C. Erggelet ] B. R. Mandelbaum. Principles of Cartilage Repair

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2 C. Erggelet ] B. R. Mandelbaum Principles of Cartilage Repair

3 C. Erggelet B. R. Mandelbaum Principles of Cartilage Repair In Collaboration with E. H. Mrosek and J. M. Scopp With 67 Figures in 177 Separate Illustrations, Most in Color 12

4 Christoph Erggelet, MD Arthrose Clinic Zürich Toblerstrasse 51 CH-8044 Zürich Switzerland Bert R. Mandelbaum, MD Santa Monica Orthopaedic & Sports Medicine Group 2020 Santa Monica Blvd. Santa Monica, California USA Eike H. Mrosek, MD Kantonsspital St. Gallen Rorschacher Strasse 95 CH-9007 St. Gallen Switzerland Jason M. Scopp, MD Peninsula Orthopaedic Associates, P.A. 111 Davis Street Salisbury, MD USA ISBN Steinkopff Verlag Bibliographic information published by Die Deutsche Nationalbibliothek Die Deutsche Bibliothek lists this publication in the Deutsche Nationalbibliografie; detailed bibliographic data is available in the Internet at This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Steinkopff Verlag. Violations are liable for prosecution under the German Copyright Law. Steinkopff Verlag a member of Springer Science+Business Media Steinkopff Verlag 2008 Printed in Germany The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about the application of operative techniques and medications contained in this book. In every individual case the user must check such information by consulting the relevant literature. Medical Editors: Dr. med. Gertrud Volkert, Petra Elster Production: Klemens Schwind Drawings: Rose Baumann, Schriesheim Cover design: Erich Kirchner, Heidelberg Typesetting: K+V Fotosatz GmbH, Beerfelden Printing and binding: Stürtz GmbH, Würzburg SPIN / Printedonacid-freepaper

5 About this Book The subject of articular cartilage defects represents an acute clinical problem. How many people during your consulting hours, in your practice or amongst your friends complain about joint pain, combined with functional limitations or a decrease in their level of performance? Clinical studies, recommendations and glossy product catalogues provide information and suggest solutions. Unfortunately, there is no quick-fix method for an instant and successful treatment of articular cartilage defects. The knowledge of orthopaedic surgeons and scientist is still fragmentary and coherence between defect morphology and pain appears to be extraordinarily complex. Only individual treatment plans combining a well balanced choice of various options will be successful. In-depth knowledge of operative and non-operative techniques is mandatory as well as preventory strategies. What are todays possibilities, how do they work and for which patients are they successful? This book should help to answer some of those questions. Acknowledgements It is impossible to compose a journal article without help and input from others and even more so a whole book. I wish to thank those who supported our project by critical questions, detailed answers, active help or patience. Special thanks go to Dr. G. Volkert and Mrs. P. Elster at Steinkopff Publishers, who have directed my ideas onto the right track with their hearty and competent support. The excellent graphics were realized by Mrs. R. Baumann, who also deserves special thanks. Zürich and Santa Monica, Spring 2008 Christoph Erggelet Bert R. Mandelbaum

6 Contents Introduction... 1 Articular Cartilage Biology... 3 ] Chondrocytes... 3 ] Collagen... 3 ] Proteoglycans... 3 ] The subchondral bone plate... 5 Etiology of Articular Cartilage Lesions... 7 ] Trauma... 7 ] Malalignments... 8 ] Meniscus... 9 ] Instability ] Osteochondrosis dissecans (OD) ] Osteoarthritis ] Rheumatoid arthritis ] Genetic factors ] Obesity ] Cartilage tumors ] Microtrauma Diagnostics ] Clinical examination ] Radiography ] Magnetic resonance tomography ] Classification of articular cartilage lesions and criteria for choosing appropriate therapy Localization Concomitant injuries Defect size/containment Radiography/MRT... 26

7 VIII ] Contents Conservative Treatment Conservative Treatment of Articular Cartilage Defects ] Drug treatment Non-steroidal anti-inflammatory drugs (NSAID) Neuroceuticals ] Physical therapy Physiotherapy Bandages and orthosis for the treatment of gonarthrosis Electrotherapy Pulsed signal therapy Ultrasound Magnetic fields Extracorporeal shock wave therapy Operative Treatment Operative Treatment of Articular Cartilage Defects ] Refixation of detached cartilage fragments ] Joint lavage/cartilage shaving/débridement ] Bone marrow stimulation techniques (drilling, abrasion, microfracture) ] Augmented microfracture techniques ] Osteochondral transplantation ] Autologous chondrocyte transplantation (ACT) ] Autologous chondrocyte transplantation (ACT) New procedures ] Correctional osteotomies ] Implantation of non-resorbable cartilage replacements Additional Reading Appendix ] Scores for the evaluation of therapy results after treatment of articular cartilage defects (selection) Important Analytic Methods ] Histology ] Immunohistochemistry ] Polymerase chain reaction (PCR) Subject Index

8 Introduction

9 Articular Cartilage Biology Intact articular cartilage is commonly called hyaline. Its thickness reaches 5 mm within the knee joint. Properties such as almost frictionless articulation of joint surfaces and the ability to absorb mechanical stress are owed to its unique and complex architecture. Histologically we can differentiate between four structural zones, which differ in both composition and arrangement of its components. The thin superficial zone hosts a relatively high number of cartilage cells (chondrocytes). They stretch out into a long, oval shape parallel to the joint surface. High cell density is characteristic for this zone. In the adjacent transitional zone cell density appears to be lower with a less organized geometric arrangement of cells. The deep zone shows the lowest cell density, leaving plenty of room for cartilage matrix. The calcified zone of articular cartilage is separated from subchondral bone by the tidemark (Fig. 1). The tidemark zone is a metabolically active layer as well. Hyaline cartilage mainly consists of chondrocytes, collagens and proteoglycans as well as 80% of water. Chondrocytes All tissue components in articular cartilage are synthesized by chondrocytes. They makeup approximately 1% of the tissue volume. The different arrangement of cells within the tissue points towards their metabolic activity. After closure of the epiphyseal gap chondrocytes loose their mitotic activity which has a major effect on intrinsic healing capacity of articular cartilage. Degenerative cells are not replaced. Chondrocytes endogenous ability to repair defects is limited to an alteration of synthetic performance which produces inferior cartilage matrix. Collagen Collagen fibrils are protein structures and resemble the largest portion of macromolecules in articular cartilage. They provide about 60% of cartilage s dry weight. The framework of hyaline cartilage predominantly consists of collagen type II and to a lesser extent of collagen types IX, X and XI. Collagen fibrils are responsible for cartilage s resilience and its ability to withstand sheer forces. Proteoglycans Proteoglycans consist of a core protein with chains of glycosaminoglycans connected to it. Both water uptake and output of articular cartilage are regulated by these molecules. This is particularly important for the absorption of mechanical stress as well as for cartilage nutrition since the majority of nutrition is accomplished via synovial diffusion. Chondroitin-sulfate, Keratan-sulfate and Dermatan-sulfate are the most important representatives of all known proteoglycans. Intact articular cartilage undergoes repetitive turnover, which is regulated by chondrocytes. Cell-matrix interactions are presumably mediated by mechanical stimulation, i.e.

10 4 ] Articular Cartilage Biology a b Fig. 1 a, b. Histological image of human articular cartilage with HE staining (a) and under polarized light (b) (with kind permission of S. Roberts, Oswestry, UK). through chondrocytes short cilia reaching into the matrix. They monitor changes in mechanical loading. This theory shows its clinical relevance for example during immobilization of a joint, which leads to rapid cartilage deterioration. Enzymatic influence through synovial diffusion is also known to affect articular cartilage. Increased synthesis if Interleukin-I promotes degradation of proteoglycans. Articular cartilage is free of nerves, blood or lymphatic vessels. Cartilage initially receives nutrients through blood perfusion from subchondral bone during early childhood. As the calcified zone forms during skeletal maturation, flow of nutrients from subchondral bone is inhibited and cartilage becomes dependent on diffusion of nutrients from the joint cavity. Intermittent mechanical loading with consequent absorption and output of fluids plays an important role. Lack of blood supply stipulates a mostly anaerobic metabolism. Chondrocytes are capable of maintaining their metabolism even under extremely low oxygen partial pressure (less than 1% of the normal oxygen partial pressure). All glycolytic processes still function under these conditions. During the fourth decade of life, intact articular cartilage begins a degradation process and cell-density decreases. Additional qualitative and quantitative changes of synovial fluids contribute to an early onset of tissue deterioration. Protein content and viscosity of synovial fluids in particular decrease with age. Chondrotoxic substances (i.e. Interleukin-I) are released from the synovial membrane causing matrix degradation such as unmasking of hyaline matrix. Proteoglycans of inferior quality are released into the matrix due to altered chondrocyte synthetic activity. Initially already slow matrix turnover (approx days) may thereafter cease completely. Macroscopic changes of tissue may be depicted by changes of both colour and altered resilience. Juvenile cartilage is commonly described as being of white-blueish colour and unique taut-resilient turgor. With increasing age, hyaline cartilage appears yellow and brittle. Mechanical stiffness tested by indentation is not only decreased in areas showing surface fibrillations.

11 The subchondral bone plate ] 5 The subchondral bone plate The subchondral bone plate resembles the tidemark between articular cartilage and subchondral bone. Although it was once assumed that cartilage nutrition is accomplished by bone marrow, we now know that this might only play a role during childhood. Moreover, resilience of the subchondral bone plate plays an important role in joint biomechanics and decreases with age. Progressing sclerosis of this thin layer is accompanied by a noticeable degeneration of the cartilage above as shown in numerous research studies. Therapeutic damage to the subchondral bone plate should be minimized during all treatment procedures.