Mylène Jansen

Clinical evidence and molecular mechanisms of KJD 203 10 joint distraction, as indicated by collagen type II markers, proteoglycan (PG) turnover and a catabolic transcription profile using a canine animal KJD model. This hints that not only during distraction but also the post-distraction period seems to be essential. It is obvious that larger studies are needed, both clinical as preclinical, with multiple time points, both during and post-treatment focusing on broader sets of markers and transcripts to further expand and value the effects found thus far. Figure 2 : Overview of joint processes/molecular mechanisms during/after distraction. Distraction changes the OA- related joint homeostasis. The reduced mechanical (over)load on the articular cartilage surfaces prevents wear and tear and might initiate intrinsic cartilage repair activity (upper part of figure). Resilience in the distraction frame causes synovial fluid pressure changes during loading and unloading of the joint, improving nutrition of cartilage and stimulating chondrocytes. Distraction also results in considerable periarticular bone changes (middle part of figure). Altered activity of bone cells may add to release of trophic factors to support cartilage repair. Restoration of the mechanical and the biochemical environment of the joint, including the loss of the hyaluranon coating from synovial fluid-resident MSCs, might therefore provide a window of opportunity in which joint-resident MSCs can attach and repair tissues (lower part). MSCs: mesenchymal stem cells; SF-MSCs: synovial fluid derived MSCs.