Effect of Non surgical Periodontal Treatment on Gingival Crevicular Fluid Interleukin-1beta and Interleukin-37 in Different Periodontal Diseases

Objective: Interleukin-37 (IL-37), which is a natural inhibitor of innate immunity, is correlated with chronic inflammation and some autoimmune diseases. Proinflammatory cytokines, for example, interleukin-1beta (IL-1 beta), which plays a key part in the periodontium, can induce IL-37. This study aimed to investigate the effect of non-surgical periodontal treatment on gingival crevicular fluid (GCF) IL-37 and IL-1 beta levels in generalized aggressive periodontitis (G-AgP) and generalized chronic periodontitis (GCP). Materials and Methods: Thirty-five patients with G-AgP, 30 patients with GCP and 30 volunteers with healthy periodontal status (C) were included in this research. Patient groups received scaling and root planning with periodontal hand instrumentations. Clinical periodontal parameters and GCF samples were collected at baseline and at six weeks following SRP. Biomarker levels in GCF were analysed by enzyme-linked immunosorbent assay. Results: Both periodontitis groups exhibited significant improvement in clinical parameters (p<0.05). GCF IL-37 levels were significantly higher in G-AgP and GCP groups than in the C group at baseline (p<0.05). Following periodontal treatment, GCF IL-37 levels were decreased and comparable in all groups. The GCF IL-1 beta levels were significantly higher at baseline in the G-AgP group than those in GCP and C groups, and after periodontal therapy, a decrease was detected in GCF IL-1 beta levels. GCF levels of IL-1 beta were positively correlated with GCF IL-37 levels. Conclusion: Clinical improvement was found in both periodontitis groups after periodontal treatment. IL-1 beta is a key regulator of periodontal inflammation and bone resorption. According to the results of our research, IL-37 may be useful marker of determining the clinical health and disease status of patients with periodontitis. However, further studies are required to determine the mechanism of IL-37 in periodontal inflammation.