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      Long-term histopathological developments in knee-joint components in a rat model of osteoarthritis induced by monosodium iodoacetate

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          Abstract

          [Purpose] This study was performed to evaluate the long-term histopathological changes in knee-joint components including synovial membrane and joint capsule in a rat model of osteoarthritis (OA) induced by monosodium iodoacetate (MIA). [Subjects and Methods] Fifty male rats were used. OA was induced through intra-articular injection of MIA, and ten rats were randomly allocated to each of five groups induced with OA for 1, 2, 4, 6, or 8 weeks. At the end of each period, the knee components were examined histopathologically. [Results] After 1 and 2 weeks, chondrocytes were weakly stained. After 4 weeks, fibrillation, fissuring, and eburnation were observed, whereas after 6 weeks, chondrocyte clustering and osteophyte formation were detected. In the synovial membrane, the proliferation of spindle-shaped cells and a multilayered structure of the surface cells were observed at 1 and 2 weeks, but the degree of these changes decreased over time. In the joint capsule, a narrowing of the space between collagen fiber bundles was observed at 4–8 weeks. [Conclusion] The long-term histopathological changes of the joint components observed in a rat model of OA induced by MIA were similar to those detected in OA, but differed at specific times and tissues.

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          Osteoarthritis cartilage histopathology: grading and staging.

          Current osteoarthritis (OA) histopathology assessment methods have difficulties in their utility for early disease, as well as their reproducibility and validity. Our objective was to devise a more useful method to assess OA histopathology that would have wide application for clinical and experimental OA assessment and would become recognized as the standard method. An OARSI Working Group deliberated on principles, standards and features for an OA cartilage pathology assessment system. Using current knowledge of the pathophysiology of OA morphologic features, a proposed system was presented at OARSI 2000. Subsequently, this was widely circulated for comments amongst experts in OA pathology. An OA cartilage pathology assessment system based on six grades, which reflect depth of the lesion and four stages reflecting extent of OA over the joint surface was developed. The OARSI cartilage OA histopathology grading system appears consistent and simple to apply. Further studies are required to confirm the system's utility.
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            Synovial inflammation, immune cells and their cytokines in osteoarthritis: a review.

            Although osteoarthritis (OA) is considered a non-inflammatory condition, it is widely accepted that synovial inflammation is a feature of OA. However, the role of immune cells and their cytokines in OA is largely unknown. This narrative systematic review summarizes the knowledge of inflammatory properties, immune cells and their cytokines in synovial tissues (STs) of OA patients. Broad literature search in different databases was performed which resulted in 100 articles. Of 100 articles 33 solely investigated inflammation in OA ST with or without comparison with normal samples; the remaining primarily focussed on rheumatoid arthritis (RA) ST. Studies investigating different severity stages or cellular source of cytokines were sparse. OA ST displayed mild/moderate grade inflammation when investigated by means of haematoxylin and eosin (H&E) staining. Most frequently found cells types were macrophages, T cells and mast cells (MCs). Overall the number of cells was lower than in RA, although the number of MCs was as high as or sometimes even higher than in RA ST. Cytokines related to T cell or macrophage function were found in OA ST. Their expression was overall higher than in normal ST, but lower than in RA ST. Their cellular source remains largely unknown in OA ST. Inflammation is common in OA ST and characterized by immune cell infiltration and cytokine secretion. This inflammation seems quantitatively and qualitatively different from inflammation in RA. Further research is needed to clarify the role of inflammation, immune cells and their cytokines in the pathogenesis of OA. Copyright © 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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              Characterization of articular cartilage and subchondral bone changes in the rat anterior cruciate ligament transection and meniscectomized models of osteoarthritis.

              Osteoarthritis (OA) is a chronic joint disease characterized by cartilage destruction, subchondral bone sclerosis, and osteophyte formation. Subchondral bone stiffness has been proposed to initiate and/or contribute to cartilage deterioration in OA. The purpose of this study was to characterize subchondral bone remodeling, cartilage damage, and osteophytosis during the disease progression in two models of surgically induced OA. Rat knee joints were subjected either to anterior cruciate ligament transection (ACLT) alone or in combination with resection of medial menisci (ACLT + MMx). Histopathological changes in the surgical joints were compared with sham at 1, 2, 4, 6, and 10 weeks post-surgery. Using a modified Mankin scoring system, we demonstrate that articular cartilage damage occurs within 2 weeks post-surgery in both surgical models. Detectable cartilage surface damage and proteoglycan loss were observed as early as 1 week post-surgery. These were followed by the increases in vascular invasion into cartilage, in loss of chondrocyte number and in cell clustering. Histomorphometric analysis revealed subchondral bone loss in both models within 2 weeks post-surgery followed by significant increases in subchondral bone volume relative to sham up to 10 weeks post-surgery. Incidence of osteophyte formation was optimally observed in ACLT joints at 10 weeks and in ACLT + MMx joints at 6 weeks post-surgery. In summary, the two surgically induced rat OA models share many characteristics seen in human and other animal models of OA, including progressive articular cartilage degradation, subchondral bone sclerosis, and osteophyte formation. Moreover, increased subchondral bone resorption is associated with early development of cartilage lesions, which precedes significant cartilage thinning and subchondral bone sclerosis. Together, these findings support a role for bone remodeling in OA pathogenesis and suggest that these rat models are suitable for evaluating bone resorption inhibitors as potential disease-modifying pharmaco-therapies.
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                Author and article information

                Journal
                J Phys Ther Sci
                J Phys Ther Sci
                JPTS
                Journal of Physical Therapy Science
                The Society of Physical Therapy Science
                0915-5287
                2187-5626
                20 April 2017
                April 2017
                : 29
                : 4
                : 590-597
                Affiliations
                [1) ] Section of Rehabilitation, Kanazawa University Hospital: 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan
                [2) ] Department of Motor Function Analysis, Human Health Sciences, Graduate School of Medicine, Kyoto University, Japan
                [3) ] Faculty of Health Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Japan
                Author notes
                [* ]Corresponding author. Ikufumi Takahashi, Section of Rehabilitation, Kanazawa University Hospital, Japan. (E-mail: t_ikuhumi@ 123456med.kanazawa-u.ac.jp )
                Article
                jpts-2016-986
                10.1589/jpts.29.590
                5430254
                28533591
                7abe9d93-37da-489f-aa82-65aa0e8859da
                2017©by the Society of Physical Therapy Science. Published by IPEC Inc.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/ ).

                History
                : 22 November 2016
                : 15 December 2016
                Categories
                Original Article

                osteoarthritis,monosodium iodoacetate,histopathology

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