[Ankle chondrocytes are more resistant to Interleukin-1 than chondrocytes derived from the knee]

Orthopade. 2006 Jul;35(7):784-90. doi: 10.1007/s00132-006-0958-2.
[Article in German]

Abstract

Background: The incidence of degenerative changes and osteoarthritis is lower in the ankle than in the knee joints. This cannot be explained exclusively with differences in anatomy and biomechanical properties of these two synovial joints. Previous studies have indicated distinct differences in the biochemical composition of the extracellular matrix of articular cartilage from knee and ankle joints. The aim of this study was to identify potential metabolic differences between knee and ankle joint chondrocytes using isolated cells to distinguish the secondary effects of the resident extracellular matrix from the primary matrix-independent effects of cellular differentiation.

Method: Isolated knee and ankle chondrocytes from the same human donor were cultured in alginate beads and subsequently exposed to a three-day pulse of the catabolic cytokine interleukin-1 (IL-1) as a model of an inflammatory episode. The metabolism of proteoglycans (PG's) was analyzed as expressed changes in 35S-sulfate incorporation into glycosaminoglycans (GAG's).

Results: The presence of IL-1 induced an inhibition of PG synthesis in knee and ankle articular chondrocytes. The 50% inhibitory concentration (IC50) of IL-1 was about 5 times lower for knee than for ankle chondrocytes.

Conclusion: Ankle chondrocytes are more resistant to IL-1 induced inhibition of PG synthesis than chondrocytes from the knee.

Publication types

  • Comparative Study
  • English Abstract

MeSH terms

  • Adult
  • Aged
  • Ankle Joint / drug effects
  • Ankle Joint / metabolism*
  • Cells, Cultured
  • Chondrocytes / drug effects
  • Chondrocytes / metabolism*
  • Dose-Response Relationship, Drug
  • Humans
  • Interleukin-1 / administration & dosage*
  • Knee Joint / drug effects
  • Knee Joint / metabolism*
  • Middle Aged
  • Organ Specificity
  • Proteoglycans / metabolism*

Substances

  • Interleukin-1
  • Proteoglycans