GCF Levels of Osteoclastogenesis-Related Cytokines in Periodontitis in Relation to Smoking During Non-Surgical Periodontal Therapy

Abstract

Objective: Interleukins (IL) -1β, -34, receptor activator of nuclear factor-kB ligand (RANKL), and osteoprotegerin (OPG) play a crucial role in osteoclastogenesis and bone resorption through modulating inflammatory processes and osteoclastogenesis. Smoking is the major risk factor in the initiation and progression of the periodontitis, and adversely affects the outcomes of non-surgical periodontal therapy. To date, there is no study investigating both gingival crevicular fluid (GCF) IL-1β, IL-34, RANKL, and OPG levels before and after non-surgical periodontal therapy in smoking and non-smoking patients with periodontitis stage 3, grade B and C. The aim of current research was to examine the GCF levels of some osteoclastogenesis-related cytokines in periodontitis in relation to smoking before and after periodontal therapy. Methods: At baseline, full-mouth periodontal status together with GCF samples were collected from 116 individuals, including 60 periodontitis patients (30 smokers and 30 nonsmokers) and 56 periodontally healthy controls (28 smokers and 28 nonsmokers). Non-surgical periodontal therapy, consisting of instruction for daily plaque control and scaling and root planing (SRP), was performed. GCF sampling and full-mouth periodontal measurements were repeated 6 weeks after completion of SRP. The GCF levels of biomarkers were measured by enzyme-linked immunosorbent assay. Results: The periodontitis groups exhibited significant improvement in clinical parameters. At baseline, the GCF IL-1β levels in periodontitis groups were significantly higher than periodontally healthy controls (p<0.05) and it was significantly decreased in periodontitis groups after non-surgical periodontal therapy. At baseline, the GCF IL-34 levels in periodontitis groups were significantly higher than periodontal healthy controls(p<0.05) and the GCF IL-34 level was significantly decreased in non-smoking periodontitis patients. At baseline and after periodontal therapy, the GCF RANKL levels were similar in all groups. The GCF OPG level was significantly lowest in non-smoking periodontitis patients at baseline and the GCF OPG level was significantly increased in smoking and non-smoking periodontitis patients after non-surgical periodontal therapy. Conclusion: In the periodontal inflammation process, GCF IL-34 level followed a similar pathway to GCF IL-1β, suggesting that IL-34 may be a marker in the pathogenesis of periodontal disease. The significant decrease in GCF IL-34 and a significant increase in GCF OPG level in the non-smoker periodontitis group after periodontal therapy suggest the negative effect of smoking on the response to periodontal therapy. More comprehensive studies are needed by increasing the number of samples included in the study groups in order to better understand the pathogenesis of periodontitis.