Odontology · 2026
Bulk RNA sequence analysis of the articular disc-retrodiscal tissue complex in a TMJ-OA rat model with anterior disc displacement.
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Kita Daiki, Hirose Naoto, Yanoshita Makoto, Ito Shota, Koizumi Yuma, Nishiyama Sayuri, Tsuboi Eri, Kubo Naoki, Oshiro Risako, Yoshida Marino, Asakawa Yuki, Tanimoto Kotaro
Аннотация
OBJECTIVE: Articular disc displacement (ADD) is a major pathology of temporomandibular disorders that increases temporomandibular joint osteoarthritis (TMJ-OA) risk. However, its effect on gene expression in the retrodiscal tissue remains unexplored. This research elucidated the genetic alterations in the articular disc-retrodiscal tissue complex (ADRC) caused by ADD and investigated their association with TMJ-OA.
METHODS: ADD was induced in the temporomandibular joints of rats, which were euthanised after 8 weeks post-op. RNA sequencing was performed on the ADRC (n = 3/group), and histological analysis was conducted on temporomandibular joints (n = 3/group).
RESULTS: Expression analysis identified 103 significantly upregulated and 129 significantly downregulated genes in the ADRC of ADD rats. Differentially expressed genes analysis revealed a significant upregulation of growth differentiation factor-10 (log2FC = 1.16), suggesting its role in mandibular condyle deformity. Gene ontology analysis revealed significant upregulation of processes related to structural and nervous system development and significant downregulation of fat metabolism processes. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed a significant increase in inflammatory and osteoclast differentiation pathways, whilst adipocytokine signalling, linoleic acid metabolism pathways, and circadian rhythm were significantly downregulated.
CONCLUSION: This is the first study to establish genetic changes with the ADRC in ADD and identify factors related to TMJ-OA pathologies.
METHODS: ADD was induced in the temporomandibular joints of rats, which were euthanised after 8 weeks post-op. RNA sequencing was performed on the ADRC (n = 3/group), and histological analysis was conducted on temporomandibular joints (n = 3/group).
RESULTS: Expression analysis identified 103 significantly upregulated and 129 significantly downregulated genes in the ADRC of ADD rats. Differentially expressed genes analysis revealed a significant upregulation of growth differentiation factor-10 (log2FC = 1.16), suggesting its role in mandibular condyle deformity. Gene ontology analysis revealed significant upregulation of processes related to structural and nervous system development and significant downregulation of fat metabolism processes. Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed a significant increase in inflammatory and osteoclast differentiation pathways, whilst adipocytokine signalling, linoleic acid metabolism pathways, and circadian rhythm were significantly downregulated.
CONCLUSION: This is the first study to establish genetic changes with the ADRC in ADD and identify factors related to TMJ-OA pathologies.