Glucocorticoid-induced bone loss in mice can be reversed by the actions of parathyroid hormone and risedronate on different pathways for bone formation and mineralization

Yao, Wei; Cheng, Zhiqiang; Pham, Aaron; Busse, Cheryl; Zimmermann, Elizabeth A.; Ritchie, Robert O.; Lane, Nancy E.

doi:10.1002/art.23954

Cited by 128Bone health and osteoporosis researchBone Metabolism and DiseasesBone health and treatments

Glucocorticoid-induced bone loss in mice can be reversed by the actions of parathyroid hormone and risedronate on different pathways for bone formation and mineralization

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Yao, Wei, Cheng, Zhiqiang, Pham, Aaron, Busse, Cheryl, Zimmermann, Elizabeth A., Ritchie, Robert O., Lane, Nancy E.·2008·Arthritis & Rheumatism

DOI 10.1002/art.23954PMC PMC2597521

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Abstract

OBJECTIVE: Glucocorticoid excess decreases bone mineralization and microarchitecture and leads to reduced bone strength. Both anabolic (parathyroid hormone [PTH]) and antiresorptive agents are used to prevent and treat glucocorticoid-induced bone loss, yet these bone-active agents alter bone turnover by very different mechanisms. This study was undertaken to determine how PTH and risedronate alter bone quality following glucocorticoid excess. METHODS: Five-month-old male Swiss-Webster mice were treated with the glucocorticoid prednisolone (5 mg/kg in a 60-day slow-release pellet) or placebo. From day 28 to day 56, 2 groups of glucocorticoid-treated animals received either PTH (5 microg/kg) or risedronate (5 microg/kg) 5 times per week. Bone quality and quantity were measured using x-ray tomography for the degree of bone mineralization, microfocal computed tomography for bone microarchitecture, compression testing for trabecular bone strength, and biochemistry and histomorphometry for bone turnover. In addition, real-time polymerase chain reaction (PCR) and immunohistochemistry were performed to monitor the expression of several key genes regulating Wnt signaling (bone formation) and mineralization. RESULTS: Compared with placebo, glucocorticoid treatment decreased trabecular bone volume (bone volume/total volume [BV/TV]) and serum osteocalcin, but increased serum CTX and osteoclast surface, with a peak at day 28. Glucocorticoids plus PTH increased BV/TV, and glucocorticoids plus risedronate restored BV/TV to placebo levels after 28 days. The average degree of bone mineralization was decreased after glucocorticoid treatment (-27%), but was restored to placebo levels after treatment with glucocorticoids plus risedronate or glucocorticoids plus PTH. On day 56, RT-PCR revealed that expression of genes that inhibit bone mineralization (Dmp1 and Phex) was increased by continuous exposure to glucocorticoids and glucocorticoids plus PTH and decreased by glucocorticoids plus risedronate, compared with placebo. Wnt signaling antagonists Dkk-1, Sost, and Wif1 were up-regulated by glucocorticoid treatment but down-regulated after glucocorticoid plus PTH treatment. Immunohistochemistry of bone sections showed that glucocorticoids increased N-terminal Dmp-1 staining while PTH treatment increased both N- and C-terminal Dmp-1 staining around osteocytes. CONCLUSION: Our findings indicate that both PTH and risedronate improve bone mass, degree of bone mineralization, and bone strength in glucocorticoid-treated mice, and that PTH increases bone formation while risedronate reverses the deterioration of bone mineralization.

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Glucocorticoids potently suppress osteoblast activities and adversely affect bone mineralization.
“As GCs potently suppress osteoblast activities and adversely affect bone mineralization [41, 46]”
From Prevention of glucocorticoid induced bone changes with beta-ecdysone (2015) · cites this paper as [41]
Compared to other studies on glucocorticoid-induced osteoporosis that used skeletal matured mice, glucocorticoid excess in young growing mice has more profound inhibition on periosteal expansion with similar degree of trabecular bone loss.
“Compared to the other studies that we and others have published on GIOP that used skeletal matured mice, we found GC excess in the young growing have more profound inhibition on periosteal expansion with similar degree of trabecular bone loss [35, 41].”
From Prevention of glucocorticoid induced bone changes with beta-ecdysone (2015) · cites this paper as [41]

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Sequential treatment of ovariectomized mice with bFGF and risedronate restored trabecular bone microarchitecture and mineralization
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Is long-term glucocorticoid therapy associated with a high prevalence of asymptomatic vertebral fractures?
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Bone Histomorphometry in Untreated and Treated Glucocorticoid-Induced Osteoporosis
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Disorders of Bone Remodeling
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Sclerostin and Dickkopf-1 as Therapeutic Targets in Bone Diseases
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Directing mesenchymal stem cells to bone to augment bone formation and increase bone mass
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Involvement of WNT/β-catenin Signaling in the Treatment of Osteoporosis
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Glucocorticoid-Induced Osteoporosis: New Insights into the Pathophysiology and Treatments
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Glucocorticoid dose determines osteocyte cell fate
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Advances in Glucocorticoid-Induced Osteoporosis
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The osteocyte plays multiple roles in bone remodeling and mineral homeostasis
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Curcumin alleviates glucocorticoid-induced osteoporosis through the regulation of the Wnt signaling pathway
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Does osteocytic SOST suppression mediate PTH bone anabolism?
Krämer, I., Keller, H., Leupin, O., & Kneissel, M. (2010) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2009.12.002 · Cited by 118 · see citing works
Intermittent Parathyroid Hormone Administration Counteracts the Adverse Effects of Glucocorticoids on Osteoblast and Osteocyte Viability, Bone Formation, and Strength in Mice
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Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength
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Recovery Versus Persistence of Disordered Mineral Metabolism in Kidney Transplant Recipients
Evenepoel, P. (2013) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2012.12.019 · Cited by 109 · see citing works
Bone Formation Regulates Circulating Concentrations of Fibroblast Growth Factor 23
Samadfam, R., Richard, C., Nguyen‐Yamamoto, L., Bolivar, I., & Goltzman, D. (2009) · Endocrinology · doi:10.1210/en.2009-0472 · Cited by 106 · see citing works
The Emerging Role of Dickkopf-1 in Bone Biology: Is It the Main Switch Controlling Bone and Joint Remodeling?
Daoussis, D., & Andonopoulos, A. P. (2011) · Seminars in Arthritis and Rheumatism · doi:10.1016/j.semarthrit.2011.01.006 · Cited by 105 · see citing works
Overexpression of secreted frizzled-related protein 1 inhibits bone formation and attenuates parathyroid hormone bone anabolic effects
Yao, W., Cheng, Z., Shahnazari, M., Dai, W., Johnson, M. L., & Lane, N. E. (2009) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.090719 · Cited by 94 · see citing works
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β2-Adrenergic receptor signaling in osteoblasts contributes to the catabolic effect of glucocorticoids on bone
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
Minireview: Live and Let Die: Molecular Effects of Glucocorticoids on Bone Cells
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Transcriptional control of Sost in bone
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Sclerostin antibody treatment enhances bone strength but does not prevent growth retardation in young mice treated with dexamethasone
Marenzana, M., Greenslade, K. J., Eddleston, A., Okoye, R., Marshall, D. R., Moore, A., & Robinson, M. K. (2011) · Arthritis & Rheumatism · doi:10.1002/art.30385 · Cited by 73 · see citing works
Anabolic and Catabolic Regimens of Human Parathyroid Hormone 1–34 Elicit Bone- and Envelope-Specific Attenuation of Skeletal Effects in Sost-Deficient Mice
Robling, A. G., Kedlaya, R., Ellis, S. N., Childress, P., Bidwell, J. P., Bellido, T., & Turner, C. H. (2011) · Endocrinology · doi:10.1210/en.2011-0049 · Cited by 67 · see citing works
Glucocorticoids activate the local renin–angiotensin system in bone: possible mechanism for glucocorticoid-induced osteoporosis
Yongtao, Z., Kunzheng, W., Jingjing, Z., Hu, S., Jianqiang, K., Ruiyu, L., & Chunsheng, W. (2014) · Endocrine · doi:10.1007/s12020-014-0196-z · Cited by 67 · see citing works
Glucocorticoid-induced osteoporosis: treatment update and review
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A new open-source tool for measuring 3D osteocyte lacunar geometries from confocal laser scanning microscopy reveals age-related changes to lacunar size and shape in cortical mouse bone
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Changes of Circulating MicroRNAs in Response to Treatment With Teriparatide or Denosumab in Postmenopausal Osteoporosis
Anastasilakis, A. D., Makras, P., Pikilidou, M. I., Tournis, S., Makris, K., Bisbinas, I., Tsave, O., Yovos, J. G., & Yavropoulou, M. P. (2017) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2017-02406 · Cited by 57 · see citing works
A joined role of canopy and reversal cells in bone remodeling — Lessons from glucocorticoid-induced osteoporosis
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Immune Suppressive and Bone Inhibitory Effects of Prednisolone in Growing and Regenerating Zebrafish Tissues
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Endogenous tissue engineering: PTH therapy for skeletal repair
Takahata, M., Awad, H. A., O’Keefe, R. J., Bukata, S. V., & Schwarz, E. M. (2011) · Cell and Tissue Research · doi:10.1007/s00441-011-1188-4 · Cited by 52 · see citing works
Pharmaceutical treatment of bone loss: From animal models and drug development to future treatment strategies
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Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo
Hildebrandt, S., Baschant, U., Thiele, S., Tuckermann, J. P., Hofbauer, L. C., & Rauner, M. (2018) · Scientific Reports · doi:10.1038/s41598-018-26300-z · Cited by 49 · see citing works
Sclerostin levels and bone turnover markers in adolescents with anorexia nervosa and healthy adolescent girls
Faje, A. T., Fazeli, P. K., Katzman, D. K., Miller, K. K., Breggia, A., Rosen, C. J., Mendes, N., Klibanski, A., & Misra, M. (2012) · Bone · doi:10.1016/j.bone.2012.06.006 · Cited by 48 · see citing works
FGF-2 targets sclerostin in bone and myostatin in skeletal muscle to mitigate the deleterious effects of glucocorticoid on musculoskeletal degradation
Adhikary, S., Choudhary, D., Tripathi, A. K., Karvande, A., Ahmad, N., Kothari, P., & Trivedi, R. (2019) · Life Sciences · doi:10.1016/j.lfs.2019.05.022 · Cited by 47 · see citing works
Higher doses of bisphosphonates further improve bone mass, architecture, and strength but not the tissue material properties in aged rats
Shahnazari, M., Yao, W., Dai, W., Wang, B., Ionova-Martin, S. S., Ritchie, R. O., Heeren, D., Burghardt, A. J., Nicolella, D. P., Kimiecik, M. G., et al. (2010) · Bone · doi:10.1016/j.bone.2009.11.019 · Cited by 46 · see citing works
Inhibition of the Progesterone Nuclear Receptor during the Bone Linear Growth Phase Increases Peak Bone Mass in Female Mice
Yao, W., Dai, W., Shahnazari, M., Pham, A., Chen, Z., Chen, H., Guan, M., & Lane, N. E. (2010) · PLoS ONE · doi:10.1371/journal.pone.0011410 · Cited by 46 · see citing works
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Glucocorticoid‐induced bone fragility
Lane, N. E., & Yao, W. (2010) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.05228.x · Cited by 44 · see citing works
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Intermittent administration of teriparatide enhances graft bone healing and accelerates spinal fusion in rats with glucocorticoid-induced osteoporosis
Sugiura, T., Kashii, M., Matsuo, Y., Morimoto, T., Honda, H., Kaito, T., Iwasaki, M., & Yoshikawa, H. (2014) · The Spine Journal · doi:10.1016/j.spinee.2014.08.001 · Cited by 43 · see citing works
Improved Mobilization of Exogenous Mesenchymal Stem Cells to Bone for Fracture Healing and Sex Difference
Yao, W., Lay, Y.-A. E., Kot, A., Liu, R., Zhang, H., Chen, H., Lam, K. S., & Lane, N. E. (2016) · Stem Cells · doi:10.1002/stem.2433 · Cited by 43 · see citing works
Self-citation
Multiscale alterations in bone matrix quality increased fragility in steroid induced osteoporosis
Karunaratne, A., Xi, L., Bentley, L., Sykes, D., BOYDE, A., Esapa, C. T., Terrill, N. J., Brown, S. D. M., Cox, R., Thakker, R. V., et al. (2015) · Bone · doi:10.1016/j.bone.2015.11.019 · Cited by 42 · see citing works
Raman spectroscopy detects deterioration in biomechanical properties of bone in a glucocorticoid-treated mouse model of rheumatoid arthritis
Maher, J. R., Berger, A. J., Takahata, M., & Awad, H. A. (2011) · Journal of Biomedical Optics · doi:10.1117/1.3613933 · Cited by 41 · see citing works
Sclerostin activity plays a key role in the negative effect of glucocorticoid signaling on osteoblast function in mice
Beier, E. E., Sheu, T., Resseguie, E. A., Takahata, M., Awad, H. A., Cory‐Slechta, D. A., & Puzas, J. E. (2017) · Bone Research · doi:10.1038/boneres.2017.13 · Cited by 40 · see citing works
Strain dependent differences in glucocorticoid-induced bone loss between C57BL/6J and CD-1 mice
Ersek, A., Santo, A. I. E., Vattakuzhi, Y., George, S., Clark, A. R., & Horwood, N. J. (2016) · Scientific Reports · doi:10.1038/srep36513 · Cited by 39 · see citing works
Role of the N- and C-terminal Fragments of Parathyroid-Hormone-Related Protein as Putative Therapies to Improve Bone Regeneration Under High Glucocorticoid Treatment
de Castro, L. F., Lozano, D., Dapía, S., Portal‐Núñez, S., Caeiro, J. R., Gómez‐Barrena, E., & Esbrit, P. (2009) · Tissue Engineering Part A · doi:10.1089/ten.tea.2009.0355 · Cited by 38 · see citing works
Mediation of nonerosive arthritis in a mouse model of lupus by interferon‐α–stimulated monocyte differentiation that is nonpermissive of osteoclastogenesis
Mensah, K. A., Mathian, A., Ma, L., Xing, L., Ritchlin, C. T., & Schwarz, E. M. (2010) · Arthritis & Rheumatism · doi:10.1002/art.27312 · Cited by 38 · see citing works
The anti-epileptic drugs valproate, carbamazepine and levetiracetam cause bone loss and modulate Wnt inhibitors in normal and ovariectomised rats
Parveen, B., Tiwari, A., Jain, M., Pal, S., Chattopadhyay, N., Tripathi, M., & Vohora, D. (2018) · Bone · doi:10.1016/j.bone.2018.05.011 · Cited by 35 · see citing works
Parathyroid Hormone (PTH) Induces Autophagy to Protect Osteocyte Cell Survival from Dexamethasone Damage
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Biodegradable intranasal nanoparticulate drug delivery system of risedronate sodium for osteoporosis
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Cannabinoid receptor 1 mediates glucocorticoid‐induced bone loss in rats by perturbing bone mineral acquisition and marrow adipogenesis
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Glucocorticoids reduce alveolar and trabecular bone in mice
Bouvard, B., Gallois, Y., Legrand, É., Audran, M., & Chappard, D. (2012) · Joint Bone Spine · doi:10.1016/j.jbspin.2012.01.009 · Cited by 31 · see citing works
Prevention of glucocorticoid induced bone changes with beta-ecdysone
Dai, W., Jiang, L., Lay, Y.-A. E., Chen, H., Jin, G., Zhang, H., Kot, A., Ritchie, R. O., Lane, N. E., & Yao, W. (2015) · Bone · doi:10.1016/j.bone.2015.01.001 · Cited by 30 · see citing works
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Molecular 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 28 · see citing works
Dexamethasone Administration in Mice Leads to Less Body Weight Gain over Time, Lower Serum Glucose, and Higher Insulin Levels Independently of NRF2
Filippopoulou, F., Habeos, G. I., Rinotas, V. E., Sophocleous, A., Sykiotis, G. P., Douni, E. K., & Chartoumpekis, D. V. (2021) · Antioxidants · doi:10.3390/antiox11010004 · Cited by 27 · see citing works
Developments in the scientific understanding of osteoporosis
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Elevated Expression of Dkk-1 by Glucocorticoid Treatment Impairs Bone Regenerative Capacity of Adipose Tissue-Derived Mesenchymal Stem Cells
Kato, T., Khánh, V. C., Sato, K., Kimura, K., Yamashita, T., Sugaya, H., Yoshioka, T., Mishima, H., & Ohneda, O. (2017) · Stem Cells and Development · doi:10.1089/scd.2017.0199 · Cited by 24 · see citing works
Strain-specific differences in the development of bone loss and incidence of osteonecrosis following glucocorticoid treatment in two different mouse strains
Shidara, K., Mohan, G., Lay, Y.-A. E., Jepsen, K. J., Yao, W., & Lane, N. E. (2018) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2018.07.001 · Cited by 22 · see citing works
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Glucocorticoid-Induced Osteoporosis ? A Disorder of Mesenchymal Stromal Cells?
Hardy, R., & Cooper, M. S. (2011) · Frontiers in Endocrinology · doi:10.3389/fendo.2011.00024 · Cited by 22 · see citing works
Intermittent PTH treatment improves bone and muscle in glucocorticoid treated Mdx mice: A model of Duchenne Muscular Dystrophy
Yoon, S.-H., Grynpas, M. D., & Mitchell, J. (2019) · Bone · doi:10.1016/j.bone.2019.01.028 · Cited by 21 · see citing works
Adjuvant drug-assisted bone healing: Part I – Modulation of inflammation
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Enhanced oral absorption of teriparatide with therapeutic potential for management of osteoporosis
Subedi, L., Pandey, P., Kang, S. H., Kim, K.-T., Cho, S., Chang, K.-Y., Byun, Y., Shim, J., & Park, J. W. (2022) · Journal of Controlled Release · doi:10.1016/j.jconrel.2022.07.012 · Cited by 20 · see citing works
A Novel Hybrid Compound LLP2A-Ale Both Prevented and Rescued the Osteoporotic Phenotype in a Mouse Model of Glucocorticoid-Induced Osteoporosis
Mohan, 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 · see citing works
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Glucocorticoids dexamethasone and prednisolone suppress fibroblast growth factor 23 (FGF23)
Feger, M., Ewendt, F., Strotmann, J. M., Schäffler, H., Kempe-Teufel, D. S., Glosse, P., Stangl, G. I., & Föller, M. (2021) · Journal of Molecular Medicine · doi:10.1007/s00109-021-02036-8 · Cited by 20 · see citing works
Glucocorticoid Attenuates the Anabolic Effects of Parathyroid Hormone on Fracture Repair
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Short-term glucocorticoid excess blunts abaloparatide-induced increase in femoral bone mass and strength in mice
Brent, M. B., Thomsen, J. S., & Brüel, A. (2021) · Scientific Reports · doi:10.1038/s41598-021-91729-8 · Cited by 19 · see citing works
The impact of glucocorticoids on bone health and growth: endocrine and non-endocrine effects in children and young patients
Cipolla, C., Sodero, G., Cammisa, I., Colonna, A. T., Giuliano, S., AMAR, I. D., BITON, R. R., Scambia, G., & Villa, P. (2022) · Minerva Pediatrics · doi:10.23736/s2724-5276.22.07074-4 · Cited by 17 · see citing works
Flemingia philippinensis Flavonoids Relieve Bone Erosion and Inflammatory Mediators in CIA Mice by Downregulating NF-κB and MAPK Pathways
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Models and screening assays for drug discovery in osteoporosis
Rissanen, J. P., & Halleen, J. M. (2010) · Expert Opinion on Drug Discovery · doi:10.1517/17460441.2010.532484 · Cited by 17 · see citing works
Basics of Bone Biology
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Prednisolone Treatment Does Not Interfere with 2′- O -Methyl Phosphorothioate Antisense-Mediated Exon Skipping in Duchenne Muscular Dystrophy
Verhaart, I. E. C., Heemskerk, H., Karnaoukh, T. G., Kolfschoten, I., Vroon, A., van Ommen, G. B., van Deutekom, J. C. T., & Aartsma-Rus, A. M. (2011) · Human Gene Therapy · doi:10.1089/hum.2011.127 · Cited by 16 · see citing works
β-Ecdysone Augments Peak Bone Mass in Mice of Both Sexes
Dai, W., Zhang, H., Zhong, Z. A., Jiang, L., Chen, H., Lay, Y.-A. E., Kot, A., Ritchie, R. O., Lane, N. E., & Yao, W. (2015) · Clinical Orthopaedics & Related Research · doi:10.1007/s11999-015-4246-5 · Cited by 15 · see citing works
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Milk kefir therapy improves the skeletal response to resistance exercise in rats submitted to glucocorticoid-induced osteoporosis
de Vasconcelos, R. F., Costa, V., Araújo, B. S., Maia, T. A. C., Dias, R., Vasconcelos, L., Silveira, H., Carneiro, B., Thiers, D., Costa, F. W. G., et al. (2022) · Experimental Gerontology · doi:10.1016/j.exger.2022.111921 · Cited by 14 · see citing works
Treatment with synthetic glucocorticoid impairs bone metabolism, as revealed by in vivo imaging of osteoblasts and osteoclasts in medaka fish
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 · see citing works
Towards novel measurements of remodeling activity in cortical bone: implications for osteoporosis and related pharmaceutical treatments
Loundagin, L. L., & Cooper, D. (2022) · European Cells and Materials · doi:10.22203/ecm.v043a15 · Cited by 14 · see citing works
Phosphocreatine Promotes Osteoblastic Activities in H2O2-Induced MC3T3-E1 Cells by Regulating SIRT1/FOXO1/PGC-1α Signaling Pathway
Jing, Z., Wang, C., Wen, S., Jin, Y., Meng, Q., Liu, Q., Wu, J., Sun, H., & Liu, M. (2020) · Current Pharmaceutical Biotechnology · doi:10.2174/1389201021999201116160247 · Cited by 14 · see citing works
Long-term safety, efficacy, and patient acceptability of teriparatide in the management of glucocorticoid-induced osteoporosis
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Sost Haploinsufficiency Provokes Peracute Lethal Cardiac Tamponade without Rescuing the Osteopenia in a Mouse Model of Excess Glucocorticoids
Javaheri, B., Herbert, E., Hopkinson, M., Aljazzar, A., & Pitsillides, A. A. (2019) · American Journal Of Pathology · doi:10.1016/j.ajpath.2018.12.007 · Cited by 13 · see citing works
Fangchinoline Promotes Autophagy and Inhibits Apoptosis in Osteoporotic Rats
Zhu, W., Ding, W., Shang, X., Zhu, D. L., & Dai, X. (2019) · Medical Science Monitor · doi:10.12659/msm.912624 · Cited by 13 · see citing works
Retracted
Glucocorticoid-Induced Osteoporosis in Growing Mice Is Not Prevented by Simultaneous Intermittent PTH Treatment
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Glucocorticoid-Induced Bone Loss in Mice Can Be Reversed by the Actions of Parathyroid Hormone and Risedronate on Different Pathways for
Formation, B., Yao, W., Cheng, Z., Pham, A., Busse, C., Zimmermann, E. A., Ritchie, R. O., & Lane, N. E. (2012)
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Authors: Yao, W., Cheng, Z., Pham, A., Busse, C., Zimmermann, E. A., Ritchie, R. O., & Lane, N. E.
Affiliations: University of California Davis Medical Center (US)
Lawrence Berkeley National Laboratory (US)
ORCID: Yao, Wei
Cheng, Zhiqiang
Zimmermann, Elizabeth A.
Ritchie, Robert O.
Lane, Nancy E.
Venue: Arthritis & Rheumatism
Publisher: Wiley
Published: 2008-10-30
Volume: 58
Issue: 11
Pages: 3485-3497
ISSN: 0004-3591 (ISSN-L)
1529-0131
DOI: 10.1002/art.23954
PMC: PMC2597521
OpenAlex: W2084395631
Cited by: 128
References: 74
Citations by year: 2025: 4 · 2024: 1 · 2023: 4 · 2022: 5 · 2021: 6 · 2020: 5 · 2019: 13 · 2018: 7 · 2017: 6 · 2016: 6 · 2015: 9 · 2014: 8 · 2013: 10 · 2012: 6
FWCI: 12.06
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Arthritis & Rheumatism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR043052, K24AR048841)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-051958-02, K12HD051958)
Topics: Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Health Sciences › Medicine › Oncology › Bone health and treatments
Keywords: prednisolone, parathyroid hormone, risedronate, bone mineralization, bone microarchitecture, trabecular bone volume, Wnt signaling, DMP1, PHEX, DKK1, sclerostin, WIF1, bone formation, bone turnover, osteoclasts, osteocalcin, antiresorptive therapy
MeSH terms: Risedronic Acid, Animals, Calcification, Physiologic, Glucocorticoids, Immunohistochemistry, Male, Osteogenesis, Parathyroid Hormone, Prednisolone, Etidronic Acid, Tomography, X-Ray Computed, Osteocalcin, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Wnt Proteins, Mice

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Glucocorticoid-induced bone loss in mice can be reversed by the actions of parathyroid hormone and risedronate on different pathways for bone formation and mineralization

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