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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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Bone fragility in male glucocorticoid-induced osteoporosis is not defined by bone mineral density
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“In vivo studies have shown that GC administration caused low bone turnover by the suppression of osteoblast function, the induction of apoptosis in osteoblasts [ 15 ], and a major loss of trabecular connectivity [16].”
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“Although the definite pathogenesis of steroid-induced ONFH has not been clarified, apoptosis has been demonstrated as one pathogeny of steroid-induced ONFH by many researches.(10,11)”
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“The coexpression of these two receptors in this osteoblastic cell line prompted the second part of the study, also in view of the preclinical and clinical opposing effects exerted by GC and CT on bone resorption.(12,13,17) In the in vitro experimentation, we focused on the RANKL/RANK system shown to have crucial prima…”
BackgroundResultGlucocorticoid Induced Osteoblast Apoptosis by Increasing E4BP4 Expression via Up-regulation of Bim
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“These findings are in line with our understanding of the effect of systemic glucocorticoids on bone, with an early and sustained inhibition of osteoblast function leading to low turnover bone loss.(49) Thus, even under current steroid-minimization protocols, glucocorticoid exposure exerts negative effects on the skele…”
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“Increased apoptosis of osteocytes is also observed [7].”
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“cides closely with mouse bone remodeling time of approximately 2 weeks.((40)) Encouragingly, human bone remodeling time ranges from 6 to 9 months,((41)) suggesting that infrequent dosing may be possible in patients with OI with this therapy.”
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“GCs have a suppressive effect on osteoblastogenesis in the bone marrow and promote the apoptosis of osteoblasts and osteocytes, thus leading to decreased bone formation [31].”
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“GCs may also promote apoptosis of osteocytes [54, 55, 58].”
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“decrease in ALPL and OCN gene expression were due to the accumulation of FPP and its subsequent activation of the glucocorticoid receptor,((19)) which is known to inhibit osteoblast proliferation and bone formation and to increase osteoblast apoptosis.((20)) In addition, the depletion of RANKL would lead to an aberran…”
BackgroundGlucocorticoid-Induced Bone Fragility Is Prevented in Female Mice by Blocking Pyk2/Anoikis Signaling
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“…have been shown to induce apoptosis in thymocytes [Ashwell et al., 2000; Chmielewski et al., 2000; Jamieson and Yamamoto, 2000], in osteoclasts and osteocytes [Mitchel et al., 1998; Weinstein et al., 1998], in dendritic cells [Brokaw et al., 1998] and in neuronal cells [Mitchel et al., 1998].”
BackgroundThe treatment of glucocorticoid-induced osteoporosis
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“Reduced BMD has been well documented in patients with Cushing’s disease, and the use of long-term exogenous synthetic GCs is one of the major causes of secondary osteoporosis [26,27].”
BackgroundPoncirin prevents bone loss in glucocorticoid-induced osteoporosis in vivo and in vitro
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“Finally, activation of caspase 3 leads to increased apoptosis of circulating osteoblasts.(18,19)”
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Necroptosis: A new target for prevention of osteoporosis
Hu, X., Wang, Z., Kong, C., Wang, Y., Zhu, W., Wang, W., Li, Y., Wang, W., & Lu, S. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1032614 · Cited by 29
CCL3 in the bone marrow microenvironment causes bone loss and bone marrow adiposity in aged mice
Yu, D., Zhang, S., Ma, C., Huang, S., Xu, L., Liang, J., Li, H., Fan, Q., Liu, G., & Zhai, Z. (2022) · JCI Insight · doi:10.1172/jci.insight.159107 · Cited by 28
“The peak bone mass of mice is achieved between 5 and 6 months of age (18), followed by progressive decline with aging (19).”
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“GC decreases the number of osteoblasts and osteocytes by enhanced apoptosis as well as suppressed turnover of cell cycle [9,12].”
BackgroundMolecular determinants of glucocorticoid actions in inflammatory joint diseases
Baschant, U., Culemann, S., & Tuckermann, J. P. (2013) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2013.06.009 · Cited by 29
Vanadate prevents glucocorticoid-induced apoptosis of osteoblasts in vitro and osteocytes in vivo
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“An increase in apoptosis of osteocytes, hypertrophic chondrocytes, and bone marrow cells was also observed in mice receiving high doses of glucocorticoids [14].”
BackgroundNew Concepts in Bone Remodeling
Dempster, D., & Zhou, H. (2006) · Elsevier eBooks · doi:10.1016/b9-78-012088-5/62650-0236 · Cited by 28
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“It is not clear why certain pieces of bone are ‘‘targeted’’ before others but one attractive hypothesis, that can be traced back to the early 1900s [4–8], is that the osteocyte acts as a mechanosensor, detecting a deterioration in the mechanical properties of the surrounding bone matrix and, having done so, communicat…”
BackgroundKaravitaki, N., Ioannidis, G., Giannakopoulos, F., Mavrokefalos, P., & Thalassinos, N. C. (2004) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2004.01968.x · Cited by 28
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“Teriparatide directly stimulates osteoblastogenesis and inhibits osteoblast apoptosis, thereby counteracting two key mechanisms through which glucocorticoid therapy promotes bone loss [12].”
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Vertebral Blood Flow and Bone Mineral Density During Long-Term Corticosteroid Treatment
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“An increase in osteoblast and/or osteocyte apoptosis would therefore be expected to compromise skeletal integrity, and may contribute to the pathogenesis of bone loss and fragility fractures associated with sex hormone deficiency and glucocorticoid excess (Weinstein et al. 1998).”
BackgroundGregorini, M., Sileno, G., Pattonieri, E. F., Corradetti, V., Abelli, M., Ticozzelli, E., Scudeller, L., Grignano, M. A., Esposito, P. B., Bogliolo, L., et al. (2017) · Transplantation Proceedings · doi:10.1016/j.transproceed.2017.02.023 · Cited by 27
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Glucocorticoid-Induced Osteoporosis
Adler, R. A., Curtis, J. R., Weinstein, R. S., & Saag, K. G. (2008) · Elsevier eBooks · doi:10.1016/b978-012370544-0.50046-x · Cited by 27
Self-citationThe effect of methotrexate on bone metabolism markers in patients with rheumatoid arthritis
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“As for osteoclastogenesis, available scientific data indicate that both the decrease and increase in this process can account for the bone loss, provided that there is a concomitant decline in the formation and functional abi lity of osteoblasts (33, 34).”
BackgroundThe skeletal impact of cancer therapies
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“On the bone resorption side of the equation, glucocorticoids induce an initial increase in osteoclast lifespan but ultimately lead to a decrease in osteoclastogenesis.(52) Due to disruption of the normal physiologic coupling that occurs between osteoclasts and osteoblasts, this decrease in osteoclastogenesis also lead…”
BackgroundMatrix regulation of skeletal cell apoptosis III: Mechanism of ion pair‐induced apoptosis
Saunders, R., Szymczyk, K. H., Shapiro, I. M., & Adams, C. S. (2006) · Journal of Cellular Biochemistry · doi:10.1002/jcb.21001 · Cited by 26
“This observation may help to explain why osteoblast apoptosis is most marked at sites of rapid bone formation or resorption [Bronckers et al., 1996; Noble et al., 1997; Jilka et al., 1998, 1999; Weinstein et al., 1998].”
BackgroundIs rheumatoid arthritis a risk factor for oral bisphosphonate-induced osteonecrosis of the jaws?
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“well-known that steroids and methotrexate (MTX) have been consistently implicated in the suppression of bone turnover through a marked inhibitory effect on osteoclastogenesis [79,80], osteoblast and osteocyte apoptosis induction by steroids [81], and osteoblastic proliferation inhibition by MTX [82].”
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Small non-coding RNAs-based bone regulation and targeting therapeutic strategies
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“However, prolonged use of GCs has been closely associated with osteoporosis, and GC-induced osteoporosis (GCOP) is the second most common aetiology of all types of osteoporosis (Kondo et al., 2008; Weinstein et al., 1998).”
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“Recent studies have suggested that apoptosis may play an important role in bone turnover [27] and the development of both type I osteoporosis [28, 29] and steroid-induced osteoporosis [ 30 ].”
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“However, glucocorticoids are also known to induce apoptosis of osteoblasts and osteocytes, which is consistent with clinical glucocorticoid-induced osteoporosis [8].”
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“Another important osteoporosis-related agent, glucocorticoids, may cause bone loss by inhibiting osteoclast apoptosis [57] and stimulating osteoblast and osteocyte apoptosis [58].”
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“Besides, it is known that the augmented bone fragility which results from glucocorticoid use [30, 31] and both estrogen [32] and androgen deficiencies [33] is also associated with a higher prevalence of osteocyte apoptosis.”
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Regulation of sclerostin in glucocorticoid-induced osteoporosis (GIO) in mice and humans
Thiele, S., Hannemann, A., Winzer, M., Baschant, U., Weidner, H., Nauck, M. A., Thakker, R. V., Bornhäuser, M., Hofbauer, L. C., & Rauner, M. (2019) · Endocrine Connections · doi:10.1530/ec-19-0104 · Cited by 25
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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