Sex Steroids and the Construction and Conservation of the Adult Skeleton
B. Lawrence Riggs,
Sundeep Khosla and
L. Joseph Melton, III
Division of Endocrinology and Metabolism (B.L.R., S.K., L.J.M.), Department of Internal Medicine, and Section of Clinical Epidemiology (L.J.M.), Department of Health Sciences Research, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, Minnesota 55905
Correspondence: Address all correspondence and requests for reprints to: B. Lawrence Riggs, M.D., Mayo Clinic and Mayo Foundation, 200 First Street SW, North 6 Plummer, Rochester, Minnesota 55905.
Here we review and extend a new unitary model for the pathophysiologyof involutional osteoporosis that identifies estrogen (E) asthe key hormone for maintaining bone mass and E deficiency asthe major cause of age-related bone loss in both sexes. Also,both E and testosterone (T) are key regulators of skeletal growthand maturation, and E, together with GH and IGF-I, initiatea 3- to 4-yr pubertal growth spurt that doubles skeletal mass.Although E is required for the attainment of maximal peak bonemass in both sexes, the additional action of T on stimulatingperiosteal apposition accounts for the larger size and thickercortices of the adult male skeleton. Aging women undergo twophases of bone loss, whereas aging men undergo only one. Inwomen, the menopause initiates an accelerated phase of predominantlycancellous bone loss that declines rapidly over 4–8 yrto become asymptotic with a subsequent slow phase that continuesindefinitely. The accelerated phase results from the loss ofthe direct restraining effects of E on bone turnover, an actionmediated by E receptors in both osteoblasts and osteoclasts.In the ensuing slow phase, the rate of cancellous bone lossis reduced, but the rate of cortical bone loss is unchangedor increased. This phase is mediated largely by secondary hyperparathyroidismthat results from the loss of E actions on extraskeletal calciummetabolism. The resultant external calcium losses increase thelevel of dietary calcium intake that is required to maintainbone balance. Impaired osteoblast function due to E deficiency,aging, or both also contributes to the slow phase of bone loss.Although both serum bioavailable (Bio) E and Bio T decline inaging men, Bio E is the major predictor of their bone loss.Thus, both sex steroids are important for developing peak bonemass, but E deficiency is the major determinant of age-relatedbone loss in both sexes.
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K. E. Ensrud, R. L. Fullman, E. Barrett-Connor, J. A. Cauley, M. L. Stefanick, H. A. Fink, C. E. Lewis, E. Orwoll, and for the Osteoporotic Fractures in Men Study Resear Voluntary Weight Reduction in Older Men Increases Hip Bone Loss: The Osteoporotic Fractures in Men Study
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