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Home / Equine Research Bank / Rheumatol Int / Variations in chondrocyte apoptosis may explain the increase...
Rheumatology international2010; 31(10); 1341-1348; doi: 10.1007/s00296-010-1471-9

Variations in chondrocyte apoptosis may explain the increased prevalence of osteoarthritis in some joints.

Abstract: To investigate whether there are any variations in chondrocyte susceptibility to an apoptotic stimulus between cells of articular cartilage (AC) from equine joints that differ in prevalence of osteoarthritis (OA). Methods: Cartilage from macroscopically normal equine metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints was used. Prior to culture, chondrocyte viability was assessed using the fluorescein diacetate (FDA) and propidium iodide paravital staining method. AC explants were subsequently treated with tumour necrosis factor-α (TNF-α) in combination with Actinomycin D to induce apoptosis. Apoptosis of chondrocytes in cartilage sections was assessed by expression of active caspase-3 using indirect immunohistochemistry and sections also histologically graded using a 'modified' Mankin scoring system. Results: Prior to culture (mean ± standard deviation) chondrocyte viability was 80.7% (3.5). The extent of chondrocyte apoptosis induced by TNF-α/Actinomycin D varied markedly according to the joint type that the cartilage was sampled from. For MCP joints, the extent of overall chondrocyte apoptosis was significantly higher (P < 0.001) in stimulated explants (26.7%, 10.3) than that observed in unstimulated control samples (9.6%, 7.5). Conversely, chondrocytes from PIP and DIP joint cartilage did not respond significantly to apoptotic stimulation (P > 0.05). Significant variations in cellularity and thickness were also evident between cartilages of different joint types. Conclusions: Data in this study demonstrate that chondrocytes from three equine joint types with varying prevalences of OA differ significantly in terms of susceptibility to apoptosis induction. This may provide a possible explanation for the joint-specific nature of the disease.
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Publication Date: 2010-04-16 PubMed ID: 20396889DOI: 10.1007/s00296-010-1471-9Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research investigates the differences in susceptibility to programmed cell death (apoptosis) in cartilage cells (chondrocytes) from various horse (equine) joints. The aim is to determine if these variations in cell behavior could provide insight into why some joints are more prone to osteoarthritis – a degenerative joint disease.

Methods

  • The research examined three types of equine joints – the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints.
  • The health of these cells was evaluated using the fluorescein diacetate and propidium iodide paravital staining method, before culture.
  • Subsequently, to understand how these cells react to factors causing programmed cell death or apoptosis, the cartilage samples were exposed to tumor necrosis factor-α (TNF-α) and Actinomycin D, known inducers of apoptosis.
  • The number of cells undergoing apoptosis were calculated by examining expression of a protein called active caspase-3, known to be involved in apoptosis, using a technique called indirect immunohistochemistry.
  • Cartilage samples were also graded histologically based on cellularity and thickness using a ‘modified’ Mankin scoring system.

Results

  • Before they were cultured and subjected to apoptosis-inducing stimulus, most of the chondrocytes were found to be viable (~80%).
  • Apoptosis varied noticeably between the cartilage from different joint types after they were exposed to the TNF-α/Actinomycin D combination.
  • In the cartilage from MCP joints, a significantly high level of chondrocyte apoptosis was observed when compared to the unstimulated samples.
  • On the other hand, the chondrocytes from PIP and DIP joints did not show a significant response in terms of apoptosis to the same stimulus.
  • Variations were also found in the cellularity and thickness of the cartilage from different joints.

Conclusions

  • This research found that chondrocytes from different types of equine joints, which have varying prevalence of osteoarthritis, differ significantly in their response to the process of apoptosis.
  • These results suggest a possible explanation for why osteoarthritis affects certain joints more than others by implying an inherent difference in how cartilage cells from these joints behave when faced with apoptotic conditions.

Cite This Article

APA
Thomas CM, Whittles CE, Fuller CJ, Sharif M. (2010). Variations in chondrocyte apoptosis may explain the increased prevalence of osteoarthritis in some joints. Rheumatol Int, 31(10), 1341-1348. https://doi.org/10.1007/s00296-010-1471-9

Publication

Rheumatology international
ISSN: 1437-160X
NlmUniqueID: 8206885
Country: Germany
Language: English
Volume: 31
Issue: 10
Pages: 1341-1348

Researcher Affiliations

Thomas, C M
  • Department of Anatomy, University of Bristol, Southwell Street, Bristol, BS2 8EJ, UK.
Whittles, C E
    Fuller, C J
      Sharif, M

        MeSH Terms

        • Animals
        • Apoptosis / physiology
        • Cartilage, Articular / pathology
        • Cells, Cultured
        • Chondrocytes / pathology
        • Disease Models, Animal
        • Female
        • Horse Diseases / pathology
        • Horses
        • Male
        • Metacarpophalangeal Joint / pathology
        • Organ Specificity
        • Osteoarthritis / epidemiology
        • Osteoarthritis / pathology
        • Prevalence
        • Toe Joint / pathology
        • Tumor Necrosis Factor-alpha / physiology

        Grant Funding

        • Biotechnology and Biological Sciences Research Council

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        Citations

        This article has been cited 7 times.
        1. Xu Y, Yang Y, Song H, Li M, Shi W, Yu T, Lin J, Yu Y. The Role of Exerkines in the Treatment of Knee Osteoarthritis: From Mechanisms to Exercise Strategies. Orthop Surg 2025 Apr;17(4):1021-1035.
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        2. Lee YT, Mohd Yunus MH, Yazid MD, Ugusman A. Unraveling the path to osteoarthritis management: targeting chondrocyte apoptosis for therapeutic intervention. Front Cell Dev Biol 2024;12:1347126.
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          doi: 10.1111/jcmm.13237pubmed: 28609022google scholar: lookup
        7. Fox B, Schantz JT, Haigh R, Wood ME, Moore PK, Viner N, Spencer JP, Winyard PG, Whiteman M. Inducible hydrogen sulfide synthesis in chondrocytes and mesenchymal progenitor cells: is H2S a novel cytoprotective mediator in the inflamed joint?. J Cell Mol Med 2012 Apr;16(4):896-910.
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