ReviewActa biochimica et biophysica Sinica2024
Subchondral osteoclasts and osteoarthritis: new insights and potential therapeutic avenues.
Review in Acta biochimica et biophysica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 26 citations in OpenAlex.
- Nanoimmunomodulation for cartilage repair in osteoarthritis: reprogramming the inflammatory joint microenvironment.International journal of pharmaceutics: X · 2026Review
- Restoring cartilage-subchondral bone metabolism with biphasic magnesium microspheres ameliorate early osteoarthritis.Bioactive materials · 2026Article
- Anti-RANKL antibody treatment mitigates subchondral bone loss and cartilage degeneration without affecting synovial inflammation in a mouse model of rotator cuff tear arthropathy.Bone & joint research · 2026Article
- Purinergic signaling in osteoarthritis: Mechanistic insights into pathogenesis and therapeutic targeting.Genes & diseases · 2026Review
- Review
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- KPT-330 alleviates osteoarthritis by inhibiting subchondral bone osteoclastogenesis via the NF-κB and MAPK signaling pathways.iScience · 2026Article
- DHA-Derived Lipid Mediators Attenuate Osteoarthritis by Resolving Inflammation and Protecting Cartilage in Association with the SIRT1 Signaling Pathway.Marine drugs · 2026Article
- Osteoclast Heterogeneity in Osteoarthritis: From Single-Cell Microenvironments to Program-Specific Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- The ganglioside GD3 and its synthase (ST8SIA1) as novel senescence markers associated with osteoarthritis.GeroScience · 2026Article
- The TRAF6/SPP1 axis participates in osteoarthritis progression through regulating the catabolism and anabolism of cartilage matrix.Scientific reports · 2026Article
- Luteolin reprograms macrophage polarization via the STING-TBK1 pathway to accelerate bone repair.Acta biochimica et biophysica Sinica · 2026Article
- Article
- Kartogenin-loaded chitosan composite scaffold with cartilage-mimetic microstructure for layered osteochondral repair and cartilage phenotype maintenance.Materials today. Bio · 2026Article
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- Association between the cartilage volume and bone mineral density in symptomatic knee osteoarthritis and the mediating role of bone mineral content.BMC musculoskeletal disorders · 2026Article
- Immunonutritional biomarkers in osteoarthritis: mechanistic insights and prognostic potential.Frontiers in immunology · 2026Review
- Exploring the intricate relationship between IL-1β and IL-18 in the context of osteoarthritis.Frontiers in immunology · 2026Review
- Epigenetic regulation in osteoarthritis: recent updates and emerging mechanisms.Frontiers in genetics · 2026Review
- Association between novel inflammatory indices and osteoporosis among older adults: evidence from a large multicenter study in China.Frontiers in medicine · 2026Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the most common joint disease, and good therapeutic results are often difficult to obtain due to its complex pathogenesis and diverse causative factors. After decades of research and exploration of OA, it has been progressively found that subchondral bone is essential for its pathogenesis, and pathological changes in subchondral bone can be observed even before cartilage lesions develop. Osteoclasts, the main cells regulating bone resorption, play a crucial role in the pathogenesis of subchondral bone. Subchondral osteoclasts regulate the homeostasis of subchondral bone through the secretion of degradative enzymes, immunomodulation, and cell signaling pathways. In OA, osteoclasts are overactivated by autophagy, ncRNAs, and Rankl/Rank/OPG signaling pathways. Excessive bone resorption disrupts the balance of bone remodeling, leading to increased subchondral bone loss, decreased bone mineral density and consequent structural damage to articular cartilage and joint pain. With increased understanding of bone biology and targeted therapies, researchers have found that the activity and function of subchondral osteoclasts are affected by multiple pathways. In this review, we summarize the roles and mechanisms of subchondral osteoclasts in OA, enumerate the latest advances in subchondral osteoclast-targeted therapy for OA, and look forward to the future trends of subchondral osteoclast-targeted therapies in clinical applications to fill the gaps in the current knowledge of OA treatment and to develop new therapeutic strategies.
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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.