osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.
Bucay N,
Sarosi I,
Dunstan CR,
Morony S,
Tarpley J,
Capparelli C,
Scully S,
Tan HL,
Xu W,
Lacey DL,
Boyle WJ,
Simonet WS.
Department of Molecular Genetics, Amgen, Inc., Thousand Oaks, California 91320-1789, USA.
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.
PMID: 9573043 [PubMed - indexed for MEDLINE]
PMCID: PMC316769