Abstract
BackgroundCartilage degradation is a typical characteristic of arthritis. This study examined whether there was a subset of phagocytic chondrocytes that expressed the specific macrophage marker, CD163, and investigated their role in cartilage degradation.MethodsCartilage from the knee and temporomandibular joints of Sprague-Dawley rats was harvested. Cartilage degradation was experimentally-induced in rat temporomandibular joints, using published biomechanical dental methods. The expression levels of CD163 and inflammatory factors within cartilage, and the ability of CD163+ chondrocytes to conduct phagocytosis were investigated. Cartilage from the knees of patients with osteoarthritis and normal cartilage from knee amputations was also investigated.ResultsIn the experimentally-induced degrading cartilage from temporomandibular joints, phagocytes were capable of engulfing neighboring apoptotic and necrotic cells, and the levels of CD163, TNF-α and MMPs were all increased (P<0.05). However, the levels of ACP-1, NO and ROS, which relate to cellular digestion capability were unchanged (P>0.05). CD163+ chondrocytes were found in the cartilage mid-zone of temporomandibular joints and knee from healthy, three-week old rats. Furthermore, an increased number of CD163+ chondrocytes with enhanced phagocytic activity were present in Col-II+ chondrocytes isolated from the degraded cartilage of temporomandibular joints in the eight-week experimental group compared with their age-matched controls. Increased number with enhanced phagocytic activity of CD163+ chondrocytes were also found in isolated Col-II+ chondrocytes stimulated with TNF-α (P<0.05). Mid-zone distribution of CD163+ cells accompanied with increased expression of CD163 and TNF-α were further confirmed in the isolated Col-II+ chondrocytes from the knee cartilage of human patients with osteoarthritis, in contrast to the controls (both P<0.05).ConclusionsAn increased number of CD163+ chondrocytes with enhanced phagocytic activity were discovered within degraded joint cartilage, indicating a role in eliminating degraded tissues. Targeting these cells provides a new strategy for the treatment of arthritis.
Highlights
Osteoarthritis (OA) is one of the main causes of chronic disability
The results showed that increased mRNA expression of tissue necrosis factor alpha (TNF-a), but not IL-1, was observed in the experimental groups compared with their agematched controls (Figure 1B)
Since chondrocytes are the only cell type within cartilage and as they remain within various stages of differentiation, we speculated that chondrocytes may take on the role of inflammatory cells within the joint cartilage
Summary
Osteoarthritis (OA) is one of the main causes of chronic disability. none of the therapies in current use appear to have an obvious impact on impeding or reversing the histopathological progression to advanced OA [1], mainly due to the limited understanding of its pathogenesis. The main functions of macrophages include phagocytosis and the production of inflammatory mediators, and these processes are tightly regulated by their surface receptors, which are heterogeneously expressed by mature tissue macrophages [6]. CD163, a member of the scavenger receptor cysteine-rich (SRCR) superfamily ( known as RM3/1, M130, or p155) [7], is one of the most specific surface markers for macrophages that is expressed at high levels in the majority of subpopulations of mature tissue macrophages across species [6,8,9,10,11]. This study examined whether there was a subset of phagocytic chondrocytes that expressed the specific macrophage marker, CD163, and investigated their role in cartilage degradation
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