Osteoarthritis: Practice Essentials, Background, Anatomy

In the normal joint, there is a balance between the continuous process of cartilage matrix degradation and repair. In OA, disruption of the homeostatic state occurs and the catabolic (breakdown) processes of chondrocytes are increased. The principal cytokines linked to the catabolism of cartilage and to the OA process are interleukin (IL)-1, tumor necrosis factor (TNF)-a, and IL-6. IL-1 is the prototypic inducer of catabolic responses in chondrocytes. This substance causes the increased secretion of proteinases (which breakdown cartilage matrix) including collagenase, the suppression of proteoglycan synthesis leading to the suppression of matrix synthesis, and ultimately the reduction of the number of chondrocytes.15, 16 (See Figure 2.)

Treatment of Deep Cartilage Defects in the Knee with Autologous Chondrocyte Transplantation

One of the earliest features of the development of osteoarthritis is degeneration of the articulating surfaces of the joint. This is characterized by fibrillation of the articular cartilage, in which the mesh of collagen fibers is disrupted. Degeneration of type II collagen is seen, as well as a decrease in the extracellular matrix.22 Loss of proteoglycan from the matrix is characteristic. The loss of aggrecan, the predominant PRG in articular cartilage imposes an increasing load on the collagen fibrils, causing further breakdown.23 Early in the course of OA, the tissue mounts an attempt at repair. Chondrocytes proliferate and there is an increase in matrix synthesis.24 However, if this repair process is disrupted for any reason including the use of NSAIDs, degradative enzymes overwhelm the synthetic capability and the repair fails. Particular compositional, molecular, and structural changes will continue to occur within the articular cartilage including decreased proteoglycan and increased water content, collagen fibril network disorganization, and proteoglycan separation, as long as the inciting issue (NSAID use) continues. (See Figure 5.)

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Journal of Biomaterials and Tissue Engineering