Differential effects of glucocorticoid on recruitment and activity of osteoclasts induced by normal and osteocalcin-deficient bone implanted in rats.
Abstract
Prolonged glucocorticoid excess is associated with bone loss. Among the contributory factors are glucocorticoids' suppression of bone formation and stimulation of bone resorption. In this study, the effects of glucocorticoids on bone resorption were evaluated in a rodent model. Subcutaneous implants of devitalized mineralized bone particles (BPs) elicit the recruitment of progenitor cells and their differentiation to osteoclasts which resorb the BPs. The effects of glucocorticoids on both the recruitment and the activity of cells induced by normal BPs were distinguished based upon when treatment was initiated. When treatment with hydrocortisone or dexamethasone was initiated at the time of BP implantation, the recruitment of bone-resorbing cells was impaired and a subsequent decrease in BP resorption was found. On the other hand, when treatment was initiated on day 7, glucocorticoids increased osteoclastic resorption and tartrate-resistant acid phosphatase activity. We also tested hydrocortisone's effect to stimulate the activity of cells associated with osteocalcin-deficient BPs. As previously reported, BPs deficient in osteocalcin were poorly resorbed as a result of decreased formation and activity of osteoclasts. Hydrocortisone had an even more pronounced effect in stimulating the low level resorption of the osteocalcin-deficient BP implants than of the normal BP implants. These findings show differential effects of glucocorticoids on two aspects of bone resorption: they inhibit the recruitment and/or differentiation of bone-resorbing cells, but they stimulate the activity of existing osteoclastic cells. The ability of glucocorticoids to increase resorption of normal bone and to overcome resistance to resorption of osteocalcin-deficient bone suggests an important regulatory effect of glucocorticoids in the activation of osteoclasts to increase bone resorption.
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In a bone xenograft model, glucocorticoids inhibited osteoclast recruitment and bone resorption, whereas delayed glucocorticoid treatment stimulated osteoclast activity and bone resorption.
“A bone xenograft model showed that glucocorticoids inhibited osteoclast recruitment and bone resorption, whereas delayed treatment with glucocorticoids resulted in stimulation of osteoclast activity and bone resorption (256).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [256]
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- Authors
- Defranco, D. J., Lian, J. B., & Glowacki, J.
- Affiliations
- Harvard University (US)
- ORCID
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1992-07
- Volume
- 131
- Issue
- 1
- Pages
- 114-121
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2107571929
- Cited by
- 50
- References
- 45
- Citations by year
- 2023: 1 · 2019: 1 · 2017: 1 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 3
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- glucocorticoids, osteoclasts, bone resorption, cortisol, dexamethasone, bone implants, tartrate-resistant acid phosphatase, osteoclast recruitment, osteoclastogenesis, glucocorticoid resistance, bone loss
- MeSH terms
- Acid Phosphatase, Animals, Bone and Bones, Bone Resorption, Cell Differentiation, Dexamethasone, Glucocorticoids, Hydrocortisone, Osteoclasts, Tartrates, Osteocalcin, Bone Transplantation, Rats
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