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      Biomechanical considerations in the pathogenesis of osteoarthritis of the knee

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          Abstract

          Osteoarthritis is the most common joint disease and a major cause of disability. The knee is the large joint most affected. While chronological age is the single most important risk factor of osteoarthritis, the pathogenesis of knee osteoarthritis in the young patient is predominantly related to an unfavorable biomechanical environment at the joint. This results in mechanical demand that exceeds the ability of a joint to repair and maintain itself, predisposing the articular cartilage to premature degeneration. This review examines the available basic science, preclinical and clinical evidence regarding several such unfavorable biomechanical conditions about the knee: malalignment, loss of meniscal tissue, cartilage defects and joint instability or laxity.

          Level of evidence IV.

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          Most cited references134

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          Osteoarthritis.

          Osteoarthritis (OA) is characterized by degeneration of articular cartilage, limited intraarticular inflammation with synovitis, and changes in peri-articular and subchondral bone. Multiple factors are involved in the pathogenesis of OA, including mechanical influences, the effects of aging on cartilage matrix composition and structure, and genetic factors. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines, and other inflammatory mediators by chondrocytes, research has focused on the chondrocyte as the cellular mediator of OA pathogenesis. The other cells and tissues of the joint, including the synovium and subchondral bone, also contribute to pathogenesis. The adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the original cartilage matrix architecture. It may attempt to recapitulate phenotypes of early stages of cartilage development, but the precise zonal variations of the original cartilage cannot be replicated. Current pharmacological interventions that address chronic pain are insufficient, and no proven structure-modifying therapy is available. Cartilage tissue engineering with or without gene therapy is the subject of intense investigation. There are multiple animal models of OA, but there is no single model that faithfully replicates the human disease. This review will focus on questions currently under study that may lead to better understanding of mechanisms of OA pathogenesis and elucidation of effective strategies for therapy, with emphasis on mechanisms that affect the function of chondrocytes and interactions with surrounding tissues. 2007 Wiley-Liss, Inc.
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            Dynamic load at baseline can predict radiographic disease progression in medial compartment knee osteoarthritis.

            To test the hypothesis that dynamic load at baseline can predict radiographic disease progression in patients with medial compartment knee osteoarthritis (OA). During 1991-93 baseline data were collected by assessment of pain, radiography, and gait analysis in 106 patients referred to hospital with medial compartment knee OA. At the six year follow up, 74 patients were again examined to assess radiographic changes. Radiographic disease progression was defined as more than one grade narrowing of minimum joint space of the medial compartment. In the 32 patients showing disease progression, pain was more severe and adduction moment was higher at baseline than in those without disease progression (n=42). Joint space narrowing of the medial compartment during the six year period correlated significantly with the adduction moment at entry. Adduction moment correlated significantly with mechanical axis (varus alignment) and negatively with joint space width and pain score. Logistic regression analysis showed that the risk of progression of knee OA increased 6.46 times with a 1% increase in adduction moment. The results suggest that the baseline adduction moment of the knee, which reflects the dynamic load on the medial compartment, can predict radiographic OA progression at the six year follow up in patients with medial compartment knee OA.
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              Aging and osteoarthritis: the role of chondrocyte senescence and aging changes in the cartilage matrix.

              Age-related changes in multiple components of the musculoskeletal system may contribute to the well established link between aging and osteoarthritis (OA). This review focused on potential mechanisms by which age-related changes in the articular cartilage could contribute to the development of OA. The peer-reviewed literature published prior to February 2009 in the PubMed database was searched using pre-defined search criteria. Articles, selected for their relevance to aging and articular chondrocytes or cartilage, were summarized. Articular chondrocytes exhibit an age-related decline in proliferative and synthetic capacity while maintaining the ability to produce pro-inflammatory mediators and matrix degrading enzymes. These findings are characteristic of the senescent secretory phenotype and are most likely a consequence of extrinsic stress-induced senescence driven by oxidative stress rather than intrinsic replicative senescence. Extracellular matrix changes with aging also contribute to the propensity to develop OA and include the accumulation of proteins modified by non-enzymatic glycation. The effects of aging on chondrocytes and their matrix result in a tissue that is less able to maintain homeostasis when stressed, resulting in breakdown and loss of the articular cartilage, a hallmark of OA. A better understanding of the basic mechanisms underlying senescence and how the process may be modified could provide novel ways to slow the development of OA.
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                Author and article information

                Contributors
                +31-20-5669111 , +31-20-5669117 , a.heijink@amc.nl
                Journal
                Knee Surg Sports Traumatol Arthrosc
                Knee Surgery, Sports Traumatology, Arthroscopy
                Springer-Verlag (Berlin/Heidelberg )
                0942-2056
                1433-7347
                16 December 2011
                16 December 2011
                March 2012
                : 20
                : 3
                : 423-435
                Affiliations
                [1 ]Department of Orthopaedic Surgery, Academic Medical Center (AMC), Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
                [2 ]Department of Orthopaedic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA USA
                [3 ]Experimental Orthopaedics and Osteoarthritis Research and Department of Orthopaedic Surgery, Saarland University Medical Center, Homburg/Saar, Germany
                [4 ]Saarland University, Homburg/Saar, Germany
                [5 ]Department of Orthopaedic Surgery, University Medical Center Ljubljana, Ljubljana, Slovenia
                [6 ]III Clinic, Biomechanics Laboratory, Rizzoli Orthopedic Institute, Bologna, Italy
                [7 ]Clínica Saúde Atlântica, Minho and Porto Universities, Porto, Portugal
                Article
                1818
                10.1007/s00167-011-1818-0
                3282009
                22173730
                f321b1e9-2679-474d-8ffe-516fbad90dea
                © The Author(s) 2011
                History
                : 8 August 2011
                : 22 November 2011
                Categories
                Knee
                Custom metadata
                © Springer-Verlag 2012

                Surgery
                joint instability,pathology,osteochondral defects,cartilage,etiology,meniscus,malalignment
                Surgery
                joint instability, pathology, osteochondral defects, cartilage, etiology, meniscus, malalignment

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