Evaluating The Salivary Cytokine Expression After Non-Surgical Periodontal Therapy In Smokers: A Clinical Followup.

Background: Smoking is a significant risk factor for periodontal disease and can influence the host's immune response. Salivary cytokines are biomarkers that reflect the inflammatory status in periodontal conditions. Non-surgical periodontal therapy (NSPT) has been shown to improve periodontal health, but its effect on salivary cytokine expression in smokers remains underexplored. This study aims to evaluate the changes in salivary cytokine levels after NSPT in smokers over a clinical follow-up period. Materials and Methods: A total of 40 smokers with moderate to severe chronic periodontitis were included in the study. Participants underwent NSPT, which included scaling and root planing. Saliva samples were collected at baseline, 3 months, and 6 months post-therapy. The levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and anti-inflammatory cytokines (IL-10) were measured using enzyme-linked immunosorbent assay (ELISA). Periodontal clinical parameters, including probing pocket depth (PPD) and clinical attachment level (CAL), were recorded at each follow-up. Results: At 3 months, there was a significant reduction in the levels of IL-1β (from 20.5 ± 2.4 pg/mL to 14.3 ± 1.8 pg/mL, p<0.05) and TNF-α (from 18.7 ± 2.3 pg/mL to 12.6 ± 1.9 pg/mL, p<0.05), along with an increase in IL-10 levels (from 5.2 ± 0.7 pg/mL to 8.9 ± 1.0 pg/mL, p<0.05). By 6 months, further reductions in IL-1β and TNF-α were observed (12.1 ± 1.5 pg/mL and 10.2 ± 1.3 pg/mL, respectively), while IL-10 levels continued to rise (10.5 ± 1.2 pg/mL, p<0.05). Improvements in periodontal parameters, with PPD reduced from 5.6 ± 0.5 mm at baseline to 3.2 ± 0.4 mm at 6 months, were also noted. Conclusion: NSPT significantly reduces pro-inflammatory salivary cytokines and enhances anti-inflammatory cytokine levels in smokers with periodontitis. These findings suggest that NSPT not only improves clinical periodontal outcomes but also modulates the local inflammatory response in smokers. [ABSTRACT FROM AUTHOR]