ArticleJCI insight2022
Increased joint loading induces subchondral bone loss of the temporomandibular joint via the RANTES-CCRs-Akt2 axis.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.
- Condylar bone regeneration following temporomandibular joint disc repositioning surgery: a systematic review and meta-analysis.BMC oral health · 2025Pooled it
- Bibliometric and visualization analysis of temporomandibular joint osteoarthritis from 2004 to 2024.Frontiers in oral health · 2025Pooled it
- ADSC-enriched adipose extract alleviates cartilage fibrosis in temporomandibular joint osteoarthritis by inhibiting chondrocyte senescence.Journal of translational medicine · 2025Trial
- Mastication-Induced Electrical Stimulation Activates Prg4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PF4 drives mechanical overload-induced temporomandibular joint osteoarthritis through TLR2-dependent activation of NF-κB.Journal of translational medicine · 2026Article
- Quantitative Imaging of the Mandibular Condyle: Radiomics and Microarchitectural Biomarkers.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026Review
- FGF19 promotes cartilage destruction in the progress of temporomandibular joint osteoarthritis.Cell and tissue research · 2026Article
- Temporomandibular Joint Osteoarthritis Modeling Methods' Efficacy in SD Rats: A Scoping Review.Oral diseases · 2026Article
- Identification of synovial lymphatic system in the temporomandibular joint and their roles in arthritis and pain.Nature communications · 2026Article
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- OX40L in endothelial cells promotes temporomandibular joint subchondral bone angiogenesis and osteoclastogenesis in mice.Bone & joint research · 2026Article
- Bilateral pseudo-disc changes in a minipig model for unilateral anterior disc displacement of the temporomandibular joint.Oral and maxillofacial surgery · 2026Article
- METTL3-mediated fibroblast-like synoviocytes senescence promotes temporomandibular joint osteoarthritis progression.Communications biology · 2026Article
- Ablation of CD38 in multiple myeloma cells leads to an aggressive phenotype in a mouse xenograft model.Blood advances · 2026Article
- Mechano-immune interactions in musculoskeletal aging: Mechanisms and translational perspectives.Theranostics · 2026Review
- Combination of High-Fat Diet and Chronic Unpredictable Stress Synergistically Induces Osteoarthritis-Like Changes in Temporomandibular Joints in Rats.Mediators of inflammation · 2026Article
- Article
- Identification of Synovial Lymphatics in the TMJ and their Roles in Arthritis and Pain.Research square · 2025Article
- Wnt/β-catenin regulates Gli1 + osteogenic progenitors in condylar subchondral bone development and osteoarthritis.BMC musculoskeletal disorders · 2025Article
- Akt2 inhibition alleviates temporomandibular joint osteoarthritis by preventing subchondral bone loss.Arthritis research & therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early-stage temporomandibular joint osteoarthritis (TMJOA) is characterized by excessive subchondral bone loss. Emerging evidence suggests that TMJ disc displacement is involved, but the pathogenic mechanism remains unclear. Here, we established a rat model of TMJOA that simulated disc displacement with a capacitance-based force-sensing system to directly measure articular surface pressure in vivo. Micro-CT, histological staining, immunofluorescence staining, IHC staining, and Western blot were used to assess pathological changes and underlying mechanisms of TMJOA in the rat model in vivo as well as in RAW264.7 cells in vitro. We found that disc displacement led to significantly higher pressure on the articular surface, which caused rapid subchondral bone loss via activation of the RANTES-chemokine receptors-Akt2 (RANTES-CCRs-Akt2) axis. Inhibition of RANTES or Akt2 attenuated subchondral bone loss and resulted in improved subchondral bone microstructure. Cytological studies substantiated that RANTES regulated osteoclast formation by binding to its receptor CCRs and activating the Akt2 pathway. The clinical evidence further supported that RANTES was a potential biomarker for predicting subchondral bone loss in early-stage TMJOA. Taken together, this study demonstrates important functions of the RANTES-CCRs-Akt2 axis in the regulation of subchondral bone remodeling and provides further knowledge of how disc displacement causes TMJOA.
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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.