FIG. 1.

Inflammation in cartilage repair. Abnormally high contact stresses such as mechanical overload transmitted to focal areas of articular cartilage result in cartilage defects and release cartilage fragments. This process stimulates the synovial membrane, leading to the activation of macrophages and inflammatory cells such as T cells, which produce interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNFα). In an autocrine–paracrine manner, these activated inflammatory factors may stimulate chondrocytes to secrete degradative enzymes like proteinases, such as matrix metalloproteinases (MMPs) and a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS), which are directly involved in degradation of type II collagen and aggrecans in cartilage matrix. In the meantime, chondrocytes can change phenotype and size in response to stimulation from inflammatory factors and undergo hypertrophy, which is an essential step in the endochondral ossification process. Color images available online at www.liebertpub.com/teb