Differential release of molecular markers in joint disease

Abstract

Cartilage and bone, the principal tissues of the diar-throdial joint, are dynamic tissues with continuous matrix turnover. These tissues, like all connective tissues, contain few cells surrounded by an abundant matrix. The cells, e.g. the chondrocytes in cartilage, regulate both synthesis and degradation of the matrix constituents in response to various environmental factors, such as hormones, nutrients, mechanical load or cytokines. Under normal conditions, the balance between matrix catabolism and anabolism is well regulated, and the tissue integrity is maintained. However, in pathological conditions, such as rheumatoid arthritis (RA), arthrosis (OA) or traumatic conditions, changes in the tissue turnover occur which disturb the balance. Thus in RA the inflammatory process induces cytokine-mediated matrix degradation of cartilage with concomitant depression of synthesis gradually leading to loss of the entire matrix (Harris 1990, Heinegård and Saxne 1991).