ABSTRACT
Vaginal atrophy develops in all women when estrogen depletion occurs at menopause. However, not all women with vaginal atrophy develop atrophic vaginitis. The estrogen concentration in perimenopausal women is approximately 120 ng/ml and after menopause begins its concentration decreases to approximately 19 ng/ ml1. The predominant hormone produced by the postmenopausal ovary is androstenedione and this hormone is converted in the peripheral fatty tissue to estrogen. Testosterone is also produced in the ovary and most of this is converted into estradiol in the ovaries. Thus there is an endogenous supply of estrogen as long as the postmenopausal ovaries continue to function. However, the decrease in estrogen is significant and the vaginal epithelial surface loses its folds, or rugae, and thickness, then becomes thin and pale. The vaginal tissue loses its elasticity and its ability to distend, thus it becomes shorter and narrower. These changes result in the patient experiencing dyspareunia and avoiding sexual intercourse.
