osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification
Abstract
Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG −/− mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly,OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.
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Footnotes
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↵Corresponding author.
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E-MAIL ssimonet{at}amgen.com; FAX (805) 447-1982.
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- Received February 9, 1998.
- Accepted March 19, 1998.
- Cold Spring Harbor Laboratory Press