ArticleMedicine2026
Genetic evidence for causal link between systemic inflammation and dental caries risk: A bidirectional Mendelian randomization study.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The causal relationship between systemic inflammation and dental caries remains unclear. This study aimed to investigate the bidirectional causal association between circulating cytokines and the risk of dental caries. A bidirectional 2-sample Mendelian randomization (MR) study was conducted. Genetic instruments for 132 circulating cytokines were obtained from 2 large-scale genome-wide association study consortia (n = 8293 and n = 14,824). Summary statistics for dental caries were sourced from the FinnGen consortium (n = 1,95,395). The inverse variance weighted method was used for the primary analysis, supplemented by a range of sensitivity analyses (e.g., MR-Egger, weighted median, MR-PRESSO) to assess the robustness of the findings and detect horizontal pleiotropy. Genetically predicted higher levels of several cytokines were causally associated with an increased risk of dental caries, including CXCL9 (odds ratio [OR] = 1.25, 95% confidence interval [CI]: 1.05-1.49 and CTACK (OR = 1.15, 95% CI: 1.04-1.27). Conversely, higher levels of IFN-γ (OR = 0.79, 95% CI: 0.65-0.96), IL-17 (OR = 0.83, 95% CI: 0.71-0.97), and RANTES (OR = 0.85, 95% CI: 0.76-0.96) were associated with a reduced risk. In the reverse analysis, genetic liability for dental caries was causally linked to increased levels of Artemin and decreased levels of Cystatin D and IL-2RA. Sensitivity analyses confirmed the robustness of these associations. Our findings reveal a bidirectional causal relationship between specific inflammatory cytokines and dental caries. This suggests that systemic inflammatory pathways both contribute to and are influenced by the pathogenesis of dental caries, highlighting potential biomarkers and therapeutic targets.
Indexed as
Identifiers
What Socratic 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 Socratic graph.