Impact of smoking on gremlin-1, syndecan-4, and IL-1β responses to non-surgical periodontal therapy in stage 3 periodontitis: a comparative study with periodontally healthy controls

This study aimed to compare the periodontal status of periodontally healthy individuals with those of smokers and non-smokers with stage 3 periodontitis before and after treatment, as well as to investigate the levels of Gremlin-1, Syndecan-4, and IL-1β in GCF samples. Another objective of the study was to evaluate the relationship between these biomarkers and periodontitis and to assess the effects of smoking on their levels. A total of 45 volunteers, 15 smokers (Group SP) and 15 non-smokers (Group NP) diagnosed with stage 3 periodontitis between the ages of 18 and 60, and 15 healthy individuals (Group H) were included in the study. All clinical parameters of the SP and NP groups were found to be significantly higher than those of the H group before NSPT (p<0.001), and a significant reduction was observed in all clinical parameters after phase I treatment (p<0.001). Following NSPT, significant improvement was observed in all periodontal parameters in both periodontitis groups (p<0.001). Gremlin-1 levels in the SP and NP groups were statistically significantly lower after treatment compared to pre-treatment levels (p<0.05). While there was no statistically significant difference in IL-1β levels before and after treatment in the SP group (p>0.05), a statistically significant reduction was observed in the NP group after treatment (p<0.05). Similarly, no statistically significant difference was found in Syndecan-4 levels before and after treatment in the SP group (p>0.05), whereas the post-treatment measurements of the NP group were statistically significantly lower (p<0.05). After NSPT, Gremlin-1 levels in GCF decreased in both groups, whereas significant reductions in Syndecan-4 and IL-1β levels were observed only in non-smokers. These findings suggest that the regulatory effect of smoking on biomarkers may negatively influence the periodontal treatment response. Smoking is a major risk factor for periodontitis and may impair healing following nonsurgical periodontal therapy. While similar clinical improvements were observed, reductions in IL-1β and Syndecan-4 occurred only in non-smokers, whereas Gremlin-1 decreased in both groups. These findings suggest that smoking may influence molecular healing responses, and biomarker monitoring may support personalized periodontal management.