ReviewCurrent rheumatology reports2019
The Role of Chondrocyte Morphology and Volume in Controlling Phenotype-Implications for Osteoarthritis, Cartilage Repair, and Cartilage Engineering.
Review in Current rheumatology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- Global research trends on macrophage polarization in osteoarthritis: a bibliometric analysis.Frontiers in immunology · 2025Pooled it
- The F-Actin of In Situ Chondrocytes in Non-Degenerate and Mildly-Degenerate Human Cartilage: Changes With Cell Volume, and Cytoplasmic Processes.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Topographical design principles for osteochondral tissue engineering.Bioactive materials · 2026Review
- Microcavitary Alginate Hydrogel Reverses Chondrocyte Dedifferentiation via Temporal Modulation of the p53 Pathway.Annals of biomedical engineering · 2026Article
- Local delivery of OSK factors enables partial cellular reprogramming to mitigate osteoarthritis and cartilage fibrosis.Experimental & molecular medicine · 2026Article
- Acupotomy Ameliorates Articular Cartilage Fibrosis in a Rabbit Model of Knee Osteoarthritis via the TGF-β1/Smad Pathway.Orthopedic research and reviews · 2026Article
- From nerve to bone: a tale of autonomic nervous system, bone cells, and beyond.Military Medical Research · 2026Review
- Bioengineered Tricomposite Hydrogel Enhances Chondrogenic Phenotype and Hyaline Matrix Formation in Human Chondrocytes.Gels (Basel, Switzerland) · 2025Article
- Recent Advances in Silk Fibroin Derived fromJournal of functional biomaterials · 2025Review
- Bioenergetic-active hydrogel drives extracellular matrix synthesis for cartilage repair.Bioactive materials · 2025Article
- Microstructure and matrix-filled lacunae impact mechanical response of temporomandibular joint cartilage under physiological loading.Osteoarthritis and cartilage · 2025Article
- Article
- Substrate Stiffness Modulates Hypertrophic Chondrocyte Reversion and Chondrogenic Phenotype Restoration.Cells · 2025Article
- Insights into chondrocyte populations in cartilaginous tissues at the single-cell level.Nature reviews. Rheumatology · 2025Review
- Article
- Cartilage-SpecificBiomedicines · 2025Article
- DDX3X Activates Chondrocyte Pyroptosis to Promote Osteoarthritis Progression.Cell biochemistry and biophysics · 2025Article
- Dynamic Col-HZ Hydrogel with efficient delivery of bioactivator promotes ECM deposition and cartilage formation.Materials today. Bio · 2025Article
- Comparison of passive and active motion: effect of myokine irisin on cartilage in knee osteoarthritis rats.Frontiers in physiology · 2025Article
- Donor ethnicity, sex, and age impact chondrogenic re-differentiation capacity: a multi-demographic study of human articular chondrocytesJournal of the Royal Society of New Zealand · 2025Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewArticular chondrocytes are exclusively responsible for the turnover of the extracellular matrix (ECM) of hyaline cartilage. However, chondrocytes are phenotypically unstable and, if they de-differentiate into hypertrophic or fibroblastic forms, will produce a defective and weak matrix. Chondrocyte volume and morphology exert a strong influence over phenotype and a full appreciation of the factors controlling chondrocyte phenotype stability is central to understanding (a) the mechanisms underlying the cartilage failure in osteoarthritis (OA), (b) the rationale for hyaline cartilage repair, and (c) the strategies for improving the engineering of resilient cartilage. The focus of this review is on the factors involved in, and the importance of regulating, chondrocyte morphology and volume as key controllers of chondrocyte phenotype. RECENT
findingsThe visualisation of fluorescently-labelled in situ chondrocytes within non-degenerate and mildly degenerate cartilage, by confocal scanning laser microscopy (CLSM) and imaging software, has identified the marked heterogeneity of chondrocyte volume and morphology. The presence of chondrocytes with cytoplasmic processes, increased volume, and clustering suggests important early changes to their phenotype. Results from experiments more closely aligned to the normal physico-chemical environment of in situ chondrocytes are emphasising the importance of understanding the factors controlling chondrocyte morphology and volume that ultimately affect phenotype. An appreciation of the importance of chondrocyte volume and morphology for controlling the chondrocyte phenotype is advancing at a rapid pace and holds particular promise for developing strategies for protecting the chondrocytes against deleterious changes and thereby maintaining healthy and resilient 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.