Atherosclerotic cardiovascular disease (ASCVD) remains a major cause of global morbidity and mortality. Emerging research suggests that oral hygiene practices, particularly dental floss use, may reduce the risk of ASCVD.

The purpose of this study was to examine the association between dental floss use and ASCVD prevalence.

Data from NHANES participants who completed home interviews and dental evaluations were analyzed. ASCVD was defined as angina, stroke, myocardial infarction, or coronary artery disease. Dental floss use was self-reported over the past seven days. Covariates included demographic, socioeconomic, lifestyle, and clinical factors. Weighted logistic regression was used to assess the relationship between dental floss use and ASCVD prevalence.

This study included a total sample of 7253 participants with a mean age of 53.8±14.6 years. The sample consisted of 47.6 % male participants. The ethnic composition included 64.3 % Non-Hispanic White. Regular dental floss use was correlated with a lower likelihood of developing ASCVD and Stringent Criteria (infarction or stroke), with ORs of 0.76 (95 % CI: 0.60, 0.97) p=0.028 and 0.68 (95 % CI: 0.49, 0.94) p=0.022, respectively. Flossing 3-4 days/week was associated with reduced ASCVD risk, OR = 0.57 (95 % CI: 0.38, 0.84) p=0.006. Similar reductions were seen for stringent criteria: flossing 3-4 days/week: OR = 0.57 (95 % CI: 0.32, 0.99) p=0.047, flossing ≥5 days/week: OR = 0.69 (95 % CI: 0.47, 1.00) p=0.049.

Regular dental floss use may reduce the risk of ASCVD. These results support the inclusion of oral hygiene practices in cardiovascular disease prevention strategies.

Atherosclerotic cardiovascular disease (ASCVD) has long been recognized as a significant contributor to mortality rates, holding a prominent position in the hierarchy of causes of death. Nevertheless, the presence of a causal relationship between serum uric acid (SUA) and the risk of ASCVD, as well as mortality rates, remains unclear.

We initially conducted a comprehensive cohort study utilizing data sourced from National Health and Nutrition Examination Survey (NHANES) 1999-2018 to investigate the specific correlation between SUA levels and ASCVD. Then, we subsequently examined the link between SUA levels and all-cause and cardio-cerebrovascular mortality among ASCVD individuals.

We identified a U-shaped relationship between SUA levels and the risk of ASCVD in all participants (inflection point at 5.399, p value = 0.014). Similarly, SUA levels showed U-shaped trends with all-cause mortality (inflection point at 5.748, p value < 0.0001) and cardio-cerebrovascular mortality (inflection point at 5.936, p value < 0.0001), respectively.

Our findings demonstrate a U-shaped association between SUA levels and the risks of ASCVD, all-cause mortality, and cardio-cerebrovascular mortality. However, further research is needed to better understand how SUA affects ASCVD and its underlying mechanisms.

It has been reported that periodontitis was a risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD). The aim of this study is to investigate the impact of periodontitis on all-cause and cause-specific mortality of MASLD patients.

We included 11,019 individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) from the National Health and Nutrition Examination Survey. Multivariable Cox proportional hazards models were utilized to analyze the estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality and cause-specific mortality among participants with different periods of periodontitis status. Additionally, we employed restricted cubic splines (RCS) curves to explore the dose-response relationship between clinical attachment level (CAL) and pocket probing depth (PPD) and mortality rates. Finally, a series of sensitivity analyses and stratification analyses were conducted to test the reliability and robustness of the results.

In this study, moderate to severe periodontitis significantly increased the all-cause mortality (HR 1.29, 95% CI 1.08-1.55; P = 0.003) and cardiovascular disease (CVD)-related mortality (HR 1.41, 95% CI 1.10-1.79; P = 0.006) among MASLD participants. However, no significant effects of different periodontal statuses on cancer mortality were observed among MASLD participants.

A nationwide large-sample longitudinal study indicated that MASLD patients with moderate to severe periodontitis experienced significantly higher all-cause and CVD-related mortality rates compared to those with no or mild periodontitis.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Despite extensive studies into the causes and therapies for CVDs, their incidence and prevalence continue to increase. Periodontitis is a multifactorial, chronic inflammatory disease related to systemic health. Current research suggests that periodontitis may be an unconventional risk factor for CVDs and it may increase the risk of CVDs such as atherosclerosis, coronary heart disease, myocardial infarction, hypertension, heart failure as well as cardiomyopathy. For all these reasons, it is quite plausible that prevention of periodontitis has an impact on the onset or progression of CVDs. Therefore, in this review, we investigated the association between periodontitis caused by oral microorganisms and different CVDs. In addition, we discuss the various mechanisms by which periodontitis contributes to the onset and progression of CVDs. Our review aims to raise global awareness of periodontitis, particularly its role in CVDs, provide a basis for the prevention and treatment of CVDs and offer potential therapeutic targets.

Chronic periodontitis is an infectious disease initiated by plaque, which affects chewing and even general health. Ozone therapy, as a complementary means in the treatment of chronic periodontitis, numerous clinical trials have been conducted. We conducted this review to evaluate the effect of the ozone use accompanied by scaling and root planning (SRP) in periodontal treatment.

Randomized controlled trials investigating the use of ozone therapy in chronic periodontitis. The search was carried out across PubMed, Cochrane Central Register of Controlled Trials, and EMBASE databases with the search period extending to July 2024. The quality of the identified studies was evaluated using the Cochrane Collaboration's Risk of Bias tool. The results were presented as weighted mean differences (WMD) with corresponding 95% confidence intervals (95% CI). Heterogeneity among the studies was assessed using the I2 test. Data analysis was performed using RevMan 5.4 and Stata 16.0.

Thirteen articles meeting the inclusion criteria. The meta-analysis revealed statistically significant differences in probing depth (PD) and gingival index (GI) reduction between ozone-assisted nonsurgical periodontal treatment and placebo-assisted treatment in patients with chronic periodontitis (P < 0.05). However, no significant differences were observed in clinical parameters such as bleeding on probing (BOP) percentage, plaque index (PI), and clinical attachment level (CAL) (P > 0.05).

Ozone therapy combined with SRP is superior to SRP alone in improving PD and GI indexes in patients with periodontitis, without increasing adverse reactions, and the effect is worthy of recognition. The research evidence indicates that ozone therapy in patients with chronic periodontitis has a positive effect.

The interface between soft and hard tissues is constituted by a gradient change of cell types and matrix compositions that are optimally designed for proper load transmission and injury protection. In the musculoskeletal system, the soft-hard tissue interfaces at tendon-bone, ligament-bone, and meniscus-bone have been extensively researched as regenerative targets. Similarly, extensive research efforts have been made to guide the regeneration of multi-tissue complexes in periodontium. However, the other soft-hard tissue interfaces in the dental and craniofacial system have been somewhat neglected. This review discusses the clinical significance of developing regenerative strategies for soft-hard tissue interfaces in the dental and craniofacial system. It also discusses the research progress in the field focused on bioengineering approaches using 3D scaffolds equipped with spatially controlled bioactivities. The remaining challenges, future perspectives, and considerations for the clinical translation of bioactive scaffolds are also discussed.

Periodontitis (PDS) is one of the most common and crippling systemic diseases. It is a chronic inflammatory condition that leads to the loss of periodontal attachment, resulting in tooth loss. In addition to its effects on oral health and nutrition, PDS is closely linked to other systemic conditions such as diabetes mellitus (DM), cardiovascular diseases (CVD), and rheumatoid arthritis (RA). The active role of inflammation and oxidation in systemic health, as well as their relationship with periodontal therapy, has been investigated. This review explores the evidence on how periodontal therapy and dietary lifestyle can help reduce chronic inflammation, limit oxidation, and prevent related pathologies. Nonsurgical periodontal therapy (NSPT) and nutrition have been extensively discussed as potential contributors to positive clinical outcomes by resolving inflammatory pathogenic pathways. NSPT, foods, and dietary supplements represent therapeutic strategies that address the underlying mechanisms of chronic inflammation and oxidation at various stages. A key finding from this review is that periodontal treatment, in conjunction with nutritional counseling, can improve clinical outcomes in PDS, DM, CVD, and RA. However, for NSPT, nutrition, and dietary composition to be effective, they should be integrated into a sustainable, long-term lifestyle.

Several epidemiological studies suggested that frequency of tooth brushing may be associated with cardiovascular disease (CVD) risk, but the results remain inconclusive. Therefore, the aim of this study was to synthesize frequency of tooth brushing and CVD risk using meta-analysis. Science Direct, PubMed, CINAHL, and OVID were searched through October 15, 2022. The random-effects model was used to quantitatively assess the combined risk estimation. In addition, we performed the sensitivity analysis to evaluate the robustness of the study results by excluding the included studies one by one. A total of 9 cohort studies containing 10 reports with 803,019 individuals were included in the meta-analysis. Pooled results showed that compared with the lowest brushing frequency, the highest brushing frequency (relative risk = 0.85, 95% confidence interval: 0.80-0.90) significantly reduced the risk of cardiovascular disease. There was moderate heterogeneity among included studies (P = .002, I2 = 65.4%). The exclusion of any one study did not materially change the combined risk estimates. Our meta-analysis supported the hypothesis that higher frequency of tooth brushing can reduce the risk of CVD, which may have important implications for conducting research on the prevention strategies of CVD.

To investigate the effect of periodontal therapy on endothelial function of subjects with periodontitis in stages III or IV and established cardiovascular disease.

A triple-blinded, parallel groups, randomized clinical trial of 6 months duration, on patients with history of coronary heart disease and periodontitis in stages III or IV was performed. Intervention consisted of steps 1 (oral hygiene instructions and professional mechanical plaque removal) and 2 (subgingival instrumentation) of periodontal therapy, including an antiseptic mouth rinse for 7 days. Patients in the control group received only step 1, with the adjunctive use of a fluoride-containing mouth rinse. Endothelial function (flow-mediated dilation [FMD]) and carotid intima-media thickness (cIMT) at baseline, 3 and 6 months, and serum markers of inflammation and cell adhesion at 3 days, 10 days, 3 and 6 months after therapy, were evaluated. Demographic characteristics, cardiovascular risk factors, history of cardiovascular diseases, medication intake, lipids profile, blood pressure, and periodontal outcomes were also evaluated. Student T, Mann-Whitney U, Chi-square and Fisher-exact tests were performed along with repeated measures ANOVA with post hoc Bonferroni's corrections.

Thirty-five patients were included. In the test group, improvements in pocket depth, bleeding on probing and suppuration at 6 months were significantly better than in control patients. Reductions in mean FMD [test group -3.43%; 95% confidence interval-CI [-2.68; 9.54], p = 0.487; control group -6.75%; 95% CI [1.29; 12.22], p = 0.012] and cIMT (test group -0.05 mm; 95% CI [0.01; 0.10], p = 0.014; control group -0.01 mm; 95% CI [-0.03; 0.05], p = 1.000) were observed in both groups from baseline to 6 months, without significant intergroup differences at any time-point. Differences between groups in serum inflammatory markers were detected at baseline and 3 days for interleukin (IL)-18, and at 10 days for IL-8.

Preliminary results from the present pilot study showed that steps 1 and 2 of periodontal treatment in subjects with periodontitis in stages III-IV and established cardiovascular disease induced improvements in cIMT and periodontal outcomes, although changes in FMD were not observed.

clinicaltrials.gov, Identifier, database (NCT02716259).

Chronic inflammatory disorders, such as periodontitis, may contribute to pro-hypertensive inflammation.

This study aimed to analyze changes in parameters for periodontitis, such as periodontal inflamed surface area (PISA) and serum inflammatory markers, following non-surgical periodontal treatment in hypertensive patients.

A quasi-experimental pre-and-post study was conducted, involving 42 controlled hypertensive patients with periodontitis. The patients underwent periodontal assessment and tests, including complete blood count, glucose, triglycerides, HDL-C, LDL-C, and serum levels of inflammatory biomarkers. All patients received scaling and root planning treatment in a single session and were reevaluated one month after the treatment.

Post-treatment evaluations showed significant improvements in periodontal inflammation parameters, such as pocket depth, attachment level, bleeding on probing, and biofilm percentage, with statistically significant differences (p < 0.001). There were decreases in serum VEGF levels (p < 0.001) and reductions in PISA associated with declines in cytokine levels such as IL-10, IL-6, IL-12p70, IL-17A, and VEGF. PISA for IL-6 and IL-10 had a positive correlation before periodontal treatment and with IL-1β and IL-10 after treatment.

Hypertensive patients with periodontitis who underwent non-surgical periodontal treatment showed improvements in their periodontal condition, a decrease in cytokine levels such as VEGF, and reductions in PISA associated with declines in cytokines such as IL-10, IL-6, IL-12p70, IL-17A, and VEGF. These findings confirm the role of inflammation in hypertensive patients with periodontitis.

To characterize the gingival crevicular fluid (GCF) and plasma extracellular vesicles (EVs) and explore their proteomic cargo in healthy pregnant women compared to those with gestational diabetes mellitus (GDM) and periodontitis.

One-hundred and four pregnant women were recruited at 24-30 gestation weeks. GDM was diagnosed by an oral glucose tolerance test. GCF and plasma samples were obtained to isolate EVs and characterized by nanoparticle tracking, immunoassays, electron microscopy and mass spectrometry.

Of the recruits,17.3% women were healthy, 50% had periodontitis and 32.7% had both GDM and periodontitis. Probing depth, clinical attachment loss and bleeding on probing were more severe in GDM and periodontitis pregnancies (p < 0.0001). Additionally, this group showed an increase concentration of total, small and large GCF-EVs (p = 0.0015, p = 0.0011 and p = 0.0008, respectively), with decreased expression of CD9, CD81 and CD81/CD63 ratio (p = 0.0461, p = 0.0164 and p = 0.0005, respectively). No differences were observed in plasmatic EVs concentration or markers expression. Proteomic analysis of GCF-EVs showed peptides of both host and bacterial origin. Gene ontology analysis revealed that proteins of GCF-EVs participate in immune inflammatory responses, glucose metabolism and insulin response mechanisms.

GCF-EVs were increased in both GDM and periodontitis, and their proteomic cargo suggest their involvement in immune inflammatory response, glucose metabolism and insulin pathways during pregnancy.

Oral and periodontal health have been linked to systemic health, cardiovascular disease and inflammation markers. Physical fitness has been linked to increased inflammatory response, but only few studies have investigated the association between oral health with physical activity. The aim of this study was to evaluate the association between oral and periodontal health status and physical fitness in British law enforcement workers.

89 subjects were recruited between November and December 2019. Cardiopulmonary fitness was measured by Maximal Oxygen Uptake (VO2max) (ml/kg/min) and Maximum Load (Loadmax) (W) generated at the end of the Bruce incremental treadmill test; physical activity levels through accelerometers; functional strength tests by Countermovement Jump (CMJ) Power (W) and Height (cm) average. Oral variables included percentage of sites with PPD > 4 mm (% PPD > 4), full-mouth bleeding score (FMBS) and Decayed, Missing, and Filled Teeth (DMFT) index. Linear regression models were adjusted for age, gender and fat %.

Mean age was 41.5 years (range 23-61; 71.9% male). Higher % PPD > 4 was consistently correlated with lower Loadmax (-4.96; p = 0.092), CMJ Height average (-0.39; p = 0.064), and press-ups in 60 s (-0.85; p = 0.052) though the associations were not statistically significant. FMBS was associated with the % of a day spent in sedentary (0.78; p = 0.030) and light activities (-0.75; p = 0.022).

Periodontitis may be negatively associated with certain components of physical performance.

Oral health status may be associated with physical fitness and functional strength.

Background: In this study, we describe a method by which a patient can independently assess their own periodontitis risk, for example, at home, with a mobile application. The aim of the study is to use active matrix metalloproteinase aMMP-8 mouth rinse cut-off 20 ng/mL point-of-care testing (POCT) and a polynomial function to reveal patients' statistical risk of periodontitis. Methods: The polynomial function presented in this study was modeled with multiple logistic regression and the function estimates the risk of periodontitis using a probability measure. To investigate variables associated with periodontitis, we used data from adult patients visiting dental clinics in Thessaloniki, Greece. Results: The research results revealed that with appropriate information it is possible to obtain sufficient accuracy about a patient's potential risk of periodontitis. The function for estimating risk of periodontitis is PERIORISK = (1 + e-(3.392×X1+0.002×X2+1.858×X3-9.151))-1, where X1 = aMMP-8 test result and tobacco smoking status, X2 = age × waist circumference and X3 = patient's individual and parental history of diabetes. Conclusions: The prediction of periodontitis risk using an aMMP-8 test and a polynomial function seems to be a useful, non-invasive, safe-to-use and cost-effective tool for all people. Overall, in the model created, mouth rinse cut-off 20 ng/mL aMMP-8 test result, age, waist circumference, tobacco smoking status and patient's individual and parental history of diabetes were found to be good factors explaining the risk of periodontitis.

Periodontitis seriously affects oral-related quality of life and overall health. Long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues. This study aimed to explore the possible pathogenesis of LINC01126 in periodontitis.

Inflammatory model of human gingival fibroblasts (HGFs) was established. Cell Counting Kit-8 (CCK-8), wound healing assay, and flow cytometry were utilized to detect biological roles of LINC01126. Binding site of miR-655-3p to LINC01126 and IL-6 was predicted. Then, subcellular localization of LINC01126 and the binding ability of miR-655-3p to LINC01126 and IL-6 in HGFs were verified. Hematoxylin-Eosin (H&E) staining and immunohistochemistry (IHC) staining were utilized to detect tissue morphology and proteins expression of clinical samples.

LINC01126 silencing can alleviate cell inflammation induced by lipopolysaccharide derived from Porphyromonas gingivalis, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. Quantitative real-time PCR, Western Blot, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK2/STAT3 was abnormally activated in periodontitis tissues.

In summary, serving as an endogenous competitive RNA of miR-655-3p, LINC01126 promotes IL-6/JAK2/STAT3 pathway activation, thereby promoting periodontitis pathogenesis.

Introduction: The incidence of obesity has dramatically increased worldwide. Obesity has been shown to exacerbate the progression of periodontal disease. Studies suggest a sex difference in periodontitis, whereby males are more sensitive to periodontal inflammation compared to females. Aim: In the current study, it was hypothesized that obesity drives periodontal inflammation and bone loss in both sexes. Methodology: Utilizing leptin receptor mutant (SSLepR mutant) rats as a genetic model of obesity, 11-12-week-old male and female lean Dahl salt-sensitive (SS) rats and obese SSLepR mutant rats were used to investigate sex differences in obesity-induced periodontal inflammation. Results: Body weight, insulin, hemoglobin A1c and cholesterol levels were significantly elevated in the obese SSLepR mutant strain vs. the lean SS strain within the same sex. Sex differences in body weight and plasma hemoglobin A1c were only observed in obese SSLepR mutant rats, with males having significantly greater body weight and hemoglobin A1c vs. females. Plasma thiobarbituric acid reactive substances (TBARs) and monocyte chemoattractant protein-1 (MCP-1), markers of systemic oxidative stress and inflammation, respectively, were significantly elevated in obese SSLepR mutant rats vs. lean SS rats, with no sex differences in these parameters in either rat strains. Although micro-CT analyses of the maxillary first molar alveolar bone from obese SSLepR mutant rats revealed no evidence of bone loss and/or sex differences, immuno-histochemical analysis revealed significant elevations in periodontal IL-6 and decreases in IL-10 in obese SSLepR mutant rats vs. lean SS rats, with no apparent sex differences in these parameters. Conclusions: Obesity increases systemic and periodontal inflammation, without evidence of bone loss or apparent sex differences in SSLepR mutant rats.

To investigate the association between periodontitis and inflammatory biomarkers, including systemic immune-inflammatory index (SII), neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio.

Our study comprised a cross-sectional analysis (an indirect evidence group and a periodontal health control group from January to October 2023) and a retrospective study (a direct evidence group and a non-maintenance group from January 2014 to March 2022). We analyzed demographic data, imaging measurements, and peripheral blood counts.

The study included 131 participants in the indirect evidence group, 132 in the healthy control group, 123 in the direct evidence group, and 76 in the non-maintenance group. The indirect evidence group exhibited significantly altered inflammatory biomarker levels compared to the healthy controls. Receiver operating characteristic curve analysis indicated that SII was the most effective biomarker for diagnosing periodontitis, with an area under the curve 0.758 and a Youden index 0.409. The optimal cut-off value was 437.07 × 10⁹/L, achieving a sensitivity 46.2% and a specificity 94.7%. Correlation analyses revealed significant associations between the biomarker levels and periodontitis grades, with SII showing the highest correlation coefficient (0.942). In the direct evidence group, supportive periodontal therapy significantly mitigated changes in these biomarkers.

An SII level exceeding 437.07 × 109/L could facilitate the periodontitis diagnosis and disease grade determination. SII can be utilized to assess and monitor periodontitis severity and treatment response.

The purpose of this Editorial is to expose the gaps in the knowledge created by a decision by the World Workshop Consensus Conference (WWCC), held in 2017, which was focused on the re-classification of periodontal diseases [...].

Periodontitis is a chronic inflammatory non-communicable disease (NCD) characterised by the destruction of the tooth-supporting apparatus (periodontium), including alveolar bone, the presence of periodontal pockets, and bleeding on probing.

To outline, for family doctors, the implications of the association between periodontal and systemic diseases; to explore the role of family doctors in managing periodontitis as an ubiquitous non-communicable disease (NCD).

The consensus reports of previous focused collaborative workshops between WONCA Europe and the European Federation of Periodontology (using previously undertaken systematic reviews), and a specifically commissioned systematic review formed the technical papers to underpin discussions. Working groups prepared proposals independently, and the proposals were subsequently discussed and approved at plenary meetings.

Periodontitis is independently associated with cardiovascular diseases, diabetes, chronic obstructive pulmonary disease, obstructive sleep apnoea, and COVID-19 complications. Treatment of periodontitis has been associated with improvements in systemic health outcomes. The article also presents evidence gaps. Oral health care professionals (OHPs) and family doctors should collaborate in managing these conditions, including implementing strategies for early case detection of periodontitis in primary medical care centres and of systemic NCDs in oral/dental care settings. There is a need to raise awareness of periodontal diseases, their consequences, and the associated risk factors amongst family doctors.

Closer collaboration between OHPs and family doctors is important in the early case detection and management of NCDs like cardiovascular diseases, diabetes mellitus, and respiratory diseases. Strategies for early case detection/prevention of NCDs, including periodontitis, should be developed for family doctors, other health professionals (OHPs), and healthcare funders. Evidence-based information on the reported associations between periodontitis and other NCDs should be made available to family doctors, OHPs, healthcare funders, patients, and the general population.

The oral microbiome-dependent nitrate (NO3 -)-nitrite (NO2 -)-nitric oxide (NO) pathway may help regulate blood pressure. NO2 --producing bacteria in subgingival plaque are reduced in relative abundance in patients with untreated periodontitis compared with periodontally healthy patients. In periodontitis patients, the NO2 --producing bacteria increase several months after periodontal treatment. The early effects of periodontal treatment on NO2 --producing bacteria and the NO3 --NO2 --NO pathway remain unknown. The aim of this study was to determine how periodontal treatment affects the oral NO2 --producing microbiome and salivary NO3 - and NO2 - levels over time.

The subgingival microbiota of 38 periodontitis patients was analysed before (baseline [BL]) and 1, 7 and 90 days after periodontal treatment. Changes in NO2 --producing bacteria and periodontitis-associated bacteria were determined by 16s rRNA Illumina sequencing. Saliva samples were collected at all-time points to determine NO3 - and NO2 - levels using gas-phase chemiluminescence.

A significant increase was observed in the relative abundance of NO2 --producing species between BL and all subsequent timepoints (all p < 0.001). Periodontitis-associated species decreased at all timepoints, relative to BL (all p < 0.02). NO2 --producing species negatively correlated with periodontitis-associated species at all timepoints, with this relationship strongest 90 days post-treatment (ρ = -0.792, p < 0.001). Despite these findings, no significant changes were found in salivary NO3 - and NO2 - over time (all p > 0.05).

Periodontal treatment induced an immediate increase in the relative abundance of health-associated NO2 --producing bacteria. This increase persisted throughout periodontal healing. Future studies should test the effect of periodontal treatment combined with NO3 - intake on periodontal and cardiovascular health.

Poor oral health negatively impacts overall health, quality of life, and well-being. Increasing evidence suggests that provision of basic dental care for elderly Americans would improve outcomes for a variety of systemic diseases and reduce the overall cost of healthcare. As a result, recent changes have been implemented to include some dental benefits in the Medicare program. This article outlines evidence, rationale, and approaches required for inclusion of dental benefits for more Americans through the Medicare program. Improving access to dental services through Medicare to help prevent and manage common chronic diseases is an important step toward integration of dental care with general healthcare to improve the overall health, quality of life, and well-being for many older Americans.

Periodontitis is a chronic inflammation of the periodontal support tissues. The typical symptoms of periodontitis are inflammation and alveolar bone resorption. Chitong Xiaoyanling Granules (CXG) is composed of 10 Chinese herbs, which have the efficacy of dispersing wind, clearing heat, cooling blood, and relieving pain. CXG is clinically used for the treatment of periodontitis and other diseases, with remarkable efficacy and broad application prospects. However, due to the lack of systematic research on its chemical constituents and metabolites, it is of great significance to characterize the various chemical components and metabolites of CXG. In this study, ultra-high-performance liquid chromatography-quadrupole time-of-flight-tandem mass spectrometry analysis was used to identify the chemical constituents and metabolites of CXG, and the differences in metabolite profiles between normal and model rats were compared. A total of 147 compounds were identified in CXG, including 53 flavonoids, 28 terpenoids, seven chromones, eight coumarins, eight organic acids, 12 phenols, 10 alcohols, nine sugars, and 12 others. In normal and model rats, 191 and 179 CXG-related xenobiotics were detected respectively. In conclusion, a rapid and accurate identification method was used to identify the chemical components and metabolites of CXG, which laid a foundation for the study of the quality control and pharmacological mechanisms of CXG.

Periodontitis suffer from inflammation-induced destruction of periodontal tissues, resulting in the serious loss of alveolar bone. Controlling inflammation and promoting bone regeneration are two crucial aspects for periodontitis-related alveolar bone defect treatment. Herein, we developed a hierarchically structured nanofibrous scaffold with a nano-embossed sheath and a bone morphogenetic protein 2-loaded core to match the periodontitis-specific features that spatiotemporally modulated the osteoimmune environment and promoted periodontal bone regeneration. We investigated the potential of this unique scaffold to treat periodontitis-related alveolar bone defects in vivo and in vitro. The results demonstrated that the hierarchically structured scaffold effectively reduced the inflammatory levels in macrophages and enhanced the osteogenic potential of bone mesenchymal stem cells in an inflammatory microenvironment. Moreover, in vivo experiments revealed that the hierarchically structured scaffold significantly ameliorated inflammation in the periodontium and inhibited alveolar bone resorption. Notably, the hierarchically structured scaffold also exhibited a prolonged effect on promoting alveolar bone regeneration. These findings highlight the significant therapeutic potential of hierarchically structured nanofibrous scaffolds for the treatment of periodontitis, and their promising role in the field of periodontal tissue regeneration. STATEMENT OF SIGNIFICANCE: We present a novel hierarchically structured nanofibrous scaffold of coupling topological and biomolecular signals for precise spatiotemporal modulation of the osteoimmune micro-environment. Specifically, the scaffold was engineered via coaxial electrospinning of the poly(ε-caprolactone) sheath and a BMP-2/polyvinyl alcohol core, followed by surface-directed epitaxial crystallization to generate cyclic nano-lamellar embossment on the sheath. With this unique hierarchical structure, the cyclic nano-lamellar sheath provided a direct nano-topographical cue to alleviate the osteoimmune environment, and the stepwise release of BMP-2 from the core provided a biological cue for bone regeneration. This research underscores the potential of hierarchically structured nanofibrous scaffolds as a promising therapeutic approach for periodontal tissue regeneration and highlights their role in advancing periodontal tissue engineering.

To investigate whether cardiovascular health (CVH) is associated with periodontitis.

We used data from the 2009 to 2014 National Health and Nutrition Examination Survey. We quantified CVH using Life's Essential 8, which includes four health behaviours (diet, smoking, physical activity and sleep) and four health factors (body mass index, blood cholesterol, glucose and pressure). We categorized scores as low (0-49), moderate (50-79) and high (80-100). We calculated subscores of health behaviours and factors and categorized them as low, moderate and high. We used logistic regression to assess the association of CVH with periodontitis, adjusting for age, gender, race/ethnicity, education, poverty index, marital status and health insurance. We computed odds ratios (ORs) and 95% confidence intervals (CIs).

This study included 9296 adults ≥30 years old. Multivariable-adjusted models showed that subjects with moderate (OR, 0.62; 95% CI: 0.52-0.74) or high (OR, 0.43; 95% CI: 0.33-0.57) CVH had significantly lower odds of periodontitis compared to those with low CVH. These results were consistent in the health behaviours model, but the estimates in the health factors model were not significant.

Improving CVH may help prevent periodontitis. Longitudinal studies are needed to confirm our findings.

Dental caries and periodontitis are among the most prevalent chronic diseases worldwide and have been associated with atherosclerotic cardiovascular diseases (ASCVD). This study aimed to determine (1) the independent associations between subclinical ASCVD markers (carotid intima media thickness [CIMT] and coronary artery calcification [CAC]) and quantitative indices of oral disease including the decayed, missing, and filled teeth (DMFT) index, gingivitis parameters, periodontal status, and number of teeth lost and (2) the extent to which metabolites altered in individuals with oral disease overlapped with those altered in individuals with ASCVD.

We used data from 552 participants recruited through the Dental Strategies Concentrating on Risk Evaluation project. Oral examinations were conducted, and CIMT and CAC were measured. Multiple linear regression models were constructed with CIMT and CAC as dependent variables in the epidemiologic analysis. In the metabolomic analysis, logistic or linear regression was used to test 1,228 metabolites for association with each phenotype adjusted for age, sex, race, blood pressure, smoking, diabetes, cholesterol, high-sensitivity C-reactive protein, and interleukin-6.

None of the oral disease markers were significant predictors of ASCVD markers in the fully adjusted models. However, critical lipid and lipid-signaling pathway metabolites were significantly associated with gingivitis, periodontitis, and DMFT: the lysophospholipid pathway (odds ratio [OR] = 2.29, false discovery rate [FDR]-adjusted P = 0.038) and arachidonate with gingivitis (OR = 2.35, FDR-adjusted P = 0.015), the sphingolipid metabolism pathway with periodontitis (OR = 2.09, FDR-adjusted P = 0.029), and borderline associations between plasmalogen and lysophospholipid pathways and DMFT (P = 0.055). Further, the same metabolite from the sphingolipid metabolism pathway, sphingomyelin (d17:1/14:0, d16:1/15:0), was inversely associated with both CIMT (β = -0.14, FDR-adjusted P = 0.014) and gingivitis (OR = 0.04, FDR-adjusted P = 0.033).

The discovery of a common sphingomyelin metabolite in both disease processes is a novel finding suggesting that gingivitis and periodontitis may be associated with some overlapping metabolic pathways associated with ASCVD and indicating potential shared mechanisms among these diseases.

The same metabolites may be altered in atherosclerosis and oral disease. Specifically, a common sphingomyelin metabolite was inversely associated with gingivitis and carotid intima media thickness, a subclinical marker of atherosclerotic cardiovascular disease. These findings can provide valuable insights for future mechanistic studies to establish potential causal relationships, with the hope of influencing disease prevention and targeted early treatment.

The aim of this study is to examine the potential correlation between periodontitis and the risk of cardiovascular mortality and all-cause mortality in individuals diagnosed with hypertension, despite the established association between periodontitis and hypertension.

The study utilized data from the National Health and Nutrition Examination Survey (NHANES) conducted in 1999-2014 involving hypertensive individuals. Following the criteria proposed by Eke et al., periodontitis was classified. Survival estimates were calculated using Kaplan Meier analyses and a Kaplan Meier curve was generated. Weighted multivariate cox regression were employed to assess the association between periodontitis and all-cause mortality, as well as cardiovascular mortality.

Of the 21,645 individuals, 6,904 individuals were diagnosed with periodontitis. The Kaplan-Meier survival analysis revealed significantly higher rates of all-cause mortality (34.766% vs. 14.739%) and cardiovascular mortality (12.469% vs. 3.736%) in the periodontitis group compared to the non-periodontitis group. Hazard ratios (HRs) for all-cause mortality were 3.19 (95% CI 2.88-3.53) and for cardiovascular mortality were 3.80 (95% CI 3.13-4.61) in individuals with periodontitis compared to those without periodontitis.

Periodontitis is a risk factor for mortality in patient with hypertension, especially if it is moderate to severe. Improving periodontal health could lead to better outcomes for these patients.

Periodontitis is the main cause of tooth loss and is related to many systemic diseases. Artificial intelligence (AI) in periodontics has the potential to improve the accuracy of risk assessment and provide personalized treatment planning for patients with periodontitis. This systematic review aims to examine the actual evidence on the accuracy of various AI models in predicting periodontitis.

Using a mix of MeSH keywords and free text words pooled by Boolean operators ('AND', 'OR'), a search strategy without a time frame setting was conducted on the following databases: Web of Science, ProQuest, PubMed, Scopus, and IEEE Explore. The QUADAS-2 risk of bias assessment was then performed.

From a total of 961 identified records screened, 8 articles were included for qualitative analysis: 4 studies showed an overall low risk of bias, 2 studies an unclear risk, and the remaining 2 studies a high risk. The most employed algorithms for periodontitis prediction were artificial neural networks, followed by support vector machines, decision trees, logistic regression, and random forest. The models showed good predictive performance for periodontitis according to different evaluation metrics, but the presented methods were heterogeneous.

AI algorithms may improve in the future the accuracy and reliability of periodontitis prediction. However, to date, most of the studies had a retrospective design and did not consider the most modern deep learning networks. Although the available evidence is limited by a lack of standardized data collection and protocols, the potential benefits of using AI in periodontics are significant and warrant further research and development in this area.

The use of AI in periodontics can lead to more accurate diagnosis and treatment planning, as well as improved patient education and engagement. Despite the current challenges and limitations of the available evidence, particularly the lack of standardized data collection and analysis protocols, the potential benefits of using AI in periodontics are significant and warrant further research and development in this area.

Inflammation is a complex physiological process that plays a pivotal role in many if not all pathological conditions, including infectious as well as inflammatory diseases, like periodontitis and autoimmune disorders. Inflammatory response to periodontal biofilms and tissue destruction in periodontitis is associated with the release of inflammatory mediators. Chronic inflammation can promote the development of cancer. Persistence of inflammatory mediators plays a crucial role in this process. Quantification and monitoring of the severity of inflammation in relation to cancer is essential. Periodontitis is mainly quantified based on the severity and extent of attachment loss and/or pocket probing depth, in addition with bleeding on probing. In recent years, studies started to investigate inflammation indices in association with periodontal diseases. To date, only few reviews have been published focusing on the relationship between blood cell count, inflammation indices, and periodontitis. This review presents a comprehensive overview of different systemic inflammation indices, their methods of measurement, and the clinical applications in relation to periodontitis and cancer. This review outlines the physiological basis of inflammation and the underlying cellular and molecular mechanisms of the parameters described. Key inflammation indices are commonly utilized in periodontology such as the neutrophil to lymphocyte ratio. Inflammation indices like the platelet to lymphocyte ratio, platelet distribution width, plateletcrit, red blood cell distribution width, lymphocyte to monocyte ratio, delta neutrophil index, and the systemic immune inflammation index are also used in hospital settings and will be discussed. The clinical roles and limitations, relationship to systemic diseases as well as their association to periodontitis and treatment response are described.

Periodontitis is one of the most common oral diseases and a major cause of tooth loss in adults. Environmental pollution is closely associated with the prevalence of periodontitis. However, few studies have focused on the association between volatile organic compounds (VOCs) and periodontitis. This cross-sectional study aims to examine whether exposure to VOCs is associated with periodontitis, based on data from the National Health and Nutrition Examination Survey (NHANES, 2011-2014).

We analysed data on blood VOC levels, periodontitis and related covariates from 2772 participants of the NHANES. The association between the blood VOCs and periodontitis was analysed using weighted logistic regression analysis, the restricted cubic spline (RCS) model and the weighted quantile sum (WQS) regression model. Interaction tests and mediation analysis were also conducted.

After adjusting for covariates, for each natural constant-fold increase in 1,4-dichlorobenzene, the odds of having periodontitis increased by 16% (odds ratio = 1.16; 95% confidence interval: 1.08-1.24, p < .001). WQS regression model indicated that 1,4-dichlorobenzene contributed the most to the association between VOC co-exposure and periodontitis. Mediation analysis further revealed that total bilirubin levels mediated the association between 1,4-dichlorobenzene and the prevalence of periodontitis, accounting for 4.32%. In addition, the positive association between o-xylene and periodontitis was more pronounced in the <65-year-old group.

This study has provided relatively little evidence to demonstrate a specific link between VOCs and periodontitis. Nonetheless, exposure to VOCs remains a non-negligible public health concern, and further research is required to investigate the association and potential mechanisms of action between VOCs and periodontitis.

The high glucose (HG) environment in diabetic periodontitis aggravates the damage of periodontal tissue. Pyroptosis has been shown to be positively correlated with the severity of periodontitis, including macrophage pyroptosis. O-GlcNAcylation is a posttranslational modification that is involved in the pathogenesis of periodontitis. However, whether HG regulates macrophage pyroptosis through O-GlcNAcylation remains uncertain. This study aimed to investigate the effect of HG on the O-GlcNAcylation level of a pyroptosis regulator GSDME in macrophages to further probe the mechanisms of diabetic periodontitis.

Blood samples were collected from patients with diabetic periodontitis. THP-1 monocytes were induced to differentiate into macrophages by phorbol 12-myristate 13-acetate and then treated with HG to simulate periodontitis in vitro. GSDME expression of blood samples and macrophages was measured by quantitative real-time PCR. Pyroptosis was assessed by propidium iodide staining, measurement of cell viability, cytotoxicity, protein levels of inflammation factors, and pyroptosis-related proteins. O-GlcNAcylation of GSDME was analyzed using co-immunoprecipitation (co-IP), IP, and western blot.

The results showed that GSDME expression was elevated in patients with periodontitis and HG-treated macrophages. HG inhibited cell viability but increased LDH content, levels of IL-1β, IL-18, TNF-α, NLRP3, GSDMD, and Caspase-1, indicating that HG promoted pyroptosis of macrophages, which was reversed by GSDME knockdown. HG treatment increased O-GlcNAcylation in macrophages. Mechanically, GSDME interacted with OGT, and OGT knockdown suppressed O-GlcNAcylation of GSDME at Ser (S)339 site. Knockdown of OGT inhibited pyroptosis in HG-treated macrophages, while GSDME overexpression partially reversed this inhibition.

HG treatment enhanced OGT-mediated GSDME O-GlcNAcylation, thereby augmenting pyroptosis in LPS-induced macrophages. These results may provide a novel sight for the treatment of periodontitis.

Background: The oral microbiota is the second largest microbial community in humans. It contributes considerably to microbial diversity and health effects, much like the gut microbiota. Despite physical and chemical barriers separating the oral cavity from the gastrointestinal tract, bidirectional microbial transmission occurs between the two regions, influencing overall host health. Method: This review explores the intricate interplay of the oral-gut-brain axis, highlighting the pivotal role of the oral microbiota in systemic health and ageing, and how it can be influenced by diet. Results: Recent research suggests a relationship between oral diseases, such as periodontitis, and gastrointestinal problems, highlighting the broader significance of the oral-gut axis in systemic diseases, as well as the oral-gut-brain axis in neurological disorders and mental health. Diet influences microbial diversity in the oral cavity and the gut. While certain diets/dietary components improve both gut and oral health, others, such as fermentable carbohydrates, can promote oral pathogens while boosting gut health. Conclusions: Understanding these dynamics is key for promoting a healthy oral-gut-brain axis through dietary interventions that support microbial diversity and mitigate age-related health risks.

The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established. However, the underlying molecular mechanisms remain unclear. Diabetic retinopathy (DR) is an important complication of diabetes, but there are few studies on the relationship between DR and periodontitis, especially on the intrinsic inflammatory pathway mechanism. This article reviews the latest clinical data on how diabetes promotes susceptibility to periodontitis from the epidemiological and molecular perspectives, with a special focus on the key roles of systemic inflammation and endothelial dysfunction in the interplay between DR and periodontitis. Comprehension of the intertwined pathogenesis of DR and periodontitis can better guide the development of comprehensive management strategies for glycemic control and periodontal health, with the aim of mitigating the progression of DR and enhancing overall well-being.

Bidirectional influences between senescence and inflammation are newly discovered. This study aimed to clarify the roles and mechanism of Porphyromonas gingivalis (P. gingivalis) in exacerbating senescence in human gingival fibroblasts (HGFs).

Subgingival plaque and gingivae were collected from twenty-four periodontitis patients and eighteen periodontally healthy subjects. Quantities of P. gingivalis in subgingival plaque were explored using real-time PCR and the expressions of p53, p21 and SIRT6 in gingivae were detected by IHC. Moreover, senescence in HGFs was induced by P. gingivalis lipopolysaccharide (LPS) and the expressions of senescence-related β-galactosidase (SA-β-gal), p53, p21 and senescence-associated secretory phenotype (IL-6 and IL-8) with or without treatment by SIRT6 activator UBCS039 were explored by IHC, western blot and ELISA, respectively. In addition, the levels of SIRT6, Nrf2, HO-1 and reactive oxygen species (ROS) were examined by western blot and flow cytometry.

Quantities of P. gingivalis in subgingival plaque and semi-quantitative scores of p53 and p21 in gingivae of periodontitis patients were increased compared with healthy controls (p < 0.05), while SIRT6 score in periodontitis patients was decreased (p < 0.001). Quantities of P. gingivalis were positively correlated with p53 and p21 scores (0.6 < r < 0.9, p < 0.01), and negatively correlated with SIRT6 score (-0.9 < r<-0.6, p < 0.01). Moreover, P. gingivalis LPS increased the levels of SA-β-gal, p53, p21, IL-6, IL-8 and ROS and decreased the levels of SIRT6, Nrf2 and HO-1 in HGFs, which was rescued by UBCS039 (p < 0.05).

P. gingivalis LPS could induce senescence of HGFs, which could be reversed by SIRT6 via Nrf2-HO-1 signaling pathway.

Periodontitis and diabetes mellitus exhibit a bidirectional relationship. This narrative review descriptively outlines the role of chlorhexidine in the periodontal treatment of diabetic patients, focusing on its antimicrobial mechanisms against microbial communities and its antiplaque effects. Although chlorhexidine is proven to be effective in combating microbial presence and improving gingivitis with substantial supporting evidence, its impact on glycemic control and insulin resistance in diabetic patients remains contentious. Additionally, the effectiveness of chlorhexidine as an adjunctive chemotherapeutic in the periodontal treatment of gestational diabetes has not yet been studied, highlighting a gap in research that necessitates further prospective studies and randomized controlled trials. Considering the interconnection between periodontal inflammation and glycemic levels, this article finally advocates for collaborative care between dental and medical professionals to manage periodontitis in diabetic patients effectively.

This pilot randomized controlled clinical trial compares the clinical outcome obtained in persistent periodontal pockets during 9-month follow-up of supportive periodontal step 4 treatment performed by either combining subgingival instrumentation with adjunctively used sodium hypochlorite/amino acid gel and crosslinked hyaluronic acid (xHyA) or subgingival instrumentation alone.

Study protocol is registered under NCT06438354 at Clinicaltrials.gov. Patients seeking further therapy after completed step 2 non-surgical periodontal treatment underwent either repeated subgingival instrumentation with adjunctive application of sodium hypochlorite/amino acid gel and crosslinked hyaluronic acid (group A) or repeated subgingival instrumentation alone (group B). One calibrated investigator performed the treatment sequence in both groups accordingly. Subgingival instrumentation of the residual pockets was carried out under local anaesthesia using hand- and ultrasonic instruments, as well as air polishing in both groups. Patients were instructed to continue oral hygiene without any restriction. At 3-month re-evaluation treatment was repeated accordingly at sites with persistent 5 mm probing depth and BoP + . Clinical attachment level (CAL), pocket probing depth (PPD), gingival recession (GR), and bleeding on probing (BoP) were recorded at baseline (T1), 3- (T2) and 9-month (T3) post-op, with CAL as a primary outcome measure.

In total 52 patients (20 females and 32 males, mean age 58.4 ± 2.4 years) presenting with 1448 sites which required further periodontal treatment were enrolled. Both groups exhibited homogeneity in terms of age, gender, smoking habit, initial number of sites, and BOP. At 9-month evaluation, PD reduction and CAL gain showed significant differences between the test and control group, favouring the adjunctive treatment. GR tended to exhibit more recovery in the test group compared to the control group. Although BOP frequency effectively reduced in both groups, there was no statistically significant difference between the two groups.

Within the limits of the study, the present data indicates that, during subgingival instrumentation of persistent pockets, the adjunctive usage of sodium hypochlorite/amino acid gel and xHyA sufficiently improves the clinical outcomes. The continuous improvement of CAL in association with the GR scores observed in group A, indicates that sites subjected to adjunctive treatment may indicate a tendency for a regenerative response to treatment within the 9-month follow-up period.

Cardiovascular diseases (CVD) is the major cause of mortality globally, with increasing evidence suggesting a link between periodontitis, and CVD. This study aims to explore the association between periodontitis and CVD, and the impact of periodontal therapy on cardiovascular health.

This review synthesized findings from preclinical and clinical studies, without publication year restrictions, examining periodontitis and CVD through various lenses. Scientific databases were inspected with keywords related to periodontitis and CVD.

The review identifies a substantial association between periodontitis and an increased risk of several CVD, supported by both epidemiological and interventional studies. Results suggest the complexity of the relationship, influenced by factors like the severity of periodontitis and the presence of other systemic conditions. Clinical data indicates that periodontal therapy, particularly non-surgical periodontal therapy, may reduce systemic inflammatory markers and thus may play a role in the primary and secondary prevention of CVD events, highlighting the potential of periodontal therapy to not only maintain oral health but also to modulate cardiovascular risk factors.

Current evidence supports a significant association between periodontitis and increased cardiovascular risk, promoting integrated healthcare approaches that consider oral health as a key-component of cardiovascular care and wellbeing.

This study aimed to compare several potential mouthrinse biomarkers for periodontitis including active matrix-metalloproteinase-8 (aMMP-8), total MMP-8, and other inflammatory biomarkers in diagnosing and monitoring the effects of nonsurgical periodontal therapy. Thirteen patients with stage III/IV periodontitis were recruited, along with thirteen periodontally and systemically healthy controls. These 13 patients were representative of the number of outpatients visiting any dentist in a single day. Full-mouth clinical periodontal parameters and biomarkers (the aMMP-8 point-of-care-test [POCT], total MMP-8, tissue inhibitor of MMPs (TIMP)-1, the aMMP-8 RFU activity assay, Myeloperoxidase, PMN elastase, calprotectin, and interleukin-6) were recorded at baseline and after nonsurgical therapy at 6 weeks. The aMMP-8 POCT was the most efficient and precise discriminator, with a cut-off of 20 ng/mL found to be optimal. Myeloperoxidase, MMP-8's oxidative activator, was also efficient. Following closely in precision was the aMMP-8 RFU activity assay and PMN elastase. In contrast, the total MMP-8 assay and the other biomarkers were less efficient and precise in distinguishing patients with periodontitis from healthy controls. aMMP-8, MPO, and PMN elastase may form a proteolytic and pro-oxidative tissue destruction cascade in periodontitis, potentially representing a therapeutic target. The aMMP-8 chair-side test with a cut-off of 20 ng/mL was the most efficient and precise discriminator between periodontal health and disease. The aMMP-8 POC test can be effectively used by dental professionals in their dental practices in online and real-time diagnoses as well as in monitoring periodontal disease and educating and encouraging good oral practices among patients.

The relationship between periodontitis and cardiovascular disease (CVD) has been extensively studied, but the role of biological aging in this relationship remains poorly understood. This study is dedicated to investigating the effect of periodontitis on the incidence of CVD and to elucidating the potential mediating role of biological aging. Furthermore, this study will seek to elucidate the causal association between periodontitis, CVD, and biological aging.

We included 3269 participants from the National Health and Nutrition Examination Survey (2009-2014) with diagnostic information on periodontitis and composite CVD events. Biological aging was evaluated by utilizing both the Klemera-Doubal method's calculated biological age (KDMAge) and phenotypic age (PhenoAge). Logistic regression, restricted cubic spline (RCS) analysis, and subgroup analysis were used for data analysis. Mediation analysis was employed to explore the mediating role of biological aging. Subsequently, Mendelian randomization (MR) analyses were performed using genome-wide association study databases to explore potential causal relationships between periodontitis, CVD, and biological aging.

Periodontitis was associated with a higher risk of CVD. Participants with periodontitis were found to have increased levels of biological aging, and elevated levels of biological aging were associated with increased CVD risk. Mediation analyses showed a partial mediating effect of biological aging (PhenoAge: 44.6%; KDMAge: 22.9%) between periodontitis and CVD risk. MR analysis showed that periodontitis played a causal role in increasing the risk of small vessel stroke, while myocardial infarction was found to increase the risk of periodontitis. In addition, reverse MR analysis showed that phenotypic aging can increase the risk of periodontitis, and there is a two-way causal relationship between CVD and biological aging.

Periodontitis is associated with an increased CVD risk, partially mediated by biological aging, with a complex causal interrelationship. Targeted interventions for periodontal health may slow the biological aging processes and reduce CVD risk.

Poor oral hygiene is associated with overall wellness, but evidence regarding associations of oral health with all-cause mortality remain inconclusive. We aimed to examine the associations of oral health with all-cause and cause-specific mortality in middle-aged and older Chinese adults.

28 006 participants were recruited from 2003-2008 and followed up until 2021. Oral health was assessed by face-to-face interview and causes of death was identified via record linkage. Cox regression yielded hazard ratios (HRs) and 95% confidence intervals (CIs) with adjustment of multiple potential confounders.

During an average of 14.3 years of follow-up, we found that a lower frequency of toothbrushing was associated with higher risks of all-cause mortality with a dose-response pattern (P for trend <0.001). Specially, the adjusted HR (95% CI) (vs. ≥ twice/d) was 1.16 (1.10, 1.22) (P < 0.001) for brushing once/d and 1.27 (1.00, 1.61) (P = 0.048) for < once/d. Similar associations were also found for cardiovascular disease (CVD), stroke, and respiratory disease mortality, but not for ischemic heart disease (IHD) and cancer mortality. A greater number of missing teeth was also associated with higher risks of all-cause, CVD, stroke, and respiratory disease mortality with a dose-response pattern (all P for trend <0.05). The association of missing teeth with all-cause mortality was stronger in lower-educated participants.

Both less frequent toothbrushing and a greater number of missing teeth were associated with higher risks of all-cause, CVD, stroke, and respiratory disease mortality, showing dose-response patterns, but not with IHD and cancer mortality. Moreover, the dose-response association of missing teeth with all-cause mortality was stronger in lower-educated participants.

(1) Background: This cross-sectional investigation appreciated the role of serum C-reactive protein (CRP), several hematologic-cell markers, and salivary inflammation-related molecules [calprotectin (S100A8/A9), interleukin-1β (IL-1β), kallikrein] to predict periodontitis in patients with atherosclerotic cardiovascular disease (ACVD), arrhythmia, or both. Also, we appreciated the relationship between the inflammatory burden and periodontal destruction with the type of cardiac pathology. (2) Methods: Demographic, behavioral characteristics, periodontal indicators, blood parameters, and saliva samples were collected. (3) Results: All 148 patients exhibited stage II or III/IV periodontitis. Stage III/IV cases exhibited significantly increased S100A8/A9 levels (p = 0.004). A positive correlation between S100A8/A9 and IL-1β [0.35 (<0.001)], kallikrein [0.55 (<0.001)], and CRP [0.28 (<0.001)] was observed. Patients with complex cardiac involvement had a significantly higher number of sites with attachment loss ≥ 5 mm [19 (3-30)] compared to individuals with only arrhythmia [9 (3.25-18)] or ACVD [5 (1-12)] [0.048♦ {0.162/0.496/0.14}]. (4) Conclusions: Severe, extensive attachment loss may be indicative of patients with complex cardiac conditions, which underscores the essential role of periodontal status in relation to systemic diseases. The correlations between the rising trends of the inflammatory parameters suggest a potential interconnection between oral and systemic inflammation.

Conduct a bibliometric analysis to review the knowledge structure and research trends regarding the association between periodontal disease and cardiovascular disease (CVD).

The Web of Science Core collection database was searched for retrieving publications related to periodontitis and CVD between January 1, 2003 and December 31, 2022. The VOSviewer, CiteSpace, and R software package "bibliometrix" were employed for the bibliometric analysis.