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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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Osteoprotegerin Prevents Glucocorticoid-Induced Osteocyte Apoptosis in Mice
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Mohammadi, Z., Fayyazbakhsh, F., Ebrahimi, M., Amoli, M. M., Khashayar, P., Dini, M., Zadeh, R. N., Keshtkar, A., & Barikani, H. (2014) · Journal of Diabetes & Metabolic Disorders · doi:10.1186/s40200-014-0098-x · Cited by 44
“Osteoporosis is a bone disease characterized by low bone density caused by increased activity of osteoclasts and decreased bone turnover [2,3].”
BackgroundCheng, Q., Morand, E. F., & Yang, Y. H. (2014) · Frontiers in Pharmacology · doi:10.3389/fphar.2014.00169 · Cited by 45
“…is reciprocally modulated, mainly via regulation of the activity of peroxisome proliferator-activated receptor gamma (PPARγ2), a master transcription factor that promotes adipogenic differentiation (Tontonoz et al., 1994; Weinstein et al., 1998; Ahdjoudj et al., 2001; Akune et al., 2004).”
BackgroundHan, Y., Zhang, L., Xing, Y., Zhang, L., Chen, X., Tang, P., & Chen, Z. (2017) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2017.3270 · Cited by 44
“Gcs also induce oB and osteocyte apoptosis in vivo (32).”
BackgroundPeng, Y., Lv, S., Li, Y., Zhu, J., Chen, S., Zhen, G., Cao, X., Wu, S., & Crane, J. L. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3987 · Cited by 43
“Therefore, the effect on bone formation may be due to the known direct effects of GCs inducing apoptosis and inhibiting differentiation of osteoblast lineage cells.((37,47))”
BackgroundProliferation, Differentiation and Apoptosis in Connexin43-Null Osteoblasts
Furlan, F., Lecanda, F., Screen, J., & Civitelli, R. (2001) · Cell Communication & Adhesion · doi:10.3109/15419060109080755 · Cited by 44
RAMPs and CRLR expressions in osteoblastic cells after dexamethasone treatment
Uzan, B., de Vernejoul, M.-C., & Cressent, M. (2004) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2004.07.037 · Cited by 43
Zheng, H., He, B., Wu, T., Cai, J., & Wei, J. (2019) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2019.11.145 · Cited by 43
Embryonic Development of Bone and Regulation of Intramembranous and Endochondral Bone Formation
Karaplis, A. C. (2008) · Elsevier eBooks · doi:10.1016/b978-0-12-373884-4.00025-2 · Cited by 48
The anabolic effect of PTH on bone is attenuated by simultaneous glucocorticoid treatment
Oxlund, H., Ørtoft, G., Thomsen, J. S., Danielsen, C. C., Ejersted, C., & Andreassen, T. T. (2006) · Bone · doi:10.1016/j.bone.2006.01.142 · Cited by 43
“GC induces apoptosis of osteoblasts and osteocytes, and this contributes to the decrease in number of mature osteoblasts [24].”
BackgroundGlucocorticoid induced osteoporosis
Hu, K., & Adachi, J. D. (2019) · Expert Review of Endocrinology & Metabolism · doi:10.1080/17446651.2019.1617131 · Cited by 44
Cunningham, J. (2006) · Journal of the American Society of Nephrology · doi:10.1681/asn.2006050427 · Cited by 44
“There also is a reduction of osteoblast proliferative activity and acceleration of apoptosis, resulting in a substantial reduction in osteoblast numbers (52,54).”
BackgroundDeterminants of bone mass in end‐stage renal failure patients at the time of kidney transplantation
Dolgos, S., Hartmann, A., Bønsnes, S., Ueland, T., Isaksen, G. A., Godang, K., Pfeffer, P. F., & Bollerslev, J. (2008) · Clinical Transplantation · doi:10.1111/j.1399-0012.2008.00810.x · Cited by 43
“Multiple fractures 10 (11) 6 (14) 16 (12) Physically active 73 (80) 35 (83) 108 (81)”
BackgroundOsteoporosis across chronic liver disease
Guarino, M., Loperto, I., Camera, S., Cossiga, V., Somma, C. D., Colao, A., Caporaso, N., & Morisco, F. (2016) · Osteoporosis International · doi:10.1007/s00198-016-3512-z · Cited by 45
“Steroids promote mature osteoblast synthesis, but also have, as explained below, an inhibitory effect on their activity, in addition also increase osteolysis and augment osteoclast recruitment [25].”
BackgroundPinto, C. M., Rojas‐Villarraga, A., Molano‐González, N., Jiménez-Herrera, E. A., Vázquez, M. D. L. L. L., Montiel-Jarquín, Á. J., García‐Carrasco, M., & Cervera, R. (2018) · PLoS ONE · doi:10.1371/journal.pone.0196113 · Cited by 43
A Second Career for Chondrocytes—Transformation into Osteoblasts
Wolff, L. I., & Hartmann, C. (2019) · Current Osteoporosis Reports · doi:10.1007/s11914-019-00511-3 · Cited by 46
Chen, L., Shi, X., Weng, S., Xie, J., Tang, J., Yan, D., Wang, B.-Z., Xie, Z.-J., Wu, Z., & Yang, L. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.01209 · Cited by 44
“The deleterious effects of GC on osteoblasts are now considered to play a major role in the development of GIOP (Weinstein et al., 1998; Canalis et al., 2007; Hartmann et al., 2016; Rizzoli, 2017).”
BackgroundUpdate on Glucocorticoid-Induced Osteoporosis
Maricic, M. J. (2011) · Rheumatic Disease Clinics of North America · doi:10.1016/j.rdc.2011.07.003 · Cited by 45
“However, there has been a study suggesting potential efficacy of intravenous ibandronate in GIOP.”
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“…and hypogonadism, GIO is mostly attributed to direct deleterious effects of GCs on cells in the osteoblast lineage, in particular inhibition of proliferation and stimulation of apoptosis (Weinstein et al. 1998; Canalis and Delany 2002; Liu et al. 2004; O’Brien et al. 2004; Mazziotti et al. 2006).”
BackgroundAggarwal, R., Lu, J., Kanji, S., Joseph, M., Das, M., Noble, G. J., McMichael, B. K., Agarwal, S., Hart, R. T., Sun, Z., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039365 · Cited by 44
“Age, endocrine malfunction or deficiency, nutrition, or lack of physical activity, all can imbalance the osteoblasts and osteoclasts activities, affecting both trabecular and cortical bone at molecular, cellular and structural levels [4,5].”
BackgroundBlanquaert, F., Pereira, R. C., & CANALIS, E. M. (2000) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.2000.278.3.e509 · Cited by 43
Glucocorticoid-Induced Osteoporosis
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Matrix Regulation of Skeletal Cell Apoptosis II: Role of Arg-Gly-Asp-Containing Peptides
Perlot, R. L., Shapiro, I. M., Mansfield, K. D., & Adams, C. S. (2002) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.2002.17.1.66 · Cited by 43
“, (6) and others (7) have shown that in vivo many osteoblasts evidence a cardinal sign of programmed cell death, nuclear fragmentation.”
BackgroundTanaka, Y., Nakayamada, S., Fujimoto, H., Okada, Y., Umehara, H., Kataoka, T., & Minami, Y. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m202238200 · Cited by 43
Bone health in glucocorticoid-treated childhood acute lymphoblastic leukemia
Velentza, L., Zaman, F., & Savendahl, L. S. (2021) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2021.103492 · Cited by 42
Risk for osteoporosis and fracture with glucocorticoids
Urquiaga, M., & Saag, K. G. (2022) · Best Practice & Research Clinical Rheumatology · doi:10.1016/j.berh.2022.101793 · Cited by 45
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“It is generally accepted that GCs can cause a rapid bone loss decreasing bone formation and increasing bone resorption in vitro as well as in vivo [reviews: Delany et al., 1994; Weinstein and Manolagas, 2000, Weinstein, 2001; Zalavras et al., 2003; Xing and Boyce, 2005].”
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“14 For example, osteoclast functions are inhibited with Dex treatment.”
Bab, I., & Yirmiya, R. (2010) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.05218.x · Cited by 43
Kuang, M., Zhang, W., He, W., Sun, L., Ma, J., Wang, D., & Ma, X. (2019) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2019.03.008 · Cited by 42
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“Age‐related bone loss in mice The peak bone mass of mice is reached between 5 and 6 month of age [13].”
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“Long-term administration of glucocorticoid therapies, especially in association with immunosuppressive agents, such as calcineurin inhibitors, are responsible for a significant bone loss, with reduction of bone mineral density (BMD), increased osteoclastic action (39, 40) and lack of osteoblasts differentiation (18, 4…”
BackgroundIncreased Bone Mass Is a Part of the Generalized Lymphoproliferative Disorder Phenotype in the Mouse
Katavić, V., Lukić, I. K., Kovačić, N., Grčević, D., Lorenzo, J., & Marušić, A. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.170.3.1540 · Cited by 42
Scholz-Ahrens, K. E., Delling, G., Stampa, B., Helfenstein, A., Hahne, H. ‐., Açil, Y., Timm, W., Barkmann, R., Hassenpflug, J., Schrezenmeir, J., et al. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00627.2006 · Cited by 42
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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