Association between hypertension and periodontitis: possible mechanisms.
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ABSTRACT:
SUBMITTER: Leong XF
PROVIDER: S-EPMC3910336 | biostudies-other | 2014
REPOSITORIES: biostudies-other
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Project description:Periodontitis is an inflammatory disease that is characterized by progressive destruction of the periodontium and causes tooth loss in adults. Periodontitis is known to be associated with dysbiosis of the oral microflora, which is often linked to various diseases. However, the complexity of plaque microbial communities of periodontitis, antibiotic resistance, and enhanced virulence make this disease difficult to treat. In this study, using metagenomic shotgun sequencing, we investigated the etiology, antibiotic resistance genes (ARGs), and virulence genes (VirGs) of periodontitis. We revealed a significant shift in the composition of oral microbiota as well as several functional pathways that were represented significantly more abundantly in periodontitis patients than in controls. In addition, we observed several positively selected ARGs and VirGs with the Ka/Ks ratio > 1 by analyzing our data and a previous periodontitis dataset, indicating that ARGs and VirGs in oral microbiota may be subjected to positive selection. Moreover, 5 of 12 positively selected ARGs and VirGs in periodontitis patients were found in the genomes of respiratory tract pathogens. Of note, 91.8% of the background VirGs with at least one non-synonymous single-nucleotide polymorphism for natural selection were also from respiratory tract pathogens. These observations suggest a potential association between periodontitis and respiratory infection at the gene level. Our study enriches the knowledge of pathogens and functional pathways as well as the positive selection of antibiotic resistance and pathogen virulence in periodontitis patients, and provides evidence at the gene level for an association between periodontitis and respiratory infection.
| S-EPMC9684085 | biostudies-literature
Project description:BackgroundHuman T-cell leukemia virus type 1 (HTLV-1) activates inflammatory cascades by activating the NF-κB pathway. The minor allele of single nucleotide polymorphism (SNP) in breast cancer suppressor BRCA1-associated protein (BRAP), which has a common etiology with HTLV-1 infection, has been reported to be positively associated with carotid atherosclerosis, but inversely associated with hypertension. Therefore, HTLV-1 infection may be inversely associated with hypertension by activating endothelial maintenance, including atherosclerosis. To clarify these associations, a cross-sectional study was conducted using 2989 Japanese individuals aged 60-99 years participating in a general health check-up.MethodsLogistic regression models were used to clarify the association between HTLV-1 and hypertension. Platelet levels stratified analyses were also performed since platelet production, which plays a crucial role in endothelium maintenance, can be stimulated by activating the NF-κB pathway.ResultsHTLV-1 infection was found to be significantly inversely associated with hypertension, particularly in subjects with high platelet levels (≥ second tertiles of platelet levels); the fully adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were 0.75 (0.62, 0.92) for total and 0.64 (0.50, 0.82) for high platelet levels, respectively. Further analysis of the non-hypertensive subjects demonstrated that HTLV-1 infection was significantly positively associated with atherosclerosis in subjects with the highest tertile of platelet levels (2.11 [1.15, 3.86]) but not in subjects with low platelet levels (first and second tertiles of platelet level) (0.89 [0.57, 1.39]).ConclusionAsymptomatic HTLV-1 infection is inversely associated with hypertension, possibly by activating endothelial maintenance, including atherosclerosis progression.
| S-EPMC7846982 | biostudies-literature
Project description:AimsInflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.Methods and resultsWe performed a two-sample Mendelian randomization analysis in the ∼750 000 UK-Biobank/International Consortium of Blood Pressure-Genome-Wide Association Studies participants using single nucleotide polymorphisms (SNPs) in SIGLEC5, DEFA1A3, MTND1P5, and LOC107984137 loci GWAS-linked to periodontitis, to ascertain their effect on blood pressure (BP) estimates. This demonstrated a significant relationship between periodontitis-linked SNPs and BP phenotypes. We then performed a randomized intervention trial on the effects of treatment of periodontitis on BP. One hundred and one hypertensive patients with moderate/severe periodontitis were randomized to intensive periodontal treatment (IPT; sub- and supragingival scaling/chlorhexidine; n = 50) or control periodontal treatment (CPT; supragingival scaling; n = 51) with mean ambulatory 24-h (ABPM) systolic BP (SBP) as primary outcome. Intensive periodontal treatment improved periodontal status at 2 months, compared to CPT. This was accompanied by a substantial reduction in mean SBP in IPT compared to the CPT (mean difference of -11.1 mmHg; 95% CI 6.5-15.8; P < 0.001). Systolic BP reduction was correlated to periodontal status improvement. Diastolic BP and endothelial function (flow-mediated dilatation) were also improved by IPT. These cardiovascular changes were accompanied by reductions in circulating IFN-γ and IL-6 as well as activated (CD38+) and immunosenescent (CD57+CD28null) CD8+T cells, previously implicated in hypertension.ConclusionA causal relationship between periodontitis and BP was observed providing proof of concept for development of clinical trial in a large cohort of hypertensive patients. ClinicalTrials.gov: NCT02131922.
| S-EPMC6837161 | biostudies-literature
Project description:ObjectiveEmerging evidence shows the clinical consequences of patient with COVID-19 and periodontitis are not promising, and periodontitis is a risk factor. Periodontitis and COVID-19 probably have a relationship. Hence, this study aimed to identify the common molecular mechanism that may help to devise potential therapeutic strategies in the future.Material and methodsWe analyzed two RNA-seq datasets for differential expressed genes, enrichment of biological processes, transcription factors (TFs) and deconvolution-based immune cell types in periodontitis, COVID-19 and healthy controls. Relationships between TFs and mRNA were established by Pearson correlation analysis, and the common TFs-mRNA regulatory network and nine co-upregulated TFs of the two diseases was obtained. The RT-PCR detected the TFs.ResultsA total of 1616 and 10201 differentially expressed gene (DEGs) from periodontitis and COVID-19 are found. Moreover, nine shared TFs and common biological processes associated with lymphocyte activation involved in immune response were identified across periodontitis and COVID-19. The cell type enrichment revealed elevated plasma cells among two diseases. The RT-PCR further confirmed the nine TFs up-regulation in periodontitis.ConclusionThe pathogenesis of periodontitis and COVID-19 is closely related to the expression of TFs and lymphocyte activation, which can provide potential targets for treatment.
| S-EPMC10369766 | biostudies-literature
Project description:This systematic review aims to investigate the association between psychological stress and periodontitis through analysis of cortisol levels and periodontal clinical parameters. This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guide and based on PECO (Participants, Exposure, Comparators, Outcomes) question and registered at PROSPERO under the code CRD42017076670. As eligibility criteria, observational studies performed in adult humans presenting periodontitis (P), which evaluated patients exposed (E) and nonexposed to psychological stress (C) and to verify the association between this type of stress and periodontitis (O) were included. The searches were performed until March 2018. The following databases were used: PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar. After searches, the duplicate results were removed. The remaining citations were selected according to eligibility criteria in two phases. In the first phase, the title/abstract was evaluated. In the second phase, the articles were chosen previously were assessed by full text. After selection, the studies were submitted to data extraction and risk of bias evaluation by Fowkes and Fulton. A total of 1,386 citations were retrieved. After duplicates removal and selection process, three articles were selected by full text. Among them, two articles reported a positive association between psychological stress and periodontitis. All articles were classified as low risk of bias. Even though two articles highlighted an association between psychological stress and the presence of a possible modulatory pattern of cortisol levels in clinical parameters of periodontitis, more studies are necessary to elucidate this question.
| S-EPMC7069755 | biostudies-literature
Project description:Background: Diabetic retinopathy is a common microvascular complication in diabetic patients and is considered the main cause of visual loss worldwide. Periodontitis is a chronic inflammatory condition, which compromises dental supporting tissues. The chronic bacterial challenge in periodontitis is a persistent source of inflammatory mediators that may be associated with insulin resistance, increasing the risk of complications of diabetes mellitus. This systematic review aimed to summarize the evidence in the association between diabetic retinopathy and periodontitis. Methods: This review was registered under the number CRD 42019142267. A search strategy in five electronic databases and a gray literature source was performed based on the PECO acronym. After data extraction, the qualitative synthesis and risk of bias analyses were performed using the Newcastle-Ottawa scale. The level of evidence of all studies taken together was evaluated through the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Results: Out of the 253 citations screened, five cross-sectional studies met the eligibility criteria and were included in the qualitative analysis, in which two were judged to be of good quality, one as fair quality, and two as poor quality. Among the included studies, a significant relationship between the severity of periodontitis (CAL > 5 mm) and the severity of diabetic retinopathy (p < 0.05) was reported by four studies. Also, an association between both diseases in non-obese adults was found after adjustments [OR 2.206 (1.114-4.366); p = 0.0232). However, the analysis of evidence by GRADE assessment was rated as low. Conclusions: Although the results of individual studies suggest an association between diabetic retinopathy and periodontitis, the quality of the body of evidence was judged to be low by the GRADE approach. Further studies with larger sample sizes, adequate models of cofounders' adjustments, and prospective analysis of periodontitis and diabetes conditions ought to be conducted to clarify this association.
| S-EPMC7820190 | biostudies-literature
Project description:BackgroundPeriodontitis is closely associated with chronic systemic diseases. Healthy lifestyle interventions have health-enhancing effects on chronic systemic disorders and periodontitis, but the extent to which healthy lifestyle combinations are associated with periodontitis is unclear. Therefore, this study aimed to investigate the association between periodontitis and different healthy lifestyle combinations.Methods5611 participants were included from the National Health and Nutrition Examination Survey (NHANES, 2009-2014). Six healthy lifestyles factors were defined as fulfilling either: non-smoking, moderate drinking, moderate body mass index (BMI), physical activity, healthy sleep and appropriate total energy intake. Then, the adjusted logistic regression models were performed to identify the association between the periodontitis and the scoring system composed of six lifestyles (0-6 scale). Finally, different scenarios were dynamically and randomly combined to identify the optimal and personalized combination mode.ResultsHigher healthy lifestyle scores were significantly associated with lower periodontitis prevalence (p < 0.05). Four lifestyle factors (smoking, drinking, BMI, and sleep) significantly varied between the periodontitis and healthy groups (p < 0.05). Smoking was considered as a strong independent risk factor for periodontitis in both former and current smokers. Results further indicated that the combination of these four lifestyles played the most essential role in determining the magnitude of periodontitis occurrence (odds ratio [OR]: 0.33; 95% confidence interval [CI]: 0.21 to 0.50). In the total population, the majority of three lifestyle combinations outperformed the two combination models, whereas the two-combination of nonsmoking-drinking (OR: 0.39; 95% CI: 0.27 to 0.58) had relatively lower periodontitis prevalence than the three-combination of healthy drinking-BMI-sleep (OR: 0.42; 95% CI: 0.26 to 0.66).ConclusionThis cross-sectional study suggests that smoking, drinking, BMI, and sleep are significantly related with periodontitis and smoking is the principal risk factor related among them. This study provides various customized lifestyle combinations for periodontitis prevention.
| S-EPMC10840229 | biostudies-literature
Project description:Periodontitis is an oral chronic infection/inflammatory condition, identified as a source of mediators of inflammation into the blood circulation, which may contribute to exacerbate several diseases. There is increasing evidence that inflammation plays a key role in the pathophysiology of Alzheimer's disease (AD). Although inflammation is present in both diseases, the exact mechanisms and crosslinks between periodontitis and AD are poorly understood. Therefore, this article aims to review possible comorbidity between periodontitis and AD. Here, the authors discuss the inflammatory aspects of periodontitis, how this oral condition produces a systemic inflammation and, finally, the contribution of this systemic inflammation for worsening neuroinflammation in the progression of AD.
| S-EPMC5649154 | biostudies-other
Project description:ObjectiveTo explore possible genes related to the development of persistent pulmonary hypertension of the newborn (PPHN).MethodsThe authors identified 285 single nucleotide polymorphisms (SNPs) of 11 candidate genes (BMPR2, EPAS1, PDE3A, VEGFA, ENG, NOTCH3, SOD3, CPS1, ABCA3, ACVRL1, and SMAD9), using an Illumina Asian Screening Array-24 v1.0 BeadChip Array. The FastLmmC and R package was used for statistical analyses. The chi-square test and Cochrane-Armitage trend test were used to compare the allele and genotype frequencies between the groups and to test the genetic models, respectively.ResultsA total of 45 PPHN infants and 294 control subjects were analyzed. The most common cause of PPHN was meconium aspiration syndrome. Among the 285 SNPs, 17 SNPs from 6 candidate genes (BMPR2, EPAS1, PDE3A, VEGFA, ENG, and NOTCH3) were significantly associated with PPHN (P < 0.05). After using the Bonferroni correction (P < 0.00018), only the rs17034984 SNP located in intron 1 of the EPAS1 gene remained significantly different between the PPHN and control subjects (P = 0.00014). The frequency of the TC/TT genotype of rs17034984 in the gene with the dominant model was significant in the patients with PPHN (OR = 5.38, 95% CI: 2.15-13.49). The T allele frequency of rs17034984 in the gene showed a significant difference compared with the control subjects (OR = 4.89, 95% CI: 2.03-11.82).ConclusionsThe present study suggests that the rs17034984 variant of EPAS1 gene is associated with PPHN.
| S-EPMC9432230 | biostudies-literature
Project description:ObjectiveTo investigate the genetic crosstalk mechanisms that link periodontitis and Alzheimer's disease (AD).BackgroundPeriodontitis, a common oral infectious disease, is associated with Alzheimer's disease (AD) and considered a putative contributory factor to its progression. However, a comprehensive investigation of potential shared genetic mechanisms between these diseases has not yet been reported.MethodsGene expression datasets related to periodontitis were downloaded from the Gene Expression Omnibus (GEO) database, and differential expression analysis was performed to identify differentially expressed genes (DEGs). Genes associated with AD were downloaded from the DisGeNET database. Overlapping genes among the DEGs in periodontitis and the AD-related genes were defined as crosstalk genes between periodontitis and AD. The Boruta algorithm was applied to perform feature selection from these crosstalk genes, and representative crosstalk genes were thus obtained. In addition, a support vector machine (SVM) model was constructed by using the scikit-learn algorithm in Python. Next, the crosstalk gene-TF network and crosstalk gene-DEP (differentially expressed pathway) network were each constructed. As a final step, shared genes among the crosstalk genes and periodontitis-related genes in DisGeNET were identified and denoted as the core crosstalk genes.ResultsFour datasets (GSE23586, GSE16134, GSE10334, and GSE79705) pertaining to periodontitis were included in the analysis. A total of 48 representative crosstalk genes were identified by using the Boruta algorithm. Three TFs (FOS, MEF2C, and USF2) and several pathways (i.e., JAK-STAT, MAPK, NF-kappa B, and natural killer cell-mediated cytotoxicity) were identified as regulators of these crosstalk genes. Among these 48 crosstalk genes and the chronic periodontitis-related genes in DisGeNET, C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 were shared and identified as the most pivotal candidate links between periodontitis and AD.ConclusionsExploration of available transcriptomic datasets revealed C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 as the top candidate molecular linkage genes between periodontitis and AD.
| S-EPMC8032519 | biostudies-literature