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There is a postulated association of periodontitis with a number of human cancers. This narrative review provides current epidemiological evidence on the association between periodontitis and cancer. A PubMed search with the relevant keywords (periodontal disease, periodontitis, cancer, and malignancy) was completed to identify relevent articles. We present a narrative review on the association between periodontal disease and a range of cancers, including oral cancer, stomach and esophageal cancer, colorectal cancer, lung cancer, pancreatic cancer, prostate cancer, hematological malignancies, liver cancer, breast cancer, and ovarian cancer. While there is a considerable body of epidemiological evidence that supports the association between periodontal disease and cancer, this is largely from cohort and case–control studies and the association may therefore be circumstantial as little evidence exists in the form of treatment trials that would validate the role of periodontal disease in the process of cancer initiation and development. [ABSTRACT FROM AUTHOR]

Background: Growing evidence suggests the type of periodontal treatment could differentially influence the reduction of key cardiovascular risk mediators in periodontitis patients. This randomized, controlled clinical trial compared the impact of minimally invasive non‐surgical therapy (MINST) with quadrant‐wise subgingival instrumentation (Q‐SI) on C‐reactive protein (CRP) together with lipoprotein‐associated phospholipase A2 (Lp‐PLA2) levels, and clinical periodontal outcomes in patients with periodontitis. Moreover, it was evaluated if baseline CRP levels impacted the efficacy of non‐surgical periodontal therapy protocols. Methods: Forty‐two periodontitis patients were enrolled and randomly treated by means of MINST (n = 21) or Q‐SI (n = 21). The outcomes assessed were serum CRP and Lp‐PLA2, and periodontal parameters (probing depth [PD], clinical attachment level [CAL], full‐mouth bleeding score [FMBS]), at baseline and at follow‐ups at 1, 3, and 6 months and at 1 year after treatment. Results: At 1 year, MINST significantly reduced, among others, mean PD (p = 0.007), mean CAL (p = 0.007), the number of pockets >4 mm (p = 0.011) and ≥6 mm (p = 0.005), and FMBS (p = 0.048) compared to Q‐SI. Generalized multivariate analysis evidenced that high baseline CRP (p = 0.039) and FMBS (p = 0.046) levels, together with MINST treatment (p = 0.007) were significant predictors of PD reduction at 1‐year follow‐up. Moreover, the Jonckheere–Terpstra test showed that patients with high baseline CRP levels gained more benefits from MINST treatment at 1‐year follow‐up than they did from Q‐SI. Conclusion: Patients receiving MINST showed a greater reduction in CRP levels than patients with Q‐SI after 1 year of follow‐up. Moreover, patients with high baseline levels of CRP and Lp‐PLA2 gained more benefits from the MINST approach at 1‐year follow‐up. [ABSTRACT FROM AUTHOR]

Objective: Periodontitis is an inflammatory oral disease that occurs as a result of the damaging effects of the immune response against the subgingival microflora. Among the mechanisms involved, the nucleotide‐binding oligomerization domain, leucine‐rich repeat‐containing proteins family member NLRP3 (NLR family pyrin domain‐containing 3), proposed as the key regulator of macrophage‐induced inflammation, is strongly associated with periodontal disease due to the bacterial activators. This paper aimed to present key general concepts of NLRP3 inflammasome activation and regulation in periodontal disease. Method: A narrative review was conducted in order to depict the current knowledge on the relationship between NLRP3 inflammasome activity and periodontal disease. In vitro and in situ studies were retrieved and commented based on their relevance in the field. Results: The NLRP3 inflammasome activity stimulated by periodontal microbiota drive periodontal disease pathogenesis and progression. This occurs through the release of proinflammatory cytokines IL‐1β, IL‐18, and DAMPs (damage‐associated molecular pattern molecules) following inflammasome activation. Moreover, the tissue expression of NLRP3 is dysregulated by oral microbiota, further exacerbating periodontal inflammation. Conclusion: The review provides new insights into the relationship between the NLRP3 inflammasome activity and periodontal disease pathogenesis, highlighting the roles and regulatory mechanism of inflammatory molecules involved in the disease process. [ABSTRACT FROM AUTHOR]

The article focuses on examining the relationship between periodontitis and dyslipidemia, demonstrating a direct association between both diseases. Topics include discussing the limitations of cross-sectional study design in determining the direction and temporality of the association, as well as the methodology used to investigate the relationship between periodontitis and dyslipidemia while considering confounding variables.

Background: Dyslipidemia, a silent multifactorial condition, is characterized by changes in blood lipid levels, affecting all socioeconomic strata, increasing the risk for atherosclerotic diseases. This study investigated whether there is an association between dyslipidemia and the combined exposure of periodontitis plus the number of remaining teeth, gingival bleeding, or caries. Methods: A two‐center cross‐sectional study was conducted involving 1270 individuals, with a minimum age of 18 years. Socioeconomic and demographic data, health conditions, lifestyle parameters, and anthropometric, biochemical, and oral clinical examinations were performed. The exposures considered were the presence of periodontitis, dental caries, number of remaining teeth, and gingival bleeding. The outcome was dyslipidemia as defined by the Brazilian Guidelines on Dyslipidemia and Prevention of Atherosclerosis. The combined associations between periodontitis plus other oral health conditions and dyslipidemia were estimated using confounder‐adjusted prevalence ratios (PRsingle, PRmultiple, for single and multiple covariable adjustments) with 95% confidence intervals (95% CIs), in a Poisson regression model with robust variance. Results: The occurrence of dyslipidemia was 70.1% and periodontitis was 84.1%. A positive association between periodontitis and dyslipidemia existed: PRsingle = 1.13; 95% CI: 1.01–1.26. Combined exposure of periodontitis plus <11 remaining teeth (PRmultiple = 1.23; 95% CI: 1.05–1.43), as well as combined exposure of periodontitis plus ≥10% gingival bleeding and <11 remaining teeth (PRmultiple = 1.22; 95% CI: 1.03–1.44), represented greater probabilities of 23% and 22% of individuals having a diagnosis of dyslipidemia. Conclusion: Periodontitis combined with fewer than 11 teeth doubled the likelihood of being diagnosed with dyslipidemia. [ABSTRACT FROM AUTHOR]

Over her near 60‐year career, Mirdza E. (Mitzi) Neiders has served as a teacher, dentist, researcher, mentor, role‐model, friend, and critic for thousands of faculty, students, and patients of the University at Buffalo School of Dental Medicine. One of the first women to serve on the dental school faculty, this article describes her journey and the great impact that she has made on dentistry and her community on the occasion of her retirement. [ABSTRACT FROM AUTHOR]

The possibility of patients using ventilators being infected by bacteria that cause respiratory diseases like pneumonia is discussed. of oral hygiene of such patients is highlighted.