Although epidemiological studies have promoted our understanding of the risk factors that predispose to OA, we do not yet understand the initiating events that trigger the disease. OA is primarily a disease of cartilage Cartilage is a unique tissue with viscoelastic and compressive properties which are imparted by its extracellular matrix, composed predominantly of type II collagen and proteoglycans (slide). Under normal conditions, this matrix is subjected to a dynamic remodeling process in which low levels arthritis - palindromic rheumatism arthritis - palindromic rheumatism of degradative and synthetic enzyme activities are balanced, such that the volume of cartilage is maintained. In OA cartilage, however, matrix degrading enzymes are overexpressed, shifting this balance in favor of net degradation, with resultant loss of collagen and proteoglycans from the matrix (slide). Presumably in response to this loss, chondrocytes initially proliferate and synthesize enhanced amounts of proteoglycan and collagen molecules. As the disease progresses, however, reparative attempts are outmatched by progressive cartilage degradation. Fibrillation, erosion and cracking initially appear side pain arthritis - palindromic rheumatism in the superficial layer of cartilage and progress over time to deeper layers, resulting eventually in large clinically observable erosions. OA, in simplistic terms, therefore, can be thought of as a process of progressive cartilage matrix degradation to which an ineffectual attempt at repair is made. (top of page) Is OA simply a process of aging of cartilage? A critical question is whether OA is truly a disease or a natural consequence of aging. Several differences between cellular therapy + arthritis arthritis - palindromic rheumatism aging cartilage and OA cartilage have been described, suggesting the former. For example, although denatured type II collagen is found in both normal aging and OA cartilage, it is more predominant in OA. In addition, OA and normal aging cartilage differ in the amount of water content and the in ratio of chondroitin-sulfate to keratin sulfate constituents. The expression of a chondroitin-sulfate epitope (epitope 846) in OA cartilage, that is otherwise only present in fetal and neonatal cartilage, provides further evidence pain info arthritis - palindromic rheumatism that OA is
