Background: Nod-like receptor family pyrin domain-containing protein-3 (NLRP3) complex inflammasome has potentially been shown to play an important role in the development of periodontitis and diabetes. The objective of this study was to analyze the association between serum and salivary NLRP3 concentrations in patients with periodontitis and type-II diabetes mellitus (DM) and to evaluate whether this association was influenced by potential confounders. Methods: : For the present study, a cohort of healthy controls (n = 32), and patients with periodontitis (n = 34), type-II DM (n = 33), and a combination of periodontitis + type-II DM (n = 34) were enrolled. Patients were characterized on the basis of their periodontal status and analyzed for demographic characteristics, serum mediators, and for serum and salivary concentrations of NLRP3. A uni-and multivariate model was established to analyze whether periodontitis, type-II DM, and CRP influenced serum and salivary NLRP3 concentrations. Results:In comparison to type-II DM patients and healthy controls, patients with periodontitis (serum, P = 0.003; saliva P = 0.012) and periodontitis + type-II DM (serum, P = 0.028; saliva, P = 0.003) had elevated serum and salivary NLRP3 concentrations. The multivariate regression model showed that periodontitis (P = 0.029) and HDL-cholesterol (P = 0.012) were significant predictors of serum NLRP3 concentrations whereas periodontitis (P = 0.036) and CRP (P = 0.012) were significant predictors of salivary NLRP3. Conclusion:The results of the present study showed that periodontitis and periodontitis + type-II DM patients had higher serum and salivary NLRP3 concentrations in comparison to healthy controls and patients with type-II DM. Periodontitis was demonstrated to be a significant predictor of both serum and salivary NLRP3 concentrations.

Malondialdehyde (MAA) within a lipid pathway has been demonstrated to possess an important role in endothelial function that undergoes periodontitis and coronary heart disease (CHD) development. This study evaluated the impact of periodontitis, CHD, or a combination of both diseases (periodontitis + CHD) on salivary and serum MAA levels. The periodontal and clinical characteristics, serum, and saliva samples were collected from 32 healthy subjects, 34 patients with periodontitis, 33 patients with CHD, and 34 patients with periodontitis and CHD. Lipid profile and levels of MDA and C-reactive protein (CRP) were assessed. Patients in the periodontitis group (serum: 3.92 (3.7–4.4) µmol/L; salivary 1.81 (1–2.1) µmol/g protein, p < 0.01) and in the periodontitis + CHD (serum: 4.34 (3.7–4.8) µmol/L; salivary 1.96 (1.7–2.3) µmol/g protein, p < 0.001) group presented higher median concentrations of salivary and serum MAA compared to patients in the CHD (serum: 3.72 (3.5–4.1) µmol/L; salivary 1.59 (0.9–1.8) µmol/g protein, p < 0.01) and control group (serum: 3.14 (2.8–3.7) µmol/L; salivary 1.41 (0.8–1.6) µmol/g protein, p < 0.01). In univariate models, periodontitis (p = 0.034), CHD (p < 0.001), and CRP (p < 0.001) were significantly associated with MAA. In the multivariate model, only CRP remained a significant predictor of serum and salivary MAA (p < 0.001) MAA levels. Patients with periodontitis and with periodontitis + CHD presented higher levels of salivary and serum MAA compared to healthy subjects and CHD patients. CRP has been found to be a significant predictor of increased salivary and serum MAA levels.

The skin, oral cavity, digestive and reproductive tracts of the human body harbor symbiotic and commensal microorganisms living harmoniously with the host. The oral cavity houses one of the most heterogeneous microbial communities found in the human organism, ranking second in terms of species diversity and complexity only to the gastrointestinal microbiota and including bacteria, archaea, fungi, and viruses. The accumulation of microbial plaque in the oral cavity may lead, in susceptible individuals, to a complex host-mediated inflammatory and immune response representing the primary etiological factor of periodontal damage that occurs in periodontitis. Periodontal disease is a chronic inflammatory condition affecting about 20–50% of people worldwide and manifesting clinically through the detection of gingival inflammation, clinical attachment loss (CAL), radiographic assessed resorption of alveolar bone, periodontal pockets, gingival bleeding upon probing, teeth mobility and their potential loss in advanced stages. This review will evaluate the changes characterizing the oral microbiota in healthy periodontal tissues and those affected by periodontal disease through the evidence present in the literature. An important focus will be placed on the immediate and future impact of these changes on the modulation of the dysbiotic oral microbiome and clinical management of periodontal disease.

Background and Objective Recent emerging evidence has shown that microRNA (miRNAs) is involved in several epigenetic processes linked with periodontitis, increased oxidative stress and cardiovascular disease (CVD). The present study aimed to assess the impact of periodontitis on gingival crevicular fluid (GCF) miRNAs expression associated with CVD risk and to evaluate possible confounders that influenced this association. Materials and Methods For the present study, healthy controls (n = 28) and subjects with CVD (n = 28), periodontitis (n = 30) and periodontitis + CVD (n = 29) were enrolled. All subjects underwent regular periodontal examinations and blood sampling. In addition, GCF sampling was performed, and miRNAs 7a‐5p, 21‐3p, 21‐5p, 100‐5p, 125‐5p, 200b‐3p, and 200b‐5p expression was analyzed using a real‐time quantitative polymerase chain reaction (RT‐PCR). Results The results showed that periodontitis and periodontitis + CVD subjects presented significantly different GCF miRNAs expression compared to healthy controls and CVD subjects. More specifically, compared to healthy controls and CVD, subjects with periodontitis and periodontitis + CVD showed higher GCF miRNA 7a‐5p, miRNA 21‐3p, miRNA 21‐5p, miRNA 200b‐3p, and miRNA 200b‐5p (p < .05) and lower miRNA 100‐5p, miRNA 125‐5p levels (p < .05). Furthermore, the multivariate regression analysis evidenced that periodontitis (miRNA 21‐3p, 100‐5p) and periodontal inflamed surface area (PISA) (miRNA 7a‐5p, 21‐3p, 21‐5p, 100‐5p, 125‐5p, 200b‐3p) were significant predictors of GCF miRNAs concentration (p < .05). Conclusion The results of the study highlighted that the periodontitis and periodontitis + CVD group showed higher GCF miRNAs expression than healthy controls and CVD subjects. Furthermore, periodontitis and its extent (PISA) were revealed as significant predictors of GCF miRNAs associated with CVD risk.

During the last few decades, it has been established that messenger ribonucleic acid (mRNA) transcription does not inevitably lead to protein translation, but there are numerous processes involved in post-transcriptional regulation, which is a continuously developing field of research. MicroRNAs (miRNAs) are a group of small non-coding RNAs, which negatively regulate protein expression and are implicated in several physiological and pathological mechanisms. Aberrant expression of miRNAs triggers dysregulation of multiple cellular processes involved in innate and adaptive immune responses. For many years, it was thought that miRNAs acted only within the cell in which they were synthesised, but, recently, they have been found outside cells bound to lipids and proteins, or enclosed in extracellular vesicles, namely exosomes. They can circulate throughout the body, transferring information between cells and altering gene expression in the recipient cells, as they can fuse with and be internalised by the recipient cells. Numerous studies on miRNAs have been conducted in order to identify possible biomarkers that can be used in the diagnosis of periodontal disease. However, as therapeutic agents, single miRNAs can target several genes and influence multiple regulatory networks. The aim of this review was to examine the molecular role of miRNAs and exosomes in the pathophysiology of periodontal disease and to evaluate possible clinical and future implications for a personalised therapeutical approach.