Evidence map›Paper›PMID 39856231›Full record

ArticlePediatric research2025

Glucocorticoids on bone remodeling in systemic lupus erythematosus mice.

Sheng Hao, Yuyun Zhang, Xiaowei Tong, Fangkai Ding, Runjie Wang, Jing Zhang, Dan Feng, Xiaoling Niu, Wenyan Huang

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Article in Pediatric research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Sheng HaoDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Yuyun ZhangDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiaowei TongDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Fangkai DingDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Runjie WangDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Jing ZhangDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Dan FengDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Xiaoling NiuDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China.
Wenyan HuangDepartment of Nephrology, Rheumatology and Immunology, Shanghai Children's Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai, China. huangwenyan@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-2197-0781

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus requires glucocorticoids for management. This study investigates how glucocorticoids influence bone in a SLE mouse model, focusing on bone mineral density (BMD), microstructure, and remodeling markers.

methodsMRL/lpr and C57BL/6 mice were administered dexamethasone or saline as a control for 4-weeks. Bone assessments included analyses of BMD, bone structure, and serum levels of RANKL and OPG.

resultsDexamethasone decreased BMD and altered cortical and trabecular bone thickness in both MRL/lpr and C57BL/6 mice. In C57BL/6 mice, cortical bone exhibited increased catabolism while trabecular bone showed signs of increased anabolism, whereas MRL/lpr mice did not show significant changes in bone turnover. Both strains experienced weight loss, with a significant decrease in femur length observed only in C57BL/6 mice. Dexamethasone exacerbated BMD reduction in MRL/lpr mice and halted its increase in C57BL/6 mice. C57BL/6 mice exhibited notable changes in cortical and trabecular bone structure, while MRL/lpr mice didn't. After receiving dexamethasone, both strains showed higher serum RANKL levels, especially in C57BL/6 mice. OPG decreased in both strains.

conclusionBoth glucocorticoids and SLE contribute to abnormal bone remodeling through RANKL/OPG pathway. IMPACT: Glucocorticoid (GC) treatment in a mouse model of systemic lupus erythematosus (SLE) leads to significant changes in bone parameters, including decreased bone mineral density (BMD) and alterations in bone structure. Those change are associated with the modulation of RANKL and OPG expression. Both GC and inflammation in SLE contribute to BMD reduction, and GC may have a certain protective effect on bone in the early stage of chronic inflammation. GC can upregulate RANKL expression and downregulate OPG expression in vivo. During a state of chronic inflammation, RANKL expression increases. However, OPG may not exert a significant influence on inflammatory stimulation.

Indexed as

Bone RemodelingDexamethasoneGlucocorticoidsLupus Erythematosus, SystemicAnimalsBone DensityCancellous BoneCortical BoneDisease Models, AnimalFemaleFemurMiceMice, Inbred C57BLMice, Inbred MRL lprOsteoprotegerinRANK LigandDexamethasoneGlucocorticoidsOsteoprotegerinRANK LigandTnfrsf11b protein, mouseTnfsf11 protein, mouse

Identifiers

PMID39856231
PMCPMC12507680

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.