The involvement of TNF-α in the pathogenesis of arthritis was initially suggested by several in vitro approaches demonstrating that TNF-α can stimulate collagenases and many other matrix metalloproteinases (MMPs) in human synovial cells and fibroblasts [27,28] and recombinant TNF-α can cause bone resorption and inhibit bone formation [29]. Here, TNF is linked to arthritic joint disease.