IL1B and rheumatic disorder: Specifically, rheumatic diseases, including OA, are often accompanied by increased tumor necrosis factor alpha (TNF-α) and interleukin 1beta (IL-1β), both shown to contribute to cartilaginous matrix breakdown, by up-regulating cartilage catabolic enzymes (e.g., matrix metalloproteinases [MMPs] and disintegrin and metalloproteinase with thrombospondin motifs [ADAMTS]), often leading to progressive articular cartilage damage and ectopic mineralization of the joint surfaces (3, , –6).