Interleukin-1β enhances cartilage-to-cartilage integration.

摘要: The failure of cartilages to fuse, particularly in the case articular cartilage under conditions repair is due morphological and structural constraints tissue. Factors that impede integration include, non-vascularisation, low cellularity, proteoglycan surrounding extracellular matrix acting as a natural barrier cellular migration. We hypothesised brief activation catabolic cascade by cytokines followed culture anabolic would promote tissue fusion ring-disk model integration. Our results show transient exposure 10 ng mL-1 interleukin-1β, two weeks post-culture conditions, enhanced cartilage-cartilage compared untreated explants. Quantitative PCR analysis catabolism-related genes ADAMTS4 MMP13 showed both were transiently upregulated these findings correlated with evidence remodelling. At level histology, we observed chondrocytes readily populated interfacial between fused explants interleukin-1β treated explants, whereas control this region was relatively acellular comparison. Catabolic cytokine exhibited 29-fold greater adhesive strength (0.859 MPa versus 0.028 MPa, P <0.05) than counterparts. Collectively, our demonstrate single short pulse an response sufficient generate mechanically robust, integrative repair.