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Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
Open accessAbstract
Glucocorticoid-induced bone disease is characterized by decreased bone formation and in situ death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess, the third most common cause of osteoporosis, may affect the birth or death rate of bone cells, thus reducing their numbers. To test this hypothesis, we administered prednisolone to 7-mo-old mice for 27 d and found decreased bone density, serum osteocalcin, and cancellous bone area along with trabecular narrowing. These changes were accompanied by diminished bone formation and turnover, as determined by histomorphometric analysis of tetracycline-labeled vertebrae, and impaired osteoblastogenesis and osteoclastogenesis, as determined by ex vivo bone marrow cell cultures. In addition, the mice exhibited a threefold increase in osteoblast apoptosis in vertebrae and showed apoptosis in 28% of the osteocytes in metaphyseal cortical bone. As in mice, an increase in osteoblast and osteocyte apoptosis was documented in patients with glucocorticoid-induced osteoporosis. Decreased production of osteoclasts explains the reduction in bone turnover, whereas decreased production and apoptosis of osteoblasts would account for the decline in bone formation and trabecular width. Furthermore, accumulation of apoptotic osteocytes may contribute to osteonecrosis. These findings provide evidence that glucocorticoid-induced bone disease arises from changes in the numbers of bone cells.
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“A high level of glucocorticoid in smokers alters bone metabolism and decreases bone mass either directly by changing the osteoblast and osteoclast activities or indirectly by altering the gastrointestinal absorption and renal reabsorption of calcium [39–42].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [39]
Experimental — accuracy not yet measuredIn the citing paper
“In mice, BMD loss with prednisolone was associated with decreased osteocalcin and decreased bone formation, with no histological or biochemical evidence for increased bone resorption (251).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“bone marrow harvested from mice treated with prednisolone showed reduced osteoclastogenic potential (251).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“One important component of glucocorticoid biology that is lacking in most cell culture models is the marked depletion of osteoblast numbers in animals treated with glucocorticoids (251).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“Bone marrow harvested from mice treated with prednisolone was shown to have markedly reduced osteoblastogenic capacity (251).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“Glucocorticoids can also inhibit osteoblast differentiation (249 -251), osteoblast attachment to bone matrix (252), and osteoblast production of IGF-I (253).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“The prednisolonerelated increase in bone volume in rats, confirmed in a study described immediately below (262), is not consistent with histological data from patients with glucocorticoid-induced osteoporosis (194) and is a recognized limitation of the model (251).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
In the citing paper
“Glucocorticoids decrease BMD in rats (262, 263), mice (251), and minipigs (264).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [251]
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“GIOP is the most common cause of secondary osteoporosis (30) and the pro-apoptotic effect of high‑dose GCs on osteoblasts has been identified as a major cause for GIOP (4,31,32).”
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“In addition, steroids may accelerate osteonecrosis by facilitating the apoptosis of osteoblasts and osteocytes, thereby partially contributing to bone cell death (14,36-38).”
BackgroundA high-fat diet aggravates osteonecrosis through a macrophage-derived IL-6 pathway
Zhou, Z., Pan, C., Wang, N., Zhou, L., Shan, H., Gao, Y., & Yu, X. (2019) · International Immunology · doi:10.1093/intimm/dxz002 · Cited by 21
The skeletal remains: porosis and necrosis of bone in the marrow transplantation setting
Mattano, L. A. (2003) · Pediatric Transplantation · doi:10.1034/j.1399-3046.7.s3.11.x · Cited by 21
Caffeine-mediated enhancement of glucocorticoid receptor activity in human osteoblastic cells
Föcking, M., Schmiegelt, D., & Trapp, T. (2005) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2005.09.067 · Cited by 21
Steroid-induced osteoporosis: how can it be avoided?
Jehle, P. M. (2003) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfg067 · Cited by 22
“As shown in Figure 1, steroids do not only reduce the lifespan and promote the apoptosis of osteoblasts and osteoclasts but also decrease the recruitment of osteoblasts and osteoclasts from progenitor cells [1].”
BackgroundBone histomorphometric changes in children with rheumatic disorders on chronic glucocorticoids
Harrington, J., Holmyard, D. P., Silverman, E. D., Sochett, E. B., & Grynpas, M. D. (2016) · Pediatric Rheumatology · doi:10.1186/s12969-016-0119-z · Cited by 22
Xue, X., Feng, Z., Li, Z., & Pan, X. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.8349 · Cited by 21
“The imbalance between osteoblast and osteoclast activity, by inhibiting osteoblastogenesis and promoting osteoblast apoptosis, will finally cause osteonecrosis (8,9).”
BackgroundJohnson, B. R., Fayad, M. I., & Witherspoon, D. E. (2011) · Elsevier eBooks · doi:10.1016/b978-0-323-06489-7.00021-7 · Cited by 21
Bone Mass And Bone Metabolism In Pediatric Gastrointestinal Disorders
Mora, S., & Barera, G. (2004) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1002/j.1536-4801.2004.tb00784.x · Cited by 21
Shane, E. J., & Epstein, S. (2001) · Transplantation Reviews · doi:10.1053/trre.2001/19535 · Cited by 21
Jiang, X., Qi, X., & Xie, C. L. (2023) · Food & Nutrition Research · doi:10.29219/fnr.v67.9064 · Cited by 20
“Furthermore, decreased osteoclasts and osteoblasts might be correlated with the suppressed turnover and formation of the bones caused by glucocorticoid as well (31).”
BackgroundResultPlesa, M., Gagné, V., Glisovic, S., Younan, M., Sharif-Askari, B., Laverdière, C., Alos, N., Leclerc, J., Sallan, S. E., Neuberg, D. S., et al. (2017) · The Pharmacogenomics Journal · doi:10.1038/s41397-017-0002-4 · Cited by 20
Jiang, Y., Xin, N., Yang, J., Wu, W., Wang, M., Feng, N., & Zhu, G. (2021) · Environmental Toxicology and Pharmacology · doi:10.1016/j.etap.2021.103719 · Cited by 19
PINK1-mediated mitophagy contributes to glucocorticoid-induced cathepsin K production in osteocytes
Yuan, J., Gao, Y., Liu, D., Tai, A. C. P., Zhou, H., Papadimitriou, J. M., Zhang, C., Zheng, M., & Gao, J. (2022) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2022.11.003 · Cited by 21
“Previous evidence suggests that GC induces bone loss by means of enhancing osteoclastic bone resorption [3] and inhibiting osteoblastic bone formation [4,5].”
BackgroundVitamin D Deficiency in Chronic Childhood Disorders: Importance of Screening and Prevention
Joshi, M., & Uday, S. (2023) · Nutrients · doi:10.3390/nu15122805 · Cited by 24
“Steroid therapy for hepatic disease negatively impacts bone mass by enhancing the lifespan of existing osteoclasts, increasing the apoptosis of osteocytes and osteoblasts [56], supressing the formation of osteoblasts in the bone marrow and promoting loss of calcium through the kidneys and gut [57].”
BackgroundKuznetsov, S. A., Mankani, M. H., & Robey, P. G. (2011) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.515 · Cited by 20
Kuriwaka-Kido, R., Kido, S., Miyatani, Y., Ito, Y., Kondo, T., Omatsu, T., Dong, B., Endo, I., Miyamoto, K., & Matsumoto, T. (2013) · Endocrinology · doi:10.1210/en.2013-1915 · Cited by 20
“Parathyroid Hormone (1-34) Counteracts the Suppression of Interleukin-11 Expression by Glucocorticoid in Murine Osteoblasts: A Possible Mechanism for Stimulating Osteoblast Differentiation Against Glucocorticoid Excess”
BackgroundInfluentialMohan, G., Lay, E. Y.-A., Berka, H., Ringwood, L. A., Kot, A., Chen, H., Yao, W., & Lane, N. E. (2016) · Calcified Tissue International · doi:10.1007/s00223-016-0195-6 · Cited by 21
“GCs reduce osteogenesis from mesenchymal stem cells (MSCs) and direct their differentiation into adipocytes, decrease terminal differentiation to osteoblasts, and reduce osteoblast function and lifespan which eventually leads to bone loss [6, 7].”
Yin, J., Han, L., & Cong, W. (2017) · Pharmacological Reports · doi:10.1016/j.pharep.2017.11.001 · Cited by 20
RetractedBrown, H. K., Allocca, G., Ottewell, P. D., Wang, N., Brown, N. J., Croucher, P. I., Eaton, C. L., & Holen, I. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19102920 · Cited by 20
“As the lifespan of osteoblasts in mice is estimated to be around 12 days [21], their number would remain increased following PTH treatment during the key period of tumour cell homing and colonization of the bone metastatic niche in our model.”
BackgroundJähn, K., & Zimmermann, E. A. (2021) · Current Osteoporosis Reports · doi:10.1007/s11914-021-00686-8 · Cited by 18
Decrease in Bone Mass in Women After Liver Transplantation: Associated Factors
Baccaro, L. F., Boin, I. D. F. S. F., Pedro, A. O., Costa‐Paiva, L., Leal, A., Ramos, C. D., & Pinto-Neto, A. M. (2011) · Transplantation Proceedings · doi:10.1016/j.transproceed.2011.02.027 · Cited by 19
Zikán, V., Týblová, M., Raška, I., Havrdová, E., Luchavova, M., Michalská, D., & Kuběna, A. A. (2012) · Physiological Research · doi:10.33549/physiolres.932299 · Cited by 21
“The central pathophysiological mechanism of bone loss during long-term use of GC is reduced bone formation and bone repair, due to actions that affect osteoblast differentiation and function (Weinstein et al. 1998).”
BackgroundLong-term results of children diagnosed with idiopathic nephrotic syndrome; single center experience
Hacıhamdioğlu, D. Ö., Kalman, S., & Gök, F. (2015) · Türk Pediatri Arşivi · doi:10.5152/tpa.2015.2086 · Cited by 20
“Glucocorticoids inhibit osteoblastogenesis and stimulate osteoblast apoptosis and this leads to a reduction in bone formation (34).”
BackgroundAnimal Models in Osteoporosis Research
Kimmel, D. B. (2002) · Elsevier eBooks · doi:10.1016/b978-012098652-1.50197-9 · Cited by 20
Hip Osteonecrosis Is Associated with Increased Plasma IL-33 Level
Ma, J., Guo, W., Li, Z., Wang, B., Li, S., & Wang, P. (2017) · Mediators of Inflammation · doi:10.1155/2017/1732638 · Cited by 20
Maratová, K., Hradský, O., Matysková, J., Čopová, I., Souček, O., Šumnı́k, Z., & Bronský, J. (2017) · European Journal of Pediatrics · doi:10.1007/s00431-017-2988-7 · Cited by 20
“The main contributing factor of low bone mass accrual is most likely the overproduction of pro-inflammatory cytokines (TNF-α, IL-1 β, and IL-6) [8], which promote osteoclastogenesis, and corticosteroid (CS) therapy, which induces osteoblast and osteocyte apoptosis [9].”
BackgroundLorenzo, J. A., CANALIS, E. M., & Raisz, L. G. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4377-0324-5.00029-8 · Cited by 20
Bone growth stimulators New tools for treating bone loss and mending fractures
Whitfield, J. F., Morley, P., & Willick, G. E. (2002) · Vitamins and hormones · doi:10.1016/s0083-6729(02)65059-9 · Cited by 21
11β-Hydroxysteroid Dehydrogenase, an Amplifier of Glucocorticoid Action in Osteoblasts
CANALIS, E. M., & Delany, A. M. (2002) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2002.17.6.987 · Cited by 20
Cellular Actions of Parathyroid Hormone on Osteoblast and Osteoclast Differentiation
Aubin, J. E., & Heersche, J. N. M. (2001) · Elsevier eBooks · doi:10.1016/b978-012098651-4/50014-6 · Cited by 20
Theruvath, A. J., Sukerkar, P. A., Bao, S., Rosenberg, J., Luna‐Fineman, S., Kharbanda, S., & Daldrup-Link, H. E. (2017) · European Radiology · doi:10.1007/s00330-017-4961-2 · Cited by 19
The skeletal consequences of epidural steroid injections: a literature review
Krez, A. N., Liu, Y., Kanbour, S., Clare, S., Waldman, S. A., & Stein, E. M. (2021) · Osteoporosis International · doi:10.1007/s00198-021-05986-4 · Cited by 20
Wen, X., Xu, C., Wang, F.-Q., Feng, Y., Zhao, X., Yan, Y., & Lei, W. (2015) · BioMed Research International · doi:10.1155/2015/263434 · Cited by 19
Glucocorticoid Attenuates the Anabolic Effects of Parathyroid Hormone on Fracture Repair
Doyon, A. R., Ferries, I. K., & Li, J. (2010) · Calcified Tissue International · doi:10.1007/s00223-010-9370-3 · Cited by 19
“One reason is that there has not been a standard animal model to test the effects of bone anabolic compounds on fracture repair in the presence of GC. The rodent model presented in this study appears useful to study fracture repair in the presence of GC. Our dose of GC was based on the effects reported to produce oste…”
BackgroundNawata, K., Nakamura, J., Ikeda, K., Furuta, S., Nakajima, H., Ohtori, S., Hagiwara, S., Wako, Y., Miura, M., Kawarai, Y., et al. (2018) · Lara D. Veeken · doi:10.1093/rheumatology/key009 · Cited by 19
Prednisolone treatment reduces the osteogenic effects of loading in mice
Bergström, I. B., Isaksson, H., Koskela, A., Tuukkanen, J., Ohlsson, C., Andersson, G. N., & Windahl, S. H. (2018) · Bone · doi:10.1016/j.bone.2018.04.002 · Cited by 19
Mineral and Bone Disease in Kidney Transplant Recipients
Altman, A. M., & Sprague, S. M. (2018) · Current Osteoporosis Reports · doi:10.1007/s11914-018-0490-4 · Cited by 19
Okawara, H., Arai, Y., Matsuno, H., Marcián, P., Borák, L., Aoki, K., & Wakabayashi, N. (2021) · Journal of the mechanical behavior of biomedical materials/Journal of mechanical behavior of biomedical materials · doi:10.1016/j.jmbbm.2021.104370 · Cited by 19
Brent, M. B., Thomsen, J. S., & Brüel, A. (2021) · Scientific Reports · doi:10.1038/s41598-021-91729-8 · Cited by 19
Metadata
- Authors
- Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1998-07-15
- Volume
- 102
- Issue
- 2
- Pages
- 274-282
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC508885
- OpenAlex
- W2002315967
- Cited by
- 1,753
- References
- 56
- Citations by year
- 2026: 25 · 2025: 35 · 2024: 44 · 2023: 63 · 2022: 55 · 2021: 69 · 2020: 65 · 2019: 60 · 2018: 59 · 2017: 63 · 2016: 72 · 2015: 59 · 2014: 77 · 2013: 70 · 2012: 74
- FWCI
- 15.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health (5r01ar043003-05)
- National Institute on Aging (P01 AG-13918, P01AG013918)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR43003)
- 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, osteoblastogenesis, osteoblast apoptosis, osteocyte apoptosis, prednisolone, avascular necrosis, bone formation, bone turnover, osteoclastogenesis, trabecular bone, bone mineral density, osteocalcin
- MeSH terms
- Adult, Animals, Bone and Bones, Bone Marrow Cells, Bone Resorption, Cells, Cultured, Female, Glucocorticoids, Humans, Male, Osteoblasts, Osteocytes, Osteoporosis, Prednisolone, Spine, Bone Density, Apoptosis, Mice
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