Publication: Effects of Smoking on the Gingival Crevicular Fluid Levels of Interleukin-17A, Interleukin-17E, and Oxidative Stress Following Periodontal Treatment Process
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Abstract
Objective and background: How smoking affects periodontal inflammation and healing still needs to be revealed with all its mechanisms. In this study, the gingival crevicular fluid (GCF) levels of: (a) interleukin-17A (IL-17A) and interleukin-17E(IL-17E) with their ratios and (b) oxidative stress by means of total oxidative stress (TOS), total anti-oxidant capacity (TAOC), and their ratios as the oxidative stress index (OSI) were evaluated and compared for smoking and non-smoking periodontitis patients after a periodontitis management process including both the non-surgical and surgical treatments. Materials and methods: Fifteen smoker and 15 non-smoker generalized periodontitis patients as 2 distinct groups participated in the study. Conventional clinical and radiographical examinations were utilized for the periodontitis diagnosis. The clinical data and GCF samples were collected at baseline, 4 week after non-surgical periodontal treatment (NSPT), and 4 weeks after surgical periodontal treatment (SPT). IL-17A, IL-17E, TOS, and TAOC were determined by ELISA and Rel Assay. Results: Clinical parameters in both smokers and non-smokers improved following periodontal treatment (P < .001) and their clinical data were similar for all the examination times (baseline, NSPT, and SPT) (P > .05). Following the treatment phases, the IL-17A concentration decreased and the IL-17E concentration increased in both the smokers and non-smokers (P < .01). The total amount of IL-17A decreased while the total amount of IL-17E increased in smokers throughout NSPT and SPT (P < .01). Such an alteration was seen only at SPT compared to NSPT and baseline in non-smokers (P < .01). The concentration and total amount of IL-17A were higher at baseline, and the concentration and total amount of IL-17E were lower at all examination time points in non-smokers as compared to smokers (P < .01). The 17A/E ratio decreased in both groups following the treatment phases and was higher in smokers at all the examination times (P < .01). TOS were higher and TAOC were lower in smokers versus non-smokers at all the time points, but the differences were significant only for TOS levels (P < .01). Throughout the treatment phases, the concentration and total amount of TOS decreased in smokers(P < .01) and only the total amount of TOS decreased in non-smokers (P < .01). The concentration and total amounts of TAOC increased throughout the treatments in both smokers and non-smokers without significant changes (P > .05). The baseline OSI was higher in smokers, and it decreased only in smokers following the treatment phases (P < .01). Conclusions: Smoking and periodontal inflammation were found to alter IL-17A, IL-17E, and oxidant/anti-oxidant statuses in periodontitis patients. The intra-group assessments in smokers demonstrated more apparent alterations in the oxidant/anti-oxidant statuses and IL-17A and IL-17E levels after periodontitis management.
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Bilgici, Birşen/0000-0001-7783-5039; Otan Özden, Feyza/0000-0003-3258-3979; Ürkmez, Sebati Sinan/0000-0002-8821-1835; Lutfioglu, Muge/0000-0003-1499-5902;
Citation
WoS Q
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Scopus Q
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Source
Journal of Periodontal Research
Volume
56
Issue
2
Start Page
388
End Page
396
