ArticleJournal of cellular and molecular medicine2020
TLR4 contributes to the damage of cartilage and subchondral bone in discectomy-induced TMJOA mice.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Correction to 'TLR4 Contributes to the Damage of Cartilage and Subchondral Bone in Discectomy-Induced TMJOA Mice'.Journal of cellular and molecular medicine · 2026Article
- Neural crest-specific disruption of Evc2 provides an animal model to study the temporomandibular joint development and homeostasis in response to jaw loading.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis.International journal of oral science · 2026Article
- Target-Specific Extracorporeal Shockwave Therapy Modulates TLR4/NF-κB/MMP13 Signaling Within the Joint Microenvironment to Improve Osteochondral Pathology in Patellofemoral Osteoarthritis.International journal of medical sciences · 2026Article
- Glutathione peroxidase 4 restrains temporomandibular joint osteoarthritis progression by inhibiting ferroptosis.Journal of cellular and molecular medicine · 2024Article
- TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL-1β-induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis.Journal of cellular and molecular medicine · 2024Article
- Inhibition of TLR4 signalling to dampen joint inflammation in osteoarthritis.Rheumatology (Oxford, England) · 2024Review
- Equine Models of Temporomandibular Joint Osteoarthritis: A Review of Feasibility, Biomarkers, and Molecular Signaling.Biomedicines · 2024Review
- TLR4 antagonism provides short-term but not long-term clinical benefit in a full-depth cartilage defect mouse model.Connective tissue research · 2024Article
- Article
- Potential pathological and molecular mechanisms of temporomandibular joint osteoarthritis.Journal of dental sciences · 2023Review
- The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Temporomandibular Joint Osteoarthritis: Pathogenic Mechanisms Involving the Cartilage and Subchondral Bone, and Potential Therapeutic Strategies for Joint Regeneration.International journal of molecular sciences · 2022Review
- Inhibition of HMGB1 suppresses inflammation and catabolism in temporomandibular joint osteoarthritis <em>via</em> NF-κB signaling pathway.European journal of histochemistry : EJH · 2022Article
- Cinnamic Aldehyde, the main monomer component of Cinnamon, exhibits anti-inflammatory property in OA synovial fibroblasts via TLR4/MyD88 pathway.Journal of cellular and molecular medicine · 2022Article
- Molecular signaling in temporomandibular joint osteoarthritis.Journal of orthopaedic translation · 2022Review
- Animal Models of Temporomandibular Joint Osteoarthritis: Classification and Selection.Frontiers in physiology · 2022Review
- TLR4 contributes to the damage of cartilage and subchondral bone in discectomy-induced TMJOA mice.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The abundance of inflammatory mediators in injured joint indicates innate immune reactions activated during temporomandibular joint osteoarthritis (TMJOA) progression. Toll-like receptor 4 (TLR4) can mediate innate immune reaction. Herein, we aimed to investigate the expression profile and effect of TLR4 in the cartilage and subchondral bone of the discectomy-induced TMJOA mice. The expression of TLR4 and NFκB p65 in the synovium of TMJOA patients was measured by immunohistochemistry, Western blotting and RT-PCR. H&E and Masson staining were utilized to assess the damage of cartilage and subchondral bone of the discectomy-induced TMJOA mice. A TLR4 inhibitor, TAK-242, was used to assess the effect of TLR4 in the cartilage and subchondral bone of the discectomy-induced TMJOA mice by Safranin O, micro-CT, immunofluorescence and immunohistochemistry. Western blotting was used to quantify the expression and effect of TLR4 in IL-1β-induced chondrocytes. The expression of TLR4 and NFκB p65 was elevated in the synovium of TMJOA patients, compared with the normal synovium. TLR4 elevated in the damaged cartilage and subchondral bone of discectomy-induced TMJOA mice, and the rate of TLR4 expressing chondrocytes positively correlated with OA score. Intraperitoneal injections of TAK-242 ameliorate the extent of TMJOA. Furthermore, TLR4 promotes the expression of MyD88/NFκB, pro-inflammatory and catabolic mediators in cartilage of discectomy-induced TMJOA. Besides, TLR4 participates in the production of MyD88/NFκB, pro-inflammatory and catabolic mediators in IL-1β-induced chondrocytes. TLR4 contributes to the damage of cartilage and subchondral bone in discectomy-induced TMJOA mice through activation of MyD88/NFκB and release of pro-inflammatory and catabolic mediators.
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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.