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Periodontitis and stroke: A Mendelian randomization study
Chaoyang Ma1, Min Wu2, Jie Gao3
1Department of Endodontology, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou, China.
Insights
Chronic periodontitis (CP) may causally increase the risk of cardioembolic stroke, a subtype of ischemic stroke. Aggressive periodontitis (AgP) showed no causal link to ischemic stroke or its subtypes.
Area of Science:
- Genetics
- Cardiovascular Disease
- Oral Health
Background:
- Periodontitis, a gum disease, is linked to ischemic stroke.
- The specific causal links between periodontitis subtypes and stroke remain unclear.
Purpose of the Study:
- To investigate the causal relationship between chronic periodontitis (CP) and aggressive periodontitis (AgP) and ischemic stroke.
- To examine the association with specific ischemic stroke subtypes using Mendelian randomization.
Main Methods:
- Utilized large-scale genetic summary statistics from UK Biobank and GWAS.
- Employed Mendelian randomization and inverse variant weighted methods.
- Conducted comprehensive sensitivity analyses to ensure result robustness.
Main Results:
- Aggressive periodontitis (AgP) showed no causal association with ischemic stroke or its subtypes.
- Chronic periodontitis (CP) did not show a significant causal link to overall ischemic stroke.
- CP demonstrated a potential causal relationship with cardioembolic stroke (OR, 1.052; P = .042).
Conclusions:
- Chronic periodontitis may have a causal effect on cardioembolic stroke.
- No causal link was found between aggressive periodontitis and ischemic stroke.
Background And Purpose:
Periodontitis has been implicated in the incidence of ischemic stroke. However, the generalizability of results to individuals with different subtypes of periodontitis is unknown. We aimed to investigate the causal relationship of chronic periodontitis (CP) and aggressive periodontitis (AgP) with ischemic stroke and its subtypes in the Mendelian randomization framework.
Methods:
The genetic proxies of CP were derived from large-scale summary statistics from the UK Biobank datasets (950 cases and 455,398 controls). The genetic associations of AgP were selected from another large genome-wide association study of European ancestry (851 cases and 6836 controls). The instruments of ischemic stroke (34,217 cases and 406,111 controls) and its subtypes were selected from the MEGASTROKE consortium of European ancestry. The inverse variant weighted method was performed to determine the causal inference and a comprehensive set of sensitivity analyses to test the robustness of the results.
Results:
In population-wide genetic analysis, there was no association of genetically predicted AgP (odds ratio [OR], 0.982; 95% confidence interval [CI], 0.956-1.009; p = .197) with ischemic stroke or its subtypes. For patients with CP, there was also no significant causal inference on ischemic stroke (OR, 1.017; 95% CI, 0.992-1.043; p = .184). However, regarding the stroke subtypes, the genetic analysis provided evidence of a causal relationship of CP with cardioembolic stroke (OR, 1.052; 95% CI, 1.002-1.104; p = .042), but not with large artery atherosclerosis (OR, 1.005; 95% CI, 0.944-1.069; p = .875) or small vessel occlusion (OR, 1.039; 95% CI, 0.981-1.101; p = .193).
Conclusion:
This study suggested that there was a potential causal effect of CP on cardioembolic stroke.
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