Skin water-holding capacity and transdermal estrogen therapy for menopause: a pilot study

Piérard-Franchimont, C; Letawe, Céline; Goffin, Veroniqué; Pierard, Gérald

doi:10.1016/0378-5122(95)00924-a

Cited by 107 publications

(57 citation statements)

References 12 publications

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“…Diminution of circulating estrogens that accompanies menopause is associated with increased skin dryness 11 and slackness, 12 and decreased skin elasticity, 13 dermal thickness of thigh skin, 14 and skin collagen content as measured in thigh, 15 abdomen, 16 and pubis. 17 Conversely, various studies have shown that estrogen therapy (ET) users have better skin hydration [18][19][20][21] and elasticity, [20][21][22][23] higher density of collagen fibers, 24 fewer fine wrinkles, 19,21 and thicker skin 20,25 than nonusers. However, other studies have failed to show any effect of ET on the prevalence or severity of cutaneous signs of menopause on the photoaged face.…”

mentioning

confidence: 99%

Induction of Collagen by Estradiol

Rittié¹,

Kang²,

Voorhees³

et al. 2008

Arch Dermatol

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To evaluate the effectiveness of topical estradiol in stimulating collagen I and III production in naturally aged and photoaged human skin of postmenopausal women and age-matched men.Design: Vehicle-controlled treatment followed by biochemical and immunohistochemical analyses of skin biopsy specimens.Setting: Academic referral center.Participants: Seventy healthy volunteers (40 postmenopausal women with a mean age of 75 years, and 30 men with a mean age of 75 years) with photodamaged skin.Interventions: Topical application of estradiol, 0.01%, 0.1%, 1%, or 2.5% or vehicle on aged or photoaged skin, with biopsy specimens taken after last treatment.Main Outcome Measures: De novo synthesis of collagen by quantitative polymerase chain reaction, immunohistochemistry, and enzyme-linked immunosorbent assay.Results: Topical estradiol increased procollagen I and III messenger RNA and collagen I protein levels in sun-protected aged hip skin in postmenopausal women and, to a lesser extent, in age-matched men. Surprisingly, no significant changes in production were observed in women or men after 2-week estradiol treatment of photoaged forearm or face skin, despite similar expression of estrogen receptors (ER-␣, ER-␤, and GPR30) in aged and photoaged skin. Estradiol treatment induced the estrogenresponsive gene GREB1, indicating that penetration of topical estradiol and genomic response to estrogen were similar in the 3 anatomic sites.Conclusions: Two-week topical estradiol treatment stimulates collagen production in sun-protected hip skin, but not in photoaged forearm or face skin, in postmenopausal women and aged-matched men. These findings suggest that menopause-associated estrogen decline is involved in reduced collagen production in sun-protected skin. Interestingly, alterations induced by long-term sun exposure hinder the ability of topical 2-week estradiol to stimulate collagen production in aged skin.

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mentioning

confidence: 99%

Induction of Collagen by Estradiol

Rittié¹,

Kang²,

Voorhees³

et al. 2008

Arch Dermatol

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“…Kanda and Watanabe [19 ]demonstrated that estradiol suppresses apoptosis in keratinocytes by promoting Bcl-2 expression and induces the expression of cyclin D2, an important cell-cycle regulatory protein [20]. Estrogen may also play a role in the stratum corneum barrier function [21,22,23,24]. …”

Section: Discussionmentioning

confidence: 99%

Intrinsic versus Extrinsic Aging: A Histopathological, Morphometric and Immunohistochemical Study of Estrogen Receptor β and Androgen Receptor

Seleit¹,

Bakry²,

Repey

et al. 2016

Skin Pharmacol Physiol

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Skin is a target organ of sex steroids which play important roles in skin health and disease. The aim of this study is to investigate the expression of estrogen receptor β (ERβ) and androgen receptor (AR) in human skin from different age groups for a better understanding of the hormonal regulation of skin aging. Using standard immunohistochemical techniques, biopsies of sun-unprotected and sun-protected skin were taken from 60 normal subjects. Sun-protected skin showed significantly higher immunoreactivity for ERβ and AR compared to sun-unprotected skin of all age groups. Significantly higher ERβ H score and percent of expression were associated with the 20-35 years age group compared to the groups that were 35-50 years and >50 years old (p < 0.02, p = 0.03, respectively) in sun-unprotected and sun-protected skin (p < 0.001, p = 0.01, respectively). AR H score showed a negative correlation with age (p = 0.04) with no significant difference in immunoreactivity in different age groups, either in sun-unprotected or sun-protected skin. There was also a significant correlation between ERβ H score and epidermal thickness in sun-unprotected (p = 0.04) and sun-protected skin (p = 0.04) in studied subjects regardless of age. The same relationships did not reach significance with AR expression. However, a significant positive correlation was detected between H scores and percent of expression of ERβ and AR in sun-unprotected (p = 0.01, p = 0.02, respectively) and sun-protected skin (p = 0.005, p = 0.02, respectively) regardless of age. In conclusion, both ERβ and AR decline gradually with intrinsic and extrinsic aging. This decline is more obvious with extrinsic aging. Further large-scaled studies are recommended to expand, validate and translate current findings to clinically significant, diagnostic and therapeutic applications. Molecular studies to investigate the probable ligand-independent action of both receptors are warranted. In addition, their gene expression patterns and associated signaling and metabolic pathways can also be tackled to provide a basis for further interventions in pathological processes that involve their dysregulation.

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“…This condition results from an altered desquamation process that is often associated with decreased hydration of the upper layers of the stratum corneum and with weakening of the barrier function of the skin. Both the skin water-holding capacity and the barrier function of the stratum corneum appear to increase following HRT [20,21].…”

Section: Hrt and Skin Epitheliamentioning

confidence: 99%

Downgrading skin climacteric aging by hormone replacement therapy

Quatresooz

Pierard

2007

Expert Review of Dermatology

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For years, hormone replacement therapy (HRT) for menopausal women appeared straightforward for the believers. It markedly improved climacteric changes in many organs, including the skin. However, emerging information suggested that combined HRT increased the risks of cardiovascular diseases and invasive breast cancer [1,2]. Many healthcare providers and women were soon impressed by the alarmist lay press regarding the use of these hormones. These pessimistic views were more recently challenged. Indeed, it was demonstrated that the administration of estrogens alone in hysterectomized women did not significantly increase the incidence of coronaropathies and breast cancer [3]. The bulk of recent studies also confirmed that estrogens or estroprogestins effectively suppress the climacteric syndrome and genital atrophy, while significantly decreasing the risk of osteoporotic fractures. The cardiovascular risk appears more prominent in late menopausal HRT users than in early menopause, and the risk of venous thromboembolism can be reduced strongly by using transdermal instead of oral estrogens [4]. Regarding the risk of breast cancer, the additional absolute risk of postmenopausal women using estroprogestins is only 0.08 per 100 women per year, whereas estrogens alone do not increase the risk [3,5].

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Skin water-holding capacity and transdermal estrogen therapy for menopause: a pilot study

Cited by 107 publications

References 12 publications

Induction of Collagen by Estradiol

Induction of Collagen by Estradiol

Intrinsic versus Extrinsic Aging: A Histopathological, Morphometric and Immunohistochemical Study of Estrogen Receptor β and Androgen Receptor

Downgrading skin climacteric aging by hormone replacement therapy

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