Cited by 2,483Bone Metabolism and DiseasesBone health and osteoporosis researchBone and Dental Protein Studies

Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.

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Bucay, N., Sarosi, I., Dunstan, C. R., Morony, S., Tarpley, J., Capparelli, C., Scully, S., Tan, H. L. +4 more·1998·Genes & Development

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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Crossref · 10.1101/gad.12.9.1260

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  • Mice overexpressing OPG get osteopetrosis, while OPG-knockout mice get severe osteoporosis and frequent fractures.

    “overexpression of OPG produced osteopetrosis, while OPG-knockout mice had a phenotype of severe osteoporosis with a high incidence of fractures”
  • OPG knockout mice have severe osteopenia with increased bone turnover, cortical porosity, reduced cortical and cancellous bone volume and density, and spontaneous fragility fractures in early life.

    “The essential physiological role of OPG in maintaining bone mass was shown by the severe osteopenic phenotype of OPG knockout mice (124 -126).These mice exhibit increased bone turnover, cortical porosity, and reductions in cortical and cancellous bone volume and density.These deleterious changes are accompanied by spontaneous fragility fractures in the first weeks of life (124).”
  • OPG knockout animals develop medial calcification of the aorta and renal arteries along with elevated bone turnover.

    “OPG knockout animals developed medial calcification of the aorta and renal arteries, in association with elevated bone turnover (124).”

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Authors
Bucay, N., Sarosi, I., Dunstan, C. R., Morony, S., Tarpley, J., Capparelli, C., Scully, S., Tan, H. L., Xu, W., Lacey, D. L., Boyle, W. J., & Simonet, W. S.
Affiliations
Amgen (United States) (US)
Venue
Genes & Development
Published
1998-05-01
Volume
12
Issue
9
Pages
1260-1268
ISSN
0890-9369 (ISSN-L)
OpenAlex
W2129651548
Cited by
2,483
References
42
Citations by year
2026: 29 · 2025: 29 · 2024: 46 · 2023: 43 · 2022: 52 · 2021: 61 · 2020: 90 · 2019: 62 · 2018: 53 · 2017: 93 · 2016: 82 · 2015: 94 · 2014: 89 · 2013: 122 · 2012: 106
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
Keywords
osteoprotegerin, osteoporosis, arterial calcification, vascular calcification, osteoclastogenesis, bone mineral density, trabecular bone, cortical bone, bone porosity, fracture, renal artery calcification
MeSH terms
Animals, Arteries, Calcinosis, Disease Models, Animal, Female, Glycoproteins, Male, Osteoporosis, Vascular Diseases, Bone Density, In Situ Hybridization, Receptors, Tumor Necrosis Factor, Receptors, Cytoplasmic and Nuclear, Mice, Knockout, Gene Targeting, Mice, Osteoprotegerin

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