Abstract
In original description of osteoporosis by Albright et al. (1), they highlighted the greater prevalence of oophorectomy among patients presenting with osteoporotic fracture, and established for the first time the importance of ovarian failure in the pathogenesis of bone loss. Since that time, considerable evidence has been accumulated documenting the rate of loss of ovarian function in the pathogenesis of osteoporotic fracture (2). This has led to the use of estrogen for prevention of bone loss and subsequent fracture (3) with dramatic success. However, about one decade ago, it became apparent that the uncontrolled use of estrogen in women who had an intact uterus led to an increased incidence of endometrial hyperplasia and malignancy. Concern that a therapeutic regimen that not only might afford protection against osteoporotic fracture, but also might reduce the frequency of ischemic heart disease, might increase the risk of other disorders, has led to a reevaluation of the use of estrogen among the postmenopausal population, and to the development of routes of administration other than the oral, as well as new prescribing habits. This review evalutes the role of estrogen in prevention of osteoporosis as well as summarizes these new attitudes toward the provision of estrogen for the postmenopausal population.
Pathogenesis of Osteoporosis: The Role of Ovarian Failure
The introduction of noninvasive techniques that allow accurate and precise measurement of bone mass enabled study of the asymptomatic process of bone loss that precedes the increase in fracture incidence in the aging population. Early studies, in which peripheral cortical bone was measured, demonstrated that bone mass is fairly constant in women until the fourth and fifth decades when there is a fairly sudden downward trend in bone mass that has been observed in virtually all cross-sectional studies of cortical bone (2).
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