Objective:This study aims to investigate the causal inference underlying this association through the application of Mendelian randomization (MR) analysis. Basic research design: A Two-Sample Mendelian Randomization Study. Clinical setting: NA. Participants: This study uses summary data from genome-wide association studies (GWAS) of seven antibodies targeting Helicobacter pylori (H. pylori) and periodontal diseases, employing a two-sample MR design. It analyzed 97,830 cases and 272,252 controls for gingivitis, 4784 cases for chronic periodontitis, and 367 cases for acute periodontitis. Interventions: NA. Main outcome measures: This study aimed to overcome the limitations of observational studies and provide insights into whether H. pylori plays a causal role in the development of periodontal disease (PD). Results:The genetic prediction results indicate a statistically significant association between H. pylori UREA antibody levels and the risk of acute periodontitis (OR = 0.7, 95% CI: 0.50–0.98, p = 0.035). In the Weighted Median method, comparable results were obtained (OR = 0.61, 95% CI: 0.39 - 0.95, p = 0.028). However, we did not identify a causal association between genetically predicted levels of other H. pylori antibodies and periodontal disease. For sensitivity analysis, heterogeneity was detected in studies of CagA antibody and acute periodontitis through Cochran’s Q tests, and one outlier was identified using MR-PRESSO. Upon exclusion of outliers, the results remained robust and were not influenced by other factors. Conclusions:The study results revealed a causal relationship between H. pylori UREA antibody levels and acute periodontitis, indicating that H. pylori UREA antibody levels are a protective factor against acute periodontitis.
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
0.00 MB
0.16 MB