Value of Gingival Crevicular Fluid Levels of Biomarkers IL-1 β, IL-22 and IL-34 for the Prediction of Severity of Periodontal Diseases and Outcome of Non-Surgical Periodontal Treatment

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Number of pages: 24-30
Year-Number: 2022-Volume: 4 Issue: 1

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Abstract

Interleukins (IL) -1β, -22 and -34 play a crucial role in osteoclastogenesis and bone resorption through modulating inflammatory processes and osteoclastogenesis. To date, there is no study investigating both gingival crevicular fluid (GCF) ILs -22 and -34 levels before and after non-surgical periodontal treatment in patients with aggressive periodontitis (AgP) and chronic periodontitis (CP). We aimed to examine the relationship of GCF levels of biomarkers IL-1 β, IL-22 and IL-34 with the clinical evidence of periodontal tissue breakdown and alveoler bone resorption and to determine the value of these biomarkers for the prediction of severity of periodontal diseases and outcome of non-surgical periodontal treatment. Thirty-five AgP patients, 30 CP patients and 30 periodontally healthy volunteers (C) were included in this research. The AgP and CP patients underwent scaling and root planning interventions, performed with periodontal hand instruments. Clinical findings and GCF samples was collected at baseline and 6 weeks later. The GCF ILs were measured by ELISA. The AgP and CP groups exhibited significant improvement in clinical parameters. The GCF ILs -1β, -22, and -34 levels were significantly higher in the CP group compared to the C group at baseline. The GCF levels of these parameters were decreased in CP group after treatment. The ILs -22 and -34 levels were lower in AgP patients at baseline, they increased after treatment. In accordance with clinical improvement of CP patients, the ILs -22 and -34 levels in GCF decreased meaningfully; however, ILs -22 and -34 were lower in AgP patients at baseline and later there were increased after treatment although IL-1β was found higher at first measurement and later it decreased. These findings require further studies to elucidate the mechanisms involved in the regulation of ILs -22 and -34 in the pathogenesis of AgP.

 

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