Cited by 384Bone Metabolism and DiseasesBone health and osteoporosis researchEstrogen and related hormone effects

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Glucocorticoids suppress bone formation via the osteoclast.

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Kim, H.-J.·2006·Journal of Clinical Investigation

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Abstract

The pathogenesis of glucocorticoid-induced (GC-induced) bone loss is unclear. For example, osteoblast apoptosis is enhanced by GCs in vivo, but they stimulate bone formation in vitro. This conundrum suggests that an intermediary cell transmits a component of the bone-suppressive effects of GCs to osteoblasts in the intact animal. Bone remodeling is characterized by tethering of the activities of osteoclasts and osteoblasts. Hence, the osteoclast is a potential modulator of the effect of GCs on osteoblasts. To define the direct impact of GCs on bone-resorptive cells, we compared the effects of dexamethasone (DEX) on WT osteoclasts with those derived from mice with disruption of the GC receptor in osteoclast lineage cells (GRoc-/- mice). While the steroid prolonged longevity of osteoclasts, their bone-degrading capacity was suppressed. The inhibitory effect of DEX on bone resorption reflects failure of osteoclasts to organize their cytoskeleton in response to M-CSF. DEX specifically arrested M-CSF activation of RhoA, Rac, and Vav3, each of which regulate the osteoclast cytoskeleton. In all circumstances GRoc-/- mice were spared the impact of DEX on osteoclasts and their precursors. Consistent with osteoclasts modulating the osteoblast-suppressive effect of DEX, GRoc-/- mice are protected from the steroid's inhibition of bone formation.

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Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.
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Additional file 3 of The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells
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Additional file 2 of The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells
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Sivapalan, P., Jørgensen, N. R., Mathioudakis, A. G., Eklöf, J. V., Lapperre, T. S., Ulrik, C. S., Andreassen, H. F., Armbruster, K., Sivapalan, P., Janner, J. H., et al. (2020) · Figshare · doi:10.6084/m9.figshare.13082939
Additional file 1 of The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells
Jiang, H., Deng, R., Deng, Y., Nie, M., Deng, Y.-X., Luo, H.-H., Yang, Y.-Y., Ni, N., Ran, C.-C., & Deng, Z.-L. (2021) · Figshare · doi:10.6084/m9.figshare.14608592
Preparation and characterization of starch-poly-epsilon-caprolactone microparticles incorporating bioactive agents for drug delivery and tissue engineering applications
Balmayor, E. R., Tuzlakoglu, K., Azevedo, H. S., & Reis, R. L. (2009) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT)
Repair of fractures in the bone of caudal fin for Xiphophorus helleri fish under the influence of hydrocortisone hormone
Al-Ali, A. A. A., & Ibrahim, M. A. (2019) · International Journal of Biosciences (IJB) · doi:10.12692/ijb/15.4.115-126
The therapeutic potential of descending regulatory pathways from brain to bone in osteoporosis: focusing on the brain-bone axis
Rong, Y., Zhang, L., Xu, M., Chen, Y., Wang, X., Li, S., Yang, G., & Chen, G. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1750464
Cushing's syndrome, glucocorticoids and bone
Kršek, M. (2019) · Clinical Osteology · doi:10.36290/clo.2019.010
The endocrine pathway during whole body vibration modulates the immune system and the osteogenesis in postmenopausal women with osteoporosis
Pyatin, V. F., & Maslova, O. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1776499
“According to literature data the glucocorticoids reduce cell replication of osteoblastic lineage and osteoblast function through direct effects on the osteoclast lineage and indirect effects on osteoblasts and T cells mediated by cytokines such as RANKL, osteoprotegerin, and TNF-a (117 – 119).”
Crosstalk with bone marrow adipocytes, but not osteoblasts, drives a cortical bone resorption phenotype in female mice with adult-onset deletion of the glucocorticoid receptor in Osterix-expressing cells
Lindsay, J., Bensreti, H., Gross, C., Tripathi, A., Maridas, D. E., Johnson, M., Shi, X., Bollag, W. B., Isales, C. M., & McGee‐Lawrence, M. E. (2026) · JBMR Plus · doi:10.1093/jbmrpl/ziag090
“27 , 28 While fully appreciating the importance of Osx-Cre + WT control mice when using the Osx-Cre model, 29 – 31 we previously demonstrated that Osx-Cre + WT control mice present with a phenotype similar to Osx-Cre − mice in this GR-floxed model, 24 and therefore used Cre − WT mice as our control…”
Recent advances in glucocorticoid regulation of bone and the bone marrow niche: Genetic and pharmacological approaches to understand and prevent bone loss
Hermsmeyer, I. D. K., Li, Z., & MacDougald, O. A. (2026) · Current Opinion in Endocrine and Metabolic Research · doi:10.1016/j.coemr.2026.100617
“Direct glucocorticoid signaling in osteoclasts also contributes to skeletal outcomes, as osteoclast-specific GR knockout mice are protected from dexamethasone-induced inhibition of bone formation, despite minimal baseline effects and additional deletion in LysM-expressing immune cells [24].”
Dexamethasone reduces osteogenic potential through suppressing retinoic acid signaling via NF-κB/CYP26B1 axis in mesenchymal stem cells
Ye, A. H., Wang, Y.-M., Wan, X.-Y., Liu, J. Y., Tang, N., Liu, W., Cai, J., He, D., He, B., He, W.-G., et al. (2026) · Stem Cell Research & Therapy · doi:10.1186/s13287-026-05131-0
“…GCs on bone formation may also contribute to inhibit the proliferation, induce apoptosis of osteoblasts [11–13], and promote differentiation and maturation of osteoclast by increasing the ratio of receptor agonists for nuclear factor-κβ ligand to osteoprotegerin to promote bone resorption [14–16].”
Klinisch-radiologische Ergebnisse eines modularen zementfreien Endoprothesensystems mit XLPE/Keramik-Gleitpaarung
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Authors: Kim, H.-J.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Kim, H.-J.
ORCID: Kim, H.-J.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2006-08-01
Volume: 116
Issue: 8
Pages: 2152-2160
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci28084
PMC: PMC1518793
OpenAlex: W2102680446
Cited by: 384
References: 47
Citations by year: 2026: 6 · 2025: 10 · 2024: 7 · 2023: 11 · 2022: 16 · 2021: 23 · 2020: 22 · 2019: 21 · 2018: 21 · 2017: 9 · 2016: 17 · 2015: 25 · 2014: 18 · 2013: 12 · 2012: 25
FWCI: 11.70
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
Funders: National Institutes of Health (DK 056341, AR046523)
National Institute of Allergy and Infectious Diseases (AI50655, R01AI050655, R21AI050655)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 056341, P30DK056341)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR 048853, AR 046852, AR 032788, R01AR048812, AR 048812, R01AR032788, R37AR046523, AR046523, R01AR048853, R01AR046852, R01AR046523)
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: glucocorticoids, glucocorticoid-induced osteoporosis, osteoclasts, bone formation, dexamethasone, glucocorticoid receptor, RhoA, Rac, Vav3, osteoclast precursors, bone remodeling, osteoblast apoptosis
MeSH terms: Animals, Bone Development, Bone Resorption, Cell Survival, Dexamethasone, Glucocorticoids, Osteoclasts, Receptors, Glucocorticoid, Mice, Knockout, Mice

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Glucocorticoids suppress bone formation via the osteoclast.

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