Involvement of the Wnt/beta-catenin signaling antagonists in the chronic periodontitis associated with risk factors

Abstract

Some molecular mechanisms that justify an increased incidence and severity of periodontitis and, consequent increased alveolar bone loss, in diabetic subjects and smokers remained unclear. The aim of this study will be to evaluate the serum and local levels of the inhibitors of Wnt-beta-catenin signaling, dickkopf-related protein 1 (DKK1) and sclerostin (SOST), and osteoimmunoinflammatory mediators related to these inhibitors (interleukin [IL]-1², tumoral necrosis factor [TNF-±], osteoprotegerin [OPG] and receptor activator of nuclear factor-kappa B ligand [RANKL]) in smokers, diabetic subjects and smoking diabetic subjects with chronic periodontitis. One hundred subjects with chronic periodontitis (25/group) will be allocated into one of the following groups: (1) uncontrolled type 2 diabetic subjects, (2) smoking subjects, (3) smoking type 2 diabetic subjects and (4) non-smoking/non-diabetic subjects (non-risk factor). The subjects will be submitted to periodontal clinical examination and periodontitis gingival tissue and blood samplings. The protein levels of DKK1, SOST, IL-1², TNF-±, OPG and RANKL in the gingival tissue and serum samples will be analyzed by enzyme-linked immunosorbent assay. The mRNA levels of DKK1, SOST, IL-1², TNF-±, OPG and RANKL in the gingival tissue were measured by real time PCR. Clinical parameters, protein and mRNA levels will be compared by ANOVA or Kruskal Wallis tests, according to data normality. Models of multivariable logistic regression analysis will be undertaken to estimate the association between diabetes, smoking, diabetes + smoking, clinical parameters and the local and systemic levels of the studied proteins. The level of significance will be set at 5% for all analysis. (AU)