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Anabolic Therapy for Osteoporosis

St. Joseph Hospital (C.J.R.), Bangor, Maine 04401; University of Maine (C.J.R.), Orono, Maine 04473; and Departments of Medicine and Pharmacology, Columbia University College of Physicians and Surgeons (J.P.B.), New York, New York 10032

Address all correspondence and requests for reprints to: Clifford J. Rosen, M.D., The Maine Center for Osteoporosis, St. Joseph Hospital, 360 Broadway, Bangor, Maine 04401. E-mail: rofe{at}aol.com

All currently available, approved therapies for osteoporosis inhibit bone resorption. By acting at this site in the bone remodeling cycle, estrogens, selective estrogen receptor modulators, calcitonin, and the bisphosphonates all have the capacity to increase bone mineral density and to reduce the risk of new fractures. There can be no doubt that these agents have had an enormous impact on our diagnostic and therapeutic approach to osteoporosis. Despite their great value, the antiresorptives are generally not associated with dramatic increases in bone mass, and their action to reduce fracture risk, although highly significant, is rarely more than 50% of the baseline risk. Another approach is anabolic therapy, in which bone formation is directly stimulated. In this review we will summarize the anabolic agents that have been studied and present a current view of their current standing. Fluoride, GH, insulin-like growth factor I, the statins, and PTH will be reviewed. Although still in development, approaches to combination therapy with antiresorptives and anabolic agents are also promising.

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