ArticleOsteoarthritis and cartilage2010
Osteochondral angiogenesis and increased protease inhibitor expression in OA.
Article in Osteoarthritis and cartilage, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 81 citations in OpenAlex.
- Mechanism driven adaptation of smart hydrogels to the osteoarthritis pathological microenvironment.Frontiers in bioengineering and biotechnology · 2026Review
- Decellularized cartilage scaffolds derived from wharton's jelly facilitate cartilage regeneration and inhibit angiogenesis.Materials today. Bio · 2025Article
- The Role ofBiomolecules · 2025Review
- Cathepsin K Inhibitors as Potential Drugs for the Treatment of Osteoarthritis.International journal of molecular sciences · 2025Review
- Platelet-Derived Growth Factor as Biomarker of Clinical Outcome for Autologous Platelet Concentrate Therapy in Grade I Knee Osteoarthritis.Biologics : targets & therapy · 2025Article
- Pathophysiological Insights Into the Role of Osteoclasts in Osteoarthritis: Mechanisms, Therapeutic Targets, and Future Directions.Journal of inflammation research · 2025Review
- Disease-Modifying Effects of Lenvatinib, a Multiple Receptor Tyrosine Kinase Inhibitor, on Posttraumatic Osteoarthritis of the Knee.International journal of molecular sciences · 2024Article
- The use of hydrogel microspheres as cell and drug delivery carriers for bone, cartilage, and soft tissue regeneration.Biomaterials translational · 2024Review
- Effects and action mechanisms of individual cytokines contained in PRP on osteoarthritis.Journal of orthopaedic surgery and research · 2023Review
- Recent development in multizonal scaffolds for osteochondral regeneration.Bioactive materials · 2023Review
- FGF receptor inhibitor BGJ398 partially rescues osteoarthritis-like phenotype in older high molecular weight FGF2 transgenic mice via multiple mechanisms.Scientific reports · 2022Article
- The essential anti-angiogenic strategies in cartilage engineering and osteoarthritic cartilage repair.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- Macro, Micro, and Molecular. Changes of the Osteochondral Interface in Osteoarthritis Development.Frontiers in cell and developmental biology · 2021Review
- Diversity of Vascular Niches in Bones and Joints During Homeostasis, Ageing, and Diseases.Frontiers in immunology · 2021Review
- Advances in the Mechanisms Affecting Meniscal Avascular Zone Repair and Therapies.Frontiers in cell and developmental biology · 2021Review
- Matrix Metalloproteinase 3: A Promoting and Destabilizing Factor in the Pathogenesis of Disease and Cell Differentiation.Frontiers in physiology · 2021Review
- Runx3 regulates chondrocyte phenotype by controlling multiple genes involved in chondrocyte proliferation and differentiation.Molecular biology reports · 2020Article
- Angiogenesis stimulated by elevated PDGF-BB in subchondral bone contributes to osteoarthritis development.JCI insight · 2020Article
- Molecular Signaling Interactions and Transport at the Osteochondral Interface: A Review.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveNormal cartilage is resistant to vascular invasion and anti-angiogenic protease inhibitors may contribute to its avascular status. We hypothesized that dysregulated expression of four key anti-angiogenic protease inhibitors may contribute to increased osteochondral vascularity in osteoarthritis (OA).
designMedial tibial plateaux from OA patients (n=40) were compared with those from non-arthritic controls collected post-mortem (PM, n=10). Immunohistochemistry was performed for protease inhibitors TIMP-1, TIMP-3, PAI-1 and SLPI and the pro-angiogenic factor vascular endothelial growth factor (VEGF). Immunoreactivity in articular chondrocytes was scored. Chondropathy was measured as a modified Mankin score, and osteochondral vascular density as number of channels crossing each mm of tidemark. Non-parametric analyses were used for all data.
resultsAll protease inhibitors and VEGF were localised to chondrocytes near the articular surface, less often in the middle zone, and rarely to deep chondrocytes. Scores for VEGF, TIMP-1, TIMP-3, SLPI and PAI-1 were all increased in OA compared with PM, and higher scores were associated with greater chondropathy. Chondrocyte expression of VEGF was associated with higher osteochondral vascular density (r=0.32, P<0.05), whereas protease inhibitors were not.
conclusionsThe resistance of normal articular cartilage to vascular invasion may be more due to its matrix environment than ongoing protease inhibitor expression. Upregulation of protease inhibitors by superficial chondrocytes in OA may moderate the angiogenic effects of growth factors such as VEGF. However, failure of deep chondrocytes to express anti-angiogenic protease inhibitors may permit vascular invasion into the articular cartilage.
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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.