Hypothesis
Phenotypic modulation of chondrocytes as a potential therapeutic target in osteoarthritis: a hypothesis
a Institute of
Pathology, University of Erlangen-Nürnberg, Germany , b Kennedy-Institute of Rheumatology, London
Correspondence to: Dr T Aigner, Institute of Pathology, University of Erlangen-Nürnberg, Krankenhausstr 8-10, D-91054 Erlangen, Germany.
Accepted for publication 11 February 1997
| The first 150 words of the full text of this article appear below. |
 |
Introduction |
|---|
One central hallmark of osteoarthritic cartilage
degeneration is the loss of matrix molecules, in particular
proteoglycans. However, chondrocytes of osteoarthritic cartilage are
generally thought to be anabolically hyperactive. Thus, in
osteoarthritic cartilage degeneration, the ongoing net loss of the
cartilage matrix components is attributed not to a lack of synthesis of cartilage matrix molecules by the cartilage cells, but to an increase in matrix catabolism by most authors.1-3 In contrast, our
in situ analysis on the single cell level showed a suppression of aggrecan and collagen type II expression in the chondrocytes in the
upper cartilage zone, which is critical for the progression of the
cartilage destruction. Phenotyping of the osteoarthritic chondrocytes
in this zone furthermore shows that the decrease in anabolic activity
was presumably not simply because of cell deactivation, but may entail
a specific cell differentiation pathway taken by the osteoarthritic
chondrocytes. Based on our in situ analyses,
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