Periodontal inflammation and tryptophan-kynurenine metabolism in Parkinson’s disease
Periodontal inflammation and tryptophan-kynurenine metabolism in Parkinson’s disease
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Kynurenine Pathway in Parkinson's Disease
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Abstract Objective The kynurenine pathway(KP) of tryptophan catabolism is a major regulator 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 (PAD) and Periodontitis (PD). Materials and methods Saliva and serum samples were collected from Stage III, Grade B periodontitis patients with PAD (Parkinson+periodontitis group, n = 20) and without PAD (periodontitis group, n = 24), and 24 periodontally and systemically healthy individuals (control group). Salivary and serum concentrations of tryptophan-kynurenine pathway metabolites, including tryptophan, kynurenine, kynurenine/tryptophan ratio, kynurenic acid, 3-hydroxykynurenine, picolinic acid, and quinolinic acid, were quantified using liquid chromatography–mass spectrometry. Periodontal status was assessed by recording plaque index, probing pocket depth, clinical attachment loss, and bleeding on probing according to standard clinical procedures. Results Clinical parameters were significantly higher in the PD groups than in the control group ( p < 0.001). The control group had the lowest BOP (3.54 ± 2.52), followed by the Parkinson+periodontitis (52.00 ± 14.91) and the periodontitis groups (70.46 ± 25.09). Salivary TRP, KYN, KYNA, PA, and QA levels were significantly higher in the Parkinson+periodontitis group than in the control. The salivary KYN/TRP ratio was significantly higher in the Parkinson+periodontitis group than in the other groups ( p < 0.05). Serum TRP levels were significantly higher in the periodontitis group compared to the other groups. The serum KYN/TRP ratio was significantly higher in the Parkinson+ periodontitis group than in the control group ( p < 0.05). Conclusions The data suggest that the metabolic regulation of immune responses via the tryptophan-kynurenine pathway may play a pathogenetic role in the link between Parkinson’s disease and periodontitis. Clinical relevance Altered tryptophan–kynurenine metabolism in patients with both Parkinson’s disease and periodontitis suggests a shared inflammatory pathway linking the two conditions. Clinical Trials ID: NCT07272564.