ArticleJournal of pain research2025
Exploring Causality Between Bone Mineral Density and Cervical Spondylosis: Bidirectional and Multivariable Mendelian Randomization Study.
Article in Journal of pain research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Recent evidence has suggested a potential link between bone mineral density (BMD) and cervical spondylosis (CS), while the specific relationship has yet to be comprehensively elucidated. Our study aimed to implement a comprehensive analytical framework incorporating bidirectional two-sample Mendelian randomization (MR) and multivariable MR (MVMR) to investigate the causal relationship between BMD and CS. Methods: Genome-wide association summary statistics for BMDs across four skeletal sites and five age groups, and CS, were obtained from public databases. Single Nucleotide Polymorphisms (SNPs) that had a significant genetic association with exposures were used as instrumental variables (IVs). We employed inverse variance weighting (IVW) analysis as the primary analytical method to estimate potential causal effects, whereas Weighted median, MR-Egger regression, weighted mode, and simple mode were served as supplements. Furthermore, several sensitivity analyses (MR-Egger intercept, MR-PRESSO, Cochran's Q test, and Leave-one-out test) were utilized to assess the robustness, heterogeneity, and horizontal pleiotropy of the findings. Results: After applying the Bonferroni correction, BMDs in three skeletal sites exhibited significant positive causal associations with CS risk, including total body (TB), femoral neck (FN), and heel bone (HB). Notably, based on MR analyses of TB-BMD data stratified by five age brackets, the positive causal relationship was especially pronounced in the 45-60-year-old group. Further MVMR analysis revealed that, even after controlling for confounding factors, higher TB-BMD (OR = 1.14, 95% CI: 1.01-1.29; P = 3.12E-02) and HB-BMD (OR = 1.11, 95% CI: 1.01-1.22; P = 2.45E-02) still maintained an independent and significant causal association with CS. However, we did not find evidence to suggest that CS has an impact on BMD in reverse MR analysis. Conclusion: This study provides genetic support for a causal relationship between BMD and CS susceptibility. Specifically, individuals with high BMD are at greater risk of developing CS, offering valuable insights for future clinical research.
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.