The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.
Lacey, D. L., Timms, E., Tan, H.-L., Kelley, M. J., Dunstan, C. R., Burgess, T., Elliott, R., Colombero, A., Elliott, G., Scully, S., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81569-x · Cited by 5,439
Bone Resorption by Osteoclasts
Teitelbaum, S. L. (2000) · Science · doi:10.1126/science.289.5484.1504 · Cited by 3,962
Conditional gene targeting in macrophages and granulocytes using LysMcre mice
Clausen, B. E., Burkhardt, C., Reith, W., Renkawitz, R., & Förster, I. (1999) · Transgenic Research · doi:10.1023/a:1008942828960 · Cited by 2,098
Weinstein, R. S., Jilka, R. L., Parfitt, A. M., & Manolagas, S. C. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2799 · Cited by 1,753 · cited 1×
“Net bone mass represents the relative activities of osteoblasts and osteoclasts, and there is little question that GCs suppress bone-forming cells, in vivo, via a process involving accelerated apoptosis (1, 2).”
BackgroundSeverely Suppressed Bone Turnover: A Potential Complication of Alendronate Therapy
Odvina, C. V., Zerwekh, J. E., Rao, D. S., Maalouf, N. M., Gottschalk, F., & Pak, C. Y. C. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0952 · Cited by 1,429
c-Fos: a Key Regulator of Osteoclast-Macrophage Lineage Determination and Bone Remodeling
Grigoriadis, A. E., Wang, Z., Cecchini, M. G., Hofstetter, W., Felix, R., Fleisch, H. A., & Wagner, E. F. (1994) · Science · doi:10.1126/science.7939685 · Cited by 1,264
Black, D. M., Greenspan, S. L., Ensrud, K. E., Palermo, L., McGowan, J., Lang, T., Garnero, P., Bouxsein, M., Bilezikian, J. P., & Rosen, C. J. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa031975 · Cited by 1,168
Udagawa, N., Takahashi, N., Akatsu, T., Tanaka, H., Sasaki, T., Nishihara, T., Koga, T., Martin, T. J., & Suda, T. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.18.7260 · Cited by 1,048
The Effects of Parathyroid Hormone, Alendronate, or Both in Men with Osteoporosis
Finkelstein, J. S., Hayes, A.-M., Hunzelman, J. L., Wyland, J. J., Lee, H., & Neer, R. M. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa035725 · Cited by 823
IL-1 mediates TNF-induced osteoclastogenesis
Shi, W., Kitaura, H., Zhou, P., Ross, F. P., & Teitelbaum, S. L. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23394 · Cited by 805
Cited by
Sorted by citations
Items 201–300 of 384
Wu, R., Lian, W., Chen, Y., Kuo, C.-W., Ke, H.-C., Hsieh, C.-K., Wang, S.-Y., Ko, J., & Wang, F. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20205141 · Cited by 20
“Osteoclast morphology was microscopically evaluated, as previously described [42].”
MethodSrc‐like adaptor protein regulates osteoclast generation and survival
Kim, H., Zou, W., Ito, Y., Kim, S., Chappel, J. C., Ross, F. P., & Teitelbaum, S. L. (2010) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22527 · Cited by 20
“Primary BMMs were prepared as described [Kim et al., 2006].”
MethodSelf-citationPark, H., Tse, S. M., Yang, W., Kelly, H. W., Kaste, S. C., Pui, C.-H., Relling, M. V., & Tantisira, K. G. (2016) · The Pharmacogenomics Journal · doi:10.1038/tpj.2015.92 · Cited by 20
Should biochemical markers of bone turnover be considered standard practice for safety pharmacology?
Henriksen, K., Bohren, K. M., Bay‐Jensen, A., & Karsdal, M. A. (2009) · Biomarkers · doi:10.3109/13547500903434519 · Cited by 20
“…to the osteoblastic lineage, i.e. mature bone-forming osteoblasts and osteocytes, and while the effect on bone appears to be dependent on osteoclasts (Kim et al. 2006), there are no indications that the glucocorticoids lead to increased bone resorption (Engvall et al. 2008, Minisola et al. 2008).”
BackgroundLoss of glucocorticoid rhythm induces an osteoporotic phenotype in female mice
Schilperoort, M., Kroon, J., Kooijman, S., Smit, A. E., Gentenaar, M., Mletzko, K., Schmidt, F. N., van Ruijven, L. J., Busse, B., Pereira, A. M., et al. (2021) · Aging Cell · doi:10.1111/acel.13474 · Cited by 19
Kim, H., Lee, D.-K., Jin, X., Che, X., Ryu, S. H., & Choi, J. (2022) · Experimental & Molecular Medicine · doi:10.1038/s12276-022-00820-1 · Cited by 20
Self-citationBone remodeling humoral networks and smart biomaterial technology for osteoporosis
Fini, M. (2009) · Frontiers in Bioscience-Scholar · doi:10.2741/s79 · Cited by 19
“Furthermore, glucocorticoid excess sensitizes bone cells to other regulators of bone remodelling and augments osteoclast recruitment (22, 23).”
BackgroundLee, J. Y., Ahn, J. K., Park, K. S., & Park, H. G. (2018) · RSC Advances · doi:10.1039/c7ra13642k · Cited by 19
The tyrosine kinase inhibitor GNF-2 suppresses osteoclast formation and activity
Kim, H., Yoon, H., Choi, J., Lee, I. K., & Kim, S. (2013) · Journal of Leukocyte Biology · doi:10.1189/jlb.0713356 · Cited by 19
“failure of osteoclasts to spread reflects cytoskeletal disorganization [29, 40].”
BackgroundMethodSelf-citationKenanidis, E. I., Potoupnis, M. E., Kakoulidis, P., Leonidou, A. O., Sakellariou, G. T., Sayegh, F. E., & Tsiridis, E. E. (2015) · Expert Opinion on Drug Safety · doi:10.1517/14740338.2015.1040387 · Cited by 20
“revealed that GC may have an adverse structural effect on osteoclasts ruffled border or disrupt the cytoskeleton thus resulting in indirect osteoclast ‘de-activation’ [51].”
BackgroundNilsson, A., Norgård, M., Andersson, G., & Fahlgren, A. (2012) · Journal of Cellular Biochemistry · doi:10.1002/jcb.23456 · Cited by 16
“…et al., 2010], and directly by influencing the osteoclast bone degrading capacity mainly through disruption of organization of the cytoskeleton [Kim et al., 2006], we cannot unequivocally conclude that the suppression of osteoclast number was solely due to inhibition of the inflammatory…”
BackgroundOwen, H. C., Ahmed, S. F., & Farquharson, C. (2009) · Calcified Tissue International · doi:10.1007/s00223-009-9276-0 · Cited by 18
“A reduction in MAR with Dex has previously been shown [38], and additional contributing factors are likely to be increased osteoblast apoptosis and increased survival of osteoclasts [39].”
BackgroundKim, H. J., Ohk, B., Kang, W. Y., Seong, S. J., Suk, K., Lim, M., Kim, S., & Yoon, Y.-R. (2016) · Journal of Bone Metabolism · doi:10.11005/jbm.2016.23.1.8 · Cited by 18
“While the mitogen-activated protein kinase (MAPK) pathway, MEK/ERK, primarily supports proliferation of macrophages (osteoclast precursors),[3-5] PI3K/Akt mediates survival,[6] proliferation,[7] and cytoskeletal organization.[8] Interaction of RANKL with its receptor, RANK, stimulates the induction and activation of s…”
BackgroundSelf-citationRisk Factors for Prevalent Vertebral Fractures in Black and White Female Densitometry Patients
Vokes, T., Gillen, D. L., Pham, A. T., & Lovett, J. M. (2006) · Journal of Clinical Densitometry · doi:10.1016/j.jocd.2006.11.002 · Cited by 18
“Since the primary mechanism of corticosteroid mediated decrease in bone strength is the impairment of osteoblastic bone formation (34,35), possibly mediated by decreased osteoclastic function (36), subjects with lower bone turnover may be more prone to fractures when exposed to corticosteroids.”
BackgroundThe conundrum of glucocorticoid-induced osteoporosis
Teitelbaum, S. L. (2012) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2012.89 · Cited by 18
Wang, W., Wang, Q., Li, W., Xu, H. Y., Liang, X., Wang, W., Li, N., Yang, H., Xu, Y., Bai, J., et al. (2024) · Journal of Advanced Research · doi:10.1016/j.jare.2024.12.033 · Cited by 19
“[2,3] Hence, the investigation of inflammatory bone loss treatment remains a significant field of research, necessitating the prompt identification of effective therapeutic targets and medications.”
Ultrastructural characteristics of glucocorticoid-induced osteoporosis
Bouvard, B., Audran, M., Legrand, É., & Chappard, D. (2009) · Osteoporosis International · doi:10.1007/s00198-009-0864-7 · Cited by 17
Inhibitory effects of sesamin on human osteoclastogenesis
Wanachewin, O., Pothacharoen, P., Kongtawelert, P., & Phitak, T. (2017) · Archives of Pharmacal Research · doi:10.1007/s12272-017-0926-x · Cited by 17
“Chemokines such as MCP-1 and RANTES, together with chemokine receptors including CCR2b and CCR4 were upregulated upon RANKL activation and may play a role in human osteoclast recruitment (Kim et al. 2006b).”
BackgroundStout, S. D., Cole, M. E., & Agnew, A. M. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-809738-0.00006-5 · Cited by 21
Rauner, M., Stein, N., & Hofbauer, L. C. (2011) · Springer eBooks · doi:10.1007/978-3-7091-0520-7_1 · Cited by 16
Yoon, H.-Y., Cho, Y.-S., Jin, Q., Kim, H.-G., Woo, E., & Chung, Y. (2012) · Biomolecules & Therapeutics · doi:10.4062/biomolther.2012.20.1.089 · Cited by 16
“Kim et al. (2006) reported that DEX regulates osteoclast precursor proliferation, but does not infl uence in functional differentiation as bone resorption through MNCs formation.”
BackgroundSelf-citationRippo, M. R., Villanova, F., Tomassoni‐Ardori, F., Graciotti, L., Amatori, S., Manzotti, S., Fanelli, M., Gigante, A. P., & Procopio, A. D. (2010) · International Journal of Immunopathology and Pharmacology · doi:10.1177/039463201002300419 · Cited by 16
Snäll, J., Apajalahti, S., Suominen, A. L., Törnwall, J., & Thorén, H. (2015) · Medicina oral, patología oral y cirugía bucal · doi:10.4317/medoral.20553 · Cited by 16
“They also suppress osteoclasts’ bone-degrading capacity (2) and increase bone resorption (1).”
BackgroundInvariant natural killer T cells in rheumatic disease: a joint dilemma
Drennan, M. B., Aspeslagh, S., & Elewaut, D. S. (2010) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2009.261 · Cited by 17
Wang, L., Lu, W., Shi, J., Zhang, H., Xu, X., Gao, B., Huang, Q., Li, X., Hu, Y., Jie, Q., et al. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.7610 · Cited by 16
Corticosteroid-Induced Osteoporosis
Clarke, B. L. (2012) · American Journal of Clinical Dermatology · doi:10.2165/11594250-000000000-00000 · Cited by 16
“Decreased bone resorption during long-term therapy is due to direct suppression of osteoclasts due to inhibition of calpain 6 by corticosteroids.([4,5]) Prolonged therapy also decreases expression of the major osteoclastogenic transcription factor, nuclear factor of activated T cells c1.”
BackgroundOsteonecrosis: A More Appropriate Term than Avascular Necrosis–Pathophysiologic Rationale
Cheng, E. Y., Mirzaei, A., Sugano, N., Hernigou, P., Jones, L. C., Koo, K., Drescher, W., Cui, Q., Sierra, R. J., Goodman, S. B., et al. (2025) · The Journal of Arthroplasty · doi:10.1016/j.arth.2025.05.064 · Cited by 15
Fu, W., Chen, M., Wang, K., Chen, Y., Cui, Y., Xie, Y., Lei, Z., Hu, W., Sun, G., Huang, G., et al. (2025) · Cell Research · doi:10.1038/s41422-024-01016-0 · Cited by 17
Ding, M. L., Danielsen, C. C., & Overgaard, S. (2011) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.448 · Cited by 15
“Kim et al. (2006) reported that higher glucocorticoid doses inhibited the ability of osteoclasts to reorganize the cytoskeleton but had no effect on osteoclast maturation.”
BackgroundPark, H.-J., Gholam-Zadeh, M., Yoon, S.-Y., Suh, J., & Choi, H. (2021) · Antioxidants · doi:10.3390/antiox10040619 · Cited by 16
Dexamethsone Suppresses Bone Formation via the Osteoclast
Kim, H., Zhao, H., Kitaura, H., Bhattacharyya, S., Brewer, J. A., Muglia, L. J., Ross, F. P., & Teitelbaum, S. L. (2007) · Advances in experimental medicine and biology · doi:10.1007/978-0-387-72009-8_5 · Cited by 15
“We, therefore, undertook a series of studies to determine whether glucocorticoids directly talk to mature OCs and, if so, does this translate into suppression of bone forming activity ( Kim, Zhao, Kitaura, et al. 2006 ).”
BackgroundSelf-citationAnimal Models of Cushing's Syndrome
Nishiyama, M., Iwasaki, Y., & Makino, S. (2022) · Endocrinology · doi:10.1210/endocr/bqac173 · Cited by 16
Azetsu, Y., Chatani, M., Dodo, Y., Karakawa, A., Sakai, N., Negishi‐Koga, T., & Takami, M. (2019) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2019.109101 · Cited by 14
Loundagin, L. L., & Cooper, D. (2022) · European Cells and Materials · doi:10.22203/ecm.v043a15 · Cited by 14
New insights into the biology of glucocorticoid-induced osteoporosis
Lane, N. E., & Yao, W. (2011) · IBMS BoneKEy · doi:10.1138/20110511 · Cited by 15
“Therefore, GC excess results in an increase in osteoclast number, but in an apparent inhibition of function with impaired spreading and degradation of mineralized matrix (17).”
BackgroundBisphosphonates in the treatment of glucocorticoid-induced osteoporosis: pros
Rossini, M., Orsolini, G., Viapiana, O., Adami, S., & Gatti, D. (2015) · Endocrine · doi:10.1007/s12020-014-0506-5 · Cited by 13
Wu, Z., Yan, D., Xie, Z.-J., Weng, S., Zhou, Q., Li, H., Bai, B.-L., Boodhun, V., Shen, Z., Tang, J., et al. (2018) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2018.10.039 · Cited by 13
Semenkovich, C. F., & Teitelbaum, S. L. (2007) · Cell · doi:10.1016/j.cell.2007.07.031 · Cited by 13
“Chronic administration of steroids affects osteoclasts and osteoblasts, suppressing bone formation and thus osteocalcin expression (Kim et al., 2006).”
BackgroundDong, S., Ge, J., Meng, Q., Yuan, T., Wang, Y., Li, Y., Lu, Q., Song, W., Li, Z., & Sun, S. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.70044 · Cited by 12
“34,35 Consequently, we induced BMMs with 10 −8 M DEX to emulate the microenvironment of ONFH.”
BackgroundMethodSharma, A. K., Shi, X., Isales, C. M., & McGee‐Lawrence, M. E. (2019) · Current Osteoporosis Reports · doi:10.1007/s11914-019-00554-6 · Cited by 12
The effects of systemic stress on orthodontic tooth movement
Gameiro, G. H., Nouer, D. F., Neto, J. S. P., Urtado, M. B., Novaes, P. D., de Castro, M., & Veiga, M. C. F. A. (2008) · Australasian Orthodontic Journal · doi:10.2478/aoj-2008-0018 · Cited by 12
Miyamoto, S., Miyamoto, Y., Shibata, Y., Yoshimura, K., Izumida, E., Suzuki, H., Miyazaki, T., Maki, K., & Kamijo, R. (2014) · Acta Biomaterialia · doi:10.1016/j.actbio.2014.10.038 · Cited by 12
Zauli, G., Rimondi, E., Celeghini, C., Milani, D., & Secchiero, P. (2009) · Journal of Cellular Physiology · doi:10.1002/jcp.21960 · Cited by 12
Park, H.-J., Park, J.-N., Yoon, S.-Y., Yu, R., Suh, J., & Choi, H. (2022) · Antioxidants · doi:10.3390/antiox11050963 · Cited by 11
“To examine the actin ring within the OCs, mature OCs were washed and incubated under the indicated conditions for 6 h to examine filamentous polymer actin (F-actin) distribution as previously described [32].”
MethodAwida, Z., Hiram‐Bab, S., Bachar, A., Saed, H., Zyc, D., Gorodov, A., Ben‐Califa, N., Omari, S., Omar, J., Younis, L., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231912051 · Cited by 13
Skeletal Implications of Chronic Obstructive Pulmonary Disease
Misof, B. M., Moreira, C. A., Klaushofer, K., & Roschger, P. (2016) · Current Osteoporosis Reports · doi:10.1007/s11914-016-0301-8 · Cited by 13
Postnatal Bone Growth: Growth Plate Biology, Bone Formation, and Remodeling
Maes, C., & Kronenberg, H. M. (2011) · Elsevier eBooks · doi:10.1016/b978-0-12-382040-2.10004-8 · Cited by 12
Jiang, H., Deng, R., Deng, Y., Nie, M., Deng, Y., Luo, H., Yang, Y., Ni, N., Ran, C.-C., & Deng, Z. (2021) · Stem Cell Research & Therapy · doi:10.1186/s13287-021-02347-0 · Cited by 11
The Skeletal Subsystem as an Integrative Physiology Paradigm
Weiss, A., Iqbal, J. Z., Zaidi, N., & Mechanick, J. I. (2010) · Current Osteoporosis Reports · doi:10.1007/s11914-010-0033-0 · Cited by 12
“Recently, it was shown that dexamethasone-treated mice lacking the glucocorticoid receptor in osteoclast lineage cells failed to develop the bone degradation seen in wild-type osteoclasts [ 40 ].”
BackgroundLi, D., Ye, C., Zhu, Y., Gou, Z., & Gao, C. (2012) · Journal of Biomedical Materials Research Part B Applied Biomaterials · doi:10.1002/jbm.b.32677 · Cited by 11
Inhibin and the regulation of bone mass
Gaddy, D. (2008) · Current Osteoporosis Reports · doi:10.1007/s11914-008-0009-5 · Cited by 11
Gymnasterkoreayne F inhibits osteoclast formation by suppressing NFATc1 and DC-STAMP expression
Kim, H., Hong, J.-M., Jung, J., Kim, T., Kim, J. A., Kim, Y. H., & Kim, S. (2010) · International Immunopharmacology · doi:10.1016/j.intimp.2010.08.017 · Cited by 10
Self-citationProtection against Ovariectomy-Induced Bone Loss by Tranilast
Phan, T. V., Ke, K., Sul, O., Park, Y.-K., Kim, K., Cho, Y.-S., Chung, H., & Choi, H. (2014) · PLoS ONE · doi:10.1371/journal.pone.0095585 · Cited by 10
“sparing effects observed could be due to stimulation of bone formation, since serum ALP and osteocalcin, in vivo bone formation marker [23], were not affected by administration of Tranilast.”
BackgroundQureshi, A. S., Yaqoob, F., & Enbergs, H. (2013) · Pakistan Veterinary Journal · Cited by 10
Circadian regulation of bone metabolism by β-adrenergic signaling, glucocorticoids, and clock genes
Kondo, H., & Togari, A. (2014) · Journal of Oral Biosciences · doi:10.1016/j.job.2014.09.003 · Cited by 10
“The mutant mice lacking the glucocorticoid receptor in osteoclast lineage cells appear indistinguishable from wild type for at least 2 months, indicating that glucocorticoid-responsive osteoclasts are not required for normal skeletal development [24].”
BackgroundXi, L., Falco, P. D., Barbieri, E., Karunaratne, A., Bentley, L., Esapa, C. T., Davis, G. R., Terrill, N. J., Cox, R., Pugno, N. M., et al. (2019) · Bone · doi:10.1016/j.bone.2019.115111 · Cited by 10
Wang, N., Wang, H., Chen, J., Wang, F., Wang, S., Zhou, Q., Ying, J., Huang, S., Wang, P., & Yuan, F. (2020) · Molecular Medicine Reports · doi:10.3892/mmr.2020.11319 · Cited by 10
Exosome-derived miR-5p-72106_14 in vascular endothelial cells regulates fate determination of BMSCs
Li, H., Wang, J., Xie, X., Chen, Y., Zheng, Q., He, J., & Lu, Q. (2023) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2023.116793 · Cited by 9
Mechanism of Glucocorticoid-Induced Osteoporosis: An Update
Shi, X., Chutkan, N. B., Mark, W., & Carlos, M. (2012) · InTech eBooks · doi:10.5772/53978 · Cited by 9
“It is now recognized that glucocorticoids increase the longevity of osteoclasts but may inhibit their bone resorptive activity [81;82].”
BackgroundGlucocorticoids exert context-dependent effects on cells of the joint in vitro
Madsen, S. H., Andreassen, K. V., Christensen, S. T., Karsdal, M. A., Sverdrup, F. M., Bay‐Jensen, A., & Henriksen, K. (2011) · Steroids · doi:10.1016/j.steroids.2011.07.018 · Cited by 9
Thyroid Hormones, Glucocorticoids, Insulin, and Bone
Lakatos, P. L., Szili, B., Bakos, B., Takács, I., Putz, Z., & Istenes, I. (2019) · Handbook of experimental pharmacology · doi:10.1007/164_2019_314 · Cited by 9
Inhibitory effects of obovatol on osteoclast differentiation and bone resorption
Kim, H., Hong, J. M., Yoon, H.-J., Kwon, B., Choi, J., Lee, I., & Kim, S. (2013) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2013.10.027 · Cited by 9
Self-citationLon, H., DuBois, D. C., Earp, J. C., Almon, R. R., & Jusko, W. J. (2015) · Pharmacology Research & Perspectives · doi:10.1002/prp2.169 · Cited by 8
“The inhibition described by Kim et al. regarding the DEX effect on osteoclast function was then applied to fit the data (Kim et al. 2006), and it appeared to capture the profiles of TRACP-5b well.”
BackgroundMethodInfluentialKe, K., Kim, W.-K., Sul, O., Phan, V. T., Lee, M., Kim, H., Kim, S., & Choi, H. (2012) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00085.2012 · Cited by 8
“Mature OCs were washed and incubated under the indicated conditions for 5 h to examine filamentous polymer actin (F-actin) distribution as previously described (19).”
MethodSelf-citationGlucocorticoid-induced Osteoporosis
Mazziotti, G., & Giustina, A. (2010) · Elsevier eBooks · doi:10.1016/b978-0-12-374602-3.00034-1 · Cited by 9
Promoting bone health in children and adolescents following solid organ transplantation
Kusumi, K., Shaikhkhalil, A. K., Patel, H. P., & Mahan, J. D. (2020) · Pediatric Transplantation · doi:10.1111/petr.13940 · Cited by 8
Bone metabolism: a note on the significance of mouse models
Raška, O., Bernášková, K., & Raška, I. (2009) · Physiological Research · doi:10.33549/physiolres.931459 · Cited by 8
Detection of Apoptosis of Bone Cells In Vitro
Bellido, T., & Plotkin, L. I. (2008) · Methods in molecular biology · doi:10.1007/978-1-59745-104-8_4 · Cited by 8
Polygonum multiflorm alleviates glucocorticoid‑induced osteoporosis and Wnt signaling pathway
Zhou, M., Wu, J., Yu, Y., Yang, Y., Li, J., Cui, L., Yao, W., & Liu, Y. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.7997 · Cited by 8
“The disruption of the bone formation-resorption balance plays a key role in osteoporosis (39).”
Zhang, Q., Fong, C., Zhang, Y., Tzang, C., Fong, W. F., & Yang, M. (2007) · Life Sciences · doi:10.1016/j.lfs.2007.10.012 · Cited by 8
The CRH‐Transgenic Cushingoid Mouse Is a Model of Glucocorticoid‐Induced Osteoporosis
Williams‐Dautovich, J., Yogendirarajah, K., Cruz, A. D., Patel, R., Tsai, R., Morgan, S., Mitchell, J., Grynpas, M. D., & Cummins, C. L. (2017) · JBMR Plus · doi:10.1002/jbm4.10009 · Cited by 9
“Mechanistically, this has been shown to be related to the direct effects of GCs on osteoblasts (to increase apoptosis and decrease differentiation to the osteoblast lineage((31))) and direct effects of GCs on osteoclasts (increasing osteoclast activity((32,33)) and promoting osteoclast survival((33,34))).”
BackgroundAntiosteoporosis and bone protective effect of nimbolide in steroid‐induced osteoporosis rats
Huo, J., Ding, Y., Wei, X., Chen, Q., & Zhao, B. (2022) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.23209 · Cited by 7
The glucocorticoid receptor in skeletal health and disease: insights from targeted knockout mice
Macfarlane, E., Zhou, H., & Seibel, M. J. (2024) · Journal of Endocrinology · doi:10.1530/joe-23-0399 · Cited by 7
Osteonecrosis Development Post Covid-19 Infection
Daltro, G. D. C. (2021) · Journal of Regenerative Biology and Medicine · doi:10.37191/mapsci-2582-385x-3(5)-087 · Cited by 7
Effects of Chronic Stress and Alendronate Therapy on the Osseointegration of Titanium Implants
Neto, N. C., de Andrade, C. R., Spolidório, L. C., Planeta, C. S., Cruz, F. C., Bastos, A. D. S., & Marcantônio, É. (2013) · Clinical Implant Dentistry and Related Research · doi:10.1111/cid.12046 · Cited by 7
Voluntary wheel running mitigates the stress-induced bone loss in ovariectomized rats
Lertsinthai, P., Charoenphandhu, J., Suntornsaratoon, P., Krishnamra, N., & Charoenphandhu, N. (2014) · Journal of Bone and Mineral Metabolism · doi:10.1007/s00774-014-0597-3 · Cited by 7
“formation, the elevated glucocorticoid level, which is known to suppress both osteoblast and osteoclast activities [31], cannot fully account for the observed CAS-induced bone loss.”
BackgroundRamli, E. S. M. (2018) · Medicine & health · doi:10.17576/mh.2018.1301.17 · Cited by 7
“Keywords: antioxidant, biomechanical, bone, histomorphometry, trabecular formation and increase bone resorption (O’Brien et al. 2004; Kim et al. 2006).”
BackgroundZhu, H. J., Wang, M., Zhao, C., Li, R., Yang, J., Pei, G., Ye, T., Zuo, X., Liu, L., Shin, O. L.-S. C. L., et al. (2018) · Europe PMC (PubMed Central) · Cited by 7
Park, H. J., Kim, H. S., & Chung, D. H. (2010) · Immune Network · doi:10.4110/in.2010.10.1.26 · Cited by 6
Self-citationDiagnosis and therapeutic approach to bone health in patients with hypopituitarism
Kuliczkowska-Płaksej, J., Zdrojowy-Wełna, A., Jawiarczyk-Przybyłowska, A., Gojny, Ł., & Bolanowski, M. (2024) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-024-09878-w · Cited by 6
“However, osteoclasts differ - entiation is inhibited during prolonged treatment with high doses of GC [11, 197, 198].”
Henning, P., Conaway, H. H., & Lerner, U. H. (2022) · Vitamins and hormones · doi:10.1016/bs.vh.2022.04.005 · Cited by 8
An Update on Medication-Related Osteonecrosis of the Jaw in Patients with Osteoporosis
Bennett, B., Tahir, H., Solanki, K., & Ali, N. (2023) · EMJ Rheumatology · doi:10.33590/emjrheumatol/10300262 · Cited by 6
Mechanism of Induction of P-gp Activity During MET Induced by DEX in Lung Cancer Cell Line
Liu, W., Zhang, X., Sunakawa, H., Perera, L. M. B., Martha, L., Mizoi, K., & Ogihara, T. (2024) · Journal of Pharmaceutical Sciences · doi:10.1016/j.xphs.2024.02.027 · Cited by 6
Venkatasamy, R., & Spina, D. (2007) · Expert Review of Clinical Immunology · doi:10.1586/1744666x.3.3.365 · Cited by 6
Lokale und systemische Knocheneffekte bei rheumatoider Arthritis
Rauner, M., Hofbauer, L. C., & Aringer, M. (2012) · Zeitschrift für Rheumatologie · doi:10.1007/s00393-011-0927-y · Cited by 7
Glucocorticoid-induced Osteoporosis; Update
Kim, S., & Kim, H. J. (2009) · The Journal of the Korean Orthopaedic Association · doi:10.4055/jkoa.2009.44.2.151 · Cited by 6
Self-citationHossein‐Nezhad, A., Nikoo, M. K., Mirzaei, K., Mokhtarei, F., & Meybodi, H. R. A. (2010) · European Journal of Inflammation · doi:10.1177/1721727x1000800203 · Cited by 6
Li, X., Yang, X., Liu, Z., Liu, H., Lv, H., Li, X., Xu, X., & Shen, Y. (2025) · Chemical Biology & Drug Design · doi:10.1111/cbdd.70069 · Cited by 6
“At the cellular level, this injury is attributed to a disruption in bone remodeling, a process involving bone-resorbing osteoclasts (OC) and bone-forming osteoblasts (OB) (Chotiyarnwong and McCloskey 2020; Kim et al. 2006; Matsuo 2014).”
Kim, H., Lee, D.-K., Jin, X., Che, X., & Choi, J. (2020) · PubMed · doi:10.14348/molcells.2020.2260 · Cited by 5
“Moreover, these findings are in agreement with our previous observations that impaired spreading in osteoclasts mirrors osteoclast cytoskeleton disorganization (Hong et al., 2011; Kim et al., 2006; 2014; 2016).”
ResultSelf-citationPang, K., Wang, S., Li, M., & Zhou, Z. (2021) · Frontiers in Veterinary Science · doi:10.3389/fvets.2021.746087 · Cited by 5
“FHN evaluation score 0, The normal femoral head with integral structure; FHN evaluation score 1, The femoral head separating from articular cartilage without any visible damage to the growth plate; FHN evaluation score 2, Femoral head separation with laceration of the growth plate (38).”
BackgroundResultExpression of long noncoding RNA Xist is induced by glucocorticoids
Su, Y., Chen, X., Zhou, H., Shaw, S., Chen, J., Isales, C. M., Zhao, J., & Shi, X. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1005944 · Cited by 5
“Conditional GR knockout (GR cKO) mice were generated by breeding a GR-floxed (GR) mouse (28) with a 3.”
MethodOsteoporosis and risk of fracture in heart transplant patients
Forien, M., Coralli, R., Verdonk, C. G., Ottaviani, S., Ebstein, E., Demaria, L., Palazzo, É., Dorent, R., & Dieudé, P. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1252966 · Cited by 6
“Glucocorticoids reduce bone formation (16), induce apoptosis of osteoblasts and osteocytes (17), increase bone resorption and reduce intestinal calcium absorption (18).”
BackgroundZhang, L., & Mager, D. E. (2018) · Journal of Pharmaceutical Sciences · doi:10.1016/j.xphs.2018.11.024 · Cited by 5
Hatano, M., Kitajima, I., Nakamura, M., Isawa, K., Suwabe, T., Hoshino, J., Kinowaki, K., Ohashi, K., Sawa, N., Yamamoto, S., et al. (2021) · Modern Rheumatology Case Reports · doi:10.1093/mrcr/rxab028 · Cited by 5
“In addition, glucocorticoids suppress bone formation via osteoclasts [9].”
BackgroundNuclear receptors in osteoclasts
Bae, S., Zeng, S. L., & Park‐Min, K. (2020) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2020.03.002 · Cited by 5
Osteogenic Evaluation of Hydroxyapatite Scaffold Loaded With Dexamethasone in Femoral Drill Holes
Park, M., JANG, S. J., & Choi, S. H. (2020) · In Vivo · doi:10.21873/invivo.11980 · Cited by 4
Chronic Kidney Disease-Mineral Bone Disease Biomarkers in Kidney Transplant Patients
Hasparyk, Ú. G., Vigil, F. M. B., Bartolomei, V. S., Nunes, V. M., & Silva, A. C. S. E. (2022) · Current Medicinal Chemistry · doi:10.2174/0929867329666220318105856 · Cited by 4
From Stem to Sternum: The Role of Shp2 in the Skeleton
Jensen, N. R., Kelly, R. R., Kelly, K. D., Khoo, S. K., Sidles, S. J., & LaRue, A. C. (2022) · Calcified Tissue International · doi:10.1007/s00223-022-01042-3 · Cited by 4
Impairment of rat tooth eruption in pups born to mothers exposed to chronic stress during pregnancy
Fontanetti, P. A., Lucca, R. C. D., Mandalunis, P., & Vermouth, N. T. (2013) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2013.08.003 · Cited by 4
“Whereas some authors have associated GCs to an increase in bone resorption,(43,44) others have found GCs to be associated with an inhibition of bone resorption, by means of a decrease in the number of osteoclasts and preosteoclasts,(45) the promotion of osteoclast apoptosis(46) or exerting an inhibitory effect on the…”
ResultIn vivo Toxicological Studies on Methanol Leaf Extract of Lantana camara
Abonyi, O. E. (2015) · Cited by 4
Metadata
- 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 › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review