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a Mount Sinai Bone Program, The Mount Sinai School of Medicine, New York, New York, USA b Departments of Pathology and Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA c Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Missouri, USA d University of Bari, Italy
Key Words: osteoclast • osteoporosis • hypogonadism
Address for correspondence: Sun Li, M.D., Ph.D., The Mount Sinai School of Medicine, Division of Endocrinology, Box 1055, One Gustave L. Levy Place, Atran Building AB4-02, New York, NY 10029. Voice: 212-241-3054; fax: 212-534-4820. Li.sun{at}mssm.edu
We review studies that propose follicle-stimulating hormone (FSH) as a physiologic stimulator of osteoclastic bone resorption. We hypothesize that, in addition to low estrogen, a rising FSH contributes to the increased bone resorption and bone loss in hypergonadism. This is of particular relevance to the perimenopausal transition, wherein profound bone loss is accompanied by trabecular perforations in the face of high FSH and normal estrogen levels. Potential therapeutic implications include the development of antagonists to both circulating FSH and its osteoclastic receptor.
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