ArticleJournal of dental research2015
Wnt5a/Ror2 mediates temporomandibular joint subchondral bone remodeling.
Article in Journal of dental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- ROR2 preserves alveolar bone homeostasis by orchestrating IRAK4-dependent suppression of CXCL8-driven osteolysis.Cell communication and signaling : CCS · 2026Article
- Article
- Immuno-Mechanical Signaling Network Integration in Temporomandibular Joint Pathology: A TMID Conceptual Framework.International journal of molecular sciences · 2026Review
- Cell communication and relevant signaling pathways in osteogenesis-angiogenesis coupling.Bone research · 2025Review
- The role of Piezo1 in bone marrow stem cells in response to elevated intraosseous pressure on regulating osteogenesis and angiogenesis of steroid-induced osteonecrosis of the femoral head.Journal of orthopaedic translation · 2025Article
- Development of animal model for anterior open bite and mechanism of temporomandibular joint morphological change: an implication for MAC surgery.BMC oral health · 2025Article
- The combination of odontogenic stem cells and mandibular advancement promotes the length of the mandible in adult rats by facilitating the development of condylar cartilage.Stem cell research & therapy · 2024Article
- The Pathogenetic Role of RANK/RANKL/OPG Signaling in Osteoarthritis and Related Targeted Therapies.Biomedicines · 2024Review
- Equine Models of Temporomandibular Joint Osteoarthritis: A Review of Feasibility, Biomarkers, and Molecular Signaling.Biomedicines · 2024Review
- Wnt5a deficiency in osteocalcin-expressing cells could not alleviate the osteoarthritic phenotype in a mouse model of post-traumatic osteoarthritis.Iranian journal of basic medical sciences · 2024Article
- Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation.Frontiers in pharmacology · 2024Review
- Potential pathological and molecular mechanisms of temporomandibular joint osteoarthritis.Journal of dental sciences · 2023Review
- Progress of Wnt Signaling Pathway in Osteoporosis.Biomolecules · 2023Review
- Global Trends and Future Research Directions for Temporomandibular Disorders and Stem Cells.Journal of functional biomaterials · 2023Review
- Review
- Temporomandibular Joint Osteoarthritis: Pathogenic Mechanisms Involving the Cartilage and Subchondral Bone, and Potential Therapeutic Strategies for Joint Regeneration.International journal of molecular sciences · 2022Review
- Noncanonical Wnt5a Signaling Suppresses Hippo/TAZ-Mediated Osteogenesis Partly Through the Canonical Wnt Pathway in SCAPs.Drug design, development and therapy · 2022Article
- The Wnt signaling cascade in the pathogenesis of osteoarthritis and related promising treatment strategies.Frontiers in physiology · 2022Review
- Molecular signaling in temporomandibular joint osteoarthritis.Journal of orthopaedic translation · 2022Review
- Role of osteoclast differentiation in the occurrence of osteoarthritis of temporomandibular joint.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Increased subchondral trabecular bone turnover due to imbalanced bone-resorbing and bone-forming activities is a hallmark of osteoarthritis (OA). Wnt5a/Ror2 signaling, which can derive from bone marrow stromal cells (BMSCs), takes a role in modulating osteoblast and osteoclast formation. We showed previously that experimentally unilateral anterior crossbites (UACs) elicited OA-like lesions in mice temporomandibular joints (TMJs), displaying as subchondral trabecular bone loss. Herein, we tested the role of BMSC-derived Wnt5a/Ror2 signaling in regulating osteoclast precursor migration and differentiation in this process. The data confirmed the decreased bone mass, increased tartrate-resistant acid phosphatase (TRAP)-positive cell number, and enhanced osteoclast activity in TMJ subchondral trabecular bone of UAC-treated rats. Interestingly, the osteoblast activity in the tissue of TMJ subchondral trabecular bone of these UAC-treated rats was also enhanced, displaying as upregulated expressions of osteoblast markers and increased proliferation, migration, and differentiation capabilities of the locally isolated BMSCs. These BMSCs showed an increased CXCL12 protein expression level and upregulated messenger RNA expressions of Rankl, Wnt5a, and Ror2. Ex vivo data showed that their capacities of inducing migration and differentiation of osteoclast precursors were enhanced, and these enhanced capabilities were restrained after blocking their Ror2 signaling using small interfering RNA (siRNA) assays. Reducing Ror2 expression in the BMSC cell line by siRNA or blocking the downstream signalings with specific inhibitors also demonstrated a suppression of the capacity of the BMSC cell line to promote Wnt5a-dependent migration (including SP600125 and cyclosporine A) and differentiation (cyclosporine A only) of osteoclast precursors. These findings support the idea that Wnt5a/Ror2 signaling in TMJ subchondral BMSCs enhanced by UAC promoted BMSCs to increase Cxcl12 and Rankl expression, in which JNK and/or Ca(2+)/NFAT pathways were involved and therefore were engaged in enhancing the migration and differentiation of osteoclast precursors, leading to increased osteoclast activity and an overall TMJ subchondral trabecular bone loss in the UAC-treated rats.
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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.