In the United States, menopause occurs in women between the ages 45 and 56, with a median age of 51.¹ Racial, ethnic, and genetic differences contribute to the variability in the timing of onset.^2,3 Approximately 60 million women in the United States are over age 45, with about 2 million women reaching menopause annually. Women typically spend about 40% of their lifespan postmenopausal, translating to roughly 30 or more years.⁴

Menopause, defined retrospectively as twelve consecutive months of amenorrhea without other pathologic causes, reflects the permanent cessation of ovarian follicular activity. The menopausal transition, often referred to as perimenopause, precedes menopause and is characterized by menstrual cycle irregularity and fluctuating ovarian hormone levels that may begin several years before the final menstrual period.⁵

In addition to natural menopause, some individuals experience surgical menopause following bilateral oophorectomy, which results in an abrupt decline in ovarian hormones.⁶ Similarly, premature ovarian insufficiency or premature menopause occurs when ovarian function declines before the age of 40, often leading to earlier and sometimes more abrupt hormonal changes. These distinct clinical contexts may influence the timing and presentation of menopause-associated symptoms.⁶ Inevitable cutaneous symptoms arise as a result of these hormonal changes, impacting many perimenopausal and menopausal women. Recent narrative reviews have highlighted that declining estrogen during menopause contributes to measurable deterioration in “skin quality,” including reduced collagen content, elasticity, hydration, and barrier function. Despite these well-recognized physiologic effects, clear clinical guidance for the dermatologic management of menopausal skin remains limited, and many patients remain unaware of menopause-associated skin changes.⁷

A narrative review was conducted to synthesize existing literature on the etiology of menopause-associated skin and hair changes and their management. The review process involved defining a targeted research scope, followed by a comprehensive literature search using databases including PubMed and Google Scholar. Studies addressing dermatologic changes in menopause were critically appraised and organized thematically to summarize current evidence, highlight knowledge gaps, and review therapeutic options. Study types included in this review were randomized controlled trials, case-control studies, cross-sectional studies, preclinical experimental studies, and review papers. A specific date range was not utilized for this narrative review. Examples of keywords utilized in the literature search include “dryness in menopause,” “itching in menopause,” “wrinkles in menopause,” “hyperpigmentation in menopause,” “acne in menopause,” “rosacea in menopause,” “hair loss in menopause,” “menopause skin management,” and “treatments for skin in menopause.” As this is a narrative review, this work does not follow a systematic review protocol and therefore may not include all available studies on this subject matter.

Menopause is associated with a wide range of dermatologic changes, including xerosis, pruritus, atrophy, hyperhidrosis, impaired wound healing, thinning, rhytides, decreased hair growth, decreased hair density, and increased unwanted facial hair growth.⁸ Mechanistically, menopause-associated dermatologic changes can be broadly understood across several interconnected biological domains: dermal extracellular matrix remodeling, epidermal barrier and lipid alterations, neurovascular and immune regulation, and pilosebaceous unit and hair follicle biology.⁹ The etiology of many of the cutaneous changes is largely attributable to decreased estrogen secondary to declining ovarian function, through effects on fibroblast activity, epidermal lipid synthesis, inflammatory mediators, and follicular cycling.⁹ Together, these mechanisms contribute to the structural, functional, and inflammatory skin changes observed during the menopause.

Estrogen is essential in dermal homeostasis, regulating collagen, elastin, water, and extracellular matrices.^10,11 The principal endogenous estrogens include estradiol (E2), estrone (E1), estriol (E3), and estetrol (E4).¹² Estradiol is the most biologically potent estrogen during the reproductive years and exhibits strong affinity for estrogen receptors in multiple tissues, including the skin. After menopause, estrone becomes the predominant circulating estrogen due to peripheral conversion of adrenal androgens in tissues such as adipose tissue. Estriol and estetrol demonstrate weaker receptor affinity and are produced primarily during pregnancy.¹² These estrogens primarily exert their biologic effects through estrogen receptors (ERα and ERβ), which are expressed in multiple skin cell populations including keratinocytes, dermal fibroblasts, melanocytes, and hair follicle cells. Activation of these receptors regulates gene transcription involved in collagen synthesis, extracellular matrix organization, epidermal lipid production, and water retention, overall supporting the structure and hydration of the skin.^10,11

Of the many biological effects of estrogen, interactions with dermal fibroblasts are particularly important in linking hormonal decline during menopause with dermal structural changes. Dermal fibroblasts are the primary producers of extracellular matrix components, including collagen, elastin, and glycosaminoglycans, that maintain dermal thickness, elasticity, and hydration. Estrogen signaling directly regulates fibroblast activity through estrogen receptors expressed in dermal cells, influencing collagen synthesis, extracellular matrix turnover, and matrix metalloproteinase activity.¹³ With estrogen deficiency during menopause, fibroblast-mediated production of collagen and other matrix components decreases, leading to reduced dermal thickness and elasticity and increased wrinkle formation. Estrogen signaling in fibroblasts also modulates cytoskeletal organization and intracellular signaling pathways, including ERK activation and G protein-coupled estrogen receptor pathways, which influence fibroblast morphology, adhesion dynamics, and matrix production.¹⁴ These mechanisms have been demonstrated in an in vitro menopause model using primary human dermal fibroblasts.¹³ Estrogen withdrawal was associated with reduced collagen and glycosaminoglycan synthesis and with alterations in fibroblast morphology and cytoskeletal organization.¹³ By these mechanisms, a decrease in estrogen contributes to transepidermal water loss (TEWL), a weakened skin barrier, a decline in skin collagen, and elastin degeneration, which can manifest as decreased skin elasticity and thickness, increased wrinkling, and increased dryness.^10,11

Research has demonstrated that estrogen stimulates collagen maturation and turnover,¹⁵ and declining levels of estrogen lead to a marked decrease in skin thickness and collagen content, particularly collagen types I and III.¹⁰ In addition to reduced collagen synthesis, estrogen deficiency may also promote extracellular matrix degradation through increased activity of matrix metalloproteinases (MMPs), enzymes that break down collagen and elastin fibers. Disruption of the balance between collagen synthesis and degradation contributes to dermal thinning, loss of elasticity, and increased formation of rhytides observed during the postmenopausal period.^13,16

Estrogen also plays a crucial role in maintaining ceramide composition and preserving skin moisture and barrier function by stimulating the production of acid mucopolysaccharides and hyaluronic acid.¹⁷ Estrogen-deficient states such as menopause are associated with changes in the skin’s ceramide profile, such as reduced abundance and shorter chain lengths. These lipid alterations also affect the lamellar organization of the stratum corneum which is essential for maintaining an effective epidermal barrier. Disruption of this lipid architecture increases TEWL and facilitates penetration of environmental irritants and allergens. Barrier impairment also may influence the cutaneous microbiome, which further contributes to irritation and inflammation.^18,19

In addition to decreasing estrogen, progesterone and testosterone also decline during menopause; however, these hormonal shifts are less well characterized compared to those of estrogen. During menopause, there is often a relative increase in androgenic activity due to the dramatic decrease in estrogen and sex hormone-binding globulin.²⁰ This relative androgen excess at the tissue level stimulates sebaceous gland growth and sebum production and may contribute to cutaneous changes such as unwanted facial hair.²¹ Overall, while these hormone-related skin changes can occur relatively rapidly during menopause, the precise biological pathways linking hormonal fluctuations to skin aging still remain incompletely understood.^7,22

In addition to responding to circulating hormones, the skin itself functions as an active endocrine organ capable of local steroid metabolism and hormone signaling. The different cutaneous cells express enzymes necessary for steroidogenesis and can locally synthesize glucocorticoids, androgens, and estrogens from circulating precursors. This local hormone production supports the concept of the skin as a neuro-endocrine-immune organ and contributes to regulation of epidermal barrier function.²³

Barrier dysfunction during menopause has been implicated in cutaneous sensitivity and irritation. Fluctuations in estrogen have been linked to the development and exacerbation of sensitive skin symptoms. In individuals with menopause, estrogen deficiency and resultant barrier dysfunction may increase susceptibility to microbial colonization and injury, impair cutaneous immune responses, and dysregulated wound healing.^24,25 In a cross-sectional survey of 278 women aged 20-65 years, peri- and postmenopausal women with pre-existing skin conditions or more severe menopausal symptoms were more likely to report increased skin sensitivity after menopause.²⁴

Given estrogen’s role in maintaining the skin’s structure and barrier function, menopause-related estrogen depletion may exacerbate or unmask underlying skin sensitivity, potentially worsening existing primary skin conditions. This review examines the relationship between menopause and skin health with a focus on common dermatologic conditions and explores potential therapeutic options for menopause-associated skin changes.

While the physiologic effects of estrogen decline are well characterized, the psychosocial implications of these changes are also important. Skin and hair symptoms during the menopausal transition can carry substantial psychosocial burden and may be under-recognized in clinical encounters.⁸ Prior literature notes that skin and hair symptoms may receive less attention than other menopausal symptoms despite a significant negative effect on quality of life.²⁶ Their concerns can affect self-image, confidence, and social functioning, and changes in appearance may contribute to distress, stress, and anxiety. Clinicians should remain attentive to the emotional changes that may accompany perimenopause and menopause, and incorporate supportive, patient-centered counseling into management.

Though widely thought to be a skin condition of adolescence, persistent acne and adult-onset acne are not uncommon.²⁷ Adult acne, typically described as acne presenting beyond age 25, has a rather large prevalence range, with studies estimating a prevalence 20-40%.²⁸ Menopausal acne, which refers to acne observed around perimenopause or menopause, affects approximately 15% of women.²⁷ Despite increasing interest in menopause-related acne, data on its management in this population remain limited. Menopausal acne can cause significant scarring and postinflammatory dyspigmentation, which are associated with impairments in quality of life and self-esteem.

A history of acne in adolescence is a strong predictor of experiencing acne during menopause, but women without this history can also experience menopausal acne, termed “late-onset acne.”^28,29 The hormonal changes of menopause, including the decline in estrogen and relative androgen excess contribute to sebum overproduction and acne development.²⁸ In addition, genetic predisposition and lifestyle factors such as high stress levels and low consumption of fruits, vegetables, and fresh fish may also play a contributory role in the development of acne during this period.²⁹

In comparative analyses, postmenopausal acne is reported to be less severe than adult-onset acne and more frequently involves the trunk and facial areas.²⁸ Adult-onset acne typically localizes to the lower face, particularly on the mandible and chin, with less frequent truncal involvement.^28,29 Despite a more mild acne presentation, menopausal women have greater skin sensitivity, resulting in a higher frequency of post-inflammatory erythema, scarring, and dyschromia.^28,29 These cosmetically unfavorable changes likely contribute to the increased severity of stress and depression associated with postmenopausal acne.

Rosacea during menopause is influenced by several factors, including hormonal changes, immune system dysregulation, neurovascular dysregulation, microbiome dysbiosis, and environmental factors.⁸ The decline in estrogen levels characteristic of menopause exacerbates rosacea through mechanisms that include skin barrier impairment, increased vasoreactivity, and resultant increased skin sensitivity and inflammation—hallmarks of rosacea.³⁰ Changes in the skin microbiome including increases in Demodex folliculorum, which may be mediated by hormonal changes of menopause, can further trigger or worsen rosacea.³⁰ Menopause associated increase in skin sensitivity increases susceptibility to oxidative damage from ultraviolet (UV) exposure, which may be implicated in the pathogenesis and exacerbation of rosacea in this population.^31,32 Compared to premenopausal adults and adolescents, menopausal women may exhibit more prominent symptoms of rosacea and may experience persistent facial redness, flushing, and telangiectasias, particularly in association with hot flashes.³³ In this population, increased skin sensitivity and dryness associated with the characteristic hormonal fluctuations of menopause may further intensify symptom burden and skin discomfort.³⁰

Neurovascular dysregulation may further contribute to rosacea symptoms during menopause. Estrogen influences vascular tone and cutaneous blood flow, and declining estrogen levels may increase vasoreactivity and flushing responses, mechanisms that overlap with the vasomotor symptoms experienced during menopause. These changes may contribute to facial erythema and flushing in individuals predisposed to rosacea.³⁴

Postmenopausal women often experience hair thinning, clinically referred to as female pattern hair loss (FPHL), which is characterized by reduced hair density and diameter in the frontal and vertex scalp regions. The estimated prevalence of FPHL among postmenopausal women is 52.2%.³⁵ Risk factors for FPHL during menopause include genetic predisposition, age, time since menopause, elevated body mass index, and increased scalp sebum levels.³⁵ Hormonal shifts, specifically the decline in estrogen and relative increase in androgens, such as testosterone, are central to the pathogenesis of FPHL.⁸ Reduced estrogen levels are associated with a shorter anagen phase of the hair cycle, resulting in miniaturized hair follicles and diminished scalp hair density.⁸ Estrogen normally helps maintain the anagen (growth) phase of the hair cycle, supporting follicular longevity and hair shaft production.⁸ During menopause, reduced estrogen signaling combined with relative androgen predominance may promote follicular miniaturization in genetically susceptible individuals.⁸ This shift contributes to the characteristic pattern of decreased scalp hair density alongside increased terminal hair growth in androgen-sensitive facial regions.⁸

Wrinkles and fine lines, also known as rhytides, are among the most prominent cutaneous manifestations of menopause, primarily attributable to a decline in estrogen. Fine lines represent superficial, early changes in the dermis, while wrinkles indicate deeper, more established structural alterations.

Estrogen plays a critical role in maintaining skin architecture by stimulating collagen synthesis, promoting dermal elasticity, and enhancing water retention.^15,36 With the onset of menopause, the abrupt decline in estrogen leads to a substantial reduction in dermal collagen content, estimated at up to 30% within the first five years.³⁷ Additional changes in menopause include decreased skin thickness, disorganized collagen structure, diminished elasticity, and impaired skin hydration.^15,36 These changes compromise the skin’s biomechanical integrity and accelerate the formation of wrinkles and fine lines. There is concurrent loss of glycosaminoglycans that further reduces moisture retention and turgor and exacerbates the clinical appearance of skin aging.^15,36

Clinical studies have demonstrated a strong correlation between the duration of menopause and the severity of facial rhytides, with postmenopausal women exhibiting more pronounced changes than their premenopausal counterparts.³⁸ Estrogen receptors in both the epidermis and dermis mediate the hormone’s effects on skin homeostasis, and their downregulation in menopause further contributes to skin fragility and increased wrinkling.^15,36 In addition to intrinsic hormonal changes, extrinsic environmental aging factors, including UV radiation, air pollution, tobacco exposure, contribute to dermal matrix degradation and oxidative damage, further exacerbating menopausal skin aging.^8,39

While hormonal replacement therapy has been shown to partially reverse these changes by restoring collagen content, increasing dermal thickness, and improving elasticity, it is not recommended solely for cosmetic purposes due to its systemic risk profile.⁴⁰ Non-hormonal interventions such as topical retinoids, antioxidants and laser devices have been studied as adjunctive and alternative therapies, particularly in women who are not candidates for HRT.⁴⁰

Xerosis and pruritus are frequent menopausal symptoms, primarily driven by estrogen deficiency and its effects on structural and functional alterations within the epidermis and dermis. These alterations include decreased surface lipids, particularly ceramides, reduced hydrophilic glycosaminoglycan content, and diminished water-holding capacity, all of which contribute to impaired skin hydration, increased transepidermal water loss, and impaired barrier function.¹⁵ This decreased skin moisture has been demonstrated with aging, and plays a key role in skin dryness, wrinkling, and atrophy and these alterations manifest clinically as xerosis, pruritus, decreased skin elasticity, and dermal atrophy.¹⁵ Histologic changes include thinning of the stratum corneum, reduced expression of the differentiation markers, and weakened epidermal cohesion, contributing to skin fragility and increased susceptibility to irritants.⁴¹

Pruritus may arise from both the mechanical consequences of xerosis and neuroinflammatory mechanisms.⁴² Estrogen deficiency has been associated with increased cutaneous nerve fiber density and the upregulation of type 2 cytokine-mediated pathways, contributing to heightened itch sensitivity and alloknesis.⁴² In the vulvar and vaginal regions, estrogen deficiency leads to an array of dermatologic changes, including thinning of the epithelium, reduced collagen and elastin content, decreased lubrication, and increased vascular fragility.⁴³ These changes contribute to vulvar pruritus, burning, soreness, and are a core component of the genitourinary syndrome of menopause. Patients frequently report these symptoms and increased vulnerability to dermatoses such as lichen sclerosus and lichen planus.⁴³ The estrogen-related loss of microbial diversity and elevation in vaginal pH further predispose menopausal individuals to inflammation, discomfort, and infection.⁴³

The psychosocial impacts of skin aging cannot be understated. In addition to rhytides, skin quality, which includes attributes such as pigmentation, redness, dullness, dryness, pores, crepiness, firmness, and hydration, has been shown to have a significant impact on self-perception, emotional health, quality of life, and interactions with others.⁴⁴ Despite how common menopausal skin aging is, many women are unaware of the skin-related impacts of menopause.⁷ As such, skin quality and the dermatologic conditions described in this paper should be discussed by clinicians treating patients during and around the menopausal period. Importantly, recent studies have shown an increasing demand for cosmetic procedures specifically among women ages 40-69, further highlighting the need for clinicians to be educated on the skin changes associated with menopause, and the management options available.⁷ In addition to skin health, clinicians should consider a holistic approach to patients when discussing the menopausal transition. A whole-person approach is necessary to manage menopause as it affects physical, psychological, and social aspects of women’s health.⁴⁵ While the menopausal impacts on skin health have been discussed in this paper, an integrative approach combining bone health, physical strength, and mental health will help improve quality of life in patients experiencing menopause.⁴⁵

Given the central role of estrogen signaling in dermal fibroblast activity, collagen synthesis, and extracellular matrix maintenance, therapeutic strategies that restore or modulate estrogen pathways represent some of the most mechanistically targeted approaches for addressing menopause-associated skin changes. The multifaceted role of estrogen in skin function underscores the impacts of its deficiency during menopause while highlighting its therapeutic potential in addressing menopause-related skin changes. Estrogen contributes to wound healing through anti-inflammatory effects and regulation of cytokine activity.⁴⁶ By alleviating excessive inflammation and promoting matrix deposition, estrogen facilitates faster re-epithelialization and improves wound healing outcomes. Both topical and systemic estrogen therapies have been associated with reversal of delayed wound healing associated with aging and estrogen deficient skin.^10,46

Despite the skin being among the organs most impacted by menopause, there are no approved therapies for menopause-related skin changes.⁴⁷ Hormone replacement therapy (HRT), consisting of estrogen alone or in combination with progestogen, in patients without a uterus, is commonly used to alleviate systemic menopause symptoms and also has been observed to improve skin thickness, hydration, collagen, and hyaluronic acid content, improving menopause-associated skin symptoms, such as skin sensitivity and irritation [Table 1].^24,47 HRT has been shown to significantly increase dermal collagen levels, improving skin thickness and reducing wrinkling.¹⁷

335068 Table 1.

While the anti-aging benefits of HRT are promising, its use is accompanied by risks that must be carefully considered before treatment initiation. In 2002, the Women’s Health Initiative (WHI) study, a large randomized controlled trial of women aged 50-77 years, published findings of a slightly increased risk of breast cancer, coronary heart disease, stroke, and venous thromboembolic events after an average of 5 years of combined therapy with conjugated equine estrogen and medroxyprogesterone acetate.^5,48 In patients receiving estrogen alone, there was an increased risk of thromboembolic events, but no increased risk of cardiovascular events or breast cancer.⁶⁹ Given the initial findings were challenging to generalize to younger women experiencing menopause, reanalysis of WHI results in women younger than 60 years old and within 10 years of menopause supported lower absolute risks and possible cardioprotective effects.⁷⁰ A follow-up study of WHI noted the risk of combined equine estrogen and medroxyprogesterone acetate outweighed the benefits, therefore it was concluded that hormone replacement therapy should not be used for primary or secondary disease prevention.⁷¹ Current guidelines, including those published by the North American Menopause Society, continue to endorse HRT for symptomatic women younger than 60 years old or within 10 years of menopause who lack contraindications.^49,50 HRT is available in many formulations, including oral, transdermal, topical preparations; however, further research is needed to determine optimal concentration, duration, and dosing to address the cutaneous manifestations of menopause specifically.

Topical estrogen application has also demonstrated local benefits, including upregulation of type I and III procollagen (a collagen precursor) synthesis.⁵¹ Animal studies support these findings by demonstrating estrogen’s regulatory role in collagen maturation and turnover.⁵¹ In both systemic and topical formulations, estrogen therapy has been shown to significantly strengthen the skin’s water-holding capacity and improve ceramide levels and quality. Consequently, these therapies mitigate cutaneous skin changes associated with menopause, including increasing epidermal thickness and decreasing fine lines.^17,18,51,72 In clinical studies, Methyl estradiol propanoate (MEP), a topical estrogen compound that becomes inactivated after being metabolized by the skin, has been studied as a means of potentially avoiding side effects of systemic estrogen absorption.⁵² In 2 studies using MEP-containing compounds applied to facial skin, improvements in skin hydration, laxity, atrophy, and dullness were reported [Table 1].^52,73 While positive effects of topical estrogen have been documented in the literature, and newer preparations such as gels and patches have been developed, concerns regarding systemic absorption and resultant adverse effects, particularly cardiovascular effects, remain.⁵⁵ Further clinical studies to understand optimal dosing regimens, long-term efficacy, and topical estrogen safety profiles are needed.

Selective estrogen receptor modulators (SERMs) are synthetic, non-steroidal compounds that bind to estrogen receptors and function as estrogen antagonists or antagonists depending on the target tissue.^40,56 They represent a potential therapeutic approach that may have dermatologic benefits similar to estrogen while minimizing the previously mentioned systemic risks associated with HRT. SERMs such as Tamoxifen and Raloxifene have been widely studied and used for the management of breast cancer and osteoporosis respectively.⁵⁶ Although studies on the effects of SERMs on the skin are limited, preclinical studies evaluating Raloxifene have demonstrated that SERMs can increase skin collagen content in vitro⁵³ and skin elasticity in vivo.^54–56 Further research is needed to clarify the efficacy, safety, and long-term impact of SERMs for menopause-related skin therapy. As with HRT, SERMs carry an increased risk of VTE and vasomotor symptoms as a result of binding to various estrogen receptors in the body [Table 1].^55–57 Nevertheless, SERMs have promising therapeutic potential and may confer the same beneficial skin effects of estrogen without the risks associated with systemic HRT.

Phytoestrogens are plant-derived compounds with structural similarity to endogenous estrogens. Although their biologic activity is weaker than endogenous estrogen, this reduced potency may confer a more favorable safety profile, including a reduced risk of hormone-related cancers.⁷⁴ Preliminary studies have demonstrated that phytoestrogens, especially isoflavones such as genistein, may confer some benefits for menopause-related skin changes.⁷⁴ These include improvements in skin hydration, elasticity, and wrinkling, albeit to a lesser extent than topical estrogen therapies.^58,74 Mechanistically, phytoestrogens appear to upregulate epidermal differentiation markers, enhance stratum corneum cohesion, and reduce oxidative stress, potentially mitigating xerosis, pruritus, and skin fragility in estrogen-deficient skin [Table 1].^40,58

Although promising, clinical evidence supporting these effects remains limited and heterogenous. Systematic reviews and meta-analyses have highlighted variability in outcomes across studies, a lack of standardized formulations or dosing regimens, and insufficient long term randomized controlled trials.⁷⁵ Due to their relative safety and accessibility, phytoestrogens have already been incorporated into many over-the-counter cosmetic formulations targeted at postmenopausal skin.⁵⁸ While mechanistically plausible and supported by preliminary data, phytoestrogens should not be considered substitutes for established therapies. Additional high quality, long-term clinical trials are needed to clarify their role in the management of menopause-related skin aging.

Exosomes, which are small, extracellular vesicles that modulate intercellular communication, have emerged as another novel option for menopause-related skin changes.⁵⁹ Mesenchymal stem cell (MSC)-derived exosomes have demonstrated therapeutic potential in several reproductive disorders, with preclinical models of premature ovarian insufficiency showing potentially enhanced estrogen production and receptor sensitivity in ovarian tissue. Although these findings are preliminary, they suggest exosome-based therapy may provide a potential non-hormonal option for treating perimenopausal symptoms.⁷⁶ In dermatologic applications, exosomes are being explored for their regenerative and anti-inflammatory properties. Their composition includes proteins and lipids and other bioactive molecules which aid in wound healing, hydration, and skin protection.⁷⁷ Preclinical and early clinical studies have shown promising results including reduced wrinkles, increased collagen synthesis, improved skin texture and hydration, enhanced skin elasticity, improved skin tone, and reduced UV radiation-associated inflammation and damage [Table 1].⁷⁷ Although further research is needed, these molecules offer promising anti-aging benefits for menopausal skin due to their unique properties, notably their ability to modulate skin cells through intercellular communication.⁷⁷

Several non-hormonal topical therapies, including retinoids and antioxidants have demonstrated efficacy in managing menopause-associated skin changes. Topical retinoids activate retinoid receptors, which modify gene expression, protein synthesis, and epithelial cell growth and differentiation.⁶⁰ Studies have shown partial reversal of signs of photodamage with improvement in fine and coarse rhytides, hyperpigmentation, roughness, and severity of photodamage [Table 1].^61,62

Antioxidants, while primarily obtained through nutrition, can also exert beneficial localized effects when applied topically. Mechanistically, antioxidants can neutralize reactive oxygen species and prevent oxidative damage.⁶³ Vitamins C, B3 (niacinamide), and E have low molecular weights that facilitate dermal penetration and help increase collagen production and promote cell regeneration.⁷³ Clinically, topical antioxidants have been shown to improve skin hydration, elasticity, and texture, all of which may be beneficial for patients with bothersome skin changes [Table 1].⁶¹

Emerging evidence supports the role of phytoestrogens and other antioxidant compounds in addressing the skin of individuals who are postmenopausal. One in vitro study demonstrated that E2 enhances collagen production and protects keratinocytes and fibroblasts from oxidative stress induced by hydrogen peroxide exposure.⁷⁸ These findings have informed the development of topical formulations containing phytoestrogens targeted at postmenopausal women with signs of skin aging.⁵⁵ Other topical formulations containing antioxidant-rich substances, including melatonin, sphingolipids, coenzyme Q10, N-Acetyl-L-cysteine, and plant-derived compounds and extracts have shown varying efficacy in reducing in vivo ROS as a means of delaying skin aging,⁷⁹ and further clinical validation of these interventions is warranted.

Cosmetic interventions such as laser resurfacing and dermal fillers also offer therapeutic benefits for postmenopausal skin.⁶⁵ Laser resurfacing is a noninvasive tool typically used for treatment of scars, pigmentation, and rhytides. Ablative lasers function through preferential energy absorption by intracellular water, resulting in vaporization of tissue and thermal injury, with resultant collagen remodeling.⁸⁰ Nonablative lasers create dermal thermal injury while preserving the epidermis, and are associated with minimal downtime and less efficacy compared to ablative lasers.⁶⁴ Fractional lasers thermally ablate microscopic columns of tissue, offering increased efficacy compared to nonablative lasers, and faster recovery compared to ablative lasers.⁶⁴ While both ablative and nonablative lasers have been used for laser skin resurfacing, ablative lasers have been shown to have superior clinical results compared to nonablative lasers [Table 1].⁶⁵

An additional option includes dermal fillers, which can help address decreased elasticity, atrophy and volume loss in estrogen-deficient skin.^47,67 While different types of fillers exist, hyaluronic acid (HA), a popular type, is able to replace lost volume by attracting water and creating a swelling pressure.⁶⁶ In addition to HA fillers, several biostimulatory fillers have also been developed, which activate fibroblasts that form new collagen and soft tissue formation.⁶⁶ Both HA and biostimulatory dermal fillers have been tested and are frequently utilized in practice for skin rejuvenation [Table 1].⁶⁸

In addition to conventional therapies, many menopausal women use complementary and alternative medicine (CAM) to manage menopause-associated symptoms. Surveys suggest that approximately half of menopausal women report using CAM modalities, including herbal supplements, dietary products, and mind-body practices.⁸¹ Commonly used botanicals include black cohosh, red clover, soy-derived phytoestrogens, and other herbal formulations, although evidence supporting their efficacy remains inconsistent, and safety profiles are not well established.⁸¹ Mind-body approaches such as cognitive behavioral therapy, meditation, and hypnosis have also been studied, particularly for vasomotor symptoms, with some evidence suggesting reductions in symptom distress.⁸¹ While these therapies are widely used and may appeal to patients seeking more natural options, evidence remains limited.⁸¹ Clinicians should counsel patients on the uncertain efficacy and potential drug interactions.

Menopause represents a significant physiological transition with profound implications for skin health. The decline in estrogen and shifts in other sex hormones initiate a cascade of dermatologic changes, including dryness, pruritus, impaired barrier function, acne, rosacea, increased facial hair, and accelerated skin aging. These changes can not only affect appearance but also contribute to discomfort, reduced quality of life, and increased vulnerability to inflammatory and infectious skin conditions.

The review highlights the multifactorial pathophysiology of menopause-associated skin changes, emphasizing estrogen’s critical role in maintaining skin structure, hydration, and immune defense. While HRT and topical estrogen applications offer some promise in reversing or mitigating these changes, their use must be balanced with individual risk profiles. Emerging non-hormonal treatments, including SERMs, retinoids, antioxidants, phytoestrogens, and exosome-based therapies, provide alternative strategies and reflect growing interest in safer, targeted dermatologic care for postmenopausal individuals [Table 1].

Given the high prevalence of cutaneous concerns in menopausal populations and the psychosocial burden they may impose, there is a pressing need for increased awareness, evidence-based treatment strategies, and continued research. A deeper understanding of the intricate relationship between menopause and skin health can enable clinicians to offer more personalized, effective, and empathetic care to those navigating this critical life stage.

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