Recommendations for the use of the lowest effective dose for the shortest duration  help to prevent adverse endometrial effects.Some treatments have been developed more recently. These include selective estrogen receptor modulators, vaginal dehydroepiandrosterone, and laser therapy. Other treatments are available without a prescription such as vaginal lubricants and moisturizers. Vaginal dilators may be helpful. Since GSM may also cause urinary problems related to pelvic floor dysfunction, a woman may benefit from pelvic floor strengthening exercises. Women and their partners have reported that estrogen therapy resulted in less painful sex, more satisfaction with sex, and an improvement in their sex life. Epidemiology
Up to 50% of postmenopausal women have at least some degree of vaginal atrophy. It is likely to be underdiagnosed and undertreated. Terminology
Vulvovaginal atrophy, and atrophic vaginitis have been the preferred terms for this condition and cluster of symptoms until recently. These terms are now regarded as inaccurate in describing changes to the entire genitourinary system occurring after menopause. The term atrophic vaginitis suggests that the vagina is inflamed or infected. Though this may be true, inflammation and infection are not the major components of postmenopausal changes to the vagina. The former terms do not describe the negative effects on the lower urinary tract which can be the most troubling symptoms of menopause for women. Genitourinary syndrome of menopause (GSM) was determined to be more accurate than vulvovaginal atrophy by two professional societies. The term atrophic vaginitis does not reflect the related changes of the labia, clitoris, vestibule, urethra and bladder.
Pharmacokinetics
As with all potent bisphosphonates, the fraction of the drug that reaches the circulatory system intact (systemic bioavailability) after oral dosing is low, averaging only 0.6–0.7% in women and in men under fasting conditions. Intake together with meals and beverages other than water further reduces the bioavailability. The absorbed drug rapidly partitions, with approximately 50% binding to the exposed bone surface; the remainder is excreted unchanged by the kidneys. Unlike with most drugs, the strong negative charge on the two phosphonate moieties limits oral bioavailability, and, in turn, the exposure to tissues other than bone is very low. After absorption in the bone, alendronate has an estimated terminal elimination half-life of 10 years. References
External links
"Alendronic acid". Drug Information Portal. U.S. National Library of Medicine. "Alendronate sodium". Drug Information Portal. U.S. National Library of Medicine.