ArticleBMC musculoskeletal disorders2024
Bone biochemical markers, bone mineral density, and the risk of osteonecrosis of the femoral head: a Mendelian randomization study.
Article in BMC musculoskeletal disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Diagnostic relevance of osteocalcin and bone alkaline phosphatase as markers of bone turnover in Sickle Cell Anaemia: A Zaria study.African health sciences · 2026Article
- Application of Machine Learning and Mendelian Randomization Analysis to Identify the Cuproptosis-Related Biomarker and Its Related Regulation in Osteonecrosis of the Femoral Head.Current genomics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAlterations in bone metabolism may play a significant role in the early stages of femoral head necrosis, yet the causal relationship remains unclear. This study utilizes a two-sample Mendelian randomization (MR) approach to explore the genetic causal links between biochemical markers of bone metabolism, bone mineral density, and the risk of femoral head necrosis.
methodsThis study utilizes publicly available genome-wide association study (GWAS) datasets, with exposure factors including biochemical bone markers (25OHD, calcium, and alkaline phosphatase) and bone mineral density (measured at the lumbar spine, heel, femoral neck, and total body). The outcome of interest is osteonecrosis of the femoral head. We selected validated single nucleotide polymorphisms that are strongly associated with the exposure factors as instrumental variables. Mendelian randomization analysis was conducted using inverse variance weighting(IVW), MR-Egger regression, and weighted median estimation. Additionally, we performed analyses for horizontal pleiotropy, heterogeneity, and sensitivity.
resultsA total of 934 SNPs were included in this study. The MR analysis results indicate that the IVW analysis of 25OHD, Ca, and ALP did not reach statistical significance (25OHD OR = 1.006, 95%CI: 0.69-1.47, P = 0.975; Ca OR = 0.856, 95%CI: 0.43-1.70, P = 0.657; ALP OR = 1.022, 95%CI: 0.86-1.21, P = 0.801). However, bone density, including heel, lumbar spine, and total body bone density, showed a protective causal relationship with the onset of ONFH, while the results for femoral neck bone density did not reach statistical significance (lumbar spine BMD OR = 0.662, 95%CI: 0.48-0.91, P = 0.010; heel BMD OR = 0.726, 95%CI: 0.62-0.85, P < 0.001; total body BMD OR = 0.726, 95%CI: 0.62-0.85, P < 0.001; femoral neck BMD OR = 0.748, 95%CI: 0.53-1.05, P = 0.096). Cochran's Q statistic for IVW and MR-Egger methods indicated no intergenic heterogeneity for all exposure outcomes' SNPs, and the tests for pleiotropy suggested a low likelihood of pleiotropy in all causal analyses.
conclusionsThe results of this study indicate that there is no genetically mediated causal relationship between serum levels of 25-hydroxyvitamin D, calcium, and alkaline phosphatase and osteonecrosis of the femoral head. However, heel, lumbar spine, and total body bone mineral density can be considered protective factors for the occurrence of ONFH. There is no genetic causality between femoral neck bone mineral density and ONFH development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.