Skin, hair and beyond: the impact of menopause

Abstract

The skin is an endocrine organ and a major target of hormones such as estrogens, androgens and cortisol. Besides vasomotor symptoms (VMS), skin and hair symptoms often receive less attention than other menopausal symptoms despite having a significant negative effect on quality of life. Skin and mucosal menopausal symptoms include dryness and pruritus, thinning and atrophy, wrinkles and sagging, poor wound healing and reduced vascularity, whereas skin premalignant and malignant lesions and skin aging signs are almost exclusively caused by environmental factors, especially solar radiation. Hair menopausal symptoms include reduced hair growth and density on the scalp (diffuse effluvium due to follicular rarefication and/or androgenetic alopecia of female pattern), altered hair quality and structure, and increased unwanted hair growth on facial areas. Hormone replacement therapy (HRT) is not indicated for skin and hair symptoms alone due to the risk–benefit balance, but wider potential benefits of HRT (beyond estrogen’s effect on VMS, bone, breast, heart and blood vessels) to include skin, hair and mucosal benefits should be discussed with women so that they will be able to make the best possible informed decisions on how to prevent or manage their menopausal symptoms.

摘要

皮肤是内分泌器官, 是雌激素、雄激素和皮质醇等激素的主要靶点。除了血管舒缩症状（VMS）, 相比其他绝经症状, 皮肤和毛发症状通常更少受到关注, 尽管这些症状对生活质量有显著的负面影响。皮肤和粘膜绝经症状包括干燥和瘙痒、变薄和萎缩、皱纹和下垂、伤口愈合不良和血供减少, 而皮肤癌前病变和恶性病变以及皮肤老化倾向几乎完全由环境因素引起, 尤其是太阳辐射。头发的绝经症状包括头皮上的头发生长减少和密度降低（由于毛囊稀疏和/或女性型雄激素性脱发引起的弥漫性脱发）、头发质量和结构改变以及面部多余毛发生长增加。由于风险-效益平衡, 激素替代疗法（HRT）不能单独适用于皮肤和头发症状, 但是HRT的这些更广泛的潜在益处（除了雌激素对VMS、骨骼、乳房、心脏和血管的作用外）包括对皮肤、头发以及粘膜的益处。应与女性探讨HRT的这些益处, 以便她们能够就如何预防或管理绝经症状做出尽可能明智的决定。

Keywords:

• Menopause
• perimenopause
• exposome
• hair
• skin
• mucosa
• hormones
• hormone replacement therapy

Introduction

The median menopausal age is 51 years and is generally preceded by a course of perimenopause (around 2–8 years) when the clinical and biological features of approaching menopause commence (this includes the 12 months following the last menstrual cycle) [1,2].

The age of onset of the menopause transition is multifactorial and is influenced by genetics [3] and exposome factors, including environmental factors like UV radiation and tobacco smoke and lifestyle factors like hormones, nutrition/alcohol consumption, stress and sleep deprivation [4,5].

In this review, we mainly focus on manifestations of skin and mucosa as well as hair changes at perimenopause and menopause, discussing which hormones play a role and how their clinical consequences can be prevented or managed.

Symptoms of menopause

Perimenopausal symptomatology is variable in different women. Generally, within 4–5 years of menopause, 80% of women will be devoid of symptoms or have only mild symptoms, while 20% may have symptoms for up to 10 years or longer. The most common climacteric symptoms in around 75% of women are vasomotor symptoms (VMS), including hot flashes, night sweats and sleep disturbance, that may start during perimenopause. VMS will often lead women to consult a physician. A multiethnic study in 3302 women enrolled at seven US sites found that the median total VMS duration was 7.4 years [6]. Risks for hot flashes include early or iatrogenic menopause, females with skin of color or Hispanic ethnic groups, high body mass index or sedentary lifestyle, smoking, anxiety, depression, psychosocial stress and use of selective estrogen receptor modulators (SERMs) or aromatase inhibitors [7].

Other common physical symptoms include genitourinary syndrome of menopause (GSM), palpitations, headaches, bone/joint/muscle pain, asthenia, tiredness, insomnia, breast tenderness, dyspareunia and skin aging/hair/mucosal disorders, while psychological symptoms include memory loss, irritability, poor concentration and loss of confidence [8]. Insomnia may contribute to neurological symptoms that emerge during perimenopause. Other risks to health associated with menopause include bone loss/osteoporosis, heart disease, diabetes, obesity and cognitive decline.

Skin, hair and mucosal changes during menopause

Besides VMS, skin and hair symptoms often receive less attention than other menopausal symptoms. In a survey of 87 women attending a menopause clinic, 64% reported skin problems and around half indicated that the menopause had caused skin changes, with dry skin being the main symptom [9]. Additionally, in a survey from 2018 in 1287 French women, 72% reported they noticed changes in their skin at perimenopause/menopause, while 50% felt they had been insufficiently informed about these symptoms, highlighting the need for educating women and healthcare professionals on the impact of menopause on the skin [10]. The visible signs of dryness, wrinkles and sagging, especially on the face, contribute to an increased perception of aging and decreased attractiveness [11] with a significant impact on quality of life (QoL). Furthermore, a woman is frequently judged, particularly in westernized societies, by the quality of her skin and hair (including hair color), both of which are seen to reflect health and well-being, and may cause a great psychological burden [12].

Large longitudinal studies have investigated the onset and duration of VMS but there is a paucity of information on studies evaluating skin, mucosal and hair symptoms and hormonal changes at different stages in menopausal women. Furthermore, it may be difficult to distinguish between so-called menopausal symptoms from loss of ovarian function or from natural aging or psychosocial factors. Actinic lentigines (‘dark spots’) are common in women of menopausal age but are caused almost exclusively by photodamage rather than hormonal changes. However, one pilot study reported that in photo-exposed areas, such as the face, menopausal women acquire a higher degree of pigmentation than premenopausal women after equal exposure time [13]. Wrinkling has been shown to correlate most closely with chronologic age and skin color rather than menopause, whereas skin rigidity (an inverse measure of dermal collagen density) was only positively correlated with the time since menopause in women with white skin [14].

During the perimenopause course, peripheral estrogen levels do not steadily decline but fluctuate around the normal range, since aromatization of androgens increases, leading to variations in sebum levels. Skin dryness may be noticed in early perimenopause, but it may initially be somewhat compensated by sebaceous gland hypertrophy. Later in menopause when sebum production is markedly reduced, the skin becomes increasingly dry and itchy, followed by sagging and atrophy.

Skin atrophy due to collagen loss is more pronounced in menopausal women [15–17]. In early menopause, skin collagen levels decrease fairly rapidly with a collagen reduction of approximately 30% in the first 5 years, followed by a further decline of 2% per year for the next 15 years [17]. A steady depletion of collagen and reduced skin thickness with yearly reductions of 2.1% and 1.1%, respectively, was observed in menopausal women [18].

Diffuse effluvium due to follicular rarefication and/or androgenetic alopecia of female pattern may be observed later in menopause due to sustained reduction of hair cycling, while the existing hair becomes thinner and drier due to aging. However, thinning may be noticeable at perimenopause in women predisposed to develop centroparietal alopecia. Hair issues at menopause include reduced scalp hair but increased (unwanted) hair growth in certain areas on the face [12].

GSM with changes in the bladder, vulva and vagina due to vulvovaginal atrophy affects almost half of postmenopausal women. Symptoms of vaginal dryness, vaginal irritation and itching may be followed by reduced elasticity, dyspareunia, urinary urgency, dysuria and recurrent urinary-tract infections, which will deteriorate with time from the menopausal transition if left untreated [19–22].

In addition, oral mucosa dryness [23] and conjunctival dryness may increase as menopause progresses.

The skin is an endocrine organ

Skin cells produce sex hormones and other steroids, such as estrogens, androgens and glucocorticoids from systemic steroid hormones originating from the adrenals [24]. In menopause, changes of sex hormones occur. The androstenedione/sex hormone-binding globulin ratio, cortisol, melatonin, insulin-like growth factor-1 (IGF-1) and norepinephrine are also related to the pathophysiology of menopause [24,25].

Role of hormones on skin, hair and mucosal menopausal symptoms and conditions

In addition to the effects of chronological aging, sun exposure and other environmental or lifestyle factors affect the menopausal skin biology.

Estrogens

Hypoestrogenism may affect various systems and plays important roles in the immune function, cancer development and other biological processes related to health and well-being [26]. Estrogens (specifically 17β-estradiol) are primarily synthesized in the ovaries in premenopausal women, while estrone comes from non-ovarian sites in menopausal women, including the adrenal glands, skin, brain, adipose tissue and pancreas [27,28]. Human skin is a major target of hormones [24,29] with glucocorticoids, cAMP analogs, growth factors and cytokines modulating local estrogen synthesis via aromatase, mainly expressed in the pilosebaceous unit [30,31]. Estrogen receptors (ERs) are abundant in both dermis and epidermis, and are most dense in the genitalia, face and lower limbs [32,33]. In human skin, there is no gender difference in the pattern or distribution of ER. Two isoforms of ER are known (i.e. ERα and ERβ). Whereas a large number of natural and synthetic estrogens show a similar binding affinity to both receptors, other ligands are more selective, such as genistein or daidzein, which induce a stronger activation of ERβ. ERα is expressed exclusively in basal and partially differentiated cells of normal sebaceous glands and is seen in only a small portion of the eccrine gland epithelia. In the axillary apocrine glands, a strong nuclear expression of ERα is seen in the secretory epithelium [34]. ERβ is expressed by sebaceous glands (in the same distribution as ERα) and by human eccrine sweat glands. ERβ is widely expressed in the skin, namely in dermal papilla cells and dermal fibroblasts, sebocytes, adipocytes, melanocytes and keratinocytes of the outer root sheath [35].

The impact of estrogen decline at menopause on aging skin has been extensively reviewed [11,15,17,33,36–38]. Estrogen deficiency during menopause alters certain skin functions: impaired skin barrier function causes skin dryness from diminished skin moisture and decreased sebum production on the face and scalp; decreased antioxidant function and impaired wound healing [15,39]; decreased collagen and elastin synthesis leading to wrinkling and dermal thinning on both skin and genital mucosa, and decreased glycosaminoglycans in the extracellular matrix, such as hyaluronic acid, leading to decreased skin turgescence and reduced hydration [40]; and thermoregulation function with pallor, reduced vascularity and hot flashes caused by vasodilation deep within the blood capillaries in the papillary dermis.

Estradiol can significantly alter both the growth and life cycle of the hair follicle by binding to ERs, thus influencing aromatase activity, which is responsible for converting androgen into estrogens [41]. Estradiol prolongs the anagen phase of the hair cycle, which enhances hair growth by increasing the synthesis of essential growth factors stimulating the proliferation of follicular keratinocytes, explaining the reduction of hair renewal, growth and thickness, and rarefication of hair observed during menopause [27].

Estrogen induces glycogen production by vaginal and cervical epithelial cells. Menopausal decline in estrogen results in urogenital atrophy and a loss of vaginal epithelial cells [21]. The resulting reduction in epithelial glycogen in menopause also leads to low levels of lactobacilli as they are unable to proliferate without glycogen, hence they no longer produce antimicrobial and anti-inflammatory products leading to an increased susceptibility to mucosal injury [19].

Androgens

Unlike estrogen and progesterone which decline rapidly, androgen secretion, which is already relatively low in women, declines gradually with menopause and aging. Androgens play a role in modulating hair growth and sebum production in the pilosebaceous unit. The relative increase of androgens during the menopause leads to clinical hyperandrogenism manifesting as sebaceous gland hypertrophy and androgenetic alopecia of female pattern due to regional reduction of hair renewal and growth, which can be aggravated by genetic and exposome factors [42].

Aging, concomitant diseases, genetic factors, environmental factors and medication, in conjunction with hormonal changes occurring during menopause, can all affect hair quality and result in cessation of hair growth activity, hair thinning, loss of trio or duo groups and hair density decline [12,43]. Androgens, such as testosterone, dihydrotestosterone and their prohormones, may play a role in miniaturization of hair follicles and a decrease in body and scalp hair or transform small, fair vellus hairs in hormone-sensitive areas on the face to darker terminal hair follicles [12,41]. Relative peripheral hyperandrogenism, secondary to androgen, estrogen and progesterone imbalance, may impact the hair growth pattern [12,44]. However, most women presenting with alopecia, particularly of the female pattern, do not have elevated androgen levels, indicating that the androgen/estrogen ratio and not androgen-dependent mechanisms may be involved [12,45,46].

Dehydroepiandrosterone (DHEA; much of which is sulfated DHEA-S) in the skin is mainly produced in the adrenal glands from cholesterol by two cytochrome P450 enzymes. DHEA is converted in sebocytes to testosterone and, finally, in all skin epithelial cells to 5α-dihydrotestosterone (DHT), which are skin active androgens with diversified activity, whereas its aromatization leads to the synthesis of skin active estrogens (estradiol and estrone) and more potent androgens, which have greater impact on skin. DHEA and DHEA-S are the most abundant sex steroids in plasma. Circulating levels of DHEA decline dramatically with age, albeit with large variability on a scale from 1 to 8 in different women, which may explain the large disparity of symptoms [47]. DHEA is the cardinal source of both androgen and estrogen synthesis for all tissues except the uterus following menopause. Supplementation has been shown to increase skin thickness, hydration and sebum production. Local synthesis of the sex steroids in the skin affects the eccrine sweat glands and hair follicles.

Cortisol

The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with adrenocorticotropic hormone (ACTH). The release of corticotrophin-releasing hormone (CRH), ACTH and cortisol from skin cells may explain some skin aging signs [48,49]. Stress hormones negatively affect the epidermal barrier [50] and cortisol suppresses the pro-inflammatory cytokines IL-1 and TNF-α, resulting in deficient cutaneous repair. The clinical effects of cortisol on the skin are dryness, inflammation and wrinkles.

Overnight urinary cortisol levels were found to increase during the late stage of perimenopause in some women, especially if they had severe hot flashes [51]. Furthermore, increased salivary cortisol levels were observed in women in menopause [52].

Another stress hormone, norepinephrine, released by the adrenal medulla, inhibits epidermal proliferation and reduces blood perfusion via α-adrenergic-induced vasoconstriction [53]. Finally, stress may also hamper hair growth, although studies in menopausal women are lacking [54].

Vitamin D

Vitamin D is a fat-soluble vitamin, characterized by synergic action of its two main metabolites: 25-OH-D₂, which is obtained from plant sources, and 25-OH-D₃, which comes from animal products and endogenous synthesis in skin through exposure to sunlight. While the prevalence of vitamin D insufficiency is more common in older, frailer women, vitamin D supplementation was not shown to affect overall health outcomes in several clinical studies [55,56], but may improve vaginal health outcomes in menopausal women with vulvo-vaginal atrophy symptoms [57] and metabolic syndrome risk profile [58]. Furthermore, in several clinical studies on vitamin D insufficiency supplementation in menopausal women, calcifediol was found to be superior to cholecalciferol in improving vitamin D status [59] and was associated with a concomitant greater improvement in muscle strangth after oral supplementation for 6 months [60].

Melatonin

Melatonin declines with menopause and/or aging and changes in melatonin concentrations related to the menopausal transition may be associated with VMS, mood, sleep and QoL [61].

Prevention and management of menopausal symptoms

Studies have shown that only 25% of women who experience symptoms consult a physician, highlighting the need to improve awareness concerning the management of menopausal symptoms [7,62]. Decisions about therapy for perimenopausal and menopausal women should be individualized and will depend on symptomatology, health status, immediate and long-term health risks, personal life expectations and availability of therapies [63,64].

Hormone replacement therapy

Since the Women’s Health Initiative (WHI) trial results in 2002 in older women (mean age 63 years) led to a dramatic reduction in the number of women receiving hormone replacement therapy (HRT), it has now become clear that the risks of HRT are low for healthy women (<60 years of age or within 10 years of menopause onset) [64–69]. HRT remains the most effective treatment for VMS, GSM (local vaginal hormone therapies for some patients) and bone protection, as well as for improving QoL [70–72]. HRT should be started early for hot flashes and painful intercourse and there is no maximum length of treatment time. For women with primary ovarian insufficiency (due to genetic, iatrogenic [e.g. surgery, chemotherapy], infectious or autoimmune causes) [2] without contraindications, HRT is recommended until at least the average age of natural menopause as the benefits on bone, heart, cognition, GSM, sexual function and mood outweigh the risks [72].

The ancillary Women’s Health Initiative Memory Study of Magnetic Resonance Imaging (WHIMS-MRI) study measured subclinical small vessel cerebrovascular disease to possibly explain the negative cognitive findings reported by the WHIMS [73,74].

HRT consists of estrogen (17β-estradiol or conjugated equine estrogen [CEE]) and, in women with an intact uterus, progestogen (micronized progesterone) is also required to protect the endometrium. In the WHI trial, women with prior hysterectomy receiving only CEE for a median of 7.2 years did not exhibit increased risk for all-cause mortality, coronary heart disease or cancer mortality, did present decreased hip fracture and diabetes rates, but presented increased stroke and venous thrombosis [75]. In women <60 years of age or within 10 years of menopause, statistically significant reductions of 23% in breast cancer and 20% in heart disease were observed after 5.9 years of CEE use and 11.8 years of follow-up; this benefit may not apply to populations at higher risk [75,76]. Hence, the increased risks of HRT were due to the progestogen and not the CEE (used in the USA but not in Europe) [64,75].

As an alternative to progestogen, SERMs are synthetic non-steroidal agents that have variable estrogen agonist and antagonist activities in different target tissues [77]. For example, bazedoxifene may provide endometrial [78] and breast protection [79] in menopausal women with a uterus, while conjugated estrogen [77,80] reduces bone loss [81,82], VMS [83] and vaginal atrophy [84]. Furthermore, CEE may exhibit SERM-like properties such as reduced breast cancer incidence and mortality.

Efficacy data are lacking on compounded bioidentical hormones for correcting menopausal hormonal imbalances and there are safety concerns about dose and purity [85].

Until there is a better understanding amongst all physicians of the minimal risks of HRT when individualized with regular evaluations, many women will continue to suffer a reduced QoL unnecessarily [86]. Furthermore, HRT may offer wider benefits, including the management of skin, hair and mucosal symptoms, as discussed below.

Non-hormonal therapies

Estrogen therapy is the gold standard for menopausal symptoms and there is limited evidence for the efficacy of non-hormonal therapies. Some efficacy in reducing hot flashes has been observed with cognitive behavioral therapy, clinical hypnosis, low-dose selective serotonin-reuptake inhibitors and serotonin–norepinephrine reuptake inhibitors, drugs that lower blood pressure (clonidine), antidepressants (paroxetine salt) and gabapentinoids [7,87]. They may be preferred by women who have contraindications to hormone therapy (e.g. a history of or an elevated risk of breast cancer, chronic venous disease or deep vein thrombosis) or unacceptable side effects with HRT.

Effects of HRT on skin

Clearly, HRT is not indicated solely for skin and hair benefits, but these should be considered in individual patient discussions concerning the treatment of menopausal symptoms. Improvements in skin surface texture, hydration, collagen content of the dermis and viscoelasticity have been shown in women receiving HRT/estrogen (oral and transdermal) [15,17,33,36,37,88]. A randomized controlled trial in menopausal women with 12 months of oral estrogen increased dermal thickness by 30% [89] and, similarly, 6 months of HRT increased skin collagen by 6.5% [90]. Minor improvements in skin elasticity, hydration and thickness, but not surface lipids, were observed after 7 months of HRT [91]. HRT appeared to mitigate the progressive enlargement of pores after menopause [92].

Results on wrinkles are less clear. In a cross-sectional analysis, improvements in skin elasticity and wrinkle severity were observed after 5 years of HRT [93]. A 24-week study reported a statistically significant improvement with CEE versus placebo for skin thickness and fine wrinkles [94]. However, other HRT studies did not show a significant improvement in wrinkles [95,96]. In a randomized controlled trial, HRT showed some benefits on skin but did improve skin wrinkles or rigidity at most facial locations when women within 36 months of their last menstrual period were treated for 4 years with HRT (oral CEE or transdermal estradiol with micronized progesterone) versus placebo [97]. The authors suggested that confounding in non-randomized studies may occur due to race/ethnicity as women with skin of color had the lowest wrinkle scores even without HRT [97].

The observation that improvement in wrinkles with HRT only occurs in non-photoaged skin highlights the importance of photoprotection. A study of 40 postmenopausal women (mean age 75 years) receiving topical estradiol or vehicle showed that principally sun-protected skin on the hip, but not photoaged forearm or facial skin, benefited from HRT [98].

Studies have also been conducted with SERMs [15,33,99,100]. Raloxifene, a SERM which is used successfully to prevent and treat postmenopausal osteoporosis, as well as reduce breast cancer risk, was also shown to increase collagen biosynthesis in human skin fibroblasts [101]. In a 12-month trial with 17 postmenopausal women (mean age 66 years), raloxifene had a similar effect to estradiol treatment (patch plus cyclic medroxyprogesterone acetate) in increasing skin elasticity [102].

Summarizing, HRT, SERMs, topical estrogens, topical isoflavones (soy-derived compounds that interact with ERs) and phytoestrogens may improve estrogen-deficient skin [37,38,99]. However, prospective, placebo-controlled clinical studies to document the efficacy and potential risks of therapeutic interventions for the skin and hair problems during menopause are required.

Finally, tibolone is a synthetic selective tissue estrogenic activity regulator used for HRT in some countries. In the tibolone patient information leaflet, unusual hair growth is listed under common side effects and itchy skin under rare ones. However, a Cochrane systematic review on short-term and long-term effects of tibolone did not report any skin and hair side effects [103].

Effects of HRT on hair

Data are lacking on the effect of HRT on hair quality and sebum production during menopause [104]. A recent review on the impact of micronized progesterone (topical or oral, with or without estradiol) found no publications on menopausal scalp hair quantity and quality or on female pattern hair loss in perimenopausal/menopausal women [105].

Management of skin, hair and mucosal symptoms

Dermo-cosmetics and adapted skin care for facial skin and other areas may be used alone or combined with HRT (if prescribed for other symptoms).

Photoprotection

Photoprotection (sunscreen, clothes, sunglasses, seeking shade) can prevent photoaging and may reduce the prevalence of premalignant and malignant skin lesions (melanoma, non-melanoma skin cancer).

Dermo-cosmetic ingredients can compensate hormonal changes on the skin

Pro-xylane

A C-xylopyranoside derivative (pro-xylane) has been shown to stimulate the synthesis of mucopolysaccharides in the dermis and epidermis to improve skin elasticity and tonicity. Reduced visible signs of skin aging and changes in sebum composition were observed in postmenopausal women after applying topical serum containing pro-xylane 3% daily for 60 days [106].

Cassia extract

Cassia extract, from a traditional medicinal plant, has anti-aging effects on skin by reducing the impact of cortisol on collagen and hyaluronic acid synthesis to stimulate extracellular matrix synthesis [107].

Hyaluronic acid

Hyaluronic acid, or hyaluronan, in the skin extracellular matrix has viscoelastic and hygroscopic properties [108], and may be a suitable alternative to vaginal estrogens for the treatment of symptoms of vaginal atrophy in women with contraindications to HRT [109].

Other ingredients

Dermo-cosmetics for skin hydration to treat dry skin may include collagen stimulators, antioxidants, or estrogen.

Dedicated dermo-cosmetics for hair and scalp conditions

Alopecia may be difficult to manage during the menopause, especially since loss of hair volume/density is age-dependent [12,110]. Dedicated shampoo may be used in combination with or after using a prescription medication. Aminexil and Stemoxydine (an antioxidant) are active dermo-cosmetic ingredients shown to decrease the percentage of hair in the resting telogen phase to maintain hair density [111,112].

Holistic approach

Increased awareness of symptoms and prevention/treatment/coping strategies might help women during menopause. The skin aging process is accelerated by menopause but also by the exposome [113]. Calcitrol (vitamin D) is synthesized in the skin exposed to UV radiation and is important for bone health; however, photoprotection is essential for preventing skin premalignant and malignant lesions and skin aging signs [114]. Photoprotection, reducing stress, healthy nutrition, weight loss, physical exercise and discontinuation of smoking early in the perimenopausal period may help to alleviate symptoms and reduce the risk of further decline before menopause is established.

Expert recommendations

Recommendations for physicians (including dermatologists and gynecologists) based on clinical literature, information from professional menopause societies and expert opinion of the authors are summarized in Table 1.

Table 1. Expert recommendations for prevention/treatment/coping strategies for symptoms of menopause, including skin, hair and mucosal symptoms.

Symptom	Recommendations		References
Vasomotor symptom management	Gynecologist follow-up and start HRT early when needed (annual follow-up if continuing after 5 years)	Estrogen and progesterone HRT Estrogen and SERM HRT	[72] [84]
	Non-hormonal therapies if HRT contraindicated	Acupuncture therapy Behavioral therapy	[64]
Genitourinary and mucosal symptoms	Gynecologist follow-up and start HRT early when needed	Estrogen and progesterone HRT Estrogen and SERM HRT	[72]
	If only genitourinary symptoms without VMS	Local vaginal estrogen therapy	[7,115,116]
Skin symptoms	Dermatologist follow-up, photoprotection to avoid/reduce photodamage and photoaging	Daily sunscreen of appropriate sun protection factor Protective clothing, sunglasses	[114]
	Adapted skin care for facial skin and other areas	Pro-xylane Cassia extract Antioxidants Other collagen stimulators Hydration for dry skin Avoid chronic application of topical corticosteroids	[106] [107] [117,118]
	HRT (if prescribed for other symptoms)	Not indicated for skin symptoms alone due to the risk–benefit balance
Hair symptoms	Dermatologist follow-up if significant androgenic alopecia	Local minoxidil medication (solution or foam)	[119,120]
	Loss of volume/density is age dependent	Specific hair dermo-cosmetics to increase volume (Aminexil, Stemoxydine) Nutricosmetics to enhance hair quality	[111,112]
	Management of facial hypertrichosis	Epilation techniques Local eflornithine	[121]
All symptoms and general well-being	Stress reduction, psychological support and improving sleep quality	Cognitive behavior therapy Mindfulness and meditation	[7]
	Advise lifestyle changes (physical exercise, weight loss, healthy eating, reduce stress, quit smoking)	Quitting smoking is essential before receiving HRT	[72]

HRT, hormone replacement therapy; SERM, selective estrogen receptor modulator; VMS, vasomotor symptoms.

Conclusions

Most previous reviews about menopause, its physiologic changes and various therapies included a paucity of information about the role of sex steroids and their replacement from a dermatologic perspective. Although HRT is not indicated for skin and hair symptoms alone due to the risk–benefit balance, a better understanding of skin, hair and mucosal changes at menopause and how to manage or prevent them will reduce the burden and improve the well-being and QoL of women at this stage in their lives. Further efforts are needed to educate physicians on these wider potential benefits of HRT on skin, hair and mucosa (beyond the benefits for VMS, bone, breast, heart and blood vessels), and this information should be discussed with women to help them make the best possible informed decisions as soon as they have any menopausal symptoms.

Potential conflict of interest

D.K. is an employee of Vichy Laboratoires and all other authors received honoraria as advisory board members for Vichy Laboratoires.

Source of funding

None.

Acknowledgements

Writing and editorial assistance for the preparation of this manuscript were provided by Helen Simpson, PhD, ISMPP CMPP™, of My Word Medical Writing and funded by Vichy Laboratoires. Advisory board and editorial assistance were supported by Vichy Laboratoires.