Comparison of Sclerostin Levels in Gingival Crevicular Fluid before and after Nonsurgical Therapy in Smokers and Nonsmokers with Chronic Periodontitis

This is the authors' abstract. We don't add key points for this paper.

This study aims to assess gingival crevicular fluid levels of sclerostin before and after nonsurgical periodontal therapy in smokers and nonsmokers with chronic generalized periodontitis. Materials and methods: Subjects with generalized chronic periodontitis were divided into two groups: Group I-nonsmokers with chronic periodontitis (n = 18) and group II-smokers with chronic periodontitis (n = 18). Baseline clinical parameters were recorded and a GCF sample was collected for assessment of sclerostin levels. All the patients received nonsurgical periodontal therapy. GCF sampling and clinical periodontal measurements were repeated 4 weeks after completion of SRP. Sclerostin levels were analyzed using an enzyme-linked immunosorbent assay (HUMAN SOST ELISA KIT). The data were tested statistically by the Student's t-test: Intragroup analysis was done using paired t-test and intergroup was done using independent t-test. Results: Probing pocket depth and clinical attachment loss were decreased significantly in both smokers and nonsmokers after nonsurgical therapy. The levels of sclerostin were higher in the smoker group when compared with nonsmokers. The mean sclerostin levels in smokers and nonsmokers at baseline were 354 141 and 164.87 59.8 pg/mL, respectively. There is a significant decrease in sclerostin levels from (164-136 pg/mL) in nonsmokers after nonsurgical therapy (p = 0.001). Conclusion: Sclerostin levels were significantly higher in smokers when compared with nonsmokers at the baseline and exhibited persistent higher levels even after periodontal therapy in smokers. Clinical significance: Sclerostin is an osteocyte secreted soluble antagonist of the wnt/ catenin signaling pathway which is a requisite for osteoblast development and osteogenesis. Increased sclerostin levels in smokers increase and hasten periodontal destruction. Therefore, sclerostin can be a promising therapeutic target for control of osteoclastic activity and promotion of osteogenesis in chronic periodontitis and more so in smokers.