Cyclic Compression of Chondrocytes Counteracts Pro-Inflammatory Tissue Remodeling Induced by Interleukin-1

Chondrocytes in tissue engineered constructs face challenging environments when first transplanted into a synovial joint, including high levels of compression/shear and pro-inflammatory cytokines. The joint level of interleukin 1 (IL-1) after trauma injury and in a repaired joint is acutely elevated. Matrix remodeling in tissue engineered constructs can be easily affected by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 11]. Several recent studies suggest that tensile loading and unconfined compression of chondrocytes has some anti-inflammatory effects against interleukin 1 (IL-1) by the downregulation of COX-2 and iNOS genes [1, 5, 6]. However, the role of loading in tissue repair at physiological levels is not clear. The objective of this study was to determine the effect of cyclic confined compression on the gene expression of MMPs and tissue inhibitors of metalloproteinases (TIMPs) in agarose-embedded chondrocytes in the presence of interleukin 1 (IL-1).