ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2021
Cartilage articulation exacerbates chondrocyte damage and death after impact injury.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Combined cartilage thickness and mechanical property mismatch drives local strain amplification at the patellar osteochondral allograft interface.Biomechanics and modeling in mechanobiology · 2026Article
- Photobiomodulation outperforms ultrasound in reducing IL-1APL bioengineering · 2026Article
- New therapeutic target for osteoarthritis: modulating immune-metabolic aberrations and micromilieu remodeling in underlying bone.Frontiers in pharmacology · 2026Review
- Time-dependent computational model of post-traumatic osteoarthritis to estimate how mechanoinflammatory mechanisms impact cartilage aggrecan content.PLoS computational biology · 2025Article
- Optical Redox Imaging Predicts Post-Loading Cartilage Mitochondrial Membrane Potential.Annals of biomedical engineering · 2025Article
- Multiscale characterization of ultrasmall fluorescent core-shell silica nanoparticles in cartilage and synovial joints reveals rapid cartilage penetration and sustained joint residence.Acta biomaterialia · 2025Article
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- Research progress of procyanidins in repairing cartilage injury after anterior cruciate ligament tear.Heliyon · 2024Review
- Inflammatory mechanisms in post-traumatic osteoarthritis: a role for CaMKK2.Immunometabolism (Cobham, Surrey) · 2023Review
- Yes-associated protein nuclear translocation promotes anabolic activity in human articular chondrocytes.Osteoarthritis and cartilage · 2023Article
- Post-traumatic osteoarthritis: A review of pathogenic mechanisms and novel targets for mitigation.Bone reports · 2023Article
- Understanding the Influence of Local Physical Stimuli on Chondrocyte Behavior.Advances in experimental medicine and biology · 2023Review
- The Risk Factors and Preventive Strategies of Poor Knee Functions and Osteoarthritis after Anterior Cruciate Ligament Reconstruction: A Narrative Review.Physical therapy research · 2023Review
- Modeling early changes associated with cartilage trauma using human-cell-laden hydrogel cartilage models.Stem cell research & therapy · 2022Article
- Bio-orthogonal Click Chemistry Methods to Evaluate the Metabolism of Inflammatory Challenged Cartilage after Traumatic Overloading.ACS biomaterials science & engineering · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Posttraumatic osteoarthritis (PTOA) is typically initiated by momentary supraphysiologic shear and compressive forces delivered to articular cartilage during acute joint injury and develops through subsequent degradation of cartilage matrix components and tissue remodeling. PTOA affects 12% of the population who experience osteoarthritis and is attributed to over $3 billion dollars annually in healthcare costs. It is currently unknown whether articulation of the joint post-injury helps tissue healing or exacerbates cellular dysfunction and eventual death. We hypothesize that post-injury cartilage articulation will lead to increased cartilage damage. Our objective was to test this hypothesis by mimicking the mechanical environment of the joint during and post-injury and determining if subsequent joint articulation exacerbates damage produced by initial injury. We use a model of PTOA that combines impact injury and repetitive sliding with confocal microscopy to quantify and track chondrocyte viability, apoptosis, and mitochondrial depolarization in a depth-dependent manner. Cartilage explants were harvested from neonatal bovine knee joints and subjected to either rapid impact injury (17.34 ± 0.99 MPa, 21.6 ± 2.45 GPa/s), sliding (60 min at 1 mm/s, under 15% axial compression), or rapid impact injury followed by sliding. Explants were then bisected and fluorescently stained for cell viability, caspase activity (apoptosis), and mitochondria polarization. Results show that compared to either impact or sliding alone, explants that were both impacted and slid experienced higher magnitudes of damage spanning greater tissue depths.
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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.