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Michael R. McClung, MD

JAMA. 1999;282:687-689.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Nearly 60 years ago, Fuller Albright originally recognized postmenopausal osteoporosis in older women who presented with height loss, kyphosis, and back pain as a result of vertebral fractures.¹ He astutely surmised that the waning of estrogen levels after menopause resulted in loss of bone tissue and increased skeletal fragility and predicted that estrogen therapy would prevent fractures. The relationship between cessation of ovarian function and loss of bone mass is now well established. An interval of relatively rapid bone loss occurs in the years immediately following menopause, and bone loss continues and even accelerates again in the very elderly. Estrogen therapy preserves bone mineral density (BMD) in both younger and older postmenopausal women.² However, to date, no large randomized clinical trials have evaluated the antifracture efficacy of estrogen.

The current image of osteoporosis has broadened over the past few years. The disorder is now viewed as . . . [Full Text of this Article]

Author Affiliation: Department of Medical Education, Providence Health System and Oregon Osteoporosis Center, Portland, Ore.

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