Research Information System
The International Association for Dental, Oral, and Craniofacial Research (IADR), California, United States Of America, 13 - 16 March 2024, pp.1-2
Objectives: The kynurenine pathway (KP) of tryptophan catabolism is one of the major regulators of the immune response. Metabolites of this pathway may have protective or degenerative effects on the nervous system. Based on our recent studies, we tested the hypothesis that KP metabolites play a role in the pathogenesis of the link between Parkinson's disease (PD) and Periodontitis (P). T
Materials and Methods: Saliva and serum samples were collected from 20 Stage III, Grade B periodontitis patients with PD (Parkinson-periodontitis group) and without PD (periodontitis group) and 20 periodontally and systemically healthy control individuals (control group). Samples were analyzed for TRP, KYN, KYN/TRP ratio, KYNA, 3OHKYN, picolinic acid (PA), and quinolinic acid (QA) by liquid chromatography–mass spectrometry. Clinical periodontal parameters (plaque index (PI), probing pocket depth (PPD), clinical attachment loss (CAL), and bleeding on probing (BOP)) were recorded.
Results: Clinical parameters were significantly higher in both periodontitis groups than in the control group (p <0.001). Salivary TRP, KYN, KYNA, PA, and QA levels were significantly higher. The KYN/TRP ratio was significantly lower in the Parkinson-periodontitis group than the other groups (p<0.05), without differences between periodontitis and control groups. In parallel, serum TRP levels were significantly lower, and the KYN, KYN/TRP ratio was significantly higher in the Parkinson-periodontitis group (p<0.05).
Conclusions: Our results suggested that the tryptophan-kynurenine metabolism may be a critical pathogenetic link between PD and periodontitis.