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Atrophic Vaginitis

Editor: Carrie A. Hall Updated: 10/31/2022 8:19:23 PM


Genitourinary syndrome of menopause, a group of chronic, progressive, hypoestrogenic conditions, includes vulvovaginal atrophy, atrophic vaginitis, and bladder and urethral dysfunctions. Urogenital tissues, derived from similar embryologic tissues, develop and mature in response to estrogen. In hypoestrogenic states, these tissues undergo physiologic change. Atrophic vaginal changes are caused by thinning vaginal epithelium, decreased vaginal rugae and elasticity, and decreased vaginal secretions. Atrophic vaginitis is a symptomatic inflammatory process involving the thinned vaginal epithelium affecting some pre-menopausal and up to 50% of post-menopausal women.


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A hypoestrogenic state may be part of natural physiological menopause or induced (secondary to surgical, radiation, or chemotherapy treatments). Premenopausal women may develop a temporary hypoestrogenic state while lactating. Other conditions, such as exposure to medications, radiation therapy, chemotherapy, or hypothalamic dysfunction, may also result in a hypoestrogenic state. Medications that may induce a hypoestrogenic state include Selective estrogen receptor modulators, Selective estrogen receptor degrader, and antigonadotropins.

Decreased estrogen levels lead to changes in the vaginal environment, which causes a shift in the normal flora. Typically there is a decrease in Lactobacillus spp. resulting in overgrowth of skin and rectal pathogens.


An estimated 10% to 50% of all postmenopausal women develop atrophic vaginitis.[1][2][3] Additionally, 15% of premenopausal women develop genitourinary syndrome symptoms. While these numbers are high, the prevalence may be significantly higher than reported given, and many women do not discuss their symptoms.[4]


The female genitalia, the lower urinary tract, and the surrounding vasculature develop from the same embryologic tissue with similar estrogen receptors. Estrogen receptor alpha is primarily found in the uterus and pituitary gland. The estrogen receptor alpha is present during premenopause and postmenopause. Estrogen receptor beta is primarily found in the ovary. The estrogen receptor beta is present predominately in the premenopausal state, leading to the ovarian failure state experienced in menopause.[4] Hypoestrogenic state results in the fusion of collagen fibers and fragmentation of elastin fibers in vulvovaginal tissue and decreased squamous cells, resulting in decreased mucosal elasticity and decreased rugae, and narrowing the vagina.

Premenopausal vaginal tissues mature in normal estrogen ranges of 30 to 40 pg/ml, which allows for adequate growth of vaginal epithelium with superficial squamous cells containing glycogen. Lactobacilli spp. utilize the glycogen from the cells and convert it into lactic acid, creating a slightly acidic environment with a pH of 3.5 to 5.0. Free glycogen is also associated with lower pH and higher levels of lactobacillus. In menopause, vaginal tissue is exposed to estrogen less than 20pg/ml resulting in fewer superficial squamous epithelial cells with an increase in parabasal cells. The higher concentration of parabasal cells and reduced Lactobacillus spp. leads to a decrease in lactic acid conversion, producing a higher pH of 5.0 to 7.5 environment. (1,2) The consequence of elevated vaginal pH is a shift in normal flora, Lactobacilli spp., and more susceptible to other pathogens such as Gardnerella, Prevoltella, Atopobium, and Streptococcus.[2][5][3]


Atrophic pattern histologic findings demonstrate decreased superficial squamous cells, increased parabasal cells, decreased Lactobacilli. However, there are normal to low numbers of neutrophils.[6] Increased neutrophils are noted in atrophic vaginitis when compared to the vaginal atrophy pattern.[1] 

The hypoestrogenic state results in loss of dermal collagen, elastin fibers, and blood vessels in the lamina propria. These changes result in decreased elasticity and vascularity. Decreased vascularity, in response to low estrogen levels, results in thin friable vaginal mucosa and decreased secretions.

History and Physical

Postmenopause women are typically greater than 50 years old unless they incurred induced menopause. Postmenopausal women have low estrogen levels, precipitating genitourinary syndrome symptoms. Symptoms appear in the early to the late postmenopausal stage.  

The STRAW staging system is a useful tool for health care members and patients to evaluate menstrual transition and postmenopause.[7] Atrophic vaginitis symptoms include vulvovaginal dryness, pruritis, dyspareunia, abnormal vaginal discharge, post-coital pain of the labia minora, or deeper in the vaginal vault, recurrent urinary tract infections, urethral pain, hematuria, urinary incontinence.[1][8][9] These symptoms may be progressive, or the patient may have just noticed the changes.


Age-related changes include a decrease in hair distribution and pigment of the hair. A decreased amount of subcutaneous fat leads to decreased volume of the mons pubis, labia majora, and labia minora. There may be fissuring or other signs of friction of the external genitalia or at the introitus. Inflammation may occur, resulting in erythematous patches, with or without petechia or friable tissue.

Collection of pH, vaginal swabs for the Vaginal Maturation Index, and cultures are obtained before the speculum exam. The exam reveals hypoestrogenic tissue with decreased secretions and elasticity, resulting in the introitus's narrowing and more susceptible to friction. Vaginal tissue will be pale pink with diminished vaginal secretions.

pH greater than 5.0 or decreased Follicular stimulating hormone is consistent with lower estrogen states. The pH of vaginal secretions should be obtained before the speculum exam.

Vaginal maturation index (VMI) is the proportional relationship between the superficial, intermediate, and parabasal cells of the vaginal tissue. A decrease in estrogen is associated with an increase in parabasal cells resulting in lower VMI. The hypoestrogenic state is noted as a VMI of 0 to 49, however, the hyperestrogenic state is noted as a VMI 65 to 100.[1][10]

Treatment / Management

Treatment of atrophic vaginitis begins with a trial of intravaginal estrogen. Intravaginal estrogen products, Conjugated estrogen cream, estradiol cream, estradiol tablet, estradiol vaginal ring, and estradiol transdermal patch show equivocal relief of symptoms and improvement in acidification of vaginal tissues.[6][7] Use the lowest effective dose to reduce systemic estrogen exposure. Taper the estrogen therapy after symptoms and function improve.[8] (B2)

Some patients may require maintenance therapy indefinitely. Contraindications to estrogen therapy include a history of estrogen receptor-positive breast cancer, other estrogen-dependent cancers (subtypes of breast and uterine cancers), thromboembolism disorders, liver disease, undiagnosed vaginal bleeding, endometrial hyperplasia, heart disease, pregnancy, migraines with aura, or allergy to the estrogen or the carrier product.[11] (A1)

The vaginal maturation index may be used as a clinical measurement to evaluate the response to estrogen therapy. Lactobacillus predominance is noted to be associated with fewer genital symptoms compared to a change in pH.[2]

Additional therapy or alternative therapy includes selective estrogen receptor modulators, tissue-selective estrogen complexes, estriol, platelet-rich plasma, herbals, and other natural products.[9] Ospemifene, a selective estrogen receptor modulator, is approved by the FDA for adjunctive therapy in patients with dyspareunia or for use in patients that are not candidates for estrogen therapy. (A1)

A patient may use lubricants for symptomatic improvement and/or if contraindicated to estrogen therapy. Lubricants can improve symptoms; however, no chemical or histologic changes occur.

Other non-hormonal forms of treatments include fractional micro-ablative carbon-dioxide laser therapy and transcutaneous temperature-controlled radiofrequency with external and internal treatments that improve vaginal dryness, vulvovaginal laxity, and dyspareunia for 6 to 12 months.[12][13][14][15][16]

Differential Diagnosis

Differentials include vaginal atrophy, vulvovaginal atrophy, vulvovaginal lichen planus or sclerosis, vulvar dermatitis, vulvovaginal candidiasis, vulvodynia, inflammatory vaginitis without atrophy, desquamative inflammatory vaginitis, vulvovaginal neoplasm, sexually transmitted infection, other infections, and urogenital dysfunction.

Pertinent Studies and Ongoing Trials

Microablative carbon-dioxide laser therapy has been noted to improve histologic changes in the lamina propria with the remodeling of collagen fibers and blood vessels and improve the vaginal flora with increased Lactobacillus spp.[15][17]

Radiofrequency temperature therapy shows potential as an alternative treatment in atrophic vaginitis. However, due to the small study sizes, follow up studies are needed to evaluate the histological changes, which improved regeneration of collagen and blood vessels.[12][13][14]


Many women see improvement with the use of intravaginal estrogen. Those refractory to treatment or who experience incomplete resolution may start adjunctive therapy with ospemifene.

Risk factors include no vaginal births, therefore no stretching of the vaginal canal. Cigarette smoking causes vasoconstriction, which decreases secretions and exacerbates symptoms.


Untreated atrophic vaginitis leads to persistent pruritis, which may cause scarring from scratching. Thinned mucosa may result in abrasions or fissures. The patient may continue to have other genitourinary complaints.

Deterrence and Patient Education

Atrophic vaginitis is an inflammatory condition associated with low estrogen levels. Pre-menopausal women may experience symptoms but more commonly experienced by postmenopausal women. Treatment is typically initiated with localized estrogen therapy to provide symptom relief. Adjunctive therapy with estrogen modulator receptors or radiofrequency treatment may further improve symptoms.

Enhancing Healthcare Team Outcomes

Atrophic vaginitis is not a life-threatening disease, but it can significantly negatively affect patients' quality of life if not diagnosed and treated appropriately. Interprofessional communication and patient education are essential. The condition can be recognized and treated by multiple clinicians to include primary care, obstetricians/gynecologists, dermatologists, and surgeons. A proper diagnosis can be challenging without a dedicated history taking, and physical exam and misdiagnosis can lead to unnecessary referrals and procedures. With adequate interprofessional communication and patient education, atrophic vaginitis can be diagnosed and treated for improved patient outcomes.



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