Mitochondrial Dysfunction In Temporomandibular Joint Osteoarthritis

Mitochondrial dysfunction drives peripheral OA via OXPHOS/ROS, yet its role in TMJ OA is unclear. Using differential gene analysis, pathway enrichment, and immune profiling, this study explores mitochondrial dysregulation in TMJ OA. We aim to identify shared mitochondrial-inflammatory pathways, uncover TMJ-specific metabolic defects, and target mitochondrial-immune crosstalk, bridging mechanisms to therapies for this understudied disorder. TMJ OA transcriptomic data (GSE205389) were processed using R (limma: DEGs, adj. p<0.05, |log2FC|>1). Enriched pathways (KEGG/GO;GSEA/GSVA, clusterProfiler) and mitochondrial genes (MitoCarta3.0) were analyzed. STRING (confidence>0.7) and CytoHubba identified PPI hub genes. CIBERSORT linked hub genes to immune infiltration. Visualizations used ggplot2/DESeq2. GSE205389 analysis revealed 1,408 OA genes (adj. p<0.05, |log2FC|>1), with six mitochondrial hubs (COX7A1,COX7C,etc) via MitoCarta3.0. KEGG/GO linked inflammation to OXPHOS dysfunction (q<0.01). COX7A1 correlated with natural killer T cells, implying immune-metabolic crosstalk. These findings unify mitochondrial failure and immune dysregulation in TMJ OA, proposing COX7A1 and OXPHOS modulation as therapeutic targets. Mitochondrial dysfunction underpins TMJ OA pathogenesis. Analysis of GSE205389 identified 1,408 OA genes, including six mitochondrial hubs (COX7A1/COX7C) linked to OXPHOS-linked inflammation. COX7A1 correlated with natural killer T cells, suggesting immune-metabolic crosstalk. Restoring OXPHOS or targeting COX7A1 may mitigate disease progression. These findings advance TMJ OA therapies, urging experimental validation to translate computational insights into clinical interventions.