# Periodontal inflammation and tryptophan-kynurenine metabolism in Parkinson’s disease

## TL;DR

The study explores how periodontal inflammation and tryptophan metabolism may be linked to Parkinson’s disease through immune system changes.

## Contribution

The study identifies altered tryptophan-kynurenine metabolism in Parkinson’s patients with periodontitis, suggesting a shared inflammatory pathway.

## Key findings

- Salivary and serum levels of tryptophan-kynurenine metabolites were higher in Parkinson’s patients with periodontitis compared to controls.
- The kynurenine/tryptophan ratio was significantly elevated in Parkinson’s patients with periodontitis.
- Periodontal clinical parameters were worse in Parkinson’s and periodontitis groups compared to healthy controls.

## Abstract

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).

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.

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).

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.

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.