Degeneration of cartilage resulting from trauma or disease processes is an increasingly prevalent problem in the aging population. Intrinsic repair of cartilage is limited and few methodologies exist, short of prosthetic replacement, for restoring damaged articular surfaces. These realities engender a need for new strategies for extrinsic repair. One strategy, tissue engineering, generates replacement cartilage composed of scaffolds and differentiated chondrocytes [1]. In addition to chondrocytes, recent work has demonstrated that mesenchymal stem cells (MSCs) isolated from bone marrow may be induced to take on a chondrocyte-like phenotype [2]. Tissue engineered constructs of either cell type can yield near-native properties (though those derived from MSCs are typically lower) [3]. While such constructs may be surgically implanted to replace areas denuded of cartilage, one factor to consider is that these defect sites exist in an already inflamed joint [4]. In addition, surgical interventions trigger further inflammatory responses, greatest in the area of intervention [5]. Recent literature has shown that pro-inflammatory cytokines, such as interleukin-1beta (IL-1β), instigate catabolic destruction not only of cartilage explants, but also of chondrocyte-based engineered cartilage constructs [6–9]. Still other studies have shown that un-differentiated MSCs themselves may exert an anti-inflammatory effect on their local environment [10–12]. Thus the current study examined the effect of varying doses of IL-1β exposure on both chondrocyte- and MSC-based engineered cartilage constructs to determine the relative sensitivity of neo-cartilage derived from each cell type to cytokine induced degradation.

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