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Effects of smoking on the gingival crevicular fluid levels of interleukin‐17A, interleukin‐17E, and oxidative stress following periodontal treatment process
Author(s) -
Lütfioğlu Muge,
Sakallıoğlu Umur,
Sakallıoğlu Eser Elif,
Özden Feyza O.,
Ürkmez Sebati Sinan,
Bilgici Birsen
Publication year - 2021
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12831
Subject(s) - medicine , periodontitis , oxidative stress , chronic periodontitis , gastroenterology , interleukin , interleukin 6 , dentistry , interleukin 17 , inflammation , cytokine
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.