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Background: The association between adverse pregnancy outcomes (APOs) and maternal apical periodontitis remains unclear as it has not been examined rigorously or reviewed systematically. Objective: To systematically review and critically evaluate the available evidence on the association of maternal apical periodontitis with several APOs. Methods: A literature search was conducted using the following electronic databases: Clarivate Analytics' Web of Science, Scopus, PubMed, and Cochrane Central Register of Controlled Trials (CENTRAL), from inception to 25 February 2021, with no language restrictions. Observational studies including longitudinal clinical trials, cohort, case–control and cross‐sectional studies of prospective and retrospective design were included. Articles with duplicate or overlapping results, abstract‐only papers, case reports, case series, animal studies and reviews were excluded. Two independent reviewers were involved in study selection, data extraction and appraising the included studies; disagreements were resolved by a third reviewer. The Newcastle–Ottawa Scale (NOS) and the adapted form of the NOS were used to assess the quality for case–control and cross‐sectional studies, respectively. Results: Two case–control and one cross‐sectional study were included in the current review. The included studies were published between 2015 and 2017, with a total of 1187 participating individuals with an approximate age range of 15 to 40 years. As the included studies reported different outcomes, the heterogeneity of data prevented a meta‐analysis being undertaken. The overall quality of the evidence was 'Fair' for two out of three included studies, while one study was categorized as 'Good'. Discussion: Two out of three included primary studies had a substantial number of methodological inconsistencies and flaws, and therefore caution should be exercised in interpreting the results of this systematic review because several important covariates were not considered in the original investigations. Conclusion: Based on a limited volume and 'Fair' and 'Good' quality of evidence, a positive association between maternal apical periodontitis and APOs was observed. However, more 'Good' quality clinical studies are needed to confirm the results of the current review. Funding: None Registration: PROSPERO database (CRD42‐2191987) [ABSTRACT FROM AUTHOR]

Background: The existence of an association between cardiovascular diseases (CVDs) and apical periodontitis (AP) remains unclear because results obtained from previous clinical studies and reviews are inconsistent or inconclusive. Objective: To conduct an umbrella review to determine whether there is an association between CVDs and the prevalence of AP in adults. Methods: The protocol of the review was registered in the PROSPERO database (CRD42020185753). The literature search was conducted using the following electronic databases: Clarivate Analytics' Web of Science Scopus, PubMed and Cochrane Database of Systematic Reviews, from inception to May, 2020, with no language restrictions. Systematic reviews with or without meta‐analysis that evaluated the association between CVDs and AP were included. Other types of studies, including narrative reviews, were excluded. Two reviewers independently performed a literature search, data extraction and quality assessment of included studies. Any disagreements or doubts were resolved by a third reviewer. The quality of the reviews was assessed using the AMSTAR 2 tool (A measurement tool to assess systematic reviews), with 16 items. A final categorization of the systematic reviews classified each as of 'high', 'moderate', 'low' or 'critically low' quality. Results: Four systematic reviews were included in the current review. Three reviews were graded by AMSTAR 2 as 'moderate' quality, whereas one review was graded as 'critically low' quality. Discussion: Only one systematic review included a meta‐analysis. Substantial heterogeneity amongst the primary studies included within each systematic review was notable in preventing a pooled analysis. Conclusions: From the limited 'moderate' to 'critically low' quality evidence available, the current umbrella review concluded that a weak association exists between CVDs and AP. In the future, well‐designed, longitudinal clinical studies with long‐term follow‐up are required. [ABSTRACT FROM AUTHOR]

Aim: To investigate the possible association between TNFα (−308 G/A) and IL‐1β (−511 C/T) single nucleotide polymorphisms (SNPs) and GSTT and GSTM deletion polymorphisms and risk of apical periodontitis (AP) development, and determine the association of different genotypes with the presence of herpesviral infection in AP. Methodology: The study included 120 periapical lesions and 200 control samples. Gene polymorphism analysis was performed using either polymerase chain reaction (PCR) or PCR/ restriction fragment length polymorphism (RFLP). Relative gene expression of TNF‐α and IL‐1β was analysed using reverse transcriptase – real‐time PCR. The presence of Epstein–Barr virus (EBV) and human cytomegalovirus (HCMV) was assessed by nested PCR. Chi‐square and Fisher's exact tests and logistic regression analyses were done for polymorphisms, whilst Mann–Whitney U‐test was performed for the expression analysis. The expected frequency of variants was analysed by the Hardy–Weinberg equilibrium test. Results: TNF‐α (−308 G/A) SNP increased AP susceptibility for heterozygous (odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.06–2.80, P = 0.027) and homozygous (OR = 8.55, 95% CI = 1.77–41.36, P < 0.001) carriers of the variant A allele. On the other hand, IL‐1β (−511 C/T) polymorphism exerted a protective effect both in heterozygotes (OR = 0.540, 95% CI = 0.332–0.880, P = 0.013) and homozygotes (OR = 0.114, 95% CI = 0.026–0.501, P < 0.001). In addition, GSTM1 and GSTT1 null genotypes separately, as well as concomitantly, were associated with an increased risk for AP development (P < 0.001). The null GSTT1 genotype increased approximately twice the risk of Epstein–Barr infection (EBV) in AP (OR = 2.17, 95% CI = 1–4.71, P = 0.048), whilst TNF‐α SNP decreased it, both in heterozygotes (OR = 0.20, 95% CI = 0.08–0.48, P < 0.001) and AA homozygotes (OR = 0.07, 95% CI = 0.01–0.37, P = 0.001). Conclusions: GSTM and GSTT deletion polymorphisms, as well as TNFα (−308 G/A) SNP, are associated with increased risk, whereas IL‐1β (−511 C/T) polymorphism decreases the risk of AP development. GSTT and TNFα polymorphisms also appear to modulate the risk of EBV infection in Serbian patients with AP. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to analyse Epstein–Barr virus (EBV) and human cytomegalovirus (HCMV) viral loads in symptomatic and asymptomatic apical periodontitis lesions, to determine levels of TNF‐α, IL‐1β and IL‐6 in these lesions and to investigate a possible correlation between herpesviral copy numbers and levels of proinflammatory cytokines. Materials and Methods: A total of 100 samples of apical periodontitis were subjected to HCMV and EBV copy numbers analysis by nested polymerase chain reaction (PCR) and TaqMan real‐time PCR. The concentrations of TNF‐α, IL‐1β and IL‐6 were determined by ELISA method. SPSS software was used for statistical analysis. Results: There were no significant differences in the occurrence of EBV and HCMV between symptomatic and asymptomatic periapical lesions (p = .686, p = .879, respectively). Only 12 of 74 EBV (16.2%) and four of 54 HCMV (13.5%) nested PCR‐positive samples showed increased viral copy numbers above the limit of 125 copies/ml. There was no significant correlation between the levels of analysed proinflammatory cytokines and herpesviral copy numbers in our sample. Conclusion: The observed low viral loads point to a relatively rare occurrence of active EBV and HCMV infection in our sample. Latent herpesviral infection does not enhance the production of investigated proinflammatory cytokines. [ABSTRACT FROM AUTHOR]

Abstract: Aim: To investigate whether apical periodontitis lesions infected by Epstein–Barr virus (EBV) exhibit higher levels of oxidative stress biomarkers [8‐hydroxydeoxyguanosine (8‐OHdG) and oxidized glutathione (GSSG)] and bone resorption regulators [receptor activator of nuclear factor (NF‐κB) ligand (RANKL) and osteoprotegerin (OPG)] compared to EBV‐negative periapical lesions and healthy pulp tissues. Methodology: The experimental group consisted of 30 EBV‐positive and 30 EBV‐negative periapical lesions collected in conjunction with apicoectomy. The pulp tissues of 20 impacted third molars were used as healthy controls. The qualitative and quantitative analysis of EBV was performed by nested and real‐time polymerase chain reaction (PCR), respectively. The levels of RANKL and OPG were analysed by reverse transcriptase real‐time PCR. The levels of 8‐OHdG and GSSG were determined by enzyme‐linked immunosorbent assay (ELISA). Mann–Whitney U‐test and Spearman's correlation were used for statistical analysis. Results: The levels of RANKL, OPG, 8‐OHdG and GSSG were significantly higher in apical periodontitis lesions compared to healthy pulp controls (P = 0.001, P < 0.001, P < 0.001 and P < 0.05, respectively). RANKL and OPG mRNA expression was significantly higher in EBV‐positive compared to EBV‐negative periapical lesions (P < 0.05). There was no significant correlation between EBV copy numbers and levels of RANKL, OPG, 8OH‐dG and GSSG in apical periodontitis. Conclusion: Levels of bone resorption regulators and oxidative stress biomarkers were increased in apical periodontitis compared to healthy pulp tissues. EBV‐positive periapical lesions exhibited higher levels of RANKL and OPG compared to EBV‐negative periapical lesions. EBV may contribute to progression of apical periodontitis via enhanced production of bone resorption regulators. [ABSTRACT FROM AUTHOR]

The oral cavity has been proposed as a reservoir for H. pylori that could be responsible for the refractoriness of gastric infection to triple therapy (antibiotics, antimicrobials, and proton pump inhibitors). The aim of this study was to evaluate the efficiency of combined periodontal and triple therapy vs. triple therapy alone, in gastric H. pylori eradication in persons with H. pylori in the subgingival biofilm. Individuals positive for H. pylori in their gastric and oral samples, as determined by nested PCR, were treated either with periodontal and triple therapy or with triple therapy alone. Our results indicate that 77.3% of those treated with the combined therapy exhibited successful eradication of gastric H. pylori, compared with 47.6% who underwent only triple therapy. Analysis of these data suggests that periodontal treatment in combination with systemic therapy could be a promising approach to increasing the therapy's efficacy and decreasing the risk of infection recurrence. [ABSTRACT FROM AUTHOR]

The application of molecular genetics in cardiology is currently producing important results in the study of the pathogenetic mechanisms underlying cardiomyopathies. Recent clinical surveys have indicated that genetic factors play a major pathogenetic role in idiopathic dilated cardiomyopathy (IDC). Familial IDC is frequent (20-30%) and is probably a heterogeneous entity, as suggested by the clinical variability and the different pattern of inheritance in the affected families. Molecular genetic studies have demonstrated the existence of heterogeneity also at the genetic level. In a series of families with X-linked IDC, the disease gene has been identified as the dystrophin gene. In familial right ventricular cardiomyopathy (or right ventricular dysplasia), a new nosological entity characterized by isolated right ventricular involvement that can mimic IDC, the disease gene has been localized in the long arm of chromosome 14. In families with matrilineal transmission, the cardiomyopathy could be linked to mitochondrial DNA alterations. Autosomal dominant familial IDC, considered to be the most frequent form, is currently under active investigation. Our preliminary data have excluded a large series of candidate genes, among which are the cardiac f3-myosin heavy chain and several other genes encoding for cardiac contractile proteins, genes of the HLA region, and about 60 genes involved in the immune regulation. [ABSTRACT FROM PUBLISHER]