Characterization of Live and Experimentally Degenerated Hyaline Cartilage with Thermal Analysis

Abstract

Osteoarthritis (OA), the most prevalent joint disease, is characterized by the progressive loss of articular cartilage that leads to chronic pain and functional restrictions in affected joints [Goldring & Goldring, 2007]. The prior notion of OA as a bland disease related to aging and “wear and tear” of the joint has given way to views of a dynamic system with multiple pathogenic contributors, as local factors, as well as crystals and inflammation [Brandt et al., 2006]. OA represents a major therapeutic challenge to medical and health-care providers. In part, this is because OA is a chronic condition in which symptoms evolve over long periods of time and in which symptomatic episodes are frequently separated by lengthy asymptomatic periods. It is likely, however, that alterations in joint structure and function continue during these relative periods of clinical quiescence. In addition, limited tools are available for the assessment of the progression of structural changes in joint tissues in association with the development of osteoarthritis. Importantly, the correlation between structural alterations and symptoms is contradictory. There is a significant difference in the expression levels of cartilage relevant molecules between specimens showing histological alterations and control samples [Lorenz et al., 2006]. A total breakdown in synthesis of matrix molecules leads to the end stage OA with further progression of cartilage loss. A number of OA models, e.g. aging animals, genetically modified mice, as well as animals with surgically, enzymatically, or chemically induced OA [van den Berg, 2001] have been developed to investigate the pathogenesis of OA and evaluate the potentials of new disease/structure-modifying drugs [Oegema et al., 2002]. Among these, monosodium iodoacetate (MIA, iodoacetic acid) model has been widely used to analyze the histological and biochemical changes observed during the progression of OA [Ameye, & Young, 2006]. Injection of the metabolic inhibitor, MIA, into joints inhibits glyceraldehye-3-phosphate dehydrogenase activity in chondrocytes, resulting in disruption of glycolysis and eventual cell death [Kalbhen, 1987]. The progressive loss of chondrocytes results in histologic and morphologic changes to the articular cartilage, closely resembling those seen in human OA [Janusz et al., 2001]. In addition, the model has been utilized by a number of investigators to test pharmacologic agents for their ability to preserve cartilage structure [Janusz et al., 2001].