Mechanism and role of nitric oxide signaling in periodontitis

Abstract

The present study investigated the role of the nitric oxide (NO) signaling pathway in the progression of periodontal disease, and explored the related genetic mechanisms. An experimental model of periodontitis was established in Sprague-Dawley rats, then they were divided into normal control, and 2, 4 and 6 weeks post-surgery groups. NO content was determined in the saliva of rats from each group by the Griess reagent method. Pathological changes of the periodontal tissue sections were evaluated with hematoxylin-eosin staining. The periodontal tissue sections were also evaluated by immunohistochemistry to detect the expression of inducible nitric oxide synthase 2 (iNOS2). Significant differences were detected in the iNOS2 expression of the periodontal tissue based on immunohistochemistry. There was a significant time-dependent increase in NO serum levels post-surgery. Two single nucleotide polymorphisms (SNP), rs2297518 in the iNOS gene and rs841 of the GTP cyclohydrolase I gene, were identified to be closely related to alveolar bone resorption, which is associated with the SNP rs1049255 of the cytochrome b-245 α chain gene. The present findings demonstrated that iNOS2 values increased and NO levels increased with the progression of periodontitis. These results are in agreement with the previous literature. It was hypothesized that NO has a role in the occurrence and development of periodontal disease by regulating the action of certain cytokines.