ABSTRACT
During the fertile premenopausal years, the endometrium is uniquely endowed with a complex monthly cycle of periodic proliferation, differentiation, breakdown and regeneration. This high cellular turnover, conditioned by ovarian hormones and growth factors, has many opportunities of losing its regulatory controls, such as during the menopausal transition when cycles are frequently irregular and anovulatory, but despite this significant endometrial disease is uncommon in premenopausal women. After the menopause and in the absence of exogenous hormone stimulation, the endometrium will generally become thin and atrophic, though still retaining the ability to respond to estrogen and progestogen. Sequential regimens of estrogen and progestogen hormone replacement therapy (HRT) are intended to mimic the cyclic stimulation of the endometrium and will usually produce a similar response with proliferative and secretory changes.
