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A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit

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Peroxisome Functional Inhibition Alleviates TMJOA Cartilage Degradation.

R Ren¹, L Xiao², H Qi¹

¹State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.

Journal of Dental Research

|October 18, 2025

Summary

This summary is machine-generated.

Peroxisomes and palmitic acid contribute to temporomandibular joint osteoarthritis (TMJOA) by activating the JNK/c-JUN/S100a4 pathway, offering new therapeutic targets for this degenerative joint disorder.

Keywords:

JNK PEX2 WNT chondrocyte lipid palmitic acid

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Area of Science:

Biochemistry
Molecular Biology
Pathology

Background:

Temporomandibular joint osteoarthritis (TMJOA) is a degenerative joint disease with poorly understood pathogenesis.
Lipid metabolism disorders in chondrocytes, involving peroxisomes, are implicated in TMJOA development.
Current TMJOA treatments are insufficient to restore joint structure.

Purpose of the Study:

To investigate the role of peroxisomes in TMJOA pathogenesis.
To elucidate the molecular mechanisms linking peroxisomes, lipid metabolism, and cartilage degradation in TMJOA.
To identify potential therapeutic targets for TMJOA.

Main Methods:

Established a TMJOA mouse model using unilateral anterior crossbite surgery.
Utilized in vitro chondrocyte cultures and conditional knockout mice (Acan-CreER^T2 Pex2^f/f) to inhibit peroxisome function.
Performed multiomics analysis, CUT&RUN qPCR, and dual-luciferase reporter assays to identify molecular pathways and interactions.

Main Results:

Abnormal peroxisome quantity and function were observed in the TMJOA mouse model.
Inhibition of peroxisome function alleviated OA-like damage and reduced palmitic acid (PA) levels.
PA exposure induced OA-like phenotypes, activating the JNK/c-JUN signaling axis, leading to increased S100a4 expression and subsequent MMP13 upregulation, promoting TMJOA.

Conclusions:

This study is the first to demonstrate the critical role of peroxisomes in TMJOA.
The peroxisome/PA/JNK/c-JUN/S100a4 axis is identified as a key pathway in TMJOA cartilage degradation.
This pathway represents a novel and promising therapeutic target for TMJOA.