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Received May 24, 2017; Accepted Jun 22, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Osteoarthritis (OA) is a degenerative joint disease in the aging population that can cause disability. The functional limitation in the affected joint, which is caused by progressive degradation of cartilage and subchondral tissue remodeling, leads to bone deformity [1]. It is reported that metabolic interactions between cartilage and bones play pivotal roles in the pathogenesis of OA [2]. During OA progression, activated osteoblasts induce the production of matrix metalloproteinases (MMPs) by chondrocytes, which leads to cartilage degradation [3]. Subchondral bone osteoblasts produce proinflammatory cytokines such as interleukin- (IL-) 1, IL-6, and tumor necrosis factor-





