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Review Article
Medical Progress
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Volume 357:905-916 August 30, 2007 Number 9
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Mechanisms of Anabolic Therapies for Osteoporosis
Ernesto Canalis, M.D., Andrea Giustina, M.D., and John P. Bilezikian, M.D.

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Osteoporosis, a major worldwide health problem, affects 4 million to 6 million women and 1 million to 2 million men in the United States. Even more people have decreased bone mass, which, in addition to other risk factors, can be a major therapeutic challenge.1 Fractures, the most important consequence of osteoporosis, are associated with enormous costs and substantial morbidity and mortality. The prevention and treatment of this disease are therefore of paramount importance. Since postmenopausal osteoporosis is characterized by bone resorption that exceeds bone formation, antiresorptive agents can help to restore skeletal balance by reducing bone turnover, primarily at the . . . [Full Text of this Article]

Bone Remodeling and Modeling

Signals That Regulate Bone Formation

Bone Morphogenetic Proteins, Wnt, and Insulin-Like Growth Factor I

Parathyroid Hormone

Clinical Relevance of Anabolic Signaling Molecules

Parathyroid Hormone

Strontium Ranelate

Growth Hormone and IGF-I

Sclerostin Antagonism

Other Candidate Molecules for Anabolic Therapy

Antagonists of Dkk-1

Soluble Activin Receptors

The Osteoblast Proteasome and Its Inhibitors

Conclusions


Source Information

From the Department of Research, Saint Francis Hospital and Medical Center, Hartford, CT (E.C.); the University of Connecticut School of Medicine, Farmington (E.C.); the Department of Internal Medicine, University of Brescia, Brescia, Italy (A.G.); and the Department of Medicine, College of Physicians and Surgeons, Columbia University, New York (J.P.B.).

Address reprint requests to Dr. Canalis at the Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland St., Hartford, CT 06105-1299, or at ecanalis@stfranciscare.org.


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