Genetic links between periodontal disease and circulating leptin and resistin: A Mendelian randomization study

ObjectiveThe relationship between periodontal disease and adipokines has been extensively investigated. Using a Mendelian randomization approach, this study aimed to determine whether circulating leptin and resistin levels are causally implicated in the etiology of periodontal disease and whether the genetic risk of periodontal disease influences circulating adipokine levels.MethodsWe obtained genetic data regarding circulating leptin and resistin and periodontal disease from comprehensive genome-wide association study meta-analyses. We selected single nucleotide polymorphisms associated with periodontal disease and adipokine levels at a stringent genome-wide significance threshold (P < 5 × 10^-6) as instrumental variables. Linkage disequilibrium clumping was applied, and F-statistics were calculated for all single nucleotide polymorphisms included in the Mendelian randomization study. Data analyses were performed using the inverse variance-weighted (IVW) method implemented in R software.ResultsThe genetic risk of periodontal disease showed a positive effect on circulating resistin levels (IVW: odds ratio = 1.061, 95% confidence interval = 1.013-1.111, P = 0.013). However, no evidence supported a causal influence of circulating leptin or resistin levels on the risk of periodontal disease (IVW: leptin, odds ratio = 0.989, 95% confidence interval = 0.869-1.124, P = 0.861; resistin, odds ratio = 0.947, 95% confidence interval = 0.854-1.051, P = 0.304). Furthermore, the genetic risk of periodontal disease showed no causal association with circulating leptin levels (IVW: odds ratio = 1.021, 95% confidence interval = 0.993-1.050, P = 0.141).ConclusionsThese findings suggest that periodontal disease may exert a causal effect on circulating resistin levels. In contrast, circulating leptin and resistin levels do not appear to causally influence the risk of periodontal disease.