Evidence map›Paper›PMID 38093316›Full record

ArticleArthritis research & therapy2023

Osteoporosis and osteoarthritis: a bi-directional Mendelian randomization study.

Yudun Qu, Shibo Chen, Mengling Han, Ziqi Gu, Yujie Zhang, Tianxiang Fan, Muhui Zeng, Guangfeng Ruan, Peihua Cao, Qian Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
10.2field-weighted citation impact, top 1% of its field
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  10. [Analysis of current status and trends of disease burden of knee osteoarthritis in China, 1990-2023].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2025
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  20. The complexities of cell death mechanisms: a new perspective in systemic sclerosis therapy.Apoptosis : an international journal on programmed cell death · 2025
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4 · The record

Corrections and comments

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

13 authors at 4 institutions in 2 countries.

Yudun Qu *Clinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Shibo Chen *Clinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Mengling HanDepartment of Rehabilitation, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Ziqi GuClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Yujie ZhangDepartment of Epidemiology, School of Public Health, Southern Medical University, Guangzhou, Guangdong, China.
Tianxiang FanClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Muhui ZengClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Guangfeng RuanDepartment of Rheumatology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510180, China.
Peihua CaoClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Qian YangMRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Changhai DingClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China. changhai.ding@utas.edu.au.
Yan ZhangClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China. yan.zhang@utas.edu.au.
Zhaohua ZhuClinical Research Centre, Zhujiang Hospital, The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China. zhaohua.zhu@utas.edu.au.
Southern Medical University · CNZhujiang Hospital · CNGuangzhou First People's Hospital · CNUniversity of Bristol · GB

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2019A1515111169Guangzhou Science and Technology Program 202002030481National Natural Science Foundation of China 32000925Wu Jieping Medical Foundation Program 3206750.2020-03-12
6 · The paper itself

Abstract

objectiveTo investigate the causal relationship between low bone mineral density (BMD) and osteoarthritis (OA) using Mendelian randomization (MR) design.

methodsTwo-sample bi-directional MR analyses were performed using summary-level information on OA traits from UK Biobank and arcOGEN. Sensitivity analyses including MR-Egger, simple median, weighted median, MR pleiotropy residual sum, and outlier approaches were utilized in conjunction with inverse variance weighting (IVW). Gene ontology (GO) enrichment analyses and expression quantitative trait locus (eQTL) colocalization analyses were used to investigate the potential mechanism and shared genes between osteoporosis (OP) and OA.

resultsThe IVW method revealed that genetically predicted low femoral neck BMD was significantly linked with hip (β = 0.105, 95% CI: 0.023-0.188) and knee OA (β = 0.117, 95% CI: 0.049-0.184), but not with other site-specific OA. Genetically predicted low lumber spine BMD was significantly associated with OA at any sites (β = 0.048, 95% CI: 0.011-0.085), knee OA (β = 0.101, 95% CI: 0.045-0.156), and hip OA (β = 0.150, 95% CI: 0.077-0.224). Only hip OA was significantly linked with genetically predicted reduced total bone BMD (β = 0.092, 95% CI: 0.010-0.174). In the reverse MR analyses, no evidence for a causal effect of OA on BMD was found. GO enrichment analysis and eQTL analysis illustrated that DDN and SMAD-3 were the most prominent co-located genes.

conclusionsThese findings suggested that OP may be causally linked to an increased risk of OA, indicating that measures to raise BMD may be effective in preventing OA. More research is required to determine the underlying processes via which OP causes OA.

Indexed as

Bone Diseases, MetabolicOsteoarthritis, HipOsteoarthritis, KneeOsteoporosisBone DensityGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideExpression quantitative trait locus analysesGene ontology enrichment analysesMendelian randomizationOsteoarthritisOsteoporosis

Identifiers

PMID38093316
PMCPMC10717893
OpenAlexW4389682356

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.