Glucocorticoids suppress bone formation via the osteoclast.
Open accessAbstract
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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DEX prolongs osteoclast lifespan while decreasing their individual capacity to degrade bone.
“DEX was recently shown to prolong the lifespan of osteoclasts, while decreasing their individual capacity to degrade bone (257).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [257]
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“Attempting to dissect the relative contribution of osteoblasts and osteoclasts to glucocorticoid-induc e bone loss, investigators have developed lineage-specific mouse models with a targeted delet ion of GR (86,87).”
BackgroundScaffold strategies for modulating immune microenvironment during bone regeneration
He, J., Chen, G., Liu, M., Xu, Z., Chen, H., Yang, L., & Lv, Y. (2019) · Materials Science and Engineering C · doi:10.1016/j.msec.2019.110411 · Cited by 127 · see citing works
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“Lysozyme-Cre (mouse) Gr [64] [67]”
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Osteoclasts protect bone blood vessels against senescence through the angiogenin/plexin-B2 axis
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Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
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Glucocorticoids Shape Macrophage Phenotype for Tissue Repair
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“Using either mice deficient for GR in osteoclasts or 11BHSD2 overexpressing mice (where the GC inactivating enzyme is over-expressed in osteoclasts), it was confirmed that GCs act directly on osteoclasts to modulate bone density, in part by increasing the life span of osteoclasts (84, 85).”
BackgroundDexamethasone promotes osteoclastogenesis by inhibiting osteoprotegerin through multiple levels
Kondo, T., Kitazawa, R., Yamaguchi, A., & Kitazawa, S. (2007) · Journal of Cellular Biochemistry · doi:10.1002/jcb.21414 · Cited by 103 · see citing works
“Also, Gr / mice are spared the impact of Dex on osteoclasts and their precursors [Kim et al., 2006].”
BackgroundCorticosteroid receptors, macrophages and cardiovascular disease
Rickard, A. J., & Young, M. J. (2009) · Journal of Molecular Endocrinology · doi:10.1677/jme-08-0144 · Cited by 101 · see citing works
“The role of GR specifically in osteoclasts has been recently defined in mice in which GR were conditionally disrupted in the bone marrow monocytes/osteoclast lineage (Kim et al. 2006).”
BackgroundGlucocorticoid receptor signaling in bone cells
Moutsatsou, P., Kassi, E. N., & Papavassiliou, A. G. (2012) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2012.04.005 · Cited by 98 · see citing works
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“Dexamethasone (DEX) has been widely used in clinical applications to treat immuno-disorders [41,42], but a more specific and common use has been the control of the inflammatory response and tissue repair during organ transplantation [43].”
BackgroundGlucocorticoids maintain human osteoclasts in the active mode of their resorption cycle
Søe, K., & Delaissé, J. (2010) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.113 · Cited by 96 · see citing works
“So also did OCs generated from mouse bone marrow cells cultured in the presence of macrophage colonystimulating factor (M-CSF) and receptor-activator of NF-kB ligand (RANKL),((10)) whereas human OCs generated from peripheral blood mononuclear cells in the presence of the same cytokines and seeded on bone slices did no…”
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Ma, Y., Nyman, J. S., Tao, H., Moss, H. H., Yang, X., & Elefteriou, F. (2011) · Endocrinology · doi:10.1210/en.2010-0881 · Cited by 92 · see citing works
Bad to the Bone: The Effects of Therapeutic Glucocorticoids on Osteoblasts and Osteocytes
Gado, M., Baschant, U., Hofbauer, L. C., & Henneicke, H. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.835720 · Cited by 93 · see citing works
“It has been shown that the early increase in osteoclastic bone resorptionmay be accounted for by an increase in the survival of mature osteoclasts and reduced predisposition to apoptosis (48, 56, 57, 157).”
BackgroundInfluentialDiseases Affecting Bone Quality: Beyond Osteoporosis
Unnanuntana, A., Rebolledo, B. J., Khair, M. M., DiCarlo, E. F., & Lane, J. M. (2010) · Clinical Orthopaedics and Related Research · doi:10.1007/s11999-010-1694-9 · Cited by 92 · see citing works
“Corticosteroids, anti-rheumatic drugs, cancer chemotherapeutic agents or even with osteoporosis medications can adversely affect bone [26, 58, 76, 106].”
BackgroundInfluentialShi, J., Wang, L., Zhang, H., Jie, Q., Li, X., Shi, Q., Huang, Q., Gao, B., Han, Y., Guo, K. X., et al. (2015) · Bone · doi:10.1016/j.bone.2015.06.014 · Cited by 90 · see citing works
Minireview: Live and Let Die: Molecular Effects of Glucocorticoids on Bone Cells
Hofbauer, L. C., & Rauner, M. (2009) · Molecular Endocrinology · doi:10.1210/me.2009-0069 · Cited by 91 · see citing works
“Disruption of the osteoclastic cytoskeleton due to decreased activation of rhoA, rac, and vav3 through macrophage colony-stimulating factor was identified as the underlying mechanism (36).”
BackgroundBone Health and the Female Athlete Triad in Adolescent Athletes
Ackerman, K. E., & Misra, M. (2011) · The Physician and Sportsmedicine · doi:10.3810/psm.2011.02.1871 · Cited by 89 · see citing works
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“marrow macrophages in a dose-dependent manner in vitro [32].”
BackgroundNuclear Receptors in Bone Physiology and Diseases
Imai, Y., Youn, M., Inoue, K., Takada, I., Kouzmenko, A., & Kato, S. (2013) · Physiological Reviews · doi:10.1152/physrev.00008.2012 · Cited by 89 · see citing works
Wetzsteon, R. J., Justine Shults, A., Zemel, B. S., Gupta, P., Burnham, J. M., Herskovitz, R. M., Howard, K. M., & Leonard, M. B. (2008) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.081101 · Cited by 87 · see citing works
“GCs promote osteoclastogenesis and inhibit osteoclast apoptosis((4)); however, GCs also directly impair osteoclast adherence to bone and bone degradation,((6)) resulting in a state of low bone turnover.”
BackgroundGlucocorticoids, Inflammation and Bone
Güler-Yüksel, M., Hoes, J. N., Bultink, I. E. M., & Lems, W. F. (2018) · Calcified Tissue International · doi:10.1007/s00223-017-0335-7 · Cited by 91 · see citing works
Molecular mechanisms of glucocorticoids on skeleton and bone regeneration after fracture
Hachemi, Y., Rapp, A. E., Picke, A., Weidinger, G., Ignatius, A. A., & Tuckermann, J. P. (2018) · Journal of Molecular Endocrinology · doi:10.1530/jme-18-0024 · Cited by 87 · see citing works
Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases
Hardy, E., & Fernández-Patrón, C. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00047 · Cited by 85 · see citing works
Osteoblast autophagy in glucocorticoid‐induced osteoporosis
Wang, L., Heckmann, B. L., Yang, X., & Long, H. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.27335 · Cited by 81 · see citing works
“It is suggested that GC administration inhibits osteoclast differentiation from macrophages and limits cytoskeletal function in a dose‐ dependent manner (Kim et al., 2006).”
BackgroundInfluentialDhawan, P., & Christakos, S. (2010) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22645 · Cited by 82 · see citing works
“It has been suggested that disruption of the cytoskeleton of the osteoclast by glucocorticoids suppresses the resorptive phase of remodeling, thus contributing to retarded bone formation [Kim et al., 2006].”
BackgroundGlucocorticoids Enhanced Osteoclast Autophagy Through the PI3K/Akt/mTOR Signaling Pathway
Fu, L., Wu, W., Sun, X., & Zhang, P. (2020) · Calcified Tissue International · doi:10.1007/s00223-020-00687-2 · Cited by 79 · see citing works
Glucocorticoids and osteocyte autophagy
Yao, W., Dai, W., Jiang, J. X., & Lane, N. E. (2013) · Bone · doi:10.1016/j.bone.2013.01.034 · Cited by 82 · see citing works
“Therefore, excess GC results in an increase in osteoclast number, but in an apparent inhibition of function with impaired spreading and degradation of mineralized matrix [19].”
BackgroundGlobal Analysis of the Impact of Environmental Perturbation on cis-Regulation of Gene Expression
Grundberg, E., Adoue, V., Kwan, T., Ge, B., Duan, Q., Lam, K. C. L., Koka, V., Kindmark, A., Weiss, S. T., Tantisira, K. G., et al. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1001279 · Cited by 79 · see citing works
“Environmental stimuli included growth factors [15,16], cytokines [17,18] and hormones [19–21], all with previous known effects on the osteoblast transcriptome.”
BackgroundAdhikary, S., Choudhary, D., Ahmad, N., Karvande, A., Kumar, A., Banala, V. T., Mishra, P. R., & Trivedi, R. (2018) · Nutrition · doi:10.1016/j.nut.2017.12.003 · Cited by 77 · see citing works
Kim, C. W., Yun, Y.-P., Lee, H. J., Hwang, Y., Kwon, I. K., & Lee, S. C. (2010) · Journal of Controlled Release · doi:10.1016/j.jconrel.2010.06.016 · Cited by 76 · see citing works
The nuclear receptor superfamily of steroid hormones and vitamin D gene regulation
Margolis, R., & Christakos, S. (2010) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.05227.x · Cited by 75 · see citing works
Extrinsic Mechanisms Involved in Age-Related Defective Bone Formation
Marie, P. J., & Kassem, M. S. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-2113 · Cited by 76 · see citing works
Hypercortisolemia and Infection
Fareau, G. G., & Vassilopoulou‐Sellin, R. (2007) · Infectious Disease Clinics of North America · doi:10.1016/j.idc.2007.06.001 · Cited by 75 · see citing works
Pasqualetti, S., Congiu, T., Banfi, G., & Mariotti, M. (2015) · International Journal of Experimental Pathology · doi:10.1111/iep.12106 · Cited by 74 · see citing works
“An additional study in mice lacking glucocorticoid receptor by osteoclasts demonstrated that glucocorticoids prolonged the life span of osteoclasts (Kim et al. 2006).”
BackgroundPhosphate Regulates Osteopontin Gene Transcription
Fatherazi, S., Matsa-Dunn, D., Foster, B. L., Rutherford, R. B., Somerman, M. J., & Presland, R. B. (2009) · Journal of Dental Research · doi:10.1177/0022034508328072 · Cited by 73 · see citing works
“Clinically, the use of glucocorticoids to treat inflammatory diseases often leads to osteoporosis, due to the inhibition of osteoclast-mediated bone resorption and arrested bone formation (Kim et al., 2006).”
BackgroundAcute Effects of Glucocorticoids on Serum Markers of Osteoclasts, Osteoblasts, and Osteocytes
Maresova, K. B., Pavelká, K., & Stepan, J. J. (2012) · Calcified Tissue International · doi:10.1007/s00223-012-9684-4 · Cited by 73 · see citing works
“Supraphysiological concentrations of GC induce an early upregulation of genes associated with osteoclast cytoskeletal reorganization and organic bone matrix degradation [5] and stimulate bone resorption by promoting osteoclast survival and activity [6, 7].”
Glucocorticoids and the Osteoclast
KIM, H., Zhao, H., Kitaura, H., Bhattacharyya, S., Brewer, J. A., Muglia, L. J., Ross, F. P., & Teitelbaum, S. L. (2007) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1402.057 · Cited by 71 · see citing works
Self-citationRole of Plasminogen Activator Inhibitor-1 in Glucocorticoid-Induced Diabetes and Osteopenia in Mice
Tamura, Y., Kawao, N., Yano, M., Okada, K., Okumoto, K., Chiba, Y., Matsuo, O., & Kaji, H. (2014) · Diabetes · doi:10.2337/db14-1192 · Cited by 70 · see citing works
“Furthermore, GC suppresses the formation of osteoclast precursors (41,42).”
BackgroundAnastasilakis, A. D., Tsourdi, E., Makras, P., Polyzos, S. A., Meier, C., McCloskey, E. V., Pepe, J., & Zillikens, M. C. (2019) · Bone · doi:10.1016/j.bone.2019.07.006 · Cited by 71 · see citing works
Rauch, A., Gossye, V., Bracke, D., Gevaert, E., Jacques, P., Beneden, K. V., Vandooren, B., Rauner, M., Hofbauer, L. C., Haegeman, G., et al. (2011) · The FASEB Journal · doi:10.1096/fj.10-173393 · Cited by 71 · see citing works
“In the initial phase of pharmacological GC exposure, it is assumed that osteoclastogenesis rises by disturbing the RANKL/OPG ratio or, more specifically, via RANKL induction and transrepression of OPG expression (38) and by a prolonged osteoclast survival (11, 39, 40).”
BackgroundCommensal-Epithelial Signaling Mediated via Formyl Peptide Receptors
Wentworth, C. C., Jones, R. M., Kwon, Y. M., Nusrat, A., & Neish, A. S. (2010) · American Journal Of Pathology · doi:10.2353/ajpath.2010.100529 · Cited by 72 · see citing works
c-Src Links a RANK/αvβ3 Integrin Complex to the Osteoclast Cytoskeleton
Izawa, T., Zou, W., Chappel, J., Ashley, J. W., Feng, X., & Teitelbaum, S. (2012) · Molecular and Cellular Biology · doi:10.1128/mcb.00077-12 · Cited by 65 · see citing works
“The cells were then incubated, cytokine free, at 37°C for 30 min, after which they were exposed to RANKL or PBS for 15, 30, 60, or 120 min (13).”
MethodDissection of platelet and myeloid cell defects by conditional targeting of the β3‐integrin subunit
Morgan, E. A., Schneider, J. G., Baroni, T. E., Uluçkan, Ö., Heller, E., Hurchla, M. A., Deng, H., Floyd, D. H., Berdy, A., Prior, J. L., et al. (2009) · The FASEB Journal · doi:10.1096/fj.09-138420 · Cited by 68 · see citing works
“The LysM-Cre mice have been successfully used to obtain a tissue-specific gene deletion in OCs (37).”
MethodCorticosterone selectively targets endo-cortical surfaces by an osteoblast-dependent mechanism
Henneicke, H., Herrmann, M., Kalak, R., Brennan‐Speranza, T. C., Heinevetter, U., Bertollo, N., Day, R. E., Huscher, D., Buttgereit, F., Dunstan, C. R., et al. (2011) · Bone · doi:10.1016/j.bone.2011.06.013 · Cited by 67 · see citing works
“Even though a contribution of direct GC effects on osteoclasts cannotbe ruledout entirely [28], our results suggest thatGCinduced osteoclast activity and bone resorption are mediated via changes inosteoblast function.”
BackgroundGlucocorticoid receptor action in metabolic and neuronal function
Garabedian, M. J., Harris, C. A., & Jeanneteau, F. D. (2017) · F1000Research · doi:10.12688/f1000research.11375.1 · Cited by 66 · see citing works
Glucocorticoid-induced autophagy and apoptosis in bone
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Wang, L., Singh, M. K., Bonewald, L. F., & Detamore, M. S. (2009) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.176 · Cited by 65 · see citing works
“However, the differentiation factors, including dexamethasone and 1α,25-dihydroxyvitamin D3, may inhibit cell proliferation (Walsh et al., 2001; Atmani et al., 2003; Chen, 2004; Kim et al., 2006) for both BMSCs and osteoblasts.”
BackgroundSiddappa, R., Fernandes, H., Liu, J., van Blitterswijk, C., & de Boer, J. (2007) · Current Stem Cell Research & Therapy · doi:10.2174/157488807781696267 · Cited by 65 · see citing works
Role of nutritional vitamin D in osteoporosis treatment
Hou, Y., Wu, C., Liao, M.-T., Shyu, J., Hung, C., Yen, T., Lu, C., & Lu, K. (2018) · Clinica Chimica Acta · doi:10.1016/j.cca.2018.05.035 · Cited by 63 · see citing works
Yang, P., Lv, S., Wang, Y., Peng, Y., Ye, Z.-X., Xia, Z., Ding, G.-X., Cao, X., & Crane, J. L. (2018) · Bone · doi:10.1016/j.bone.2018.05.025 · Cited by 60 · see citing works
“The direct effect of glucocorticoids on osteoclasts appear to contribute significantly to skeletal fragility [14, 15, 34].”
BackgroundCurrent Treatments and New Developments in the Management of Glucocorticoid-induced Osteoporosis
Raterman, H. G., Bultink, I. E. M., & Lems, W. F. (2019) · Drugs · doi:10.1007/s40265-019-01145-6 · Cited by 64 · see citing works
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Tsampalieros, A. K., Gupta, P., Denburg, M., Justine Shults, A., Zemel, B. S., Mostoufi‐Moab, S., Wetzsteon, R. J., Herskovitz, R. M., Whitehead, K., & Leonard, M. B. (2012) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.1785 · Cited by 65 · see citing works
“GCs promote osteoclastogenesis and inhibit osteoclast apoptosis,((3)) but GCs also directly impair osteoclast adherence to bone and bone degradation, resulting in an eventual state of low bone turnover.((5)) In this study, we demonstrated that GC therapy was associated with declines in BSAP Z-scores but was not associ…”
BackgroundThe Role of Sclerostin in Bone Diseases
Vasiliadis, E. S., Evangelopoulos, D.-S., Kaspiris, A., Benetos, I. S., Vlachos, C., & Pneumaticos, S. G. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11030806 · Cited by 61 · see citing works
“Thus, targeting sclerostin with an antisclerostin antibody could be beneficial for the treatment of glucocorticoid-induced osteoporosis [54].”
Background
- 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
- Published
- 2006-08-01
- Volume
- 116
- Issue
- 8
- Pages
- 2152-2160
- ISSN
- 0021-9738 (ISSN-L)
- 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 › Genetics › 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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