Fast Facts. Fast Facts: Osteoarthritis. Philip G Conaghan and Leena Sharma Health Press Ltd.

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1 Fast Facts Fast Facts: Osteoarthritis Philip G Conaghan and Leena Sharma

2 Fast Facts Fast Facts: Osteoarthritis Philip G Conaghan MB BS PhD FRACP FRCP Professor of Musculoskeletal Medicine University of Leeds Consultant Rheumatologist Leeds Teaching Hospitals NHS Trust & Leeds Primary Care Trust Leeds, West Yorkshire, UK Leena Sharma MD Professor of Medicine Division of Rheumatology Feinberg School of Medicine Northwestern University Chicago, Illinois, USA Declaration of Independence This book is as balanced and as practical as we can make it. Ideas for improvement are always welcome: feedback@fastfacts.com

3 Fast Facts: Osteoarthritis First published April 2009 Text 2009 Philip G Conaghan, Leena Sharma 2009 in this edition Health Press Limited Health Press Limited, Elizabeth House, Queen Street, Abingdon, Oxford OX14 3LN, UK Tel: +44 (0) Fax: +44 (0) Book orders can be placed by telephone or via the website. For regional distributors or to order via the website, please go to: For telephone orders, please call +44 (0) (UK and Europe), (USA, toll free), (Americas) or +61 (0) (Asia Pacific). Fast Facts is a trademark of Health Press Limited. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the express permission of the publisher. The rights of Philip G Conaghan and Leena Sharma to be identified as the authors of this work have been asserted in accordance with the Copyright, Designs & Patents Act 1988 Sections 77 and 78. The publisher and the authors have made every effort to ensure the accuracy of this book, but cannot accept responsibility for any errors or omissions. For all drugs, please consult the product labeling approved in your country for prescribing information. Registered names, trademarks, etc. used in this book, even when not marked as such, are not to be considered unprotected by law. A CIP record for this title is available from the British Library. ISBN Conaghan PG (Philip) Fast Facts: Osteoarthritis/ Philip G Conaghan, Leena Sharma Medical illustrations by Dee McLean, London, UK. Typesetting and page layout by Zed, Oxford, UK. Printed by Print Bound Pty Ltd, Oakleigh South, Victoria, AUS. Text printed with vegetable inks on biodegradable and recyclable paper manufactured from sustainable forests. Low chlorine Sustainable forests

4 Glossary of abbreviations and terms 4 Introduction 5 The normal joint 7 The OA joint 16 Epidemiology 28 Etiology 36 Diagnosis 46 Principles of management 60 Non-pharmacological management 67 Pharmacological management 75 Joint-specific management (including injections) 83 Surgical management 90 Future trends 96 Useful addresses 100 Index 102

5 Glossary of abbreviations and terms ADAMTS protease: a disintegrin and a metalloproteinase with thrombospondin motifs BMD: bone mineral density Bouchard s nodes: firm or bony swellings that develop in the proximal interphalangeal joints, caused by the formation of calcific spurs of the articular cartilage; less common than Heberden s nodes (see below) Chondrocalcinosis: calcifications in joint cartilage, often diagnosed on radiographs CMC joint: carpometacarpal joint or base of thumb COX: cyclooxygenase; the COX enzymes are involved in the synthesis of prostaglandin derivatives CPPD: calcium pyrophosphate dihydrate CRP: C-reactive protein DMOADs: disease-modifying OA drugs ESR: erythrocyte sedimentation rate HA: hyaluronan or hyaluronic acid Heberden s nodes: firm or bony swellings that develop in the distal interphalangeal joints, caused by the formation of calcific spurs of the articular cartilage IL: interleukin IL-1RA: interleukin-1 receptor antagonist MCID: minimal clinically important difference MMP: matrix metalloproteinase MRI: magnetic resonance imaging NICE: National Institute for Health and Clinical Excellence (UK) NSAID: non-steroidal anti-inflammatory drug OA: osteoarthritis Osteophytes: outgrowths of new bone and cartilage, usually at the margins of osteoarthritic joints (see also Bouchard s and Heberden s nodes) PPI: proton pump inhibitor Primary OA: OA of unknown cause RA: rheumatoid arthritis TENS: Transcutaneous electrical nerve stimulation TGF: transforming growth factor TIMP: tissue inhibitor of matrix metalloproteinase TNFα: tumor necrosis factor α Valgus deformity of knees: knock knees Varus deformity of knees: bow legs 4

6 Introduction Osteoarthritis (OA) represents a massive problem in our aging society: all health professionals reading this book will have encountered OA in the clinic if not personally. For most people, OA is a syndrome of joint pain and stiffness with associated functional problems that have a substantial effect on quality of life. In terms of structural abnormalities, OA is probably best thought of as joint failure, just as we consider other age-related organ failures. However, the distinction between symptomatic and structural (often radiographic) evidence of OA is worth considering when evaluating the OA literature, as there is often a discordant relationship between the presence of symptoms and radiographic findings. The OA process has been recognized since ancient times, affecting both humans and animals, and is strongly associated with age and trauma. Research is constantly under way to better understand the OA process and to develop new therapeutic approaches. The increased use of MRI in OA research has already begun to affect our understanding of structural features associated with both pain and disease progression, with particular relevance to bone-marrow edema. From the treatment strategies currently available, including patient education and support, pain-relief medication and surgical intervention, it is important that management plans are tailored to individual patients needs, enabling them to lead active and productive lives. Although there is no cure for OA, for those clinicians who find it challenging to deal with people s OA pain, we hope Fast Facts: Osteoarthritis provides support for our view that something can be done to help every person with OA! Disclosures. Professor Conaghan has provided expert advice (advisory boards and/or presentations) for BMS, Centocor, GSK, IDEA, MSD, Mundipharma, Napp Pharmaceuticals, Negma, Novartis, Roche, Schering Plough and Wyeth. Professor Sharma has no disclosures. 5

7 1 The normal joint An understanding of the key structures in the normal joint (Figure 1.1), including their composition and function, is a prerequisite for understanding any arthritic process. Articular cartilage The end of each bone within a joint is lined with hyaline cartilage. Normal articular hyaline cartilage varies in thickness at different sites, not only within a given joint but at the same site between individuals, possibly between men and women and at different ages. The only cells in cartilage are chondrocytes. These cells are rather sparse, making up less than 5% of the tissue volume, and their density decreases with Femur Suprapatellar bursa Patellar Articular hyaline cartilage Menisci Fat Tibia Prepatellar bursa Synovial membrane Fibrous membrane Deep infrapatellar bursa Subcutaneous infrapatellar bursa Figure 1.1 Lateral view of a normal knee joint. 7

8 Fast Facts: Osteoarthritis distance from the joint cavity. Cartilage tissue is largely composed of an extracellular matrix that is produced by the chondrocytes. This matrix is very well hydrated, consisting of 70 80% water, protein collagen fibers, proteoglycans, glycosaminoglycans and some non-collagen proteins (Figure 1.2). Articular cartilage has no blood vessels, lymphatics or nerves, so the chondrocytes receive nutrition by diffusion of molecules from the synovial fluid in the joint cavity through the extracellular matrix. Histologically, the cartilage is seen as an upper non-calcified layer divided into the following zones: superficial, with few cells and tangential collagen fibers (zone I) intermediate, with oblique fiber orientation (zone II) deep, with vertical fibers (zone III). These zones are separated from the deeper calcified cartilage (zone IV) abutting subchondral bone by a basophilic-staining tidemark, the point at which the cartilage starts to become calcified (Figures 1.2 and 1.3). Lamina splendens (a) (b) Zone I Superficial Matrix Chondrocytes in lacuna Zones II and III Intermediate and Deep Tidemark Calcified cartilage Subchondral bone Zone IV End plate Trabecular bone 8 Figure 1.2 Composition and structure of normal articular hyaline cartilage and subchondral bone, showing (a) the histology and (b) the orientation of the collagen fibers.

9 3 Epidemiology OA is the most common joint disorder and represents a major cause of pain and disability for the individual, as well as resulting in enormous health expenditure in Western countries. In the UK and USA, an estimated 8.5 million and 20 million people are affected by the disorder, respectively. The joints most commonly affected are the: hands: base of thumb, distal and proximal interphalangeal joints spine: cervical and lumbosacral hips knees first metatarsophalangeal joint. Definition OA is not an acquired disease in the traditional medical model, and definitions have not always been clear. As stated in the Introduction, OA is a syndrome of joint pain and stiffness with associated functional problems, which can have a substantial effect on quality of life. In terms of structural abnormalities, OA encompasses a number of problems that result in common pathological and radiological features. The OA disease process in synovial joints is classically characterized in its later stages by focal cartilage degradation, involvement of the subchondral bone and synovium, and the formation of marginal osteophytes; in reality, all components of the joint are affected. Importantly, periarticular tissue, especially muscle, is often affected as well. 28 Prevalence Estimates of incidence and prevalence vary according to the definition of OA used; for example, symptomatic versus radiographic criteria. Even when radiographic definitions are used, different radiographic features may be emphasized (e.g. osteophytes vs joint-space narrowing). It is interesting to note that the correlation between pain and radiographic OA features is not as strong as expected, for reasons discussed in Chapter 4 (see page 44).

10 Epidemiology Radiographic OA is more common than symptomatic OA, and detection rates in a given joint may increase when more radiographic views are obtained. Recent studies on the distribution of radiographic OA have suggested that right-sided hand and knee OA are more common than left-sided disease (consistent with a biomechanical cause). Even within a specific joint (the knee), the distribution of osteophytes or joint-space narrowing differs in prevalence, probably again reflecting biomechanical factors (Figure 3.1). Effect of age. Individual joints demonstrate a striking age-related rise in the prevalence of radiographic OA. About a third of all adults have radiographic OA of the hands, with two-thirds over 75 years of age exhibiting OA of the distal interphalangeal joints. Radiographic OA of the knees has also been found in about a third of adults over 60 years of age (Figure 3.2). Effect of sex. The prevalence of radiographic OA (particularly of the hand and knee) is higher in women than men, especially in individuals over 50 years of age. Effect of ethnicity. The prevalence of radiographic OA is higher in African-American individuals than in American white individuals. Ethnic differences have also been demonstrated in (mainland) Chinese people, with the prevalence of hip OA being substantially lower in Lateral femoral 11.9 Medial femoral 13.1 Lateral tibial 16.6 Medial tibial 24.2 Figure 3.1 The prevalence distribution of radiographic osteophytosis by right knee joint compartment in US adults over 60 years of age. The medial compartments have greater prevalences than the lateral compartments, and tibial osteophytosis is more prevalent than femoral. Adapted from Dillon et al