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      Histomorphology and Innate Immunity during the Progression of Osteoarthritis: Does Synovitis Affect Cartilage Degradation?

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          Abstract

          Osteoarthritis (OA) is a common chronic degenerative disease that affects all joints. At present, the pathological processes and mechanisms of OA are still unclear. Innate immunity, a key player in damage to the structure of the joint and the mechanism by which the host attempts to repair OA, affects all pathological stages of the disease. In the present study, our aim was to assess changes in innate immunity during the pathological processes of OA in articular cartilage (AC) and the synovial membrane (SM), which are the major structures in joints, and to systematically examine the histological changes in AC and SM in mild, moderate and severe cases of OA, in order to further speculate about the manner in which the interactions of AC and SM are facilitated by innate immunity. Histological methods (including HE and Safranin O-fast green staining) were used to assess the morphological changes within AC and SM tissues in healthy and mild, moderate or severe OA rats. Mankin's and Wakitani scorings were conducted on the AC to assess the degradation of the cartilage and the extent of synovial inflammation. Localization and intensity of expression of the three key proteins: TLR4 (upstream), MyD88 (midstream) and NF-κB (downstream) of the inflammatory pathway believed to be involved in innate immune system-induced AC and SM structural degeneration, were examined using immunofluorescent staining. This technique allows a more stereoscopic visualization of the cellular structure by labeling the relative positions of the proteins of interest using fluorescent markers. In addition, significantly enhanced fluorescence signals could be detected by fluorescence microscopy in areas with more severe tissue damage. Combined with the terminal-deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, the phenomenon of apoptosis in chondrocytes and synoviocytes was observed. We found that TLR4, MyD88 and NF-κB were significantly expressed in the AC and SM of the OA rats, while very little expression was detected in healthy rats. We speculate that innate immunity is programmed to play a role in mediating the repair of tissue damage. Considering the differences in the expression levels of these proteins in AC and SM during different stages of the disease, the SM might play a driving role in the process of creating lesions. Western blots (WBs) were combined to confirm the trend of expression of TLR4, MyD88 and NF-κB in SM tissues during different stages of OA. The expression of an important specificity protein TRAF6, in addition to IL-1β and TNF-α, representative downstream inflammatory mediators, were also measured in order to verify the key role of the signaling pathway in OA. In addition, we systematically describe the principal cell types in the SM which participate in innate immunity. Our results showed that the damage to AC and SM within the joints progressively worsened during the course of the disease, and that the innate immune system was closely involved in the AC and SM during each stage of OA. These findings also confirmed that SM may affect the pathological changes in AC through the innate immune system, and therefore affect the progress of OA. This article is protected by copyright. All rights reserved.

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          Author and article information

          Journal
          J. Cell. Physiol.
          Journal of cellular physiology
          Wiley-Blackwell
          1097-4652
          0021-9541
          May 17 2017
          Affiliations
          [1 ] Beijing University of Chinese Medicine, Beijing, China.
          [2 ] China-Japan Friendship Hospital, Beijing, China.
          [3 ] The Third Affiliated Hospital of Beijing, University of Chinese Medicine, Beijing, China.
          Article
          10.1002/jcp.26011
          28513840

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