Impact Of Notch Signalling Molecules And Bone Resorption Regulators On Clinical Parameters In Periodontitis

Background and objective Notch signalling cascade has recently been connected to alveolar bone resorption in periodontitis. Hence, the present cross-sectional study aimed to analyze the expression of Notch signalling pathway (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1) and periodontitis-related (tumor necrosis factor alpha- TNF-alpha, interleukin 17-IL-17, receptor activator of nuclear factor-kappa B ligand-RANKL, osteoprotegerin-OPG) molecules and correlate it with clinical parameters in aggressive (AP) and chronic (CP) periodontitis. Additionally, the aforementioned markers' expression was evaluated in periodontitis patients with different RANKL/OPG ratios. Material and methods Eighty patients were enrolled either in AP or CP group. Clinical attachment level (CAL), bleeding on probing (BOP), periodontal probing depth (PPD) and plaque index (PI) were recorded for each patient. Total RNA was extracted from gingival crevicular fluid samples. Relative gene expression of investigated markers was determined by reverse transcriptase-real-time polymerase chain reaction. Results Significantly higher values of PPD were observed in AP compared to CP (P = .010). Negative correlations between OPG and CAL, and OPG and PI, were found in AP (P = .045,P = .006, respectively), while Hey 1 and PI had a positive correlation (P = .049). In multivariate linear regression analysis, OPG and Notch 2 were predictors of CAL in AP group. TNF-alpha and IL-17 were higher in RANKL predominant than in OPG predominant cases (P = .007,P = .001, respectively). In RANKL predominant lesions Notch 1 and Jagged 1 were down-regulated in AP compared to CP patients (P = .010,P = .025, respectively). Conclusion The present study demonstrated that changes in Notch 2 expression affected CAL in AP cases hence this molecule could be considered as a contributor to alveolar bone loss. In RANKL-activated settings, the down-regulation of Notch 1 might participate in more severe bone resorption in AP.