ArticleEuropean cells & materials2014
Activation of β-catenin signalling leads to temporomandibular joint defects.
Article in European cells & materials, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 33 citations in OpenAlex.
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Epigenetic Biomarkers in Temporomandibular Joint Osteoarthritis: An Emerging Target in Treatment.International journal of molecular sciences · 2025Review
- MSAB limits osteoarthritis development and progression through inhibition of β-catenin-DDR2 signaling.Bioactive materials · 2025Article
- Development of novel osteoarthritis therapy by targeting AMPK-β-catenin-Runx2 signaling.Genes & diseases · 2025Review
- Type V collagen exhibits distinct regulatory activities in TMJ articular disc versus condylar cartilage during postnatal growth and remodeling.Acta biomaterialia · 2024Article
- Circadian rhythm disruption upregulating Per1 in mandibular condylar chondrocytes mediating temporomandibular joint osteoarthritis via GSK3β/β-CATENIN pathway.Journal of translational medicine · 2024Article
- Mechanisms Underlying Sex Differences in Temporomandibular Disorders and Their Comorbidity with Migraine.Brain sciences · 2024Review
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- Loss of miR-204 and miR-211 shifts osteochondral balance and causes temporomandibular joint osteoarthritis.Journal of cellular physiology · 2023Article
- Sex-dependent variation in cartilage adaptation: from degeneration to regeneration.Biology of sex differences · 2023Review
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- The adaptive response of the mandibular condyle to increased load is disrupted by ADAMTS5 deficiency.Connective tissue research · 2023Article
- Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice.International journal of oral science · 2022Article
- Animal Models of Temporomandibular Joint Osteoarthritis: Classification and Selection.Frontiers in physiology · 2022Review
- Molecular signaling in temporomandibular joint osteoarthritis.Journal of orthopaedic translation · 2022Review
- Type V collagen regulates the structure and biomechanics of TMJ condylar cartilage: A fibrous-hyaline hybrid.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint.Journal of cellular and molecular medicine · 2021Review
- Deletion of Axin1 in condylar chondrocytes leads to osteoarthritis-like phenotype in temporomandibular joint via activation of β-catenin and FGF signaling.Journal of cellular physiology · 2019Article
- Epigenetic and therapeutic implications of dnmt3b in temporomandibular joint osteoarthritis.American journal of translational research · 2019Article
- Estrogen Promotes Mandibular Condylar Fibrocartilage Chondrogenesis and Inhibits Degeneration via Estrogen Receptor Alpha in Female Mice.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Despite extensive research in knee and hip osteoarthritis (OA), the underlying mechanism of temporomandibular joint (TMJ) disorder remains largely unknown. The purpose of this study was to determine whether the constitutive activation of β-catenin in the middle and deep layers of the articular cartilage can compromise the homeostasis of this tissue in the TMJ. Col2CreERT2 transgenic mice were bred with RosamT/mG reporter mice to determine Cre recombination efficiency. Col2CreERT2 mice were then crossed with β-cateninflox(ex3)+ mice to generate β-catenin conditional activation mice, β-catenin(ex3)Col2ER. TMJ samples were harvested when the mice were 1-, 3- or 6-month-old and evaluated using histology, histomorphometry and immunohistochemistry. β-catenin(ex3)Col2ER mice were further crossed with Mmp13flox/flox and Adamts5-/- mice to generate (β-catenin(ex3)/Mmp13)Col2ER and β-catenin(ex3)Col2ER)/Adamts5-/- double mutant mice to investigate the role of Mmp13 and Adamts5 in the development of TMJ disorder. High levels of Cre-recombination were seen in Col2CreERT2;RosamT/mGmice. Progressive TMJ defects developed in 1-, 3- and 6-month-old β-catenin(ex3)Col2ER mice, as revealed by histology and histomorphometry. Results further demonstrated that the defects observed in β-catenin(ex3)Col2ER mice were significantly decelerated after deletion of the Mmp13 or Adamts5 gene in (β-catenin(ex3)/Mmp13)Col2ER or β-catenin(ex3)Col2ER/Adamts5-/- double mutant mice. In summary, we found that β-catenin is a critical gene in the induction of TMJ cartilage degeneration, and over-expressing β-catenin in TMJ cartilage leads to defects assembling an OA-like phenotype. Deletion of Mmp13 and Adamts5 in β-catenin(ex3)Col2ER mice ameliorates the development of TMJ defects. This study suggests that Mmp13 and Adamts5 could be potential therapeutic targets for the treatment of TMJ disorders.
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Registered trials
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