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      Age-dependent ferritin elevations and HFE C282Y mutation as risk factors for symptomatic knee osteoarthritis in males: a longitudinal cohort study

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          Abstract

          Background

          Age, gender and genetic predisposition are major intrinsic risk factors for osteoarthritis (OA). Iron increases are associated with age and gene mutation. In the present study, we examined whether serum ferritin, an indicator of total body iron stores, correlates with clinical features in patients with OA, and whether the hemochromatosis Fe (HFE) gene mutation plays a role.

          Methods

          In a 2-year longitudinal observational study, 127 patients with knee OA and 20 healthy individuals (controls) were enrolled. All patients underwent standardized weight-bearing fixed-flexion posteroanterior knee radiographs. Peripheral blood samples were analyzed for serum ferritin, and genotyped for HFE using allelic discrimination methods.

          Results

          Higher levels of serum ferritin were found in patients older than 56 years ( P =0.0186) and males ( P =0.0006), with a trend toward higher ferritin in patients with OA. HFE gene mutation carriers were more prevalent among patients with OA than among healthy controls. When stratified further by gender, we found that male patients with OA had higher levels of serum ferritin than male control subjects [odds ratio = 4.18 (limits of 95% confidence interval: 0.86–27.69, P = 0.048)]. Analyses of radiographic data indicated that higher ferritin was associated with narrower joint space width at baseline ( P = 0.032) in male patients. Additionally, among men, risk prediction of radiographic severity [Kellgren-Lawrence (KL) grade >2)] in the higher ferritin group was almost five times that of the lower ferritin group (odds ratio = 4.74, P = 0.023).

          Conclusion

          Our data suggest that increased ferritin levels are associated with symptomatic knee OA in males. This finding needs to be validated in a larger cohort of patients.

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          Most cited references38

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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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            Atlas of individual radiographic features in osteoarthritis, revised.

            Develop a radiographic atlas of osteoarthritis (OA) to be used as a template and guide for grading radiographs of osteoarthritic lesions of the hand, hip and knee. The 1995 atlas was reviewed for the images most useful for clinical trials. Replacement images were selected from the Stanford University Radiology Department Picture Archive and Communications System by reviewing consecutive radiographs obtained from patients. Selected images were downloaded without patient identification information. Images were organized by hand, hip and knee. They were reviewed for findings of OA and images grouped into image files by individual findings and degree of change. Both investigators individually selected the most promising images. Final images were selected by consensus. Original electronic images were then cropped and placed in sequence. Individual radiographic features (e.g., osteophytes, joint space narrowing) were recorded for hand (distal interphalangeal joint, proximal interphalangeal joint, trapeziometacarpal joint), hip (acetabular, femoral) and knee (medial compartment, lateral compartment, tibial, femoral); they were also sequenced for normal, 1+, 2+, and 3+ change. Images were made available in print and electronic formats. An updated atlas of radiographic images was produced to assist in grading individual radiographic features of the hand, hip and knee for clinicians and for use in clinical trials.
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              Systemic iron homeostasis and the iron-responsive element/iron-regulatory protein (IRE/IRP) regulatory network.

              The regulation and maintenance of systemic iron homeostasis is critical to human health. Iron overload and deficiency diseases belong to the most common nutrition-related pathologies across the globe. It is now well appreciated that the hormonal hepcidin/ferroportin system plays an important regulatory role for systemic iron metabolism. We review recent data that uncover the importance of the cellular iron-responsive element/iron-regulatory protein (IRE/IRP) regulatory network in systemic iron homeostasis. We also discuss how the IRE/IRP regulatory system communicates with the hepcidin/ferroportin system to connect the control networks for systemic and cellular iron balance.
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                Author and article information

                Journal
                BMC Musculoskelet Disord
                BMC Musculoskelet Disord
                BMC Musculoskeletal Disorders
                BioMed Central
                1471-2474
                2014
                8 January 2014
                : 15
                : 8
                Affiliations
                [1 ]Division of Rheumatology, Department of Medicine, New York University School of Medicine, NYU Hospital for Joint Diseases, New York, NY, USA
                [2 ]Department of Population Health, Division of Biostatistics, New York University School of Medicine, New York, NY, USA
                [3 ]Division of Rheumatology, NYU Hospital for Joint Diseases, 301 East 17th Street, Suite 1410, New York, NY 10003, USA
                Article
                1471-2474-15-8
                10.1186/1471-2474-15-8
                3893611
                24401005
                6e79961d-b553-412a-84a0-83f213562652
                Copyright © 2014 Kennish et al.; licensee BioMed Central Ltd.

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 August 2013
                : 11 December 2013
                Categories
                Research Article

                Orthopedics
                hypoxia inducible factor,hemochromatosis,iron,osteoarthritis,radiographic progression
                Orthopedics
                hypoxia inducible factor, hemochromatosis, iron, osteoarthritis, radiographic progression

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