Our findings reveal a new regulatory pathway of YY1/HDACs/miR-155/HBP1 in macrophage-derived foam cell formation during early atherogenesis and suggest that miR-155 is a potential therapeutic target for atherosclerosis.
Aim
To investigate the association between dietary inflammatory potential and poor periodontal health.
Material and Methods
A cross‐sectional analysis of a nationally representative sample of participants was performed. NHANES 2011–2014 (n = 7081) and NHANES 2001–2004 (n = 5098) were used as discovery and validation datasets, respectively. The energy‐adjusted dietary inflammatory index (E‐DII) score was calculated for each participant based on 24‐h dietary recalls to assess diet‐associated inflammation. Periodontitis was defined by the CDC/AAP using clinical periodontal parameters. Natural cubic spline was applied to identify any non‐linear associations of the E‐DII score with moderate/severe periodontitis. Furthermore, interaction analyses were performed by age, gender, and race/ethnicity to explore the moderating roles of these factors.
Results
In the discovery dataset, a non‐linear positive relationship with periodontitis was identified for the E‐DII score (pnon‐linearity < .001) after adjustment for potential confounders. Compared with those individuals in the lowest tertile of E‐DII, participants in the highest tertile who consumed a pro‐inflammatory diet were 53% more likely to be periodontitis (OR tertile3vs1 = 1.53, 95% CI: 1.33–1.77). The validation dataset showed similar associations. Relatively stronger associations were seen in older adults and males.
Conclusion
Consuming a pro‐inflammatory diet indicated by the E‐DII score is associated with periodontal disease in the U.S. general adult population.
Background
Systemic effects of periodontal infection may increase the risk of central neuroinflammation, aggravating impaired cognition. This study aims to examine whether systemic inflammatory factors mediate the possible association between periodontal inflammation and cognitive function
Methods
We conducted a cross-sectional analysis of 766 participants aged > 60 years and who had complete periodontal and cognitive examinations in the NHANES 2001–2002. We used multivariable linear regression to investigate the overall association between periodontal health and cognitive function as measured by the digit symbol substitution test (DSST). Bleeding on probing (BOP) and periodontal inflamed surface area (PISA) were used to assess the periodontal inflammatory activity and burden, respectively. Mediation analyses were used to test the indirect effects of the BOP/PISA on DSST via C-reactive protein, white blood cell (WBC) count, and fibrinogen
Results
Participants with superior periodontal health obtained higher DSST scores than those with poorer periodontal health, adjusting for demographic factors and chronic conditions. Concerning the inflammatory activity, WBC count acted as a full mediator in the association between BOP and DSST (β = -0.091; 95% CI = -0.174 to -0.008) and mediated 27.5% of the total association. Regarding the inflammatory burden, WBC count acted as a partial mediator in the association between PISA and DSST (β = -0.059; 95% CI = -0.087 to -0.031) and mediated 20.3% of the total association
Conclusion
Our study indicated the potential role of systemic inflammatory factors as a mediator of associations between periodontal inflammation and cognitive function in the U.S. geriatric population
We recently demonstrated that a co-culture system of human umbilical vein endothelial cells (HUVECs) and human dental pulp stem cells (hDPSCs) could enhance angiogenesis ability in vitro. However, whether tumor necrosis factor α (TNF-α) could promote blood vessel formation during pulp regeneration remained unknown. The aim of this study was to investigate the effects of TNF-α on the formation of endothelial tubules and vascular networks in a co-culture system of hDPSCs and HUVECs. hDPSCs were co-cultured with HUVECs at a ratio of 1:5. The Matrigel assay was performed to detect the total tubule branching lengths and numbers of branches, and the Cell-Counting Kit 8 assay was performed to examine the effect of TNF-α on cell proliferation. Real-time polymerase chain reactions and western blot were used to detect vascular endothelial growth factor (VEGF) mRNA and protein expression. The Matrigel assay showed significantly greater total branching lengths and numbers of branches formed in the experimental groups treated with different concentrations of TNF-α compared with the control group. The decomposition times of the tubule structures were also significantly prolonged (P < 0.05). Treatment with 50 ng/ml TNF-α did not significantly change the proliferation of co-cultured cells, but it significantly increased the VEGF mRNA and protein expression levels (p < 0.05). In addition, the migration abilities of HUVECs and hDPSCs increased after co-culture with TNF-α (p < 0.05). TNF-α enhanced angiogenic ability in vitro in the co-culture system of hDPSCs and HUVECs.
Background: Cognitive impairment and poor oral health are frequently seen among older adults. Both conditions have been identified as risk factors for mortality. However, the combined associations of cognitive impairment and poor oral health with mortality have not been well studied and are therefore the aim of this cohort study. Methods: We analyzed data from the National Health and Nutrition Examination Survey (1999 linked with mortality data obtained from the 2015 public-use linked mortality file. Cognitive impairment was defined as a digit symbol substitution test score lower than the lowest quartile. Oral health status was assessed based on presence of untreated caries, moderate to severe periodontitis, and edentulism. The combined effects of caries/periodontitis or edentulism and cognitive impairment on all-cause and cardiometabolic mortality were examined using the Cox proportional hazard models after adjusting for potential confounders including demographic characteristics, lifestyle, biomarkers, and comorbidities.
Results:In total, 1973 participants were enrolled in the prospective study. At a median follow-up of 13.4 years, 978 participants had died (264 deaths because of cardiometabolic disease). Cognitive impairment, periodontitis, and edentulism were each found to be significant predictors of all-cause mortality. Caries, however, was not significantly related to mortality. When analyzing these predictors in combination, a diagnosis of cognitive impairment and periodontitis was associated with an 83.1% increase in all-cause mortality risk and an 87.7% increase in cardiometabolic mortality risk compared with healthy controls. Similarly, the risk for all-cause mortality was highest in cases where impaired cognition and edentulism co-occurred (adjusted hazard ratio = 1.701, 1.338-2.161).
The main objective of periodontal care is to reach and maintain a healthy periodontium. The definition of periodontal health plays a crucial role in population surveillance and the determination of critical therapeutic targets for clinicians. 1 Most studies traditionally regarded that a healthy periodontium is the opposite of case definitions of periodontal disease, as does the World Health Organization (WHO) defining health as an absence of illness. 2 Specifically, periodontal health refers to a state free from inflammation and characterized by shallow pockets and the absence of gingival bleeding. 3 However, there are a variety of case definitions, 4-6 and these definitions refer to an array of clinical signs and symptoms, such as probing pocket depth (PPD), clinical attachment loss (CAL) and bleeding on probing (BOP). 7 Consequently, we assume that there is heterogeneity in the definitions of periodontal health. The definition of
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