The Biology of Articular Cartilage: An Overview?

In normal adult cartilage, the chondrocytes do not show proliferative activity and the network of type-II collagen fibers is extremely stable, with a half-life of several years, and also the turnover of aggrecan is not excessive (months to years) [3], making cartilage a very consistent tissue. Nevertheless, the adult chondrocytes are capable of adjusting the metabolic (structural and functional) cartilage homeostasis by regulating the balance of ECM components (synthesis versus degradation) depending on the (complex) presence and influence of various factors including the composition of the matrix itself, mechanical loads, local hormones, growth factors (transforming growth factor beta TGF-β, insulin-like growth factor I IGF-I, the bone morphogenetic proteins 2 and 7 BMP-2, -7), and cytokines (interleukin 1 IL-1, tumor necrosis factor alpha TNF-α), disease (osteoarthritis) (Figure 1) or injury, and aging [3,5,7-16]. The chondrocytes respond for instance to mechanical forces by interactions between their cell surface integrins and the components of the matrix or to local factors (hormones, growth factors, cytokines) by interactions with specific cell surface receptors. As a consequence, these cells can either secrete matrix molecules or the enzymes that degrade them (matrix metalloproteinase’s MMPs, aggrecanases) by undergoing phenotypic changes [3,7,17,18]. Increased chondrocyte proliferation activity is also often observed in altered physiological conditions [3], but cell death by apoptosis has also been reported when the cartilage undergoes pathological processes like in the case of osteoarthritis [3,19,20]. The molecular mechanisms of cartilage remodeling are under active investigation but still only partly understood, showing the need for continuous research to improve our understanding of these processes in this highly specialized tissue.