BACKGROUND

To explore the causal association between () infection, herpesvirus infection and periodontitis (PD) from a genetic perspective using Mendelian randomization (MR).

METHODS

The PD data were derived from genome-wide association study (GWAS) from the Dental Endpoints (GLIDE) consortium, and the FinnGen Biobank provided data on and herpesvirus infections. In addition, we examined GWAS data for subtypes of and herpesvirus infection. Inverse variance weighting (IVW) was selected as a major analysis technique, and weighted median (WM), weighted model, simple model, and MR-Egger regression were added as supplementary methods. To verify the findings, the effects of pleiotropy and heterogeneity were assessed.

RESULTS

Genetically predicted infection (OR = 0.914, 95%CI = 0.693-1.205, P = 0.523), anti- VacA (OR = 0.973, 95%CI = 0.895-1.057, P  0.515), anti- CagA (OR = 1.072, 95%CI = 0.986-1.164; P = 0.102), Epstein-Barr virus (EBV) infection (OR = 1.026, 95%CI = 0.940-1.120, P = 0.567), Herpes simplex virus (HSV) infection (OR = 0.962, 95%CI = 0.883-1.048, P = 0.372), cytomegalovirus (CMV) infection (OR = 1.025, 95%CI = 0.967-1.088, P = 0.415), EBV nuclear antigen-1 (EBNA1) (OR = 1.061, 95%CI = 0.930-1.209, P = 0.378), EBV virus capsid antigen (VCA) (OR = 1.043, 95CI% = 0.890-1.222, P = 0.603), HSV-1 (OR = 1.251, 95%CI = 0.782-2.001, P = 0.351), HSV-2 (OR = 1.020, 95%CI = 0.950-1.096, P = 0.585), CMV IgG (OR = 0.990, 95CI% = 0.882-1.111, P = 0.861) were not associated with PD, indicated that and herpesvirus infection had no causal relationship to PD. Reverse studies also found no cause effect of PD on or herpesvirus infection. The results of the sensitivity analysis suggested the robustness of the MR results.

CONCLUSION

This study offered preliminary proof that and herpesvirus infections were not causally linked to PD, and vice versa. However, more robust instrumental variables (IVs) and larger samples of GWAS data were necessary for further MR analysis.