The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Mechanisms of glucocorticoid-induced osteoporosis.
Abstract
Glucocorticoids modify osteoblastic cell differentiation, number, and function. Glucocorticoids stimulate osteoclastogenesis and increase the expression of receptor activator of Nuclear factor-kappaB ligand and colony-stimulating factor-1, and decrease the expression of osteoprotegerin. However, the most significant effect of glucocorticoids in bone is an inhibition of bone formation. This inhibition is caused by a decrease in the number of osteoblasts secondary to a shift in the differentiation of mesenchymal cells away from the osteoblastic lineage, and an increase in the death of mature osteoblasts. Glucocorticoids decrease the function of the remaining osteoblasts directly and indirectly through the inhibition of insulin-like growth factor I expression. The stimulation of bone resorption is likely responsible for the initial bone loss after glucocorticoid exposure. Eventually, the inhibition of bone formation will cause a decrease in bone remodeling and a continued increased risk of fractures.
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“Glucocorticoids also have remarkably complex effects on bone, virtually all of which are detrimental, and these influences have been summarized in recent reviews (241,242).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [241]
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Use of Inhaled Corticosteroids and Risk of Fractures
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Use of oral corticosteroids and risk of fractures
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Defective adipocyte differentiation in mice lacking the C/EBPβ and/or C/EBPδ gene
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Cellular Mechanisms for Human Procollagenase-3 (MMP-13) Activation
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Estrogen deficiency induces bone loss by enhancing T-cell production of TNF-α
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Kearns, A. E., Khosla, S., & Kostenuik, P. J. (2008) · Endocrine Reviews · doi:10.1210/er.2007-0014 · Cited by 824
Cheng, C.-H., Chen, L.-R., & Chen, K.-H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031376 · Cited by 595
MANAGEMENT OF ENDOCRINE DISEASE: Secondary osteoporosis: pathophysiology and management
Mirza, F., & CANALIS, E. M. (2015) · European Journal of Endocrinology · doi:10.1530/eje-15-0118 · Cited by 343
Self-citationOsteoblast physiology in normal and pathological conditions
Neve, A., Corrado, A., & Cantatore, F. P. (2010) · Cell and Tissue Research · doi:10.1007/s00441-010-1086-1 · Cited by 354
Bioresponsive drug delivery systems for the treatment of inflammatory diseases
Dou, Y., Li, C., Li, L., Guo, J., & Zhang, J. (2020) · Journal of Controlled Release · doi:10.1016/j.jconrel.2020.09.008 · Cited by 226
Metadata
- Authors
- Canalis, E.
- Affiliations
- University of Connecticut (US)
- Corresponding author
- Canalis, Ernesto
- ORCID
- Canalis, Ernesto
- Venue
- Current Opinion in Rheumatology
- Published
- 2003-07
- Volume
- 15
- Issue
- 4
- Pages
- 454-457
- ISSN
- 1040-8711 (ISSN-L)
- OpenAlex
- W3005079460
- Cited by
- 164
- References
- 40
- Citations by year
- 2026: 11 · 2025: 7 · 2024: 9 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 10 · 2019: 6 · 2018: 9 · 2017: 5 · 2016: 1 · 2015: 3 · 2013: 3 · 2012: 6
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK045227, DK 45227)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- glucocorticoid-induced osteoporosis, osteogenic differentiation, osteoclastogenesis, RANKL, CSF-1, osteoprotegerin, bone formation inhibition, osteoblast apoptosis, mesenchymal differentiation, insulin-like growth factor I, bone resorption, bone remodeling, fracture risk
- MeSH terms
- Animals, Bone Resorption, Glucocorticoids, Humans, Osteoblasts, Osteoclasts, Osteogenesis, Osteoporosis, Mice
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