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At a glance
- Although common in postmenopausal women, symptoms associated with vaginal atrophy are often untreated.
- Estrogen deficiency interferes with many physiologic responses associated with sexual arousal.
- Symptoms are progressive over time and will not resolve without treatment.
- To reduce exposure to exogenous hormones, local estrogen therapy is recommended.
Vaginal atrophy is a collection of symptoms—including vaginal dryness, dysuria, and vulvovaginal irritation and itching—that are generally associated with declining estrogen levels attributable to menopause. However, adverse vaginal changes may also result from other conditions associated with low estrogen levels, including surgical removal of the ovaries (before the natural age of menopause), breastfeeding, and the use of certain medications that affect estrogen levels (e.g., treatments for breast cancer or endometriosis).1,2 The Women’s Health Initiative observational study and clinical trial surveyed 98,705 postmenopausal women aged 50 to 79 years. Data from this U.S.-based study indicated that 27% of the population experience vaginal or genital dryness, 18.6% vaginal or genital irritation or itching, 11.1% vaginal or genital discharge, and 5.2% dysuria.3
Although symptoms associated with vaginal atrophy in postmenopausal women are a relatively common complaint, they often remain untreated. Because estrogen is required for normal genital tissue structure and function, hypoestrogenism found during menopause causes significant problems. Several therapeutic options exist, including both nonhormonal and hormonal treatments that should be carefully considered in terms of each patient’s medical history and personal preferences. Education regarding the physiologic changes associated with vaginal atrophy should help clinicians identify and encourage implementation of appropriate treatment regimens in postmenopausal women.
As women progress through peri- and postmenopause, significant hormonal insufficiency leads to vaginal and urogenital symptoms. The occurrence of vaginal atrophy during menopause is associated with declining estrogen levels that cause structural and functional changes in vaginal tissue, including atrophy of vaginal tissue, an upward shift in vaginal pH, decreased blood flow to tissues, shortening and narrowing of the vagina, and reduced vestibular sensation.2,4 Some estrogen is produced during menopause via conversion of androgens to estrogen. Androgen levels do not change significantly in association with the menopausal transition, but they do gradually decline as women continue to age and eventually may result in complaints of decreased libido and impaired sexual functioning as well as muscle wasting, osteoporosis, loss of energy, changes in mood, and depression.5,6 This loss of vaginal estrogen production during menopause plays a major role in the development of various physiologic changes associated with vaginal atrophy.
Decreased availability of circulating estrogen results in the shortening and narrowing of the vagina, with a loss of elasticity and rugal folds leading to smoother epithelial surfaces.7,8 In the vaginal tissues, loss of collagen, adipose tissue, and the ability to retain water are common with estrogen deficiency, resulting in thinning of the epithelial surface.8,9 Thinned tissue is more susceptible to irritation, and the vaginal surface becomes friable, with petechiae, ulcerations, and increased bleeding occurring after only minimal trauma.7,9 At the cytologic level, fewer superficial epithelial cells are observed, but an increased percentage of intermediate and parabasal cells are found as a result of estrogen deficiency.7,8 In the presence of estrogen, epithelial cells produce glycogen, which is broken down into glucose; the Lactobacillus species metabolize the glucose and produce lactic acid. The incidence of epithelial thinning caused by lower estrogen levels during menopause results in decreased availability of glycogen-rich cells. The ensuing decrease in metabolism of lactic acid may be involved in increasing the pH of the vagina (to >5.0), resulting in a heightened risk of colonization of the vagina by fecal flora and other pathogens, which in turn raises the risk of urinary tract infections (UTIs).1,7 Another theory regarding changes in vaginal pH involves the presence of an estrogen-dependent proton-secreting mechanism found in vaginal epithelial cells. Epithelial cells from postmenopausal women were found to have a reduced capacity to control the vaginal pH compared with cells from premenopausal women; however, this effect was only partially restored following treatment with estrogen.10,11 Additional studies are needed to more clearly define the mechanisms involved in vaginal pH changes found throughout a woman’s life cycle.
Estrogen deficiency also interferes with many physiologic responses associated with sexual arousal, including smooth muscle relaxation, vasocongestion, and vaginal lubrication.5 One epidemiologic study found that women experiencing sexual dysfunction were 3.84 times more likely to have vaginal atrophy than women without sexual dysfunction.12 In this study, an association was found between vaginal atrophy and difficulties with sexual desire, arousal, and orgasm.12 Decreased blood flow to the urogenital tissues is associated with atrophy of the lamina propria blood vessels, contributing to vaginal dryness and reduced tissue elasticity, which can lead to painful, unpleasant, and unsatisfactory intercourse, or dyspareunia.5 In a review of the literature, dyspareunia occurring with vaginal atrophy was often found to be associated with a lack of estrogen (generally <50 pg/mL) in the genitourinary tract.13