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Progesterone as a Bone-Trophic Hormone

Division of Endocrinology and Metabolism, University of British Columbia, Vancouver British Columbia, Canada, V5Z 1M9

Correspondence: Address requests for reprints to: Dr. J. C. Prior, Department of Medicine, 910 West 10th Avenue, Suite 3318, Vancouver, British Columbia, Canada V5Z 1M9.

Abstract

Introduction: FULLER Albright's observation that women developed osteoporosis after, but rarely before the menopause, led him to assert that osteoporosis was caused by hormonal changes around the time of the climacteric (1). Although his first clinical trial tested progesterone and testosterone, as well as estrogen treatment, Albright believed that it was estrogen deficiency that resulted in decreased bone formation and caused osteoporosis, "a condition in which the osteoblasts were primarily deficient in laying down osteoid tissue" (2).

Kinetic and histomorphometric data suggest that bone formation and resorption are closely linked (3, 4). Increased resorption, which occurs after the menopause, will not cause a net loss of bone if formation is equally increased. Studies of bone histology suggest that bone formation in postmenopausal women is not increased but is inappropriately "normal" or low (5, 6). Estrogen treatment is associated with decreased resorption and with no change or a slight decrease in formation (5, 7). The long term net response to estrogen therapy appears to be decreased remodeling and the creation of a relatively inactive bone mass (5–7). Despite Albright's assumption that estrogen deficiency caused decreased bone formation, it is now clear that estrogen's predominant effect is to decrease bone resorption.

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