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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.

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]

Objective: To investigate the association between the severity of periodontitis (exposure) and dyslipidemia (outcome). Methods: This was a cross‐sectional study of users of public health services. Periodontitis was defined using the Center for Disease Prevention and Control and the American Academy of Periodontology criteria. Lipid evaluation used data on systemic biomarkers. Dyslipidemia diagnosis was based on the Guidelines of total cardiovascular risk of the World Health Organization. Weight, height, waist circumference, and blood pressure were measured, and socioeconomic–demographic, lifestyle behavior factors, general and oral health conditions of the participants were collected. Hierarchical and logistic regression analyzes were used to determine the association between the exposures and the outcome. Odds Ratios, unadjusted and adjusted, and 95% confidence intervals were estimated. Results: Of 1,011 individuals examined, 75.17% had dyslipidemia, and 84.17% had periodontitis, 0.2% with mild, 48.56% moderate, and 35.41% severe disease. The association between periodontitis and dyslipidemia was maintained through hierarchical analysis and in the multiple regression modeling, showing that the occurrences of dyslipidemia in the group with periodontitis, and its moderate and severe levels, were, respectively, 14%, 30%, and 16% higher compared with those without periodontitis. Conclusions: The results showed a positive association between moderate and severe periodontitis and dyslipidemia. [ABSTRACT FROM AUTHOR]

Objective: To conduct a systematic review and meta‐analysis to evaluate the recent scientific literature addressing the association between periodontitis and asthma, chronic obstructive pulmonary disease (COPD), and pneumonia. Materials and Methods: The search for studies was carried out using MEDLINE/PubMed, EMBASE, Lilacs, Web of Science, Scopus, and SciELO databases, including the gray literature (ProQuest). Reference lists of selected articles were also searched. Studies having varying epidemiological designs assessing the association between periodontitis and respiratory diseases in human subjects were eligible for inclusion. Three independent reviewers performed the selection of articles and data extraction. Fixed and random effects meta‐analysis were performed for the calculation of the association measurements (Odds Ratio—OR) and 95% confidence intervals (95% CI). Results: A total of 3,234 records were identified in the database search, with only 13 studies meeting the eligibility criteria and 10 studies contributed data for meta‐analysis. Using a random effects models periodontitis was associated with asthma: ORadjusted: 3.54 (95% CI: 2.47–5.07), I2 = 0%; with COPD: OR adjusted: 1.78 (95% CI: 1.04–3.05), I2 = 37.9%; and with pneumonia: OR adjusted: 3.21 (95% CI: 1.997–5.17), I2 = 0%. Conclusions: The main findings of this systematic review validated an association between periodontitis and asthma, COPD and pneumonia. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the association between periodontitis and severe asthma, with participants in treatment for severe asthma, controlled by therapy. Methods: A case–control investigation was performed to compare 130 adults with severe asthma with 130 without asthma. Individuals with periodontitis were those with ≥4 teeth with ≥1 site with probing depth ≥4 mm, clinical attachment level ≥3 mm, and bleeding upon probing at the same site. Severe asthma diagnosis was based on Global Initiative for Asthma criteria. Results: Association between exposure to periodontitis and severe asthma was found: ORcrude = 2.98 (95% CI: 1.74–5.11). When confounders were considered, the association between exposure to periodontitis and severe asthma was maintained: ORadjusted = 3.01–3.25. Individuals with periodontitis had about a threefold increased risk of severe asthma than those without periodontitis. Frequency of periodontitis in participants with severe asthma was greater than that of those without asthma (46.6% vs 22.3%, p ≤ .05). Conclusions: Association between periodontitis and severe asthma was observed. Further investigation is required to determine the direction of this relationship. It may be causal, but it may also be a consequence of the immunopathological process that characterizes asthma, or else, consequence of the medication used for treatment. [ABSTRACT FROM AUTHOR]