DOI: 10.1097/pr9.0000000000001466 ISSN: 2471-2531

Repetitive tooth-clenching triggers kynurenine pathway activation in masseter muscle of women with temporomandibular disorders myalgia

Golnaz Barjandi, Jacob Ahlberg Weidenfors, Lilly Schwieler, Sophie Erhardt, Sofia Louca Jounger, Malin Ernberg
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Abstract

Background:

Inflammation alters the kynurenine pathway (KP), producing metabolites related to pain regulation. Previous microdialysis studies indicate increased levels of inflammatory markers in temporomandibular disorders myalgia (TMDM) that increase in response to tooth-clenching. This study aimed to elucidate the role of the KP in TMDM by investigating intramuscular KP metabolites in response to tooth-clenching.

Methods:

This study included 41 women; 15 TMDM myofascial pain with referral (MFP), 13 TMDM local myalgia (MYA), and 13 controls (CTR). Microdialysis was applied to the masseter muscle for 220 minutes to analyze tryptophan (TRP),

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-kynurenine (KYN), 3-hydroxykynurenine (3-HK), quinolinic acid (QUIN) and nicotinamide (NAM). After baseline (140 minutes), participants performed a 20-minute tooth-clenching exercise followed by 1 hour of recovery. Pain variables were assessed throughout the experiment.

Results:

NAM levels increased significantly in response to tooth-clenching across all groups ( P < 0.001), while TRP, KYN, QUIN, and 3-HK increased only in MFP ( P < 0.001 to P = 0.041). Supervised multivariate analysis showed that changes in TRP, KYN, and QUIN levels in response to exercise, and NAM levels at baseline and recovery, significantly separated MFP from CTR and MYA ( P = 0.040). In addition, decreased concentration levels of mainly NAM and TRP were significantly associated with increased widespread pain ( P = 0.02) and pain during recovery ( P = 0.030).

Conclusion:

These findings indicate that intramuscular KP metabolites increase in response to tooth-clenching, particularly in MFP, distinguishing them from both CTR and MYA. This supports the link between intramuscular inflammation and exercise-induced alterations in the KP, providing further insights in the TMDM pathophysiology and differentiation of its subdiagnosis.

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