ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2016
Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength.
Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Animal Model for Glucocorticoid Induced Osteoporosis: A Systematic Review from 2011 to 2021.International journal of molecular sciences · 2021Pooled it
- mClinical and translational medicine · 2026Article
- The vinculin-β-catenin axis promotes bone formation and repair: an essential prerequisite for the anti-osteoporotic efficacy of sclerostin-neutralizing antibody.Science China. Life sciences · 2026Article
- Glucocorticoid-Induced Osteoporosis: Pathogenesis, the Impact of Different Administration Routes on Bone Mineral Density, and Fracture Risk and Treatment Options-A Narrative Review.Journal of clinical medicine · 2026Review
- Mechanisms of dexamethasone-induced bone toxicity in developing bone: a single-cell perspective.JBMR plus · 2025Article
- Review
- Asperuloside alleviates osteoporosis by promoting autophagy and regulating Nrf2 activation.Journal of orthopaedic surgery and research · 2024Article
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease.JCI insight · 2024Article
- Treatment of glucocorticoid-induced osteoporosis with concurrent denosumab and romosozumab: a case report.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024Article
- Protein kinase G2 activation restores Wnt signaling and bone mass in glucocorticoid-induced osteoporosis in mice.JCI insight · 2024Article
- Treating the Side Effects of Exogenous Glucocorticoids; Can We Separate the Good From the Bad?Endocrine reviews · 2023Review
- Management of Adrenal Cortical Adenomas: Assessment of Bone Status in Patients with (Non-Functioning) Adrenal Incidentalomas.Journal of clinical medicine · 2023Review
- Pathogenic mechanisms of glucocorticoid-induced osteoporosis.Cytokine & growth factor reviews · 2023Review
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Alpinetin alleviates osteoporosis by promoting osteogenic differentiation in BMSCs by triggering autophagy via PKA/mTOR/ULK1 signaling.Phytotherapy research : PTR · 2023Article
- Combined growth hormone and insulin-like growth factor-1 rescues growth retardation in glucocorticoid-treated mdxmice but does not prevent osteopenia.The Journal of endocrinology · 2022Article
- The Role of Sclerostin in Bone Diseases.Journal of clinical medicine · 2022Review
- Bad to the Bone: The Effects of Therapeutic Glucocorticoids on Osteoblasts and Osteocytes.Frontiers in endocrinology · 2022Review
- Trabecular bone score and sclerostin concentrations in patients with primary adrenal insufficiency.Frontiers in endocrinology · 2022Article
- Effect of adrenocorticotropic hormone infusion on circulating sclerostin levels.Endocrine connections · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
unlabelledThis study was to determine if antibody against sclerostin (Scl-Ab) could prevent glucocorticoid (GC)-induced osteoporosis in mice. We found that Scl-Ab prevented GC-induced reduction in bone mass and bone strength and that the anabolic effects of Scl-Ab might be partially achieved through the preservation of osteoblast activity through autophagy.
introductionGlucocorticoids (GCs) inhibit bone formation by altering osteoblast and osteocyte cell activity and lifespan. A monoclonal antibody against sclerostin, Scl-Ab, increased bone mass in both preclinical animal and clinical studies in subjects with low bone mass. The objectives of this study were to determine if treatment with the Scl-Ab could prevent loss of bone mass and strength in a mouse model of GC excess and to elucidate if Scl-Ab modulated bone cell activity through autophagy.
methodsWe generated reporter mice that globally expressed dsRed fused to LC3, a protein marker for autophagosomes, and evaluated the dose-dependent effects of GCs (0, 0.8, 2.8, and 4 mg/kg/day) and Scl-Ab on autophagic osteoblasts, bone mass, and bone strength.
resultsGC treatment at 2.8 and 4 mg/kg/day of methylprednisolone significantly lowered trabecular bone volume (Tb-BV/TV) at the lumbar vertebrae and distal femurs, cortical bone mass at the mid-shaft femur (FS), and cortical bone strength compared to placebo (PL). In mice treated with GC and Scl-Ab, Tb-BV/TV increased by 60-125 %, apparent bone strength of the lumbar vertebrae by 30-70 %, FS-BV by 10-18 %, and FS-apparent strength by 13-15 %, as compared to GC vehicle-treated mice. GC treatment at 4 mg/kg/day reduced the number of autophagic osteoblasts by 70 % on the vertebral trabecular bone surface compared to the placebo group (PL, GC 0 mg), and GC + Scl-Ab treatment.
conclusionsTreatment with Scl-Ab prevented GC-induced reduction in both trabecular and cortical bone mass and strength and appeared to maintain osteoblast activity through autophagy.
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