Journal of endodontics · 2025
Unraveling the Association between Apical Periodontitis and Inflammatory Bowel Disease Through Mendelian Randomization.
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Wang Yuqiang, Zhou Yueli, Song Fangfang, Tang Ying, Huang Cui
Аннотация
INTRODUCTION: The objective of this investigation was to assess the genetic predispositions linking apical periodontitis to inflammatory bowel disease (encompassing ulcerative colitis [UC] and Crohn's disease [CD]).
METHODS: Single nucleotide polymorphisms were used as instrumental variables, and the radial inverse-variance weighted method was utilized as the primary analytical approach. Steiger filtering and additional sensitivity analyses were conducted to assess the robustness of the primary results, while also accounting for various common confounders to minimize inherent pleiotropic effects.
RESULTS: Upon the evaluation of specific confounding variables, findings combined by mete-analysis indicated that genetically predicted apical periodontitis had no significant correlation with inflammatory bowel disease (OR = 0.99, 95% CI: 0.89-1.10, P > .05), UC (OR = 1.08, 95% CI: 0.97-1.20, P > .05), and CD (OR = 1.05, 95% CI: 0.94-1.18, P > .05). Conversely, in the inverse analyses, CD was genetically predicted to exert a weak influence on apical periodontitis (OR = 1.07, 95% CI: 1.02-1.12, P < .05), whereas the impact of inflammatory bowel disease on apical periodontitis risk was deemed nonsignificant (OR = 1.03, 95% CI: 1.00-1.07, P > .05). There was no discernible association between genetically influenced UC and apical periodontitis (OR = 0.98, 95% CI: 0.93-1.04, P > .05). Sensitivity analyses corroborated the primary outcomes, aligning with the direction of the estimates and thereby bolstering the robustness of the findings.
CONCLUSIONS: Despite the limitations acknowledged within this study, our results provided evidence suggesting a potential role of CD in the risk of apical periodontitis.
METHODS: Single nucleotide polymorphisms were used as instrumental variables, and the radial inverse-variance weighted method was utilized as the primary analytical approach. Steiger filtering and additional sensitivity analyses were conducted to assess the robustness of the primary results, while also accounting for various common confounders to minimize inherent pleiotropic effects.
RESULTS: Upon the evaluation of specific confounding variables, findings combined by mete-analysis indicated that genetically predicted apical periodontitis had no significant correlation with inflammatory bowel disease (OR = 0.99, 95% CI: 0.89-1.10, P > .05), UC (OR = 1.08, 95% CI: 0.97-1.20, P > .05), and CD (OR = 1.05, 95% CI: 0.94-1.18, P > .05). Conversely, in the inverse analyses, CD was genetically predicted to exert a weak influence on apical periodontitis (OR = 1.07, 95% CI: 1.02-1.12, P < .05), whereas the impact of inflammatory bowel disease on apical periodontitis risk was deemed nonsignificant (OR = 1.03, 95% CI: 1.00-1.07, P > .05). There was no discernible association between genetically influenced UC and apical periodontitis (OR = 0.98, 95% CI: 0.93-1.04, P > .05). Sensitivity analyses corroborated the primary outcomes, aligning with the direction of the estimates and thereby bolstering the robustness of the findings.
CONCLUSIONS: Despite the limitations acknowledged within this study, our results provided evidence suggesting a potential role of CD in the risk of apical periodontitis.