Abstract
ObjectiveTo explore the molecular function of Osteopontin (OPN) in the pathogenesis of human OA, we compared the expression levels of OPN in synovial fluid with clinical parameters such as arthroscopic observation of cartilage damage and joint pain after joint injury.MethodsSynovial fluid was obtained from patients who underwent anterior cruciate ligament (ACL) reconstruction surgery from 2009 through 2011 in our university hospital. The amounts of intact OPN (OPN Full) and it’s N-terminal fragment (OPN N-half) in synovial fluid from each patient were quantified by ELISA and compared with clinical parameters such as severity of articular cartilage damage (TMDU cartilage score) and severity of joint pain (Visual Analogue Scale and Lysholm score).ResultsWithin a month after ACL rupture, both OPN Full and N-half levels in patient synovial fluid were positively correlated with the severity of joint pain. In contrast, patients with ACL injuries greater than one month ago felt less pain if they had higher amounts of OPN N-half in synovial fluid. OPN Full levels were positively correlated with articular cartilage damage in lateral tibial plateau.ConclusionOur data suggest that OPN Full and N-half have distinct functions in articular cartilage homeostasis and in human joint pain.
Highlights
Osteoarthritis (OA) is a group of diseases and mechanical abnormalities involving degradation of articular cartilage and subchondral bone
One approach to understand the molecular pathogenesis of OA may be the identification and characterization of the genes involved in joint development and homeostasis
Kinetics of OPN Levels in Synovial Fluid after Joint Injury As shown in Fig. 1, OPN Full levels were significantly decreased with time after anterior cruciate ligament (ACL) rupture
Summary
Osteoarthritis (OA) is a group of diseases and mechanical abnormalities involving degradation of articular cartilage and subchondral bone. It was reported that OA affects 27 million people in the U.S in 2005 and it is estimated that 80% of the U.S population will have radiographic evidence of OA by age 65 [1] These statistics strongly indicate that both prevention of cartilage loss and promotion of cartilage repair in the recovery of joint function are important issues to address [2]. The major therapeutic strategy for OA is based on conservative treatments, such as muscle exercise with medications, to relieve joint inflammation and pain [3] These treatments are not always satisfactory because they are not powerful enough to inhibit OA progression nor can they promote cartilage repair. We focused on analyzing the molecular function of OPN in the pathogenesis of human OA
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