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      Knee osteoarthritis: pathophysiology and current treatment modalities

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          Abstract

          For decades, multiple attempts to fully understand knee osteoarthritis pathophysiology and natural history have been attempted. Despite the extensive amount of research regarding this topic, there are still marked controversies. This multifactorial condition gets influenced by local, systemic, and external factors and its progression and/or response to treatments widely varies from patient to patient. Multiple therapies have been studied in the past, low impact physical activity seems to be supported by all the current medical societies while other interventions have shown conflicting findings. Newer therapies and routes of administration are under investigation and some of them have shown promising preliminary reports. This review intends to give an overview of the current knowledge of pathophysiology and non-surgical therapies available for knee osteoarthritis.

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          Most cited references 52

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          The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis.

          Osteoarthritis (OA), one of the most common rheumatic disorders, is characterized by cartilage breakdown and by synovial inflammation that is directly linked to clinical symptoms such as joint swelling, synovitis and inflammatory pain. The gold-standard method for detecting synovitis is histological analysis of samples obtained by biopsy, but the noninvasive imaging techniques MRI and ultrasonography might also perform well. The inflammation of the synovial membrane that occurs in both the early and late phases of OA is associated with alterations in the adjacent cartilage that are similar to those seen in rheumatoid arthritis. Catabolic and proinflammatory mediators such as cytokines, nitric oxide, prostaglandin E(2) and neuropeptides are produced by the inflamed synovium and alter the balance of cartilage matrix degradation and repair, leading to excess production of the proteolytic enzymes responsible for cartilage breakdown. Cartilage alteration in turn amplifies synovial inflammation, creating a vicious circle. As synovitis is associated with clinical symptoms and also reflects joint degradation in OA, synovium-targeted therapy could help alleviate the symptoms of the disease and perhaps also prevent structural progression.
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            Effect of Intra-articular Triamcinolone vs Saline on Knee Cartilage Volume and Pain in Patients With Knee Osteoarthritis: A Randomized Clinical Trial.

             Timothy McAlindon (corresponding) ,  Michael LaValley,  William F Harvey (2017)
            Synovitis is common and is associated with progression of structural characteristics of knee osteoarthritis. Intra-articular corticosteroids could reduce cartilage damage associated with synovitis but might have adverse effects on cartilage and periarticular bone.
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              Treatment of osteoarthritis of the knee: evidence-based guideline, 2nd edition.

              Treatment of Osteoarthritis of the Knee: Evidence-Based Guideline, 2nd Edition, is based on a systematic review of the current scientific and clinical research. This guideline contains 15 recommendations, replaces the 2008 AAOS clinical practice guideline, and was reevaluated earlier than the 5-year recommendation of the National Guideline Clearinghouse because of methodologic concerns regarding the evidence used in the first guideline. The current guideline does not support the use of viscosupplementation for the treatment of osteoarthritis of the knee. In addition, the work group highlighted the need for better research in the treatment of knee osteoarthritis.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2018
                05 October 2018
                : 11
                : 2189-2196
                Affiliations
                [1 ]Department of Anesthesiology, Division of Pain Medicine, University of Florida, Gainesville, FL, USA, jmora@ 123456anest.ufl.edu
                [2 ]Department of Aging and Geriatric Research, Institute on Aging, Pain Research and Intervention Center of Excellence, University of Florida, Gainesville, FL, USA
                Author notes
                Correspondence: Juan C Mora, Department of Anesthesiology, Division of Pain Medicine, University of Florida, PO Box 100254, Room 2036, Gainesville, FL 32610-0254, USA, Tel +1 352 265 0077, Fax +1 352 265 6922, Email jmora@ 123456anest.ufl.edu
                Article
                jpr-11-2189
                10.2147/JPR.S154002
                6179584
                © 2018 Mora et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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