both androgens and estrogens affect hair growth. DHT acts on hair follicles to release growth factors in androgen dependent areas (beard, axilla, pubis) [131].
In male androgenetic alopecia, DHT causes susceptible scalp follicles miniaturize; the number of follicles in anagen phase decreases.
In women, scalp hair follicles have lower 5α-reductase levels, lower AR levels, and higher aromatase activity, limiting the impact of DHT.
Estrogens act on hair follicles through ERβ, which is present at sites of hair renewal in follicles of women but not of men. |
| Wound healing |
Skin is more susceptible to mechanical damage [141] and wound healing declines [142] |
Men display lower rates of wound healing at all ages. |
Androgens depress wound healing by increasing inflammation, proteolysis, and matrix degradation [148].
Estrogens promote wound healing by inhibiting inflammation and promoting keratinocyte mitogenesis, deposition of matrix components, and angiogenesis [170]
Subcutaneous DHEA restores wound healing rates in ovarectomized mice and promoted wound healing in aged mice, likely through local conversion to estrogen [158] |
