This study queried whether chondrocytes contribute to joint damage through soluble factors that activate synovial fibroblasts (SF). SF were isolated from 2 patients with RA and implanted into severe combined immunodeficient (SCID) mice together with fresh articular cartilage or with cartilage that had been stored for 24 hrs at either 40^oC or 37^oC. [SCID mice are used because they cannot reject the transplanted tissue.] After 60 days the invasion of RA-SF into the cartilage specimens was compared histologically and by a scoring system.

Results: RA-SF that were implanted with fresh cartilage showed a higher invasion score than RA-SF implanted with stored cartilage (regardless of temperature of storage) (3.2 ± 0.2 vs 2.1 ± 0.3 respectively). In an in vitro model, cycloheximide treatment of chondrocytes in a 3-dimensional matrix suppressed the invasiveness of RA-SF by 48%. This inhibition was partially reversed by the addition of interleukin-1 but not by tumor necrosis factor-a.

Editorial Comment: In the synovium, macrophages are believed to be the major producers of IL-1 and TNF-athat activate synovial fibroblasts. In these models, synovial fibroblasts have been separated from monocytes/macrophages. It is perhaps not surprising that chondrocytes, which are also known to produce IL-1 and TNF-a, can substitute for macrophages in inducing an activated phenotype in synovial fibroblasts. Perhaps the more interesting question is what role the chondrocytes play in directly degrading their surrounding matrix.

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