ReviewJournal of cellular and molecular medicine2021
Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint.
Review in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
83 citing papers in PubMed, 2 syntheses or guidelines pooled it, 140 citations in OpenAlex.
- Hyaluronic Acid/Platelet-Rich Plasma Mixture Improves Temporomandibular Joint Biomechanics: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Evaluating the Effect of Hypoxia on Human Adult Mesenchymal Stromal Cell Chondrogenesis In VitroInternational journal of molecular sciences · 2022Pooled it
- Classification, Structure-Activity Relationship, and Anti-Osteoarthritis Mechanism of Natural Flavonoids.Chemistry & biodiversity · 2026Review
- Mastication-Induced Electrical Stimulation Activates Prg4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Is the temporomandibular joint affected by rheumatoid arthritis? A comparative investigation with knee arthritis in an experimental rat model.Journal of anatomy · 2026Article
- Abnormal Stress Reduced miR-330 Supplementation Alleviates Osteoarthritis Progression by Suppressing Osteochondral Catabolism.Aging cell · 2026Article
- Temporomandibular Joint Osteoarthritis Modeling Methods' Efficacy in SD Rats: A Scoping Review.Oral diseases · 2026Article
- Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway.Bioactive materials · 2026Article
- Interleukin-1β-induced arthritis involves chondrocyte oxiapoptophagy.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- PLGA Nanoparticle-Mediated Sustained Release of Fisetin for Intra-Articular Therapy of Temporomandibular Joint Osteoarthritis.International journal of molecular sciences · 2026Article
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Defining subcellular synovial responses in TMJ osteoarthritis onset via mechanical stress and articular disk derangement models.International journal of oral science · 2026Article
- Punicalagin with anti-inflammatory activities affects Brd-4 mediated chromatin remodeling for attenuating inflammatory osteolysis.Scientific reports · 2026Article
- Lubricin maintains temporomandibular joint homeostasis by regulating synovial inflammation.Regenerative therapy · 2026Article
- Single-cell transcriptional atlas reveals distinct immune-chondrocyte crosstalk mechanisms in temporomandibular joint osteoarthritis induced by different types of occlusal disorder.International journal of oral science · 2026Article
- USP34 attenuates cartilage degradation in temporomandibular joint osteoarthritis by ANT1-mediated mitophagy.JBMR plus · 2026Article
- The role of lactate on arthritis-associated cells: physiology, pathology, and therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- PRKACB Attenuates Chondrocyte Loss and Inflammation in Osteoarthritis.Immunity, inflammation and disease · 2026Article
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- SGK1 triggers cartilage degradation in TMJOA via FoxO1/autophagy.Arthritis research & therapy · 2025Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Temporomandibular joint (TMJ) osteoarthritis is a common chronic degenerative disease of the TMJ. In order to explore its aetiology and pathological mechanism, many animal models and cell models have been constructed to simulate the pathological process of TMJ osteoarthritis. The main pathological features of TMJ osteoarthritis include chondrocyte death, extracellular matrix (ECM) degradation and subchondral bone remodelling. Chondrocyte apoptosis accelerates the destruction of cartilage. However, autophagy has a protective effect on condylar chondrocytes. Degradation of ECM not only changes the properties of cartilage but also affects the phenotype of chondrocytes. The loss of subchondral bone in the early stages of TMJ osteoarthritis plays an aetiological role in the onset of osteoarthritis. In recent years, increasing evidence has suggested that chondrocyte hypertrophy and endochondral angiogenesis promote TMJ osteoarthritis. Hypertrophic chondrocytes secrete many factors that promote cartilage degeneration. These chondrocytes can further differentiate into osteoblasts and osteocytes and accelerate cartilage ossification. Intrachondral angiogenesis and neoneurogenesis are considered to be important triggers of arthralgia in TMJ osteoarthritis. Many molecular signalling pathways in endochondral osteogenesis are responsible for TMJ osteoarthritis. These latest discoveries in TMJ osteoarthritis have further enhanced the understanding of this disease and contributed to the development of molecular therapies. This paper summarizes recent cognition on the pathogenesis of TMJ osteoarthritis, focusing on the role of chondrocyte hypertrophy degeneration and cartilage angiogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.