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Background: Periodontitis is associated with increased oxidative stress, which may impair treatment outcomes. Ozone therapy has shown promise in reducing oxidative stress and improving periodontal health. This study examined the impact of adjunctive gaseous ozone administration on salivary oxidative stress markers in patients with periodontitis stages II–IV and grades A–C undergoing non-surgical periodontal treatment (NSPT). Methods: Ninety patients with periodontitis were randomly allocated to either the test group (NSPT with gaseous ozone administration) or the control group (NSPT alone) using computer-generated randomization. The OzoneDTA system was used to deliver ozone at 2100 ppm for 60 s per site once weekly for 4 weeks. Clinical periodontal parameters (probing depth [PD], clinical attachment level [CAL], plaque index [PI], gingival index [GI]) and salivary oxidative stress markers (malondialdehyde [MDA], total antioxidant capacity [TAC], superoxide dismutase [SOD]) were assessed by blinded examiners at baseline, 3, and 6 months post-treatment. Results: Mixed ANOVA revealed significant three-way interactions between time, treatment, and stage or grade for clinical and biochemical measures (p < 0.001). The test group exhibited significant improvements in TAC (mean difference: 0.45 ± 0.12 mmol/L, p = 0.002), MDA (−0.38 ± 0.09 nmol/mL, p = 0.001), and SOD (65 ± 18 U/mL, p < 0.001) compared with the control group, with more pronounced effects in stages III and IV. Large effect sizes (Cohen's d > 0.8) were observed for the test group between baseline and 6 months for all markers. Conclusions: Gaseous ozone administration as an adjunct to NSPT can effectively improve clinical periodontal parameters and salivary oxidative stress markers, particularly in stages III and IV periodontitis. The enhanced outcomes may be attributed to ozone's antimicrobial and immunomodulatory properties, which synergistically reduce oxidative stress and promote periodontal healing. [ABSTRACT FROM AUTHOR]

Background: Periodontitis, a chronic inflammatory disease, has been associated with an elevated risk of cardiovascular disease (CVD). Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has emerged as a potential biomarker linking periodontitis, endothelial dysfunction, and CVD. This systematic review aimed to synthesize the existing evidence on the relationship between ADMA, periodontitis, and CVD, and to evaluate ADMA's potential as a biomarker for periodontal disease progression and its correlation with endothelial dysfunction. Methods: A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science databases from their inception to March 2023. Observational and interventional studies assessing ADMA levels in patients with periodontitis and/or CVD were included. The methodological quality of the included studies was evaluated using the NIH Quality Assessment Tools. Due to the heterogeneity of the included studies, a qualitative synthesis was performed. Results: Cross-sectional studies consistently demonstrated significantly elevated ADMA levels in patients with periodontitis and CVD compared to healthy controls. The prospective cohort study indicated that successful periodontal treatment was associated with a significant reduction in ADMA levels and concomitant improvement in endothelial function. The pilot cohort study reported a significant decrease in ADMA levels following periodontal therapy in patients with chronic kidney disease. However, the randomized controlled trials did not demonstrate significant alterations in ADMA levels or endothelial function subsequent to periodontal treatment in patients with periodontitis alone. Conclusions: Periodontal treatment may effectively reduce ADMA levels and improve endothelial function, particularly in patients with comorbidities. These findings suggest that ADMA is a promising biomarker linking periodontitis, endothelial dysfunction, and CVD. However, the limitations of this study include the small number of studies, heterogeneity in the study designs, and a lack of long-term follow-up data. Further high-quality, longitudinal studies are required to confirm its clinical utility and elucidate the underlying mechanisms of these relationships. The integration of periodontal care into CVD prevention and management strategies warrants consideration, as it may contribute to mitigating the cardiovascular risk associated with periodontitis. [ABSTRACT FROM AUTHOR]

Background: Local eradication of periodontal infection could potentially have a much broader impact on the diabetic condition by also contributing to the modification of the lipid profile, which is directly compromised in the alteration of endothelium-dependent vasodilation. The aim of this trial was to assess the benefits of intensive periodontal treatment (IPT) on the lipid profile and endothelial function of diabetic patients. Methods: This was a 6-month, randomized controlled trial involving diabetic patients with generalized periodontitis. The study group comprised 290 individuals who were randomly assigned to receive Intensive Periodontal Treatment (IPT, Intervention Group) or conventional adult prophylaxis (Control Periodontal Treatment, CPT, Control Group). Outcomes encompassed lipid profile involving serum total cholesterol, serum triglyceride, low-density lipoprotein cholesterol, high-density lipo-protein cholesterol, and flow-mediated vasodilation (FMD) as an index of endothelium-dependent vasodilation (primary outcomes); periodontal indices and high-sensitive C-reactive protein were evaluated at baseline, 3 and 6 months after periodontal treatment. Results: An increase in endothelium-dependent flow-mediated dilatation (FMD) was observed in the Intensive Periodontal Treatment group in comparison with Control (p < 0.001), but results are not statistically different. There were no differences in lipid profile in individuals of both groups. Conclusions: An intensive periodontal treatment might improve endothelial function, suggesting a direct beneficial effect on the vasculature, possibly mediated by systemic inflammatory reduction. However, no statistically significant differences between groups were observed, and no benefits were proved on lipid profile. [ABSTRACT FROM AUTHOR]

Background: Endothelial dysfunction is one of the early pathogenic events of the atherosclerotic process. Severe periodontitis is considered to be an independent contributing risk factor for the pathophysiology of endothelial dysfunction. High blood concentration of asymmetric dimethylarginine (ADMA), an L-arginine analogue that inhibits nitric oxide (NO) formation, has emerged as one of the most powerful independent risk predictors of cardiovascular disease. Abrogation of periodontal inflammation might have clinical relevance, affecting the ADMA. Insufficient clinical evidence exists for drawing clear conclusions regarding the long-term effects of periodontal disease on endothelial function, and even less evidence is available specifically on ADMA concentrations and their relationship with periodontitis. The objective of this study was to evaluate the effects of intensive periodontal treatment in modulating the endothelial function via the assessment of plasma ADMA concentration in patients diagnosed severe periodontitis. Methods: This was a 6-month randomized controlled trial, including 140 patients between 41 and 63 years old who were diagnosed with severe periodontitis, free from cardiovascular disease (CVD), and had traditional cardiovascular risk factors. All patients underwent a complete medical and clinical periodontal examination, a laboratory analysis of ADMA, and an ultrasound assessment of FMD of the right brachial artery. After the screening, they were randomly assigned to receive either intensive periodontal treatment (test group, n = 70) or community-based periodontal care (control group, n = 70). A full examination was carried out at baseline, 3 and 6 months after the periodontal treatment. Results: A total of 236 individuals diagnosed with periodontitis were screened. One hundred forty participants were enrolled. No statistically significant difference was observed over the time in ADMA concentration after the intensive periodontal treatment within the test group. No differences were revealed between the groups in the ADMA concentration at baseline and during follow-up. Conclusions: Intensive periodontal treatment does not affect the plasma levels of ADMA in patients without any risk for cardiovascular disease. [ABSTRACT FROM AUTHOR]