Background: Examinations on blood samples and gingival crevicular fluid of subjects with chronic periodontitis showed that smoking increased production of cytokines.
Objective: To evaluate the expression of immune markers on mononuclear inflammatory cell infiltrate at periodontitis and healthy tissue among smoking and non-smoking subjects.
Methods: This case-control study was performed on 41 patients who referred to a clinic of periodontology at a Mashhad dental school in Iran in 2016. The participants were all of Iranian Khorasanian ethnicity with age range of 35-65 years. Gingival biopsies were obtained during routine periodontal flap procedure. Immunohistochemistry using markers of CD20, CD3, CD68, and CD45RO was carried out. Data was analyzed by SPSS version 15, using one-way ANOVA and Tukey HSD test.
Results: Nonsmoker subjects showed significantly greater numbers of CD20+, CD68+, CD3+ cells compared to smoker subjects, both at healthy and periodontitis tissue biopsies (p<0.00), whereas there was no significant difference in terms of CD45RO (p=0.120).
Conclusion: Cigarette smoking, results in infiltrative mononuclear chronic inflammatory cells reduction in connective periodontium.
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http://dx.doi.org/10.19082/4961 | DOI Listing |
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Department of Materials Engineering, Isfahan University of Technology, Isfahan 84156-83111, Iran.
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Cardiovascular Center, College of Medicine, University of Cincinnati, Ohio-45267, United States of America; School of Chemical and Biotechnology, SASTRA Deemed University, Tirumalaisamudram, Thanjavur-613401, Tamil Nadu, India. Electronic address:
Multiple forms of cell death contribute significantly to cardiovascular pathologies, negatively impacting cardiac remodeling and leading to heart failure. While myocardial cell death has been associated with PM induced cardiotoxicity, the temporal dynamics of various cell death forms, such as apoptosis, ferroptosis, necroptosis, and pyroptosis, in relation to inflammatory processes, remain underexplored. This study examines the time-dependent onset and progression of these cell death pathways in the myocardium and their correlation with inflammation in a Wistar rat model.
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