106 research outputs found

    Interferon-gamma promoter hypomethylation and increased expression in chronic periodontitis: IFNG hypomethylation in periodontal disease

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    The goal of this investigation was to determine whether epigenetic modifications in the IFNG promoter are associated with an increase of IFNG transcription in different stages of periodontal diseases

    Obstructive airway disease and edentulism in the atherosclerosis risk in communities (ARIC) study

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    ObjectivesWe examined the potential association between prior chronic obstructive pulmonary disease (COPD) and edentulism, and whether the association varied by COPD severity using data from the Dental Atherosclerosis Risk in Communities Study.DesignCross-sectional.SettingCommunity dwelling subjects from four US communities.Participants and measurementsCases were identified as edentulous (without teeth) and subjects with one or more natural teeth were identified as dentate. COPD cases were defined by spirometry measurements that showed the ratio of forced expiratory volume (1 s) to vital capacity to be less than 0.7. The severity of COPD cases was also determined using a modified Global Initiative for Chronic Obstructive Lung Disease classification criteria (GOLD stage I–IV). Multiple logistic regression was used to examine the association between COPD and edentulism, while adjusting for age, gender, centre/race, ethnicity, education level, income, diabetes, hypertension, coronary heart disease and congestive heart failure, body mass index, smoking, smokeless tobacco use and alcohol consumption.Results13 465 participants were included in this analysis (2087 edentulous; 11 378 dentate). Approximately 28.3% of edentulous participants had prior COPD compared with 19.6% among dentate participants (p<0.0001). After adjustment for potential confounders, we observed a 1.3 (1.08 to 1.62) and 2.5 (1.68 to 3.63) fold increased risk of edentulism among GOLD II and GOLD III/IV COPD, respectively, as compared with the non-COPD/dentate referent. Given the short period of time between the measurements of COPD (visit 2) and dentate status (visit 4) relative to the natural history of both diseases, neither temporality nor insight as to the directionality of the association can be ascertained.ConclusionsWe found a statistically significant association between prior COPD and edentulism, with evidence of a positive incremental effect seen with increasing GOLD classification

    Genome-wide association study of biologically informed periodontal complex traits offers novel insights into the genetic basis of periodontal disease

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    Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria alone have had modest success to-date. Here, we refine the CP phenotype by supplementing clinical data with biological intermediates of microbial burden (levels of eight periodontal pathogens) and local inflammatory response (gingival crevicular fluid IL-1β) and derive periodontal complex traits (PCTs) via principal component analysis. PCTs were carried forward to GWAS (∼2.5 million markers) to identify PCT-associated loci among 975 European American adult participants of the Dental ARIC study. We sought to validate these findings for CP in the larger ARIC cohort (n = 821 participants with severe CP, 2031—moderate CP, 1914—healthy/mild disease) and an independent German sample including 717 aggressive periodontitis cases and 4210 controls. We identified six PCTs with distinct microbial community/IL-1β structures, although with overlapping clinical presentations. PCT1 was characterized by a uniformly high pathogen load, whereas PCT3 and PCT5 were dominated by Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, respectively. We detected genome-wide significant signals for PCT1 (CLEC19A, TRA, GGTA2P, TM9SF2, IFI16, RBMS3), PCT4 (HPVC1) and PCT5 (SLC15A4, PKP2, SNRPN). Overall, the highlighted loci included genes associated with immune response and epithelial barrier function. With the exception of associations of BEGAIN with severe and UBE3D with moderate CP, no other loci were associated with CP in ARIC or aggressive periodontitis in the German sample. Although not associated with current clinically determined periodontal disease taxonomies, upon replication and mechanistic validation these candidate loci may highlight dysbiotic microbial community structures and altered inflammatory/immune responses underlying biological sub-types of CP

    Epigenetic Regulation of TNFA Expression in Periodontal Disease

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    Tumor necrosis factor-alpha (TNF-α) plays a central role in the molecular pathogenesis of periodontal disease. However, the epigenetic regulation attributable to microbial and inflammatory signals at the biofilm gingival interface are poorly understood. In this study, we investigated the DNA methylation alteration within the TNFA promoter in human gingival biopsies from different stages of periodontal disease, and explored the regulatory mechanism of TNFA transcription by DNA methylation

    A Randomized Controlled Trial of Intensive Periodontal Therapy on Metabolic and Inflammatory Markers in Patients With ESRD: Results of an Exploratory Study

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    Periodontitis is a novel risk factor for inflammation and cardiovascular disease in the dialysis population. Limited information about the impact of periodontal therapy in patients receiving dialysis exists

    Salivary Biomarkers in a Biofilm Overgrowth Model

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    The purpose of this study was to determine whether baseline salivary inflammatory biomarkers could discriminate between different clinical levels of disease and/or predict clinical progression over a 3-week stent-induced biofilm overgrowth (SIBO) period

    Elaboration of handbook about dietary fibers and bowel constipation

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    Objective: to elaborate a handbook with high-fiber foods to be used in the composition of the homogeneous liquid diet for patients in postoperative period to reduce or prevent the bowel constipation. Methods: the handbook highlights the importance of dietary fibers, classification, food sources, amount of use, interaction with other nutrients, directions for preparation, solubility, functions and problems caused by the excess ingestion. It also contains a list of food with fibers quantities present in 100 grams of each food. Such data were obtained from the Tabela Brasileira de Composição de Alimentos of Unicamp and Tabela Brasileira de Composição de Alimentos of University of São Paulo. The handbook was elaborated by students from Fundap Professional Improvement Program and distributed for free for all patients of the Hospital for Rehabilitation of Craniofacial Anomalies, in postoperative period, receiving homogeneous liquid diet. The handbook was also made available in the homepages www.centrinho.usp/manual and www.redeprofis.com.br for consultation and free copies. The handbook art and illustrations were made by a student of Marketing rom USC. Results: The use of fibers will be oriented in a preventive form for patients not showing bowel constipation and in a corrective form for those already constipated. Conclusions: Bowel constipation is a public health problem in Brazil, mainly among women, and it becomes worse when individuals are submitted to a homogeneous liquid diet in which the foods are liquefied and filtered and the residues (fibers) are rejected. In such case, the composition of this diet needs to be enriched with dietary fibers to prevent or correct the bowel constipation

    Using genetics to test the causal relationship of total adiposity and periodontitis: Mendelian randomization analyses in the Gene-Lifestyle Interactions and Dental Endpoints (GLIDE) Consortium

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    Background: The observational relationship between obesity and periodontitis is widely known, yet causal evidence is lacking. Our objective was to investigate causal associations between periodontitis and body mass index (BMI).Methods: We performed Mendelian randomization analyses with BMI-associated loci combined in a genetic risk score (GRS) as the instrument for BMI. All analyses were conducted within the Gene-Lifestyle Interactions and Dental Endpoints (GLIDE) Consortium in 13 studies from Europe and the USA, including 49 066 participants with clinically assessed (seven studies, 42.1% of participants) and self-reported (six studies, 57.9% of participants) periodontitis and genotype data (17 672/31 394 with/without periodontitis); 68 761 participants with BMI and genotype data; and 57 871 participants (18 881/38 990 with/without periodontitis) with data on BMI and periodontitis.Results: In the observational meta-analysis of all participants, the pooled crude observational odds ratio (OR) for periodontitis was 1.13 [95% confidence interval (CI): 1.03, 1.24] per standard deviation increase of BMI. Controlling for potential confounders attenuated this estimate (OR = 1.08; 95% CI:1.03, 1.12). For clinically assessed periodontitis, corresponding ORs were 1.25 (95% CI: 1.10, 1.42) and 1.13 (95% CI: 1.10, 1.17), respectively. In the genetic association meta-analysis, the OR for periodontitis was 1.01 (95% CI: 0.99, 1.03) per GRS unit (per one effect allele) in all participants and 1.00 (95% CI: 0.97, 1.03) in participants with clinically assessed periodontitis. The instrumental variable meta-analysis of all participants yielded an OR of 1.05 (95% CI: 0.80, 1.38) per BMI standard deviation, and 0.90 (95% CI: 0.56, 1.46) in participants with clinical data.Conclusions: Our study does not support total adiposity as a causal risk factor for periodontitis, as the point estimate is very close to the null in the causal inference analysis, with wide confidence intervals
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