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Related Experiment Videos

Osteoarthritic cartilage fibrillation is associated with a decrease in chondrocyte adhesion to fibronectin.

M Piperno1, P Reboul, M P Hellio le Graverand

  • 1Claude Bernard University, Centre Hospitalier Lyon Sud, Pierre Bénite, France.

Osteoarthritis and Cartilage
|May 27, 1999
PubMed
Summary
This summary is machine-generated.

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Osteoarthritis (OA) cartilage destruction involves failed repair. Chondrocyte (cartilage cell) adhesion to fibronectin is defective in fibrillated OA cartilage, but glucosamine sulfate may reverse this defect, potentially aiding OA treatment.

Area of Science:

  • Biomedical Science
  • Orthopedics
  • Cell Biology

Background:

  • Osteoarthritis (OA) is characterized by cartilage destruction, often viewed as a failed tissue repair process.
  • Cell adhesion to the extracellular matrix is crucial for tissue repair mechanisms.
  • Understanding chondrocyte adhesion in OA is key to exploring potential therapeutic interventions.

Purpose of the Study:

  • To investigate the adhesion of chondrocytes from human OA cartilage to extracellular matrix proteins.
  • To compare chondrocyte adhesion from intact versus fibrillated cartilage surfaces.
  • To examine the effects of protein kinase C (PKC) inhibitors and glucosamine sulfate (GS) on chondrocyte adhesion.

Main Methods:

  • Chondrocytes were isolated from human OA femoral head cartilage with intact or fibrillated surfaces.

Related Experiment Videos

  • Cell adhesion assays were performed using fibronectin and type II collagen as substrates.
  • The impact of PKC inhibitors (W7, sphingosine) and glucosamine sulfate (GS) on cell adhesion was evaluated.

    • Main Results:

    • Chondrocytes from fibrillated OA cartilage exhibited significantly decreased adhesion to fibronectin compared to those from intact cartilage.
    • Adhesion to type II collagen was not significantly different between cells from intact and fibrillated cartilage.
    • PKC inhibitors reduced fibronectin adhesion in cells from intact cartilage, while GS treatment increased fibronectin adhesion in cells from fibrillated cartilage.

    Conclusions:

    • Fibrillation of OA cartilage is associated with impaired chondrocyte adhesion to fibronectin.
    • This defective adhesion appears to involve protein kinase C (PKC) and/or calmodulin-dependent kinases.
    • Glucosamine sulfate treatment may offer a potential therapeutic strategy by restoring chondrocyte adhesion in OA.