The Evaluation Of Hypoxia And Kynurenine Pathway Interaction in Periodontal Inflammation

Periodontitis is an infectious inflammatory disease that is very common all over the world, and there are many points that need to be clarified in its pathophysiology. When the available literature data is evaluated, it is seen that various host-derived enzymes and free oxygen radicals are important factors in the pathogenesis of the disease. KY is the primary pathway by which TRP is metabolized and produces several bioactive metabolites (such as KYN, KYNA, 3OHKYN) to regulate biological processes involving host-microbiome interaction. In our study, we evaluated the relationship between periodontal inflammation parameters, hypoxia, KP and its metabolites. In line with the data we obtained from this study, we think that KP may play a critical role in oral bacterial infection and periodontitis, an immune inflammatory disease, and act as a bridge in the periodontal disease-systemic disease relationship. For this reason, it is thought that the relationship of hypoxia and oxidative stress, which is important in periodontal disease, with this pathway and the investigation of its effects on periodontal disease will provide important contributions to the literature. In accordance with our aim, 20 patients with systemically healthy periodontitis diagnosed with generalized stage III and 20 periodontally healthy individuals were included in our study. We evaluated the obtained materials by Tandem Mass Mass Spectrometry (LC-MS/MS) and ELISA method. As a result of our study, all clinical periodontal parameters were found to be statistically significantly higher in the periodontitis group (p<0.05). Serum and saliva TRP levels were statistically significantly lower in the periodontitis group than in the control group (p<0.05). Serum KYN/TRP ratio, KYN, KYNA and PA levels were found to be statistically significantly higher in the periodontitis group than in the control group (p<0.05). The salivary KYN/TRP ratio, 3OHKYN and PA levels were statistically significantly higher in the periodontitis group than in the control group (p<0.05). Our study shows that KP is activated in periondontal disease. Dysregulation of this pathway may play an important role in the periodontal inflammation and pathogenesis.