Inflammation-modulating elements are recognized periodontitis (PD) risk factors, nevertheless, the association between dietary inflammatory index (DII) and PD has never been appraised. We aimed to assess the association between DII and PD and the mediation effect of DII in the association of PD with systemic inflammation. Using the National Health and Nutrition Examination Survey 2009–2010, 2011–2012 and 2013–2014, participants who received periodontal exam and provided dietary recall data were included. The inflammatory potential of diet was calculated via DII. PD was defined according to the 2012 case definition. White blood cells (WBC), segmented neutrophils and C-reactive protein (CRP) were used as proxies for systemic inflammation. The periodontal measures were regressed across DII values using adjusted multivariate linear regression and adjusted mediation analysis. Overall, 10,178 participants were included. DII was significantly correlated with mean periodontal probing depth (PPD), mean clinical attachment loss (CAL), thresholds of PPD and CAL, WBC, segmented neutrophils and DII (p < 0.01). A linear regression logistic adjusted for multiple confounding variables confirmed the association between DII and mean PPD (B = 0.02, Standard Error [SE]: 0.02, p < 0.001) and CAL (B = −0.02, SE: 0.01, p < 0.001). The association of mean PPD and mean CAL with both WBC and segmented neutrophils were mediated by DII (from 2.1 to 3.5%, p < 0.001). In the 2009–2010 subset, the association of mean CAL with serum CRP was mediated by DII (52.0%, p < 0.01). Inflammatory diet and PD may be associated. Also, the inflammatory diet significantly mediated the association of leukocyte counts and systemic inflammation with PD.

We aimed to investigate the association between blood pressure (BP) and tooth loss and the mediation effect of age. A cross-sectional study from a reference dental hospital was conducted from September 2017 to July 2020. Single measures of BP were taken via an automated sphygmomanometer device. Tooth loss was assessed through oral examination and confirmed radiographically. Severe tooth loss was defined as 10 or more teeth lost. Additional study covariates were collected via sociodemographic and medical questionnaires. A total of 10,576 patients were included. Hypertension was more prevalent in severe tooth loss patients than nonsevere tooth lost (56.1% vs. 39.3%, p < 0.001). The frequency of likely undiagnosed hypertension was 43.4%. The adjusted logistic model for sex, smoking habits and body mass index confirmed the association between continuous measures of high BP and continuous measures of tooth loss (odds ratio (OR) = 1.05, 95% CI: 1.03–1.06, p < 0.001). Age mediated 80.0% and 87.5% of the association between periodontitis with both systolic BP (p < 0.001) and diastolic BP (p < 0.001), respectively. Therefore, hypertension and tooth loss are associated, with a consistent mediation effect of age. Frequency of undiagnosed hypertension was elevated. Age, gender, active smoking, and BMI were independently associated with raised BP.

Oral diseases are highly prevalent worldwide. Recent studies have been supporting a potential bidirectional association of oral diseases with systemic noncommunicable diseases (NCDs). Available evidence supports that people with NCDs have a greater prevalence of oral diseases particularly those with limited ability of oral self-care. Regarding the reverse relationship, the lines of evidence pointing out NCDs as putative risk factors for oral diseases have increased significantly but not with a consistent agreement. This umbrella review of meta-analyses appraises the strength and validity of the evidence for the association between oral health and systemic health (registered at PROSPERO, ID: CRD42022300740). An extensive search included systematic reviews that have provided meta-analytic estimates on the association of oral diseases with NCDs. The overall strength of evidence was found to be unfavorable and with methodological inconsistencies. Twenty-eight NCDs were strongly associated with oral diseases. Among those NCDs are five types of cancer, diabetes mellitus, cardiovascular diseases, depression, neurodegenerative conditions, rheumatic diseases, inflammatory bowel disease, gastric helicobacter pylori, obesity, and asthma. According to fail-safe number statistics, the evidence levels are unlikely to change in the future, indicating a fairly robust consistency.

Patients suffering from periodontitis are at a higher risk of developing cognitive dysfunction. However, the mediation effect of an inflammatory diet and serum vitamin D levels in this link is unclear. In total, 2062 participants aged 60 years or older with complete periodontal diagnosis and cognitive tests from the National Health and Nutrition Examination Survey (NHANES) 2011–2012 and 2013–2014 were enrolled. The Consortium to Establish a Registry for Alzheimer’s disease (CERAD) word learning subtest (WLT) and CERAD delayed recall test (DRT), the animal fluency test (AFT) and the digit symbol substitution test (DSST) was used. Dietary inflammatory index (DII) was computed via nutrition datasets. Mediation analysis tested the effects of DII and vitamin D levels in the association of mean probing depth (PD) and attachment loss (AL) in all four cognitive tests. Periodontitis patients obtained worse cognitive test scores than periodontally healthy individuals. DII was negatively associated with CERAD-WLT, CERAD-DRT, AFT and DSST, and was estimated to mediate between 9.2% and 36.4% of the total association between periodontitis with cognitive dysfunction (p < 0.05). Vitamin D showed a weak association between CERAD-DRT, AFT and DSST and was estimated to between 8.1% and 73.2% of the association between periodontitis and cognitive dysfunction (p < 0.05). The association between periodontitis and impaired cognitive function seems to be mediated both by a proinflammatory dietary load and vitamin D deficiency. Future studies should further explore these mediators in the periodontitis-cognitive decline link.

Background: We aimed to assess the association between DII and PD and the mediation effect of DII in the association of PD with systemic inflammation. Using the National Health and Nutrition Examination Survey (NHANES) 2009-2010, 2011-2012 and 2013-2014, participants that received periodontal exam and provided dietary recall data were included. The inflammatory potential of diet was calculated via DII. Periodontitis was defined according to the 2012 case definition. The clinical outcomes of interest were mean periodontal probing (PPD), mean clinical attachment loss (CAL) and thresholds of PPD and CAL. White blood cells (WBC), segmented neutrophils and C-reactive protein (CRP) were used as proxies for systemic inflammation. The periodontal measures were regressed across DII values using adjusted multivariate linear regression. Adjusted mediation analysis appraised the influence of DII in the association of periodontitis and systemic inflammation. 10,178 participants were included. DII was significantly correlated with mean PPD, mean CAL, thresholds of PPD and CAL, WBC, segmented neutrophils and DII (p&amp;lt;0.01). A linear regression logistic adjusted for multiple confounding variables confirmed the association between DII and mean PPD (B = 0.02, Standard Error [SE]: 0.02, p&amp;lt;0.001) and CAL (B = -0.02, SE: 0.01, p&amp;lt;0.001). The association of mean PPD and mean CAL with both white blood cells and segmented neutrophils were mediated by DII (from 2.1 to 3.5%, p&amp;lt;0.001). In the 2009-2010 subset, the association of mean CAL with serum CRP was mediated by DII (52.0%, p&amp;lt;0.01). In conclusion, inflammatory diet and PD may be associated. Also, the inflammatory diet significantly mediated the association of leukocyte counts and systemic inflammation with periodontitis.