Evaluation of In Vivo Proteolytic Activity

Osteoarthritis (OA) is a degenerative articular disease primarily observed in older adults, and is the leading cause of physical disability and impaired quality of life. OA is characterized by softening, fibrillation, erosion, defect of the articular cartilage, bone hypertrophy at the margins with osteophyte formation, subchondral sclerosis, and chronic inflammation of the synovial membrane and joint capsule (Zhang et al., 2010). These alterations are thought to be caused by biochemical and biomechanical factors leading to a failure in the balance of synthesis and degradation (Martel-Pelletier et al., 2010). Pathogenesis of OA is based on an imbalance of the functional requirements and morphologic alterations, and these statuses progressively and chronically evoke subsequent alterations (Lorenz et al., 2005). Although the etiology of OA is not completely understood, the accompanying biochemical, structural, and metabolic alterations of the articular cartilage have been well described (de Seny et al., 2011; Kraus 2010; Reeves et al., 2011; Sobczak et al., 2010). Recently, it has been revealed that proteolytic enzymes, cytokines, biomechanical stress, and altered genetics are involved in its pathogenesis, and proteolytic activity is particularly important in regards to the morphologic alterations of the articular structures, and is considered as an internalfactor of the disease (Takei et al., 1999; Kevorkian et al., 2004). It has been suggested that proteolytic activity in the constituent of the joint, such as synovium, joint fluid, cartilage, is continuously involved in the articular alterations of the disease, as its progression is gradual. Although it is extremely difficult to accurately predict future articular OA alterations, it is possible to evaluate the present phenomenon, which may lead to speculation of possible further alterations by evaluating proteolytic activity in the joint.