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We estimated effects of diabetes mellitus and metabolic control on long-term change in coronal caries and restorative status using 11-year-follow-up data from the population-based Study of Health in Pomerania. Data of 3731 participants with baseline and 5- and 11-year follow-up information were included. Diabetes was defined via self-reported physician´s diagnosis or intake of glucose-lowering drugs or hemoglobin A1c (HbA1c) ≥6.5% or fasting blood glucose levels ≥11.1 mmol/l. The diabetes status was defined as no diabetes (HbA1c < 6.5% or non-fasting blood glucose <11.1 mmol/l), subjects with known or undetected diabetes mellitus and HbA1c ≤ 7% (well-controlled diabetes), and subjects with known or undetected diabetes mellitus and HbA1c > 7% (poorly-controlled diabetes). The caries status was clinically assessed using the half-mouth method and the Decayed Missing Filled Surfaces (DMFS) index and its component scores were determined. Covariate-adjusted linear mixed models were evaluated. Rates in change in DMFS were significantly higher in subjects with poorly-controlled diabetes compared to subjects without diabetes. Subjects with poorly- and well-controlled diabetes had significantly higher rates in change in Missing Surfaces (MS) compared to subjects without diabetes. For the DFS, rates in change were significantly lower for subjects with well-controlled diabetes and higher for subjects with poorly-controlled diabetes as compared to subjects without diabetes. Concordantly, all rates in change increased proportional to HbA1c levels. Effects were even more pronounced in subjects with diabetes duration of ≥5 years. Subjects with poorly-controlled diabetes are at higher risk for caries progression compared to subjects without diabetes, especially in case of longer disease duration.

Evidence for a shared genetic basis of association between coronary artery disease (CAD) and periodontitis (PD) exists. To explore the joint genetic basis, we performed a GWAS meta-analysis. In the discovery stage, we used a German aggressive periodontitis sample (AgP-Ger; 680 cases vs 3,973 controls) and the CARDIoGRAMplusC4D CAD meta-analysis dataset (60,801 cases vs 123,504 controls). Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (P AgP-Ger  < 0.05; P CAD  < 5 × 10 -8 ; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls). SNP rs1561198 showed significant association (PD[Replication]: P = 0.008 OR = 1.09, 95% CI = [1.02-1.16]; PD [Discovery + Replication]: P = 0.0002, OR = 1.11, 95% CI = [1.05-1.17]). For the associated haplotype block, allele specific cis-effects on VAMP8 expression were reported. Our data adds to the shared genetic basis of CAD and PD and indicate that the observed association of the two disease conditions cannot be solely explained by shared environmental risk factors. We conclude that the molecular pathway shared by CAD and PD involves VAMP8 function, which has a role in membrane vesicular trafficking, and is manipulated by pathogens to corrupt host immune defense.