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      Serum Lipid Levels and Risk Of Hand Osteoarthritis: The Chingford Prospective Cohort Study

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          Abstract

          The development of hand osteoarthritis (HOA) could be linked to hyperlipidaemia. No longitudinal studies have addressed the relationship between serum lipid profile and HOA. The study aim was to determine the association between serum lipid profile and the incidence of radiographic hand osteoarthritis (RHOA). All women in a prospective population-based cohort from the Chingford study with available baseline lipid measurements and without RHOA on a baseline were included. Study outcome was the incidence of RHOA in year 11 of follow-up. Serum lipid profile variables were analysed as continuous variables and categorised into quartiles. The association between serum lipid profile and RHOA was modeled using multivariable logistic regression. Overall RHOA incidence was 51.6% (45.7–57.4%). An inverse association between HDL cholesterol levels and the incidence of RHOA was observed by quartile: OR of 0.36 [95%CI 0.17–0.75], 0.52 [95%CI 0.26–1.06], and 0.48 [95%CI 0.22–1.03]. Triglycerides levels showed a significant trend. No relationship was found with total or LDL cholesterol. Higher levels of HDL cholesterol appear to protect against RHOA after 11 years of follow-up. More research is needed to elucidate HOA risk factors, the mechanisms related to the lipid pathway, and the effects of lipid-lowering agents on reducing the incidence of OA.

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          Obesity and osteoarthritis in knee, hip and/or hand: An epidemiological study in the general population with 10 years follow-up

          Background Obesity is one of the most important risk factors for osteoarthritis (OA) in knee(s). However, the relationship between obesity and OA in hand(s) and hip(s) remains controversial and needs further investigation. The purpose of this study was to investigate the impact of obesity on incident osteoarthritis (OA) in hip, knee, and hand in a general population followed in 10 years. Methods A total of 1854 people aged 24–76 years in 1994 participated in a Norwegian study on musculoskeletal pain in both 1994 and 2004. Participants with OA or rheumatoid arthritis in 1994 and those above 74 years in 1994 were excluded, leaving n = 1675 for the analyses. The main outcome measure was OA diagnosis at follow-up based on self-report. Obesity was defined by a body mass index (BMI) of 30 and above. Results At 10-years follow-up the incidence rates were 5.8% (CI 4.3–7.3) for hip OA, 7.3% (CI 5.7–9.0) for knee OA, and 5.6% (CI 4.2–7.1) for hand OA. When adjusting for age, gender, work status and leisure time activities, a high BMI (> 30) was significantly associated with knee OA (OR 2.81; 95%CI 1.32–5.96), and a dose-response relationship was found for this association. Obesity was also significantly associated with hand OA (OR 2.59; 1.08–6.19), but not with hip OA (OR 1.11; 0.41–2.97). There was no statistically significant interaction effect between BMI and gender, age or any of the other confounding variables. Conclusion A high BMI was significantly associated with knee OA and hand OA, but not with hip OA.
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            Evidence for a key role of leptin in osteoarthritis.

            To evaluate the contribution of leptin (an adipose tissue-derived hormone) to the pathophysiology of osteoarthritis (OA), by determining the level of leptin in both synovial fluid (SF) and cartilage specimens obtained from human joints. We also investigated the effect of leptin on cartilage, using intraarticular injections of leptin in rats. Leptin levels in SF samples obtained from OA patients undergoing either knee replacement surgery or knee arthroscopy were measured by enzyme-linked immunosorbent assay. In addition, histologic sections of articular cartilage and osteophytes obtained during surgery for total knee replacement were graded using the Mankin score, and were immunostained using antibodies to leptin, transforming growth factor beta (TGFbeta), and insulin-like growth factor 1 (IGF-1). For experimental studies, various doses of leptin (10, 30, 100, and 300 microg) were injected into the knee joints of rats. Tibial plateaus were collected and processed for proteoglycan synthesis by radiolabeled sulfate incorporation, and for expression of leptin, its receptor (Ob-Rb), and growth factors by reverse transcriptase-polymerase chain reaction and immunohistochemical analysis. Leptin was observed in SF obtained from human OA-affected joints, and leptin concentrations correlated with the body mass index. Marked expression of the protein was observed in OA cartilage and in osteophytes, while in normal cartilage, few chondrocytes produced leptin. Furthermore, the pattern and level of leptin expression were related to the grade of cartilage destruction and paralleled those of growth factors (IGF-1 and TGFbeta1). Animal studies showed that leptin strongly stimulated anabolic functions of chondrocytes and induced the synthesis of IGF-1 and TGFbeta1 in cartilage at both the messenger RNA and the protein levels. These findings suggest a new peripheral function of leptin as a key regulator of chondrocyte metabolism, and indicate that leptin may play an important role in the pathophysiology of OA.
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              Accumulation of metabolic risk factors such as overweight, hypertension, dyslipidaemia, and impaired glucose tolerance raises the risk of occurrence and progression of knee osteoarthritis: a 3-year follow-up of the ROAD study.

              To clarify the association between the occurrence and progression of knee osteoarthritis (KOA) with components of metabolic syndrome (MS), including overweight (OW), hypertension (HT), dyslipidaemia (DL), and impaired glucose tolerance (IGT), in a general population. From the large-scale population-based cohort study entitled Research on Osteoarthritis/Osteoporosis Against Disability (ROAD) initiated in 2005, 1,690 participants (596 men, 1,094 women) residing in mountainous and coastal areas were enrolled. Of these, 1,384 individuals (81.9%; 466 men, 918 women) completed the second survey, including knee radiography, 3 years later. KOA was defined as Kellgren-Lawrence (KL) grade ≥ 2 using paired X-ray films. Based on changes in KL grades between the baseline and second surveys, cumulative incidence and progression of KOA were determined. OW, HT, DL, and IGT at baseline were assessed using standard criteria. The cumulative incidence of KOA among 1,384 completers over 3 years was 3.3%/year, and progression in KL grades for either knee, 8.0%/year. Logistic regression analyses after adjusting for potential risk factors revealed that the odds ratio (OR) for the occurrence of KOA significantly increased according to the number of MS components present (OR vs no component: one component, 2.33; two components, 2.82; ≥three components, 9.83). Similarly, progression of KOA significantly increased according to the number of MS components present (OR vs no component: one component, 1.38; two components, 2.29; ≥three components: 2.80). Accumulation of MS components is significantly related to both occurrence and progression of KOA. MS prevention may be useful in reducing future KOA risk. Copyright © 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Daniel.prietoalhambra@ndorms.ox.ac.uk
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                9 June 2017
                9 June 2017
                2017
                : 7
                : 3147
                Affiliations
                [1 ]Research Unit, Family Medicine. Institut Universitari d’Investigació en Atenció Primària Jordi Gol (IDIAP Jordi Gol), Girona, Spain
                [2 ]ISNI 0000 0001 2179 7512, GRID grid.5319.e, Translab Research Group. Department of Medical Sciences, School of Medicine, , University of Girona, ; Girona, Spain
                [3 ]GRID grid.452479.9, GREMPAL Research Group, , Institut Universitari d’Investigació en Atenció Primària Jordi Gol [IDIAP Jordi Gol], ; Barcelona, Spain
                [4 ]CIBERFes, Universitat Autònoma de Barcelona and Instituto de Salud Carlos III, Barcelona, Spain
                [5 ]Primary Care Services, Catalan Institute of Health (ICS), Girona, Spain
                [6 ]ISNI 0000 0004 1936 8948, GRID grid.4991.5, Nuffield Department of Orthopaedics, , Rheumatology and Musculoskeletal Sciences, University of Oxford, ; Oxford, United Kingdom
                [7 ]ISNI 0000 0004 1936 8948, GRID grid.4991.5, Arthritis Research UK Sports Exercise and Osteoarthritis Centre of Excellence, , University of Oxford, ; Oxford, United Kingdom
                [8 ]ISNI 0000 0004 1936 9297, GRID grid.5491.9, MRC Lifecourse Epidemiology Unit, , University of Southampton, ; Oxford, United Kingdom
                [9 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, Department of Twin Research & Genetic Epidemiology, , King’s College London, ; Oxford, United Kingdom
                Author information
                http://orcid.org/0000-0002-3452-3382
                Article
                3317
                10.1038/s41598-017-03317-4
                5466681
                28600494
                74fc81d3-8bf8-4f85-bb01-6f4699a5f07d
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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                : 28 November 2016
                : 29 March 2017
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