Tea is often discussed as either helpful or harmful for oral health. This study uses genetic evidence to test whether drinking more tea is actually linked to cavities, periodontitis, or tooth loss. Oral conditions affect 3.9 billion people worldwide, with dental caries, periodontitis, and tooth loss being the most common issues.

Dental caries is chronic destruction of dental hard tissues produced by bacterial fermentation, and carious teeth are often characterized by demineralization and cavities. Periodontitis is a chronic inflammatory disease caused by bacteria and spirochetes in periodontal tissues.

Its diagnosis is determined by periodontal pockets, loss of clinical attachment, alveolar bone loss, or a combination of these factors. In advanced caries and periodontitis, tooth loss frequently occurs, affecting aesthetics, mastication, and social development. As one of the most consumed beverages globally, tea’s potential effect on oral diseases is still debatable.

On one side, tea was regarded as beneficial: EGCG can inhibit pathogenic bacteria linked to dental caries and periodontitis, and tea increases fluoride consumption, which helps prevent dental caries. A randomized clinical trial also found lower probing depth and bleeding index after patients with periodontitis received six weeks of green tea intake following scaling and root planning.

On the other side, tea was regarded as a caries risk because of enamel erosion, while caffeine could accelerate bone loss and exacerbate periodontitis progression. Mendelian randomization applies genetic variation to infer whether phenotypic traits or exposures affect diseases or health-related outcomes.

MR is generally independent of confounders or the processes of disease, and two-sample MR can explore causality between independent databases while saving cost. Genetics plays important roles in tea intake and the causes of oral diseases, so MR analysis allows more comprehensive insight into the causality of tea intake on oral diseases.

Figure one illustrates the authors’ two-sample Mendelian randomization design, using thirty-eight SNPs as instrumental variables for tea intake and examining dental caries and periodontitis outcomes, including DFSS, DMFS, and natural teeth remaining. The diagram highlights three requirements: the SNPs must relate to tea intake, remain independent of confounders, and affect the oral outcomes only through tea intake.

This framework matters because it uses genetic variation to investigate potential causal relationships across separate GWAS datasets. SNPs associated with routine tea intake were identified at the genome-wide significance level of less than five times ten to the power of minus eight.

To select independent SNPs as instrumental variables, strict clumping required the linkage-disequilibrium r-squared coefficient to be less than 0.001 in a 10,000-kilobase window, referring to the European 1000 Genomes panel. The PhenoScanner tool checked whether selected SNPs were associated with potential confounders such as sugar, sweetener, or milk intake, smoking, diabetes, body mass index, and socioeconomic factors.

SNPs with a minor allele frequency below 0.01 were excluded, and an F statistic greater than 10 indicated limited bias from weak instruments. The study extracted tea-intake and oral-disease datasets from genome-wide association studies conducted by the UK Biobank and the Gene Lifestyle Interactions in Dental Endpoints consortium.

It selected 38 single-nucleotide polymorphisms significantly associated with tea intake as instrumental variables, using a threshold of less than five times ten to the power of minus eight. Mendelian randomization investigated potential causality between tea intake, caries, and periodontitis, while multivariable MR adjusted for smoking, body mass index, and socioeconomic factors.

At a significance threshold of 0.05, tea intake frequency was negatively associated with natural teeth, with a beta of minus 0.203 and a P value of 0.029. Tea intake frequency was positively associated with the presence of periodontitis, with an odds ratio of 1.622, a 95 percent confidence interval from 1.194 to 2.205, and a P value of 0.002.

Tea intake had no association with DFSS or DMFS based on the fixed-effect inverse-variance weighted model, and MR-PRESSO found no outliers in each outcome dataset. After Bonferroni correction, the association between tea intake and periodontitis remained statistically significant, but the association with natural teeth was not significant at the adjusted threshold.

Figure three shows SNP-level Mendelian randomization estimates linking genetically predicted tea intake with caries in panels A and B, and periodontitis in panels C and D. Each point compares a SNP’s effect on tea intake with its effect on an oral-health measure, while the cross-shaped bars show ninety-five percent confidence intervals.

Colored lines represent estimates from several MR methods, allowing readers to assess how consistently the SNP-specific evidence supports the reported associations. Sensitivity analysis found no sufficient evidence of heterogeneity among the analyses, based on the P values for Cochran’s Q and I-squared.

The P value for the MR-Egger intercept was higher than 0.05 in each group, demonstrating no significant horizontal pleiotropy in this study. Table one reports sensitivity checks for tea intake’s associations with dental outcomes, after excluding a potentially pleiotropic SNP.

Across DFSS, DMFS, number of natural teeth, and periodontitis, Cochran’s Q P-values range from zero point three six six to zero point six three six, with I-squared values from zero to six percent. MR-Egger intercept P-values range from zero point two five nine to zero point eight seven three, providing no significant evidence of horizontal pleiotropy according to the authors.

The causal association of tea intake on periodontitis had an odds ratio of 1.603, with a 95 percent confidence interval from 0.964 to 2.666 and a P value of 0.069, after adjustment for years of schooling and average total household income before tax. That association was attenuated after adjusting for the two socioeconomic factors, indicating that causality might be partly mediated by socioeconomic factors.

Using MR analysis can reduce some confounders and avoid reverse causality compared with traditional cross-sectional studies. The exposure and outcome datasets were both European, which can reduce ethnic differences affecting gene polymorphisms, but the European study population may limit extrapolation of the results.

The study could not assess whether the association between genetically predicted tea intake and tooth loss differs by causes such as caries, periodontitis, or trauma, because data on what resulted in tooth loss were lacking. More explicit mechanisms for how tea intake acts on caries and periodontitis should be studied in the future.

Collectively, frequent tea consumption may increase the risk of periodontitis through genetic evidence. Tea intake was suggested as a novel target in the prevention of periodontitis and tooth loss, while relevant mechanisms require further exploration.

The genetic analysis found no association between tea intake and caries, while the periodontitis signal weakened after socioeconomic adjustment. Tea may be relevant, but the result is not a simple causal verdict.