ArticleScientific reports2021
Loss of mutual protection between human osteoclasts and chondrocytes in damaged joints initiates osteoclast-mediated cartilage degradation by MMPs.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 14 citations in OpenAlex.
- Restoring cartilage-subchondral bone metabolism with biphasic magnesium microspheres ameliorate early osteoarthritis.Bioactive materials · 2026Article
- Clinically relevant intra-articular corticosteroid doses impair equine osteoclast function in vitro.Veterinary surgery : VS · 2026Article
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- KPT-330 alleviates osteoarthritis by inhibiting subchondral bone osteoclastogenesis via the NF-κB and MAPK signaling pathways.iScience · 2026Article
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved During Osteoclast Differentiation.Molecular biotechnology · 2026Article
- Integrating network toxicology and in vitro validation to elucidate PET microplastic-induced osteoarthritis pathogenesis.Frontiers in pharmacology · 2026Article
- Gender-related differences in spontaneous osteoclastogenesis in knee osteoarthritis: A potential peripheral biomarker for early disease progression.Journal of experimental orthopaedics · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- Macrophages and osteoclasts: similarity and divergence between bone phagocytes.Frontiers in immunology · 2025Review
- Evaluation of changes in plasma levels of MMP-8, MMP-13, and Thrombospondin 2 in patients with Osgood-Schlatter disease (OSD).Frontiers in molecular biosciences · 2025Article
- Exosomal communication: a pivotal regulator of bone homeostasis and a potential therapeutic target.Frontiers in pharmacology · 2024Review
- Impaired fracture healing is associated with callus chondro-osseous junction abnormalities in periostin-null and osteopontin-null mice.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.Bone reports · 2023Article
- Molecular Assessment of Healthy Pathological Articular Cartilages in Physically Active People: A Scoping Review.International journal of molecular sciences · 2023Article
- Article
- Utilizing the codon adaptation index to evaluate the susceptibility to HIV-1 and SARS-CoV-2 related coronaviruses in possible target cells in humans.Frontiers in cellular and infection microbiology · 2022Article
- Zebrafish mutants reveal unexpected role of Lrp5 in osteoclast regulation.Frontiers in endocrinology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Osteoclasts are multinucleated, bone-resorbing cells. However, they also digest cartilage during skeletal maintenance, development and in degradative conditions including osteoarthritis, rheumatoid arthritis and primary bone sarcoma. This study explores the mechanisms behind the osteoclast-cartilage interaction. Human osteoclasts differentiated on acellular human cartilage expressed osteoclast marker genes (e.g. CTSK, MMP9) and proteins (TRAP, VNR), visibly damaged the cartilage surface and released glycosaminoglycan in a contact-dependent manner. Direct co-culture with chondrocytes during differentiation increased large osteoclast formation (p < 0.0001) except when co-cultured on dentine, when osteoclast formation was inhibited (p = 0.0002). Osteoclasts cultured on dentine inhibited basal cartilage degradation (p = 0.012). RNA-seq identified MMP8 overexpression in osteoclasts differentiated on cartilage versus dentine (8.89-fold, p = 0.0133), while MMP9 was the most highly expressed MMP. Both MMP8 and MMP9 were produced by osteoclasts in osteosarcoma tissue. This study suggests that bone-resident osteoclasts and chondrocytes exert mutually protective effects on their 'native' tissue. However, when osteoclasts contact non-native cartilage they cause degradation via MMPs. Understanding the role of osteoclasts in cartilage maintenance and degradation might identify new therapeutic approaches for pathologies characterized by cartilage degeneration.
Indexed as
Identifiers
What OpenQuestion holds
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.