Anterior Knee Pain and Patellar Instability [3 ed.] 3031097661, 9783031097669

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Anterior Knee Pain and Patellar Instability

Vicente Sanchis-Alfonso Editor

Anterior Knee Pain and Patellar Instability Third Edition

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Editor Vicente Sanchis-Alfonso Department of Orthopedic Surgery Hospital Arnau de Vilanova Valencia, Spain

ISBN 978-3-031-09766-9 ISBN 978-3-031-09767-6 https://doi.org/10.1007/978-3-031-09767-6

(eBook)

1st edition: © Springer-Verlag London Limited 2006 2nd edition: © Springer-Verlag London Limited 2011 3rd edition: © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, 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. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

To my mother, my maternal aunt and my little sister with all my love In memoriam (†)

It is very difficult to accept that my little sister is no longer by my side and that I will never see her again, at least in this life. My mother used to say that one only dies when we no longer think of them. If that is true, I can say that my sister is more alive than ever for me. I think about her all the hours of the day. I have very vivid and intense memories, and anecdotes of our times together during the 11 years that her disease lasted. Some memories are painful, but others make me smile without realizing it. She was a great sister, an amazing person, brave and determined. She was even generous when dying as she gave us

time to prepare ourselves and say goodbye. The time that she gave us has made her loss more bearable. I cannot even imagine how I would be right now if she had died suddenly being healthy. Mari Carmen, I carry you deeply within me and time will never erase you from my memory. You will be forever in my heart; having you close has been the greatest gift I have ever been bestowed.

Foreword to the Third Edition

It has been a great pleasure to witness the development of this book over these past few years. This book is much improved over previous editions as Vicente has incorporated many new ideas and concepts. Moreover, as in previous editions, he has been able to gather a group of extremely talented experts to help him write this book. This edition will establish him as the unchallenged leader in understanding the workings of the Patellofemoral Joint, why it fails, how it fails, and what we now think are the best approaches to treatment. I call him a leader. But what constitutes a leader? For Warren Bennis, an American academic who focused his entire life on the study of leadership, it is clear. Returning from World War II to enter university eventually with a Ph.D. from the Massachusetts Institute of Technology, he studied leadership in all its facets. He wrote 30 books and left behind a legacy of an almost 17-meter-long shelf of published and working papers in the archives of the University of Southern California. Once when asked in an interview to say what it takes to be a great leader, he replied “That’s easy! A great leader has a vision for accomplishment and a particular passion for a profession and for persisting in pursuit of his vision in spite of failures. Integrity is imperative and a leader never lies…about anything. Equally necessary he is curious and daring. A true leader wonders about everything, wants to learn as much as he can, experiments and takes risks” (The New York Times, Warren G. Bennis Obituary, August 1, 2014). Leaders possessing these attributes are indeed uncommon. Communicating with Vicente, it is clear he possesses vision, passion, integrity, curiosity, and daring. A vision to understand the Patellofemoral Joint and the passion to follow that dream and deliver perfection for his patients. Integrity and curiosity, he listens intensely to his patients, examines them carefully. Moreover, he questions his poor results. Although he may be quiet, he is daring and courageous to enter uncharted areas performing seemingly foolish complex surgeries. However, only after intense

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Foreword to the Third Edition

and deep study has he rejected standard approaches and revealed that the indications are not so foolish as our conventional treatments. With these attributes, he is indeed a leader, and this brilliant book should lead us all forward. Robert A. Teitge, M.D. Professor Emeritus of Orthopedic Surgery Wayne State University Detroit, Michigan, USA

Foreword to the Second Edition

I am particularly pleased to write the introduction to this fine compendium of ideas, as Dr. Sanchis Alfonso has been a leader in the understanding of patellofemoral pain origins. This topic has fascinated me my entire career in orthopedic surgery, and has been a focus of most of my research and teaching. In 1985, I published our findings of nerve injury in the peripatellar retinaculum of patients with patellar imbalance and anterior knee pain, helping to establish the link between pain and patellofemoral malalignment. Dr. Sanchis Alfonso has not only added substance and scientific evidence to the link between musculoskeletal stress and neural changes causing pain, he has now brought together many good thinkers and scientists to present interesting and sometimes divergent points of view in this current volume. The great philosopher Hegel stated “it is through the tension of opposites that we come to a higher truth”. Through computer simulated knee mechanical function noted in this book, Elias and Cosgarea demonstrate how articular loads can be tracked accurately and that even small aberrations of mechanical function can cause considerable alterations of stress transmitted through articular surfaces. Similarly, retinacular restraints around the patellofemoral joint will experience profound changes of loading when alignment is off, overuse is extreme, surgical balancing is not precise, and at extremes of laxity or tightness. Such is the nature of patellar and peripatellar stress and the relative anoxia caused by abnormal loading of peripatellar structure leading to cytokine elaboration and resulting pain. Thank you Dr. Sanchis Alfonso. I believe this book is a wonderful compendium of current patellofemoral thought, not designed as a cookbook with easy answers, because there are many complex problems around the anterior knee and few easy answers. Rather, Dr. Sanchis-Alfonso’s text contains many independent thinkers and scientists with a variety of approaches and concepts, some validated, some not, but all important in our search of the patellofemoral “holy grail”. I encourage the reader to think, along with the authors of this textbook, synthesizing ideas and considering carefully how each concept presented here applies to the individual patient, always emphasizing non-operative and simple measures whenever possible, but recognizing the importance of appropriate surgery when necessary for the relief of pain and suffering in the challenging patients with recalcitrant patellofemoral pain and instability.

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In closing, I want to summarize my 32 years of experience with patellofemoral patients by saying that I believe a critical underlying concept for treating many patients with patellofemoral dysfunction is to recognize that the structural imbalance we see in patients with patellofemoral malalignment is at the root of much patellofemoral pain and instability. Therefore, our challenge is to restore balance and reduce excessive patellofemoral stress in these patients, using non-operative measures including rest when possible, but designing necessary surgery to absolutely minimize both articular and periarticular damages while restoring patellofemoral balance as precisely as possible. John P. Fulkerson, M.D. Clinical Professor of Orthopaedic Surgery University of Connecticut School of Medicine Farmington, Connecticut, USA

Foreword to the First Edition

Anterior knee pain is one of the really big problems in my specialty, sports orthopedic surgery, but also in all other types of orthopedic surgery. Many years ago Sakkari Orava in Finland showed that among some 1311 Finnish runners, anterior knee pain was the second most common complaint. In young school girls around 15 years of age, anterior knee pain is a common complaint. In ballet classes of the same age as much as 60–70% of the students complain of anterior knee pain. It is therefore an excellent idea of Dr. Sanchis-Alfonso to publish a book about anterior knee pain and patellofemoral instability in the active young. He has been able to gather a group of extremely talented experts to help him write this book. I am particularly happy that he has devoted so much space to the non-operative treatment of anterior knee pain. During my active years as a knee surgeon, one of my worst problems was young girls referred to me for surgery of anterior knee pain. Girls that already had had 8–12 surgeries for their knee problem–surgeries that had rendered them more and more incapacitated after each operation. They now came to me for another operation. In all these cases, I referred them to our pain clinic for careful analysis, pain treatment followed by physical therapy. All recovered but had been the victims of lots of unnecessary knee surgery before they came to me. I am also happy that Suzanne Werner in her chapter refers to our study on the personality of these anterior knee pain patients. She found that the patients differ from a normal control group of the same age. I think this is very important to keep in mind when you treat young patients with anterior knee pain. In my mind physical therapy should always be the first choice of treatment. Not until this treatment has completely failed and a pain clinic recommends surgery, do I think surgery should be considered. In patellofemoral instability the situation is different. When young patients suffer from frank dislocations of the patella, surgery should be considered. From my many years of treating this type of patients, I recommend that the patients undergo an arthroscopy before any attempts to treat the instability begins. The reason is that I have seen so many cases with normal X-rays that have 10–15 loose bodies in their knees. If these pieces consist of just cartilage, they cannot be seen on X-ray. When a dislocated patella jumps back, it often hits the lateral femoral condyle with considerable force. Small cartilage pieces are blasted away as well from femur as from the patella. If they are overlooked they will eventually lead to blockings of the knee in the future. xi

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Foreword to the First Edition

The role of the medial patellofemoral ligament can also not be overstressed. When I was taught to operate on these cases, this ligament was not even known. I also feel that when patellar instability is going to be operated on, it is extremely important that the surgeon carefully controls in what direction the instability takes place. All instability is not in lateral direction. Some patellae have medial instability. If someone performs a routine lateral release in a case of medial instability, he will end up having to repair the lateral retinaculum in order to treat the medial dislocation that eventually occurs. Hughston and also Teitge have warned against this in the past. It is a pleasure for me to recommend this excellent textbook by Dr. Vicente Sanchis-Alfonso. Ejnar Eriksson, M.D., Ph.D. Professor Emeritus of Sports Medicine Karolinska Institute Stockholm, Sweden

Preface

Take good care of your patients and they will take good care of you —Freddie Fu Medicine is meant to help people! It is OK to make some money but it´s not the key —Peter Lauterbur

Santiago Ramón y Cajal, Spanish Nobel Laureate in Medicine, in his book, “The Tonics of the Will”, he said: “What a great tonic it would be for the young researcher that his mentor, instead of astonishing him and discouraging him with the sublimity of great completed projects, would explain the genesis of each scientific creation along with the mistakes and doubts that preceded them”. This is why I think it is interesting for you to know how the book you are holding in your hands came to be. This book is not only the fruit of my effort and perseverance and, clearly, the generosity of all my colleagues but also of chance. Many years ago, my good friend Donald Fithian from San Diego told me that to stand out in something I had to focus on a topic not well known and that many did not like. In those years, patellofemoral disorders fulfilled both. Paraphrasing a great American poet Robert Frost in his poem “The Road Not Taken”, I took the least traveled road 24 years ago, that is, I focused on the patella. As in this poem, it made all the difference. Without a doubt, I do not regret having chosen this road. The patella has led to very satisfactory experiences with my patients and other colleagues. In 2003, I wrote a book in Spanish with the “Editorial Médica Panamericana”, one of the most prestigious publishing houses in the Spanish language. It was entitled “Dolor Anterior de Rodilla e Inestabilidad Rotuliana en el Paciente Joven” (Anterior Knee Pain and Patellar Instability in the Young Patient). Frankly, I never thought it would be very successful. That attitude was not due to its quality, of which I was convinced, but due to its subject matter. This book was the germ for the one I am now referring to. In 2004, I had the fortune of meeting Prof. Ejnar Eriksson, from the Karolinska Institute of Stockholm, at an international meeting in Sardinia, Italy. My good friend, Roland Biedert from Switzerland, had invited me to participate in a panel session about patellofemoral pain. During the coffee break, Prof. Eriksson approached me and encouraged me to translate this book into English. I was quite delighted by his suggestion. So, as soon as I returned to Spain, I prepared a project and presented it to Springer. I was lucky that this renowned publishing house accepted the challenge of xiii

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publishing, in English, an extension of the Spanish edition. It was quite successful both with regard to sales and the book critics. They even said it was a model for what a book for specialists should be. That first English edition was published in December 2005. However, getting there is only half the battle, as it must be kept up to date. Therefore, in 2011, a second edition of the book was published in English. I donated my author’s royalties to the research foundation of the Hospital Clínico Universitario in Valencia, Spain. It was specifically given for the line of research in breast cancer, which made my sister very happy. Sadly, she recently died from breast cancer. For this reason, I proposed doing this third and last edition to Springer, as a tribute to my sister. This book is, in fact, the third edition in English. Notwithstanding, we are really before a fourth edition of this book since the first edition was the one that was published in Spanish. This monograph reflects my deep interest in the pathology of the knee, particularly that of the extensor mechanism, and emphasizes the great importance I give to the concept of subspecialization. This is the only way to confront the deterioration and the mediocrity of our specialty, Orthopedic Surgery, and to give our patients better care. In line with the concept of subspecialization, this book clearly required the participation of various authors. They are of different nationalities as well as from different schools of thought. Moreover, the participation of diverse specialists, from a multidisciplinary perspective, affords us a wider vision of this pathology. With this book, we draw upon the most common pathology of the knee even though it is the most neglected, the least known, the most problematic and controversial topic (The Black Hole of Orthopedics). Our knowledge of its etiopathogenesis is limited. Therefore, its treatment is one of the most complex among the different pathologies of the knee. On the other hand, we also face the problem of frequent and serious diagnostic errors that may lead to unnecessary operations. This book is organized into four parts. Unlike other publications, it gives great importance to etiopathogenesis. Albeit in an eminently clinical and practical manner, the latest theories are presented regarding the pathogenesis of anterior knee pain and patellar instability (Part I “Etiopathogenic Bases, Prevention and Therapeutic Implications”). In agreement with John Hunter, I think that to know the effects of an illness is to know very little. To know the cause of the effects is what is important. In Part II (“Surgical techniques-Why, When and How I Do It”), the surgical techniques that are in use today for the patellofemoral joint are described in detail. They are described by the surgeons who have designed the technique and who are recognized by their colleagues as “masters” in their specialty. The third part of this monograph is given over to the discussion of complex clinical cases. I believe we learn far more from our own mistakes (“To Err is Human”, Marcus Tullius Cicero), and those of other specialists than from our own success (“Learn from the mistakes of others-you can never live long enough to make them all yourself”, John Luther). The diagnoses reached and how the cases were resolved are explained in detail (“Good results come from experience, experience from bad results”, Prof. Erwin Morscher). Finally, in

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Part IV, new frontiers in anterior knee pain, patellar instability, and patellofemoral osteoarthritis evaluation and treatment are analyzed. The first objective I have laid out in this book is to highlight the soaring incidence of this pathology and its impact on young people, athletes, workers, and the economy. The second goal is to improve prevention and diagnosis to reduce the economic and social costs of this condition. The final objective is to improve health care for these patients. “Anterior Knee Pain and Patellar Instability” is addressed to orthopedic surgeons (both general and those specialized in knee surgery), specialists in sports medicine, rehabilitation specialist MDs, and physiotherapists. Thus, we feel that this monograph will fill an important gap in the literature about the pathology of the extensor mechanism of the knee with this approach. However, we do not intend to substitute any books on patellofemoral pathology but rather to complement them (“All in all, you’re just another brick in the wall”, Pink Floyd, The Wall). Although the information contained herein will evidently require future revision, it serves as an authoritative reference on one of the most problematic entities in the pathology of the knee at this time. We hope this book will be a reference in the future from our youngest to our oldest colleagues. We trust that the reader will find this book useful and, consequently, be indirectly valuable for patients. Valencia, Spain April 2022

Vicente Sanchis-Alfonso, M.D., Ph.D.

Acknowledgments

At times our own light goes out and is rekindled by a spark from another person. Each of us has cause to think with deep gratitude of those who have lighted the flame within us —Albert Schweitzer (Nobel Peace Prize)

I wish to express my sincere gratitude to my good friends and colleagues Don Fithian, John Fulkerson, and Bob Teitge. My journey in knee surgery began in 1992 in San Diego, California, USA. When I got to San Diego, pure serendipity put Donald Fithian in my path. Quoting William Shakespeare, destiny is the one that shuffles the cards, but we are the ones who play them. But someone has to give us a chance to play. Donald gave me this opportunity. He shuffled the cards. He introduced me in the International Patellofemoral Study Group. I was his guest at the meeting in Lyon, France, in 1998. I will be forever grateful for his invaluable help and friendship. The next year, in 1999, I was selected to become a member of this organization and where else but in St. Helena, in Napa County. California again. Belonging to this group has motivated me to study every day and to stay updated, in order to keep up with the rest of my colleagues. I have had a deep respect and admiration for John Fulkerson ever since I read the second edition of his book ``Disorders of the Patellofemoral Joint'' when I was a resident in Orthopedic Surgery. For me this book was a real page-turner, a kind of Harry Potter for today´s teenagers. Reading this book was a breakthrough. John Fulkerson made the patellofemoral joint my professional passion. Despite being the most important and recognized surgeon in this field, he turned out to be the most modest and closest to me. He gave me a lot of support and guidance. Bob Teitge got me into thinking outside of the box. He gave me the gift of his friendship and all the necessary tools for my complete professional development. With his incredible generosity, he shared all his knowledge without expecting anything in return. He also showed me techniques I had not heard of before that made it possible for me to help many patients who were considered lost-causes by others. Bob, thank you for always being there, for helping me improve day by day and for teaching me to row against the tide. I am extremely lucky to be surrounded by incredible people who support me unconditionally. They have provided me with the means and thus the opportunities to fully develop in my professional life. I would like to acknowledge Julio Domenech-Fernandez, Erik Montesinos-Berry, Cristina Ramírez-Fuentes, and Maria Jose Sanguesa-Nebot for their friendship and invaluable help. Thank you, Julio, you are the best boss that one can have. Thank you for your understanding. You are truly a motivating and inspiring xvii

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person. Thank you, Maria Jose, for being the way you are, marvelous, keep it up. I also want to commend my colleague at the Knee Unit of my hospital, Alejandro Roselló-Añón. Undoubtedly, he has a bright future ahead of him. All of you are, in part, responsible for this book. My gratitude also goes out to my friends Jack Andrish, Roland Biedert, Antonio Darder-Prats, David Dejour, Scott F. Dye, João Espregueira-Mendes, Jack Farr, Christian Fink, Ronald Grelsamer, Laura López-Company, Luis Martí-Bonmatí, Al Merchant, Joan Carles Monllau, James Selfe and to all the members of the International Patellofemoral Study Group for their constant encouragement and inspiration. Furthermore, I have had the privilege and honor to count on the participation of outstanding specialists who have lent prestige to this monograph. I thank all of them for their time, effort, dedication, kindness, as well as for the excellent quality of their contributing chapters. They all have demonstrated generosity in sharing their great clinical experience in a clear and concise way. I am in debt to you all. Personally, and on behalf of those patients who will undoubtedly benefit from this work, thank you. My sincere gratitude to Eric L. Goode and Justyna Mazurek for their inestimable collaboration. Last but not least, I am extremely grateful to both Springer London and to the production team for the confidence shown in this project and for completing this project with excellence from the time the cover is opened until the final chapter is presented.

Spring 1993, photograph at the Albufera Natural Park (Valencia, Spain). Donald Fithian (right), his wife M.E. (left), and the editor of this book, Vicente Sanchis-Alfonso (in the middle)

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Mount Sinai Medical Center, New York City, NY, USA, 2009. Vicente Sanchis-Alfonso (right), Ronald Grelsamer (left), and John Fulkerson (in the middle)

Vicente Sanchis-Alfonso, M.D., Ph.D.

Contents

Etiopathogenic Bases, Prevention and Therapeutic Implications Patellofemoral Pain: An Overview . . . . . . . . . . . . . . . . . . . . . . . . . . Vicente Sanchis-Alfonso and Ronald P. Grelsamer

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Pathophysiology of Anterior Knee Pain . . . . . . . . . . . . . . . . . . . . . . Vicente Sanchis-Alfonso, Esther Roselló-Sastre, Scott F. Dye, and Robert A. Teitge

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Femoral and Tibial Rotational Abnormalities Are the Most Ignored Factors in the Diagnosis and Treatment of Anterior Knee Pain Patients. A Critical Analysis Review . . . . . . . . . . . . . . . Vicente Sanchis-Alfonso and Robert A. Teitge Why is Torsion Important in the Genesis of Anterior Knee Pain? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Robert A. Teitge Clinical and Radiological Assessment of the Anterior Knee Pain Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vicente Sanchis-Alfonso, Cristina Ramírez-Fuentes, Laura López-Company, and Pablo Sopena-Novales

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Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat These Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vicente Sanchis-Alfonso, Julio Doménech-Fernández, Benjamin E. Smith, and James Selfe

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Management of Anterior Knee Pain from the Physical Therapist’s Perspective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Jenny McConnell

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Targeted Treatment in Anterior Knee Pain Patients According to Subgroups Versus Multimodal Treatment . . . . . . . . . . . . . . . . . 119 James Selfe Surgical Treatment of Anterior Knee Pain. When is Surgery Needed? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133 Vicente Sanchis-Alfonso and Robert A. Teitge

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The Failed Patella. What Can We Do? . . . . . . . . . . . . . . . . . . . . . . 151 Vicente Sanchis-Alfonso, Julio Domenech-Fernandez, and Robert A. Teitge Risk Factors for Patellofemoral Pain: Prevention Programs . . . . . 175 Michelle C. Boling and Neal R. Glaviano Anterior Knee Pain After Arthroscopic Meniscectomy: Risk Factors, Prevention and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . 187 Jorge Amestoy, Daniel Pérez-Prieto, and Joan Carles Monllau Anterior Knee Pain Prevalence After Anterior Cruciate Ligament Reconstruction: Risk Factors and Prevention. . . . . . . . . 197 Antonio Darder-Sanchez, Antonio Darder-Prats, and Vicente Sanchis-Alfonso Patellar Tendinopathy: Risk Factors, Prevention, and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207 Rochelle Kennedy and Jill Cook Pathophysiology of Patellar Instability . . . . . . . . . . . . . . . . . . . . . . 225 William R. Post Evaluation of the Patient with Patellar Instability: Clinical and Radiological Assessment . . . . . . . . . . . . . . . . . . . . . . . 235 Andrew E. Jimenez, Lee Pace, and Donald C. Fithian Evolving Management of Acute Dislocations of the Patella . . . . . . 251 Vicente Sanchis-Alfonso, Erik Montesinos-Berry, and Marc Tompkins How to Deal with Chronic Patellar Instability . . . . . . . . . . . . . . . . 259 Vicente Sanchis-Alfonso and Erik Montesinos-Berry Limitations of Patellofemoral Surgery in Children . . . . . . . . . . . . . 277 Mahad Hassan and Marc Tompkins The Failed Medial Patellofemoral Ligament Reconstruction. What Can We Do? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 Vicente Sanchis-Alfonso and Cristina Ramírez-Fuentes Surgical Treatment of Recurrent Patellar Instability: History and Current Concepts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305 Christopher A. Schneble, David A. Molho, and John P. Fulkerson Chondral and Osteochondral Lesions in the Patellofemoral Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315 Kevin Credille, Dhanur Damodar, Zachary Wang, Andrew Gudeman, and Adam Yanke Patellofemoral Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 329 Christopher S. Frey, Augustine W. Kang, Kenneth Lin, Doug W. Bartels, Jack Farr, and Seth L. Sherman

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Fresh Osteochondral Allografts in Patellofemoral Surgery . . . . . . 349 Suhas P. Dasari, Enzo S. Mameri, Bhargavi Maheshwer, Safa Gursoy, Jorge Chahla, and William Bugbee Extensor Mechanism Complications After Total Knee Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 Jobe Shatrov, Cécile Batailler, Gaspard Fournier, Elvire Servien, and Sebastien Lustig Surgical Techniques: Why, When and How I Do It Sonosurgery Ultrasound-Guided Arthroscopic Shaving for the Treatment of Patellar Tendinopathy When Conservative Treatment Fails . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 Ferran Abat and Håkan Alfredson Medial Patellofemoral Ligament Reconstruction: Anatomical Versus Quasi-anatomical Femoral Fixation . . . . . . . . . . . . . . . . . . . 415 Vicente Sanchis-Alfonso, Maximiliano Ibañez, Cristina Ramirez-Fuentes, and Joan Carles Monllau Minimal Invasive MPFL Reconstruction Using Quadriceps Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431 Christian Fink Combined Medial Patellofemoral Ligament and Medial Patellotibial Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . 445 Robert S. Dean, Betina B. Hinckel, and Elizabeth A. Arendt Warning: Lateral Retinacular Release Can Cause Medial Patellar Dislocation—Lateral Patellofemoral Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 461 Robert A. Teitge Reconstruction of the Lateral Patellofemoral Ligament . . . . . . . . . 469 David S. Zhu and Lutul D. Farrow Patellar Tendon Imbrication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 477 Ronak M. Patel, Sneh Patel, and Jack Andrish Quadricepsplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483 Jason Koh Sulcus Deepening Trochleoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . 491 Edoardo Giovannetti de Sanctis and David H. Dejour Arthroscopic Deepening Trochleoplasty. . . . . . . . . . . . . . . . . . . . . . 503 Lars Blønd Lengthening Trochleoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521 Roland M. Biedert Tibial Tubercle Osteotomy in Patients with Patella Supera or Infera . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533 Joan Carles Monllau and Enrique Sanchez-Muñoz

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Tibial Tubercle Anteromedialization Osteotomy (Fulkerson Osteotomy) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 543 Andrew Gudeman and Jack Farr Rotational Osteotomy. Principles, Surgical Technique, Outcomes and Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555 Vicente Sanchis-Alfonso, Alejandro Roselló-Añón, Cristina Ramírez-Fuentes, and Robert A. Teitge Bipolar Fresh Osteochondral Allograft Transplantation of the Patellofemoral Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 585 Vicente Sanchis-Alfonso and Joan Carles Monllau Patellofemoral Arthroplasty. Pearls and Pitfalls . . . . . . . . . . . . . . . 593 Pedro Hinarejos Clinical Cases—Primary and Revision Patellofemoral Surgery Patellofemoral Joint Preservation Surgery A Case-Based Approach Case # 1: Disabling Anterior Knee Pain After Failed MPFL Reconstruction in a Patient with Patellar Chondropathy, Femoral Anteversion and External Tibial Torsion . . . . . . . . . . . . . 615 Vicente Sanchis-Alfonso and Alejandro Roselló-Añón Case # 2: Disabling Anterior Knee Pain Recalcitrant to Conservative Treatment in a Patient with Patellofemoral Osteoarthritis and Structural Femoral Retrotorsion and Genu Varum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 623 Vicente Sanchis-Alfonso and Alejandro Roselló-Añón Case # 3: Severe Anterior Knee Pain Recalcitrant to Conservative Treatment in a Patient with Functional Femoral Retrotorsion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 629 Vicente Sanchis-Alfonso, Marc Tey-Pons, and Joan Carles Monllau Case # 4: Disabling Anterior Knee Pain in a Multi-operated Young Patient with Severe Patellofemoral Osteoarthritis and Medial Patellar Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 635 Vicente Sanchis-Alfonso Case # 5: Multidirectional Patellar Instability After Over-Medialization of the Tibial Tubercle in a Patient with Severe Trochlear Dysplasia and Patella Alta . . . . . . . . . . . . . 639 Vicente Sanchis-Alfonso Case # 6: Failed MPFL Reconstruction in a Patient with Severe Trochlear Dysplasia and Malpositioning of the Femoral Attachment Point. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645 Vicente Sanchis-Alfonso

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Case # 7: Lateral Patellar Instability in a Multi-operated Young Patient with Severe Patellofemoral Osteoarthritis and Severe Trochlear Dysplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 651 Vicente Sanchis-Alfonso and Joan Carles Monllau Case # 8: Extensor Mechanism Reconstruction After Resection of a Soft Tissue Sarcoma that Infiltrates the Patellar Tendon . . . . 657 Vicente Sanchis-Alfonso, Alejandro Roselló-Añón, Eloisa Villaverde-Doménech, Onofre Sanmartin, and Juan Pablo Aracil-Kessler Case # 9: Severe Patellofemoral Chondropathy in an Active 47-Year-Old Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 663 Erik Montesinos-Berry Case # 10: Dislocated Patella After Revision Total Knee Arthroplasty. Case # 11: Patella Baja and Valgus Limb 56 Years After Tibial Tubercle Transfer . . . . . . . . . . . . . . . . . . . . . 667 Robert A. Teitge New Frontiers in Anterior Knee Pain, Patellar Instability and Patellofemoral Osteoarthritis Evaluation and Treatment Kinetic and Kinematic Analysis in Evaluating Anterior Knee Pain Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675 Vicente Sanchis-Alfonso and Jose María Baydal-Bertomeu Patellofemoral Instrumented Stress Testing . . . . . . . . . . . . . . . . . . 689 Ana Leal, Renato Andrade, Cristina Valente, André Gismonti, Rogério Pereira, and João Espregueira-Mendes Anterior Knee Pain and Functional Femoral Maltorsion in Patients with Cam Femoroacetabular Impingement . . . . . . . . . . 699 Marc Tey-Pons, Vicente Sanchis-Alfonso, and Joan Carles Monllau Finite Element Technology in Evaluating Medial Patellofemoral Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 705 Vicente Sanchis-Alfonso, Diego Alastruey-López, Cristina Ramirez-Fuentes, Erik Montesinos-Berry, Gerard Ginovart, Joan Carles Monllau, and María Angeles Perez Biomechanical Analysis of the Influence of Trochlear Dysplasia on Patellar Tracking and Pressure Applied to Cartilage . . . . . . . . 721 John J. Elias Brain Network Functional Connectivity Clinical Relevance and Predictive Diagnostic Models in Anterior Knee Pain Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 731 María Beser-Robles, Vicente Sanchis-Alfonso, and Luis Martí-Bonmatí

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Robotic-Assisted Patellofemoral Arthroplasty . . . . . . . . . . . . . . . . . 745 Joseph C. Brinkman, Christian Rosenow, Matthew Anastasi, Don Dulle, and Anikar Chhabra Modern Patellofemoral Inlay Arthroplasty—A Silver Lining in the Treatment of Isolated Patellofemoral Arthritis . . . . . . . . . . . 757 Marco-Christopher Rupp, Jonas Pogorzelski, and Andreas B. Imhoff Virtual Orthopaedic Examination in Patellofemoral Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 765 Casey L. Wright and Miho J. Tanaka Epilogue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 781

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Contributors

Ferran Abat ReSport Clinic Barcelona. Blanquerna-Ramon Llull University School of Health Science. Rosselló, Barcelona, Spain Diego Alastruey-López Instituto de Investigación en Ingeniería de Aragón (I3A), Instituto de Investigación Sanitaria Aragón (IIS Aragón), Multiscale in Mechanical and Biological Engineering, University of Zaragoza, Zaragoza, Spain Håkan Alfredson Department of Community Medicine and Rehabilitation, Sports Medicine, Umeå University, Umeå, Sweden Jorge Amestoy Department of Orthopaedic Surgery, Hospital del Mar, Barcelona, Spain; Catalan Institute of Traumatology and Sports Medicine (ICATME), Hospital Universitari Dexeus, Barcelona, Spain; Universitat Autònoma de Barcelona (UAB), Barcelona, Spain Matthew Anastasi Department of Orthopaedic Surgery, Mayo Clinic, Phoenix, AZ, USA; Department of Sports Medicine, Mayo Clinic, Tempe, Phoenix, AZ, USA; Alix School of Medicine, Mayo Clinic, Phoenix, AZ, USA Renato Andrade Dom Henrique Research Centre, Porto, Portugal; Clínica Espregueira - FIFA Medical Centre of Excellence, Porto, Portugal; Porto Biomechanics Laboratory (LABIOMEP), Faculty of Sports, University of Porto, Porto, Portugal Jack Andrish The Cleveland Clinic Foundation, Cleveland, OH, USA Juan Pablo Aracil-Kessler Plastic and Reconstructive Surgery Department, Hospital Provincial de Castellón, Castellón, Spain Elizabeth A. Arendt University of Minnesota, Minneapolis, MN, USA Doug W. Bartels Department of Orthopaedic Surgery, Stanford University, Stanford, CA, USA Cécile Batailler Albert Trillat Center, Lyon North University Hospital, Lyon, France Jose María Baydal-Bertomeu Instituto de Biomecánica de Valencia (IBV), Valencia, Spain xxvii

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María Beser-Robles Biomedical Imaging Research Group at Health Research Institute, Valencia, Spain Roland M. Biedert Sportsclinic 1, Wankdorf Center, Bern, Switzerland Lars Blønd Department of Orthopaedic Surgery, The Zealand University Hospital, Koege, Denmark; Department of Orthopaedic Surgery, Aleris-Hamlet, Copenhagen, Denmark Michelle C. Boling Clinical and Applied Movement Sciences, Brooks College of Health, University of North Florida, Jacksonville, USA Joseph C. Brinkman Department of Orthopaedic Surgery, Mayo Clinic, Phoenix, AZ, USA; Department of Sports Medicine, Mayo Clinic, Tempe, Phoenix, AZ, USA; Alix School of Medicine, Mayo Clinic, Phoenix, AZ, USA William Bugbee Department of Orthopaedic Surgery, Scripps Clinic, La Jolla, CA, USA Jorge Chahla Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA Anikar Chhabra Department of Orthopaedic Surgery, Mayo Clinic, Phoenix, AZ, USA; Department of Sports Medicine, Mayo Clinic, Tempe, Phoenix, AZ, USA; Alix School of Medicine, Mayo Clinic, Phoenix, AZ, USA Jill Cook La Trobe University, Melbourne, Australia Kevin Credille Midwest Orthopedics at Rush University Medical Center, Chicago, IL, USA Dhanur Damodar Midwest Orthopedics at Rush University Medical Center, Chicago, IL, USA Antonio Darder-Prats Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain Antonio Darder-Sanchez Department of Orthopaedic Surgery, Hospital Clínico Universitario, Valencia, Spain Suhas P. Dasari Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA Robert S. Dean Beaumont Health, Royal Oak, MI, USA David H. Dejour Lyon-Ortho-Clinic: Clinique de La Sauvegarde, Lyon, France Julio Doménech-Fernández Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain

Contributors

Contributors

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Don Dulle Department of Orthopaedic Surgery, Mayo Clinic, Phoenix, AZ, USA; Department of Sports Medicine, Mayo Clinic, Tempe, Phoenix, AZ, USA; Alix School of Medicine, Mayo Clinic, Phoenix, AZ, USA Scott F. Dye University of California San Francisco, San Francisco, CA, USA John J. Elias Department of Health Sciences, Cleveland Clinic Akron General, Akron, OH, USA João Espregueira-Mendes Dom Henrique Research Centre, Porto, Portugal; Clínica Espregueira - FIFA Medical Centre of Excellence, Porto, Portugal; 3B’s Research Group–Biomaterials, Biodegradables and Biomimetics, Headquarters of the European Institute of Excellence on Tissue Engineering and Regenerative Medicine, AvePark, Parque de Ciência e Tecnologia, Zona Industrial da Gandra, University of Minho, Barco, Guimarães, Portugal; ICVS/3B’s–PT Government Associate Laboratory, Braga/Guimarães, Portugal; School of Medicine, University of Minho, Braga, Portugal Jack Farr Knee Preservation and Cartilage Restoration Center, OrthoIndy, Indianapolis, IN, USA Lutul D. Farrow Cleveland Clinic Orthopaedic and Rheumatologic Institute, Cleveland, OH, USA; Cleveland Clinic Lerner College of Medicine, Cleveland Clinic Sports Health Center, Ohio, USA Christian Fink Gelenkpunkt Sport and Joint Surgery, Innsbruck, Austria; Research Unit for Orthopedic Sports Medicine and Injury Prevention, UMIT Hall, Tirol, Austria Donald C. Fithian Senta Clinic, San Diego, CA, USA Gaspard Fournier Albert Trillat Center, Lyon North University Hospital, Lyon, France Christopher S. Frey Department of Orthopaedic Surgery, Stanford University, Stanford, CA, USA John P. Fulkerson Department of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, USA Gerard Ginovart Department of Orthopaedic Surgery, Hospital Terres de l’Ebre, Tortosa, Spain Edoardo Giovannetti de Sanctis Lyon-Ortho-Clinic: Clinique de La Sauvegarde, Lyon, France André Gismonti Clínica Espregueira - FIFA Medical Centre of Excellence, Porto, Portugal

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Contributors

Neal R. Glaviano Department of Kinesiology, College of Agriculture, Health and Natural Resources, University of Connecticut, Mansfield, USA Ronald P. Grelsamer The Icahn School of Medicine at the Mount Sinai Medical Center, New York, NY, USA Andrew Gudeman Indiana University School of Medicine, Indianapolis, IN, USA Safa Gursoy Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA Mahad Hassan University of Minnesota, Minneapolis, MN, USA Pedro Hinarejos Consorci Parc de Salut Mar. Barcelona Universitat Pompeu Fabra, Barcelona, Spain Betina B. Hinckel Beaumont Health, Royal Oak, MI, USA Maximiliano Ibañez ICATME, Hospital Universitari Dexeus, UAB, Barcelona, Spain Andreas B. Imhoff Department of Orthopaedic Sports Medicine, Hospital Rechts der Isar, Technical University of Munich, Munich, Germany Andrew E. Jimenez Department of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, USA Augustine W. Kang Stanford School of Medicine, Stanford, CA, USA Rochelle Kennedy La Trobe University, Melbourne, Australia Jason Koh Department of Orthopaedic Surgery, NorthShore University HealthSystem, Skokie, IL, USA Ana Leal CMEMS—Center for MicroElectroMechanical University of Minho, Guimarães, Portugal

Systems,

Kenneth Lin Department of Orthopaedic Surgery, Stanford University, Stanford, CA, USA Laura López-Company Department of Rehabilitation and Physical Therapy, Hospital Arnau de Vilanova, Valencia, Spain Sebastien Lustig Albert Trillat Center, Lyon North University Hospital, Lyon, France Bhargavi Maheshwer Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA Enzo S. Mameri Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL, USA Luis Martí-Bonmatí Medical Imaging Department and Biomedical Imaging Research Group at Hospital, Universitario y Politecnico La Fe and Health Research Institute, Valencia, Spain Jenny McConnell Private Practice, Sydney, NSW, Australia

Contributors

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David A. Molho Department of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, USA Joan Carles Monllau Department of Orthopaedic Surgery, Hospital del Mar, Barcelona, Spain; Catalan Institute of Traumatology and Sports Medicine (ICATME), Hospital Universitari Dexeus, Barcelona, Spain; Universitat Autònoma de Barcelona (UAB), Barcelona, Spain Erik Montesinos-Berry ArthroCentre–Agoriaz, Riaz and Clinique CIC Riviera, Montreux, Switzerland Lee Pace Children’s Health Andrews Institute, Plano, TX, USA Ronak M. Patel Illinois Center for Orthopaedic Research and Education, Hinsdale, IL, USA Sneh Patel University of Illinois College of Medicine at Chicago, Chicago, IL, USA Rogério Pereira Dom Henrique Research Centre, Porto, Portugal; Clínica Espregueira - FIFA Medical Centre of Excellence, Porto, Portugal; Faculty of Sports, University of Porto, Porto, Portugal; Health Science Faculty, University Fernando Pessoa, Porto, Portugal María Angeles Perez Instituto de Investigación en Ingeniería de Aragón (I3A), Instituto de Investigación Sanitaria Aragón (IIS Aragón), Multiscale in Mechanical and Biological Engineering, University of Zaragoza, Zaragoza, Spain Daniel Pérez-Prieto Department of Orthopaedic Surgery, Hospital del Mar, Barcelona, Spain; Catalan Institute of Traumatology and Sports Medicine (ICATME), Hospital Universitari Dexeus, Barcelona, Spain; Universitat Autònoma de Barcelona (UAB), Barcelona, Spain Jonas Pogorzelski Department of Orthopaedic Sports Medicine, Hospital Rechts der Isar, Technical University of Munich, Munich, Germany William R. Post Mountaineer Orthopedic Specialists, LLC, Morgantown, WV, USA Cristina Ramírez-Fuentes Medical Imaging Department, Universitario y Politecnico La Fe, Valencia, Spain

Hospital

Alejandro Roselló-Añón Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain Esther Roselló-Sastre Department of Pathology, Hospital General de Castellón, Castellón, Spain

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Christian Rosenow Department of Orthopaedic Surgery, Mayo Clinic, Phoenix, AZ, USA; Department of Sports Medicine, Mayo Clinic, Tempe, Phoenix, AZ, USA; Alix School of Medicine, Mayo Clinic, Phoenix, AZ, USA Marco-Christopher Rupp Department of Orthopaedic Sports Medicine, Hospital Rechts der Isar, Technical University of Munich, Munich, Germany Enrique Sanchez-Muñoz Knee Unit, Department of Trauma and Orthopaedic Surgery, Toledo University Hospital, Toledo, Spain Vicente Sanchis-Alfonso Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain Onofre Sanmartin IVO’s Dermatology Department, Instituto Valenciano de Oncología (IVO), Valencia, Spain Christopher A. Schneble Department of Orthopaedics and Rehabilitation, Yale School of Medicine, New Haven, CT, USA James Selfe Faculty of Health and Education, Department of Health Professions, Manchester Metropolitan University, Manchester, UK; Visiting Academic in Physiotherapy Studies, Satakunta University of Applied Sciences, Pori, Finland Elvire Servien Albert Trillat Center, Lyon North University Hospital, Lyon, France Jobe Shatrov Albert Trillat Center, Lyon North University Hospital, Lyon, France; Sydney Orthopedic Research Institute, St. Leonard’s, Sydney, NSW, Australia Seth L. Sherman Department of Orthopaedic Surgery, Stanford University, Stanford, CA, USA Benjamin E. Smith Physiotherapy Outpatients, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, UK Pablo Sopena-Novales Department of Nuclear Medicine, Hospital Vithas 9 Octubre, Valencia, Spain Miho J. Tanaka Department of Orthopaedic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA Robert A. Teitge Department of Orthopaedic Surgery, Wayne State University, Detroit, MI, USA Marc Tey-Pons Department of Orthopaedic Surgery, Hospital del Mar, Barcelona, Spain; Department of Orthopaedic Surgery, iMove orthopaedics, Hospital Mi Tres Torres, Barcelona, Spain Marc Tompkins University of Minnesota, TRIA Orthopedic Center, Minneapolis, MN, USA

Contributors

Contributors

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Cristina Valente Dom Henrique Research Centre, Porto, Portugal; Clínica Espregueira - FIFA Medical Centre of Excellence, Porto, Portugal Eloisa Villaverde-Doménech Plastic and Reconstructive Surgery Department, Hospital Provincial de Castellón, Castellón, Spain Zachary Wang Midwest Orthopedics at Rush University Medical Center, Chicago, IL, USA Casey L. Wright Department of Orthopaedic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA Adam Yanke Midwest Orthopedics at Rush University Medical Center, Chicago, IL, USA David S. Zhu Cleveland Clinic Orthopaedic and Rheumatologic Institute, Cleveland, OH, USA

Etiopathogenic Bases, Prevention and Therapeutic Implications

Patellofemoral Pain: An Overview Vicente Sanchis-Alfonso and Ronald P. Grelsamer

That those who know her, know her less, the nearer her they get. Emily Elizabeth Dickinson

1

Anterior Knee Pain—So Common a Symptom, so Misunderstood

Patellofemoral pain (PFP) or anterior knee pain (AKP) is defined as “pain around or behind the patella, which is aggravated by at least one activity that loads the patellofemoral joint (PFJ) during weight-bearing on a flexed knee (e.g., squatting, stair ambulation, jogging/running, hopping/jumping)” [1]. The best available test is “anterior knee pain elicited during a squatting manoeuvre: PFP is evident in 80% of people who are positive on this test” [1]. According to the International patellofemoral pain research retreat “people with a history of dislocation, or who report perceptions of subluxation, should not be included in studies of PFP, unless the study is specifically evaluating these subgroups” [1]. Although it typically occurs in physically active people lesser than 40 years, it also affects people of all activity levels and ages [2]. In a systematic review with meta-analysis, Smith and colleagues [3] have recently found high incidence and prevalence levels for AKP. Subjects were excluded “if the study

V. Sanchis-Alfonso (&) Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain e-mail: [email protected] R. P. Grelsamer The Icahn School of Medicine at the Mount Sinai Medical Center, New York, NY, USA

population was selected from a specific disease area (e.g. diabetes, rheumatoid arthritis, osteoarthritis); if the study population comprised of participants with other knee pathology (e.g. knee ligamentous instability, history of patella dislocations, true knee locking or giving way, patella or iliotibial tract tendinopathy, osteoarthritis)”. The results of that systematic review confirmed that AKP is a common pathology among adolescents and adults. That is the case in both the general population as well as those who practice sports or perform physically demanding activities such as those performed by the military. The prevalence in the general population is reported to stand at 23%, in professional cyclists at 35.7% and in the general adolescent population at 30% [3]. Moreover, a woman is twice as likely to develop AKP than a man [3]. The mean prevalence of low-back pain in the general population is 18% and goes up to 20% among runners [4]. Overall, the prevalence of knee osteoarthritis (OA) has been found to be 16% [5]. Although the prevalence of these three pathological entities is very similar, the interest they arouse in researchers is very different: There have been more than 14,000 articles on knee OA indexed on MEDLINE in the last 20 years. Compare that to only 1,500 indexed articles on AKP [3]. It seems clear that PFP or AKP is of less interest than other conditions of the musculoskeletal system. Despite its high incidence and prevalence, AKP is the most neglected, the least understood, and the most problematic pathological knee condition.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_1

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V. Sanchis-Alfonso and R. P. Grelsamer

The Problem. Anterior Knee Pain—A Paradigm of Aversion Towards a Diagnosis

Implicated factors in AKP include the loss of homeostasis as well as functional, mechanical and structural alterations (see chapters “Pathophysiology of Anterior Knee Pain”, “Femoral and Tibial Rotational Abnormalities are the Most Ignored Factors in the Diagnosis and Treatment of Anterior Knee Pain Patients. A Critical Analysis Review” and “Why is Torsion Important in the Genesis of Anterior Knee Pain?”). The etiology of AKP is multifactorial with not only local (e.g., knee) factors but also proximal (e.g., hip and trunk) and distal ones (e.g., foot and ankle). In fact, the primary cause of AKP in many patients does not lie within the PFJ. There are several subgroups within the AKP population. Therefore, the optimum treatment must be tailored to the individual patient (see chapter “Targeted Treatment in Anterior Knee Pain Patients According to Subgroups Versus Multimodal Treatment”). Among all the subsets of patients with AKP, the most challenging type of AKP, from a therapeutic point of view, is neuropathic. Rathleff and colleagues [6] have shown that young female adults with long-standing AKP demonstrated impaired conditioned pain modulation, meaning that AKP might have important central components that need to be further studied. Another challenge we face is patellar nomenclature. The study of the PFJ is complicated by the use of terms that have different meanings depending on who reads them (The Tower of Babel) [7]. There are terms that must be clarified such as the terms patellar malalignment and skeletal malalignment of the lower limb. There are other terms that should be abandoned, such as “chondromalacia patellae” and “patellofemoral pain syndrome.” AKP is a nemesis to both the patient and the treating physician, creating chronic disability, limited participation in sports, diminished quality of life, psychological impairment, and the basis for sick leave. Collins and colleagues [8] showed

that 40% of AKP patients had a less-thanfavorable recovery at 12 months from the time of diagnosis. AKP negatively influences the quality of life of the patient in the same way as knee OA, another affection that is considered more serious. However, since AKP affects younger populations, it can have a greater impact on their lives than knee OA [9]. The World Health Organization (WHO) defines disability as “a limitation of function that compromises an individual’s ability to perform an activity within the range considered normal”. Because AKP frequently occurs in young working adults, it has an important societal impact due to absenteeism from work and lowered productivity as well as the economic expense of treating these patients [10]. Moreover, people including friends and family might consider AKP patients to be malingering, which only makes things worse. Furthermore, making this worse, we must point out that it is a source of iatrogenic pathology (e.g., medial patellar instability) [11]. We must be very cautious when recommending surgical treatment for AKP patients (see chapter “The Failed Patella. What Can We Do?”). This caution is particularly directed to those “wellmeaning trigger-happy orthopedic surgeons” (a term coined by Scott F. Dye, MD) educated in a purely structural/biomechanical view of this pathology. These surgeons base their surgical decisions solely on Computed tomography (CT) or Magnetic resonance imaging (MRI) findings. This approach is misguided. The patient who began with just mild, intermittent symptoms may get even worse. We must note that the vast majority of AKP patients only need non-operative treatment. The current best evidence-based non-surgical treatment for AKP is multimodal therapy. The core components of this approach include a diverse mix of exercise therapies (e.g., strengthening, stretching), patellar taping or bracing and foot orthoses depending on the sub-group that the patient falls into. There is limited evidence supporting the long-term outcomes of any single approach. Over the years, there have been many attempts to define subgroups within the AKP population. Despite these

Patellofemoral Pain: An Overview

efforts, there is currently no consensus on what the optimal treatments are for the various subgroups. Nonetheless, there is emerging evidence that tailoring treatments to each subgroup can improve the treatment outcomes when compared to currently common multimodal approaches (see chapter “Targeted Treatment in Anterior Knee Pain Patients According to Subgroups Versus Multimodal Treatment”). Finally, we are convinced that the so-called biopsychosocial model currently used in chronic lumbar pain will soon be applied to AKP patients. According to this model, anatomic, biological and biomechanical factors as well as psychological and social factors must be considered (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat These Patients”). Among all the psychological factors that have been analyzed in the AKP patient, the most relevant one is catastrophizing (exaggerated worrying), which relates to pain and disability (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”). Consequently, cognitive behavioral interventions that have brought on a reduction of catastrophizing pain in patients with arthritis or lumbar pain may also be helpful in patients suffering from AKP (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”). Therefore, treatments for this should be incorporated into conventional approaches. Of course, catastrophizing can come from repeated doctors’ failures to diagnose and treat (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”). Unfortunately, the criteria for proper treatment of the AKP patient have largely been anecdotal. More studies with a high level of evidence are needed. These patients bring to the office “a bag full of MRIs or CTs” in which the radiologist reports a patellar subluxation or a patellar tilt. As a last resort, they have been advised to undergo surgery to correct a supposed “lateral displacement of the patella” or the “lateral tilt” diagnosed

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with the MRI or CT alone. This can be problematic when no adequate physical examination has been performed. The malalignment theory, which is strongly supported by many orthopedic surgeons, has enormously damaged many AKP patients and has given this pathology a bad reputation. Of course, a structural anomaly can be responsible for AKP. For example, a rotational osteotomy ought to be considered for that AKP patient with a significant torsional deformity (transverse plane) of the limb (see chapters “Femoral and Tibial Rotational Abnormalities are the Most Ignored Factors in the Diagnosis and Treatment of Anterior Knee Pain Patients. A Critical Analysis Review”, “Why is Torsion Important in the Genesis of Anterior Knee Pain?”, “Surgical Treatment of Anterior Knee Pain. When is Surgery Needed?” and “Rotational Osteotomy. Principles, Surgical Technique, Outcomes and Complications”). We must note that this biomechanical approach is compatible with the biological perspective (“Tissue Homeostasis Theory”) (see chapter “Pathophysiology of Anterior Knee Pain”). We should not be distracted by structural findings manifested on an MRI—but neither should we ignore them. Van der Heijden and colleagues [12] have shown that the structural abnormalities of the PFJ seen on MRIs are not automatically associated with AKP. Thus, AKP patients often undergo treatments with little scientific basis. A number of patients receive intra-articular injections of platelet-rich-plasma (PRP). A plethora of treatment options with different levels of agreement have been described. The great number of variables associated with AKP, most of which lack valid measurement tools, can explain this confusion. All of this makes this pathology an urgent research priority. Moreover, this all explains why many orthopedic surgeons have an aversion to treating AKP patients. Doctors do not want to spend the time evaluating these patients—it’s just not cost-effective. They order an MRI and read the report. Moreover, in some parts of the world, radiologists do not appreciate patellar pathology unless it is extreme; therefore, orthopedists relying completely on the MRI report also miss

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V. Sanchis-Alfonso and R. P. Grelsamer

structural issues. Not uncommonly, AKP patients are quickly shunted off to orthopedic surgeons with a particular interest in the topic.

3

Patellofemoral Pain—A Pathologic Condition with Many Clichés and False Beliefs

There are many myths surrounding this condition, false collective beliefs that are transmitted from generation to generation. One of these myths is that the AKP patient is a person with peculiar psychological traits that are responsible for the genesis of pain. This belief is reinforced by the fact that many patients have very disabling pain but insignificant radiological findings and unremarkable physical signs. The psychological explanation as the cause of pain could not be further from the truth. Psychological factors in AKP patients are only modulators of pain and disability and should be addressed in combination with the search for structural causes (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”). Another misconception is that AKP is always a self-limiting and benign condition, which is why some physicians believe that an active treatment is unnecessary. It is frequently said to that AKP is related to growth. Therefore, symptoms will disappear once the patient reaches adulthood. For this reason, some physicians recommend “expectation”. That approach is a great mistake. Collins and colleagues [8] have shown that success in treating the AKP patient depends on how early the treatment starts. Patients with pain of less than 2 months duration have a better prognosis than those who have had pain for more than 2 months. Rathleff and colleagues [13] have shown that AKP is not a self-limiting knee condition. Those authors observed that adolescents with PFP were more likely to reduce or stop participation in sports compared to adolescents with other types of knee pain. They also found that a majority of their AKP patients had been symptomatic for more than two years, suggesting

that it is not a self-limited condition. In other words, early detection and treatment are advisable. In addition, when possible it is essential to implement prevention measures during adolescence. This will help us prevent years of pain and functional impairment as well as considerable health care expenditures. Given the importance we attach to prevention, we dedicate four chapters in the first section of this book to this topic (chapters “Risk Factors for Patellofemoral Pain. Prevention Programs”, “Anterior Knee Pain After Arthroscopic Meniscectomy. Risk Factors, Prevention and Treatment”, “Anterior Knee Pain Prevalence After Anterior Cruciate Ligament Reconstruction. Risk Factors and Prevention” and “Patellar Tendinopathy. Risk Factors, Prevention, and Treatment”). Furthermore, AKP in an adolescent has a high potential for becoming chronic. Between 70 and 90% of individuals with AKP have recurrent or chronic pain [14]. Conchie and colleagues [15] brought into question the traditional belief that AKP in adolescence is a benign pathology by showing that it is associated with patellofemoral osteoarthritis (PFOA) in adulthood. An individual is 7.5 times more likely to develop PFOA if they have suffered from adolescent AKP. The results of this study are perhaps debatable, as it was a retrospective study rather than a longitudinal one. Moreover, the follow-up time for a longitudinal study of this type should be 50 years and this is impossible. Furthermore, the diagnosis of AKP was based on mailed questionnaires with all their limitations. The paper by Conchie and colleagues [15] nevertheless questions the traditional belief that adolescent AKP is a benign pathology. Thus, AKP and PFOA may form a continuum of disease. Sadly, many orthopedic surgeons do not focus enough attention on this pathology, which reflects their limited understanding. A very common symptom of great concern to AKP patients is patellofemoral crepitation (a.k.a. crepitus). Johnson and colleagues [16] published a paper in Arthroscopy in 1998 on the assessment of asymptomatic knees. Indeed, patellofemoral crepitation has a high incidence rate in asymptomatic women (94% in females vs. 45% in males). Patellofemoral crepitation has been

Patellofemoral Pain: An Overview

associated with the lateral subluxation of the patella. However, Johnson and colleagues [16] have observed that lateral subluxation of the patella (radiographic finding) in asymptomatic people is more common in males than in females (35% and 19%, respectively). It leads some to think that crepitus is not of major importance. We currently know that this is not the case. Crepitus is an important symptom: Women with AKP and pain-free controls with knee crepitus had lower functional performance compared to pain-free controls without knee crepitus. This is an indication that both pain and crepitus may negatively influence function [17]. Crepitus is a poorly understood sign and symptom that creates negative emotions (no one likes a noisy joint), inaccurate etiological theories, and ultimately leads to fear-avoidance behaviors (see chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”) [18].

4

Chondromalacia Patellae. A Symbol of Our Helplessness in Regards to a Diagnosis and Our Ignorance on AKP

Proof that AKP is not well understood is that an obsolete diagnosis like chondromalacia is still used by many doctors and physical therapists today for any pain in the anterior aspect of the knee. More than a century (116 years) has passed since the term chondromalacia was coined, and this term is still used by clinicians, by the staff in charge of codifying the different pathologies for our hospital databases, as well as on private health insurers’ lists of covered services. The term “Chondromalacia Patellae” continues in use in the “International Statistical Classification of Diseases and Related Health Problems (ICD-10, Version 2019)”, its code being M22.4 (Table 1) [19]. AKP has historically been associated with the terms “internal derangement of the knee” and “chondromalacia patellae”. Surprisingly, the term “internal derangement of the knee” also continues in use in the “International Statistical

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Classification of Diseases and Related Health Problems (ICD-10, Version 2019)”, its code M23.9 [19]. The expression “internal derangement of the knee” was coined in 1784 by the British surgeon from Leeds, William Hey [20]. This term was later discredited by the German school surgeon Konrad Büdinger, Dr Billroth’s assistant in Vienna. It was he who described fissuring and degeneration of the patellar articular cartilage of spontaneous origin in 1906 and similar lesions of traumatic origin in another paper in 1908 [21, 22]. Büdinger considered that the expression “internal derangement of the knee” was a “wastebasket” term. He was right since the expression lacks any etiological, therapeutic or prognostic significance. Until the end of the 1960s, AKP was attributed to chondromalacia patellae. However, not all the patients with AKP suffer from “chondromalacia patellae”, and at the same time many patients with “chondromalacia patellae” do not have AKP. In 1978, Leslie and Bentley [23] reported that only 51% of patients with a clinical diagnosis of “chondromalacia” had changes on the patellar surface when examined by means of arthroscopy. In 1991, Royle and colleagues [24] published a study in Arthroscopy, with special reference made to the PFJ, in which they analysed 500 arthroscopies performed over a 2- period. In those patients with pain thought to have its origin in this joint, 63% had “chondromalacia patellae” compared with a 45% incidence in those with meniscal pathological findings at arthroscopy. They concluded that AKP patients do not always have patellar articular changes, and patellar pathology is often asymptomatic. Consistent with this, Scott F. Dye did not feel any pain during arthroscopic palpation of his extensive lesion of the patellar cartilage without intraarticular anesthesia [25]. In this regard, it should be remembered that the articular cartilage is devoid of nerve fibres and, therefore, cannot cause pain. Van der Heijden and colleagues [26] have not detected any differences in the composition of the patellofemoral cartilage between AKP patients and healthy controls. Moreover, even patients with severe patellofemoral chondropathy may not suffer from AKP (Fig. 1).

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Table 1 Codification of patellofemoral disorders by the International Statistical Classification of Diseases and Related Health Problems in 2019 [19]

M22

Disorders of patella Excl.: Dislocation of patella (S83.0)

M22.0

Recurrent dislocation of patella

M22.1

Recurrent subluxation of patella

M22.2

Patellofemoral disorders

M22.3

Other derangements of patella

M22.4

Chondromalacia patellae

M22.8

Other disorders of patella

M22.9

Disorder of patella, unspecified

A

B

Fig. 1 The intensity of preoperative pain is not related to the severity or the extension of the chondral lesion found during surgery. The most serious cases of chondromalacia arise in patients with a recurrent patellar dislocation who feel little or no pain between their dislocation episodes

(A). Chondral lesion of the patella with fragmentation and fissuring of the cartilage in a patient with AKP (B). (Reprinted by permission from Springer Nature, Anterior Knee Pain and Patellar Instability by Vicente SanchisAlfonso, 2011)

Consequently, the International Patellofemoral Study Group (IPSG) advises against using chondromalacia as a diagnosis and suggests the term “anterior knee pain” as it is only descriptive without implying a specific diagnosis. Chondromalacia should not be used to describe a clinical condition. It is merely a descriptive term for morphological softening of the patellar articular cartilage. The term “chondromalacia” comes from the Greek “chondros” and “malakia” and means “softened articular cartilage”. In conclusion, this is a finding that can be made only upon palpation with open surgery or by arthroscopic means, and it is irrelevant. In short, chondromalacia patellae is not synonymous with PFP or AKP. Although traditions die hard, the term

“chondromalacia patellae” should be excluded from the clinical terminology for the reasons we have stated. The following unfavorable 1908 comment of Büdinger about “internal derangement of the knee”, might be applied to “chondromalacia patellae”: “[It] will simply not disappear from the surgical literature. It is the symbol of our helplessness in regard to a diagnosis and our ignorance of the pathology” [27]. The term chondromalacia is a twentieth century mistake. Unfortunately, we always make the same mistakes, as evidenced by the expression “patellofemoral pain syndrome” having replaced “chondromalacia patellae.” Thus, one nonsense has been replaced by another.

Patellofemoral Pain: An Overview

5

Patellar Malalignment Versus Skeletal Lower Limb Malalignment

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In the 1970s, AKP was correlated with the presence of patellar malalignment (PM). PM “is the abnormal positioning of the patella in any plane” (Fig. 2) [28]. The most common type of patellar malalignment is patellar tilt [27]. Moreover, a lateralized tibial tuberosity is included in the patellar malalignment category because it leads to a lateral force vector on the patella that might be responsible for pain and/or lateral displacement of the patella. In 1968, Jack C. Hughston (Fig. 3) published an article on subluxation of the patella that represented a major turning point in the recognition and treatment of patellofemoral disorders [29]. In 1974, Al Merchant (Fig. 4), in an attempt to better understand patellofemoral biomechanics, introduced his version of the patellofemoral axial radiograph [30]. The same author suggested, also in 1974, the open lateral retinacular release as a way of treating recurrent patellar subluxation [31]. In 1975, the French orthopedist Paul Ficat popularized the concept of patellar tilt, always associated with increased tightness of the lateral retinaculum, which causes excessive pressure on the lateral facet of the patella leading to the “lateral patellar compression syndrome”

(“Syndrome d’Hyperpression Externe de la Rotule”) [32]. In fact, the excessive lateral pressure syndrome represents a type of PM. According to Ficat, the lateral patellar compression syndrome causes hyperpressure in the lateral patellofemoral compartment and hypopressure in the medial patellofemoral compartment. Hypopressure and the disuse of the medial patellar facet cause malnutrition and early degenerative cartilage changes. This may explain the early cartilage degeneration found in the medial patellar facet. Hyperpression also leads to cartilage degeneration, thus the degeneration of the lateral cartilage. In 1977, Ficat and Hungerford published “Disorders of the Patellofemoral Joint.” It is a classic of knee extensor mechanism surgery and the first book in English devoted exclusively to the extensor mechanism of the knee [27]. In the preface of the book, these authors refer to the PFJ as “the forgotten compartment of the knee” reflecting the situation through the 1970s. In fact, only two diagnoses were used relating to AKP or patellar instability before the 1970s: chondromalacia patellae and recurrent dislocation of the patella. What’s more, the initial designs for knee arthroplasties ignored the PFJ. In Fig. 5, you can see the logo of the International Knee Society in the late 1980s. There is no patella. In 1995, in Hong Kong, the International Society of the

Fig. 2 CT at 0º of a patient with AKP and functional patellofemoral instability in the right knee. However, the left knee was completely asymptomatic. The PM was

symmetric in both knees. (Reprinted by permission from Springer Nature, Anterior Knee Pain and Patellar Instability by Vicente Sanchis-Alfonso, 2011)

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Fig. 3 Jack C. Hughston, MD (1917–2004). One of the founding fathers of Sports Medicine (The Hughston Foundation, Inc. © 2022)

V. Sanchis-Alfonso and R. P. Grelsamer

Knee (ISK) and the International Arthroscopy Association (IAA) merged to found ISAKOS. Curiously, the ISAKOS logo, which is relatively modern, does not show the patella either. The same goes for the logos of ESSKA and of the Asia–Pacific Knee Arthroscopy Sports Medicine Society. This reflects the little importance knee surgeons have placed on the PFJ. In 1979, John Insall published a paper on the “patellar malalignment syndrome” and his proximal patellar realignment technique used to treat this “syndrome” [33, 34]. According to Insall, lateral loading of the patella is increased in the malalignment syndrome. In some cases, this causes “chondromalacia patellae” but this does not correlate with the presence/absence of pain. Accordingly, Insall and colleagues [35] reported in 1983 that AKP correlates better with malalignment rather than with the severity of cartilage changes found at surgery. Fulkerson and colleagues have also emphasized the importance of PM and an excessively tight lateral

Fig. 4 John Fulkerson (left) and Alan C Merchant (right), IPSG Meeting, Boston, MA, USA, 2006

Patellofemoral Pain: An Overview

Fig. 5 Logo of the International Knee Society. 6th Congress of the International Society of the Knee, Rome, 8th-12th May 1989—Cavalieri Hilton Hotel

retinaculum as a source of AKP [36, 37]. Moreover, John Fulkerson (Fig. 4) popularized the anteromedialization (AMZ) of the tibial tuberosity in 1983 to address pain from patellofemoral chondropathy with patellofemoral tilt and/or chronic patellar subluxation [38]. This technique is indicated when restoring normal patellar tracking. This widely appreciated procedure is not only used for isolated PFOA but for chronic lateral patellar instability. For many years, PM has been widely accepted as an explanation for the genesis of AKP in the young patient. Moreover, this theory had a great influence on orthopedic surgeons who developed several surgical procedures to “correct the malalignment.” Unfortunately, PM has too often been treated surgically. Many surgical treatments have been described yielding extremely variable results. Consequently, the PM concept is currently questioned, and is not universally accepted as a source of AKP. In fact, the number of realignment surgeries performed has dropped dramatically in recent years, at least in Spain, due to a reassessment of this paradigm. To think of AKP as somehow being necessarily tied to PM is an oversimplification that has stultified progress toward better diagnosis and treatment. Overreliance on PM as a diagnosis leads to misguided surgical procedures that can aggravate a patient’s condition. At the end of 1970s, skeletal malalignment of the lower limb was suggested as one of the causes of AKP in some young patients [39]. It must be acknowledged that skeletal malalignment is not an abnormal Q-angle or an increased

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TT-TG distance [40]. It is also not the position of the patella in the trochlea. Neither is it its increased shift (subluxation) or increased tilt [40]. Skeletal malalignment is malalignment of the limb measured on the transverse, coronal, and sagittal planes [40]. For example, the presence of femoral torsion, excessive external tibial torsion, or increased varus or valgus abnormalities have a great impact on PFJ biomechanics. Rotational abnormalities are particularly important [40–42]. In 1979, Stan James presented a comprehensive review of AKP in which the condition of “miserable malalignment” was described, being increased femoral anteversion and increased external tibial torsion [39]. In 1995, he reported on seven patients with “miserable malalignment” who had been treated with internal tibial rotational osteotomy over an 18-year period [43]. Several years earlier, in 1990, Cooke and colleagues described internal proximal tibial rotational osteotomy in seven patients presenting with AKP and drew attention to the inwardly pointing knee (“squinting patella”) as an unrecognized cause of AKP [44]. However, the concept of skeletal malalignment was almost unnoticed and has had extremely little influence on orthopedic surgeons even until a few years ago. In fact, very few publications refer to skeletal malalignment as a cause of AKP. From 1990 to June of 2021, only 22 published papers in English in which the association between patellofemoral disorders in young patients and in which torsional abnormalities of the femur and/or tibia are analyzed from a clinical point of view could be found [45]. One of the world's greatest exponents of the skeletal malalignment theory in the genesis of patellofemoral pain is Robert A. Teitge, MD (Fig. 6), one of the prominent members of the International Patellofemoral Study Group (IPSG). In short, structural abnormalities predispose to pain but are not automatically the source of pain in any given patient. If you have flat feet and foot pain, your foot pain does not necessarily relate to your flat feet. Structural abnormalities are only a predisposing factor just as hypertension predisposes to strokes—even though not everyone with hypertension suffers from a stroke.

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V. Sanchis-Alfonso and R. P. Grelsamer

Fig. 6 Vicente SanchisAlfonso (left) and Robert A. Teitge (right), IPSG Meeting, Banff, Canada, 2019 (Courtesy of Ronald P. Grelsamer, MD)

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Tissue Homeostasis Theory. An Alternative to the Structural/Biomechanic Paradigm

In the 1990s, Scott F. Dye (Fig. 7), of the University of California, San Francisco, and his research group came up with the tissue homeostasis theory [46, 47]. The initial observation that led to the development of the tissue homeostasis theory of patellofemoral pain was made by Dye when a patient with complaints of AKP without evidence of chondromalacia or malalignment underwent a technetium 99 m methylene diphosphonate bone scan evaluation of the knees. It was an attempt to assess the possible presence of covert osseous pathology; and indeed, the bone scan of that individual manifested an intense diffuse patellar uptake despite normal radiographic images. The tissue homeostasis theory states that joints are more than mechanical structures; they are living metabolically active systems. This theory attributes pain to a physiopathological mosaic of causes such as increased osseous remodelling, increased intraosseous pressure, or peripatellar synovitis that leads to a decrease in what he called the “Envelope of Function” (or “Envelope of Load Acceptance”). The “Envelope of Function” describes a range of loading and energy absorption that is compatible with tissue homeostasis of an entire joint system; that is, with the mechanisms of healing and maintenance

Fig. 7 Scott F. Dye, IPSG Meeting, San Diego, CA, USA, 2011 (Courtesy of Ronald P. Grelsamer, MD)

of normal tissues. Obviously, the Envelope of Function for a young athlete will be greater than that of sedentary elderly individual. Within the Envelope of Function is the region termed Zone of Homeostasis. Loads that exceed the Envelope of Function but are insufficient to cause a macrostructural failure are termed the Zone of Supraphysiologic Overload. If sufficiently great forces are put on the patellofemoral system, macrostructural failure can occur. For Dye [46], the following four factors determine the Envelope of Function or Zone of Homeostasis: (1) anatomic factors (the morphology, structural integrity and biomechanical characteristics of tissue); (2) kinematic factors (dynamic control of the joint involving proprioceptive sensory output, cerebral and cerebellar

Patellofemoral Pain: An Overview

sequencing of motor units, spinal reflex mechanisms, and muscle strength and motor control); (3) physiological factors (the genetically determined mechanisms of molecular and cellular homeostasis that determine the quality and rate of repair of damaged tissues); and (4) treatment factors (type of rehabilitation or surgery received). According to Dye, the loss of both osseous and soft tissue homeostasis is more important in the genesis of AKP than structural characteristics. To him, it matters little which specific structural factors may be present (i.e., patellar cartilage lesions, PM, etc.) if the joint is being loaded within its Envelope of Function and is therefore asymptomatic. He suggests that patients with AKP are often symptomatic due to supraphysiological loading of anatomically normal knee components [47]. In fact, AKP patients often lack an easily identifiable structural abnormality to account for the symptoms. The Envelope of Function frequently diminishes after an episode of injury to the point where previously well-tolerated activities of daily living (e.g., stair climbing, sitting down in and arising out of chairs, pushing the clutch of a car) become supraphysiological loads for that patient, leading to ineffective tissue healing and continued symptoms. Bringing loads down within the newly diminished Envelope of Function allows for the normal tissue healing processes to go forward.

7

Creation of Study Groups: An Inflection Point in the Knowledge of Patellofemoral Pain

We are therefore faced with a very prevalent symptom with multiple possible etiologies. This is fertile ground for a study group. In 1994, Jean Yves Dupont from France, travelled to Farmington, Connecticut in the USA to visit John Fulkerson. They decided to gather “a group of friends” from different countries with a proven interest in the academic study of patellofemoral problems. They would meet

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informally to take stock of their patellofemoral opinions. Dr. Fulkerson served as the first secretary and organizer of the study group and set up an initial meeting in Orlando, Florida on February 17, 1995. Thus was born the International Patellofemoral Study Group (IPSG). The second meeting of the IPSG was held near Dupont’s home in beautiful Benodet in Brittany (France) in the fall of 1995 (Fig. 8). Each participant was encouraged to speak on a patellofemoral topic of his choice, and the group was encouraged to discuss, debate, and critique. Around this time, Joan and Al Merchant designed the logo for the IPSG. Patellofemoral pain is of such complexity that even within this group there are opposing approaches and theories with surgeons, therapists and engineers often holding dogmatic positions. Perhaps less dogmatic over time. Moreover, in 2003, John Fulkerson created with the help of Eric Dahlinger, Dr. Peter Jokl, and tennis legend Ivan Lendl, the Patellofemoral Foundation (www.patellofemoral.org). to stimulate research efforts, education, and fundraising. The Patellofemoral Foundation sponsors the “Patellofemoral Research Excellence Award” to encourage outstanding PF research. Moreover, this foundation sponsors the “Patellofemoral Traveling Fellowship” to stimulate global patellofemoral communication. Finally, the Patellofemoral Foundation awards the “Patellofemoral Lifetime Achievement Award” every year in recognition of those surgeons who have dedicated their career to the understanding and treatment of patients with patellofemoral disorders along with organizing the “Comprehensive Patellofemoral Online Education Course.” In 2009, the International Patellofemoral Research Network (iPFRN), a group of researchers and clinicians with a specific interest in patellofemoral pain, was founded. The iPFRN was established by five global leaders in patellofemoral pain research. They are Irene Davis, Chris Powers, Kay Crossley, Jenny McConnell and Erik Witvrouw. This group has published 7 consensus statements in high impact journals since 2009 [1, 14, 48–52].

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V. Sanchis-Alfonso and R. P. Grelsamer

Fig. 8 IPSG Meeting, Benodet, France, Fall 1995. (Courtesy of Ronald P. Grelsamer, MD)

8

The “Proximal Control” Concept—A Turning Point

Historically, the patella has been considered a mobile structure that sits on a fixed structure that is the femur. That thinking is based on kinematic studies done without weight-bearing or in studies in which the femur has been considered a fixed structure. In the 2000s, Chris Powers, of the University of Southern California, Los Angeles, and his working group conducted studies of the PFJ with weight-bearing and suggested that the main factor contributing to patella tilt and lateral displacement during weight-bearing is the internal rotation of the femur. Powers and colleagues [53] published a study in 2003 in which the objective was to compare PFJ kinematics during non-weight-bearing and weight-bearing knee extension in people with AKP and lateral patellar subluxation. They demonstrated that lateral patellar displacement was more pronounced during non-weight-bearing (open chain)

compared to weight-bearing (closed chain) knee extension. However, PFJ kinematics during nonweight-bearing was characterized by the rotation of the patella on the femur, while it was characterized by the femur rotating underneath the patella during weight-bearing. In 2010, Chris Powers and colleagues published another study comparing PFJ kinematics, femoral rotation, and patella rotation between females with AKP and pain-free controls using weight-bearing kinematic MRI [54]. The results of that study suggest that the control of femur rotation may be important to restoring normal PFJ kinematics. That is, the problem of PM is not in the patella but in the femur. In other words, the primary contributor to lateral patellar subluxation and patellar tilt is the internal rotation of the femur underneath the patella. Therefore, control of the rotation of the femur is fundamental to guaranteeing normal patellofemoral kinematics. This theory supposes a change in mentality relative to the concept of PM. It is a true turning point. These findings suggest that control of the rotation of the femur is essential to restoring the normal

Patellofemoral Pain: An Overview

kinematics of the PFJ. In addition, normalizing femoral rotation can affect the tension of peripatellar soft structures, including the lateral retinaculum, and can also affect patellofemoral pressures. Lee and colleagues [55] have demonstrated that femoral rotation results in an increase in PFJ contact pressures on the contralateral facet of the patella (i.e., lateral PFJ during internal rotation of the femur and vice versa). Using a finite element model, Liao and colleagues [56] have demonstrated that internal rotation of the femur provokes an increment in PFJ stress. We are thus facing a paradigm shift. It has been shown that excessive internal rotation of the femur can cause (1) a decrease in the patellofemoral contact area and therefore an increase in patellofemoral pressure and (2) tightness of the lateral retinaculum. Thus, a new concept was born: the “proximal control” concept that is currently fundamental to understanding the physiotherapeutic treatment of an important subgroup of AKP patients. Therefore, a treatment that addresses the control of femoral motion may play a crucial role in the treatment of some AKP patients. This way of thinking is diametrically opposed to the one that had been maintained until this moment, which was to consider patella tracking as the relative motion of the patella on a fixed femur.

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Take Home Message

To summarize, the high incidence and prevalence of AKP along with its high associated disability, its high potential for becoming chronic, and its association with PFOA in adulthood makes PFP an urgent research priority.

References 1. Crossley KM, Stefanik JJ, Selfe J, et al. Patellofemoral pain consensus statement from the 4th International Patellofemoral Pain Research Retreat, Manchester. Part 1: Terminology, definitions, clinical examination, natural history, patellofemoral osteoarthritis and patient-reported outcome m. Br J Sports Med 2016;50:839–843.

15 2. Crossley KM, Callaghan MJ, van Linschoten R. Patellofemoral pain. Br J Sports Med. 2016;50 (4):247–50. 3. Smith BE, Selfe J, Thacker D, et al. Incidence and prevalence of patellofemoral pain: a systematic review and meta-analysis. PLoS ONE. 2018;13(1): e0190892. https://doi.org/10.1371/journal.pone. 0190892. 4. Maselli F, Storari L, Barbari V, et al. Prevalence and incidence of low back pain among runners: a systematic review. BMC Musculoskelet Disord. 2020;21(1):343. 5. Wallace IJ, Worthington S, Felson DT, et al. Knee osteoarthritis has doubled in prevalence since the mid-20th century. Proc Natl Acad Sci USA. 2017;114(35):9332–6. 6. Rathleff MS, Petersen KK, Arendt-Nielsen L, et al. Impaired conditioned pain modulation in young female adults with long-standing patellofemoral pain: a single blinded cross-sectional study. Pain Med. 2016;17(5):980–8. 7. Grelsamer RP. Patellar nomenclature. The tower of babel revisited. Clin Orthop. 2005;436:60–65. 8. Collins NJ, Bierma-Zeinstra SM, Crossley KM, et al. Prognostic factors for patellofemoral pain: a multicentre observational analysis. Br J Sports Med. 2013;47(4):227–33. 9. Reijnders L, van de Groes SA. The quality of life of patients with patellofemoral pain—a systematic review. Acta Orthop Belg. 2020;86(4):678–87. 10. Tan SS, van Linschoten RL, van Middelkoop M, et al. Cost-utility of exercise therapy in adolescents and young adults suffering from the patellofemoral pain syndrome. Scand J Med Sci Sports. 2010;20:568–79. 11. Sanchis-Alfonso V, Merchant AC. Iatrogenic medial patellar instability: an avoidable injury. Arthroscopy. 2015;31(8):1628–32. 12. van der Heijden RA, de Kanter JL, Bierma-Zeinstra SM, et al. Structural abnormalities on magnetic resonance imaging in patients with patellofemoral pain: A cross-sectional case-control study. Am J Sports Med. 2016. pii: 0363546516646107. 13. Rathleff MS, Rathleff CR, Olesen JL, et al. Is knee pain during adolescence a self-limiting condition? Prognosis of patellofemoral pain and other types of knee pain. Am J Sports Med. 2016;44(5):1165–71. 14. Powers CM, Bolgla LA, Callaghan MJ, et al. Patellofemoral pain: proximal, distal, and local factors, 2nd International Research Retreat. J Orthop Sports Phys Ther. 2012;42:A1-54. 15. Conchie H, Clark D, Metcalfe A, et al. Adolescent knee pain and patellar dislocations are associated with patellofemoral osteoarthritis in adulthood: A case control study. Knee. 2016. https://doi.org/10. 1016/j.knee.2016.04.009. 16. Johnson, LL. van Dyk E, Green JR et al. Clinical assessment of asymptomatic knees: comparison of men and women. Arthroscopy. 1998;14:347–359.

16 17. De Oliveira SD, Barton C, Crossley K, et al. Implications of knee crepitus to the overall clinical presentation of women with and without patellofemoral pain. Phys Ther Sport. 2018;33:89–95. 18. Robertson CJ, Hurley M, Jones F. People’s beliefs about the meaning of crepitus in patellofemoral pain and the impact of these beliefs on their behaviour: a qualitative study. Musculoskelet Sci Pract. 2017;28:59–64. 19. International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10)WHO Version 2019. 20. Levay D. The history of orthopaedics. New Jersey: The Parthenon Publishing Group; 1990. 21. Budinger K. Üeber ablösung von gelenkteilen und verwandte prozesse. Dtsch Z Chir. 1906;84:311–65. 22. Budinger K. Üeber traumatische knorpelrisse im kniegelenk. Dtsch Z Chir. 1908;92:510. 23. Leslie IJ, Bentley G. Arthroscopy in the diagnosis of chondromalacia patellae. Ann Rheum Dis. 1978;37:540–7. 24. Royle SG, Noble J, Davies DR, et al. The significance of chondromalacic changes on the patella. Arthroscopy. 1991;7:158–60. 25. Dye SF, Vaupel GL, Dye CC. Conscious neurosensory mapping of the internal structures of the human knee without intra-articular anesthesia. Am J Sports Med. 1998;26:773–7. 26. van der Heijden RA, Oei EHG, Bron EE, et al. No difference on quantitative magnetic resonance imaging in patellofemoral cartilage composition between patients with patellofemoral pain and healthy controls. Am J Sports Med. 2015;44(5):1172–8. 27. Ficat P, Hungerford DS. Disorders of the PatelloFemoral Joint. Baltimore: Williams & Wilkins; 1977. 28. Grelsamer R. Patellar malalignment: current Concepts Review. J Bone Joint Surg. 2000;82A:1639– 50. 29. Hughston JC. Subluxation of the patella. J Bone Joint Surg. 1968;50-A: 1003–1026. 30. Merchant AC, Mercer RL, Jacobsen RH et al. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg. 1974; 56-A: 391–1396. 31. Merchant AC, Mercer RL. Lateral release of the patella: a preliminary report. Clin Orthop. 1974;103:40. 32. Ficat P, Ficat C, Bailleux A. Syndrome d’hyperpression externe de la rotule (S.H.P.E). Rev Chir Orthop. 1975;61: 39–59. 33. Insall J. “Chondromalacia Patellae”: Patellar malalignment syndrome. Orthop Clin North Am. 1979;10:117–27. 34. Insall J, Bullough PG, Burnstein AH. Proximal “tube” realignment of the patella for chondromalacia patellae. Clin Orthop. 1979;144:63–9. 35. Insall JN, Aglietti P, Tria AJ Jr. Patellar pain and incongruence. II: Clinical application. Clin Orthop. 1983;176:225–232.

V. Sanchis-Alfonso and R. P. Grelsamer 36. Fulkerson JP. The etiology of patellofemoral pain in young, active patients: a prospective study. Clin Orthop. 1983;179:129–33. 37. Fulkerson JP, Tennant R, Jaivin JS. Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop. 1985;197:196–205. 38. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;177:176–81. 39. James, S.L. Chondromalacia of the Patella in the Adolescent. In: Kennedy JC. editor. The Injured Adolescent Knee. Baltimore: The Williams & Wilkins Company, 1979. 40. Teitge RA. Patellofemoral disorders correction of rotational malalignment of the lower extremity. In: Noyess, knee disorders: surgery, rehabilitation, clinical outcomes, Elsevier, 2017. 41. Teitge RA. Does lower limb torsion matter? Tech Knee Surg. 2012;11:137–46. 42. Teitge RA. The power of transverse plane limb malalignment in the genesis of anterior knee pain— clinical relevance. Ann Joint. 2018;3:70. 43. Meister K, James SL. Proximal tibial derotation osteotomy for anterior knee pain in the miserably malaligned extremity. Am J Orthop (Belle Mead NJ). 1995;24:149–55. 44. Cooke TD, Price N, Fisher B. The inwardly pointing knee. An unrecognized problem of external rotational malalignment. Clin. Orthop Relat. 1990;56–60. 45. Sanchis-Alfonso V, Domenech-Fernández J, FerràsTarragó J, et al. The incidence of complications after derotational femoral and/or tibial osteotomies in patellofemoral disorders in adolescents and active adult patients. A Systematic Review with MetaAnalysis. (In press). 46. Dye SF. The knee as a biologic transmission with an envelope of function: a theory. Clin Orthop. 1996;325:10–8. 47. Dye SF, Staubli HU, Biedert RM, et al. The mosaic of pathophysiology causing patellofemoral pain: therapeutic implications. Operative Techn Sports Med. 1999;7:46–54. 48. Davis IS, Powers C. Patellofemoral pain syndrome: proximal, distal, and local factors—an international research retreat: April 30–May 2, 2009, Fells Point, Baltimore. MD J Orthop Sports Phys Ther. 2010;40 (3):A1–48. 49. Witvrouw E, Callaghan MJ, Stefanik JJ, et al. Patellofemoral pain: consensus statement from the 3rd International Patellofemoral Pain Research Retreat held in Vancouver. Br J Sports Med. 2014;48(6):411–4. 50. Crossley KM, van Middelkoop M, Callaghan MJ, et al. 2016 Patellofemoral pain consensus statement from the 4th International Patellofemoral Pain Research Retreat, Manchester. Part 2: recommended physical interventions (exercise, taping, bracing, foot

Patellofemoral Pain: An Overview orthoses and combined interventions). Br J Sports Med. 2016;50(14):844–852. 51. Powers C, Witvrouw E, Davis IS, et al. Evidencebased framework for a pathomechanical model of patellofemoral pain: 2017 patellofemoral pain consensus statement from the 4th International Patellofemoral Pain Research Retreat, Manchester, UK: part 3. Br J Sports Med. 2017;51(24):1713–23. 52. Collins NJ, Barton ChJ, van Middelkoop M, et al. 2018 Consensus statement on exercise therapy and physical interventions (orthoses, taping and manual therapy) to treat patellofemoral pain: recommendations from the 5th International Patellofemoral Pain Research Retreat, Gold Coast, Australia, 2017. Br J Sports Med. 2018;52(18):1170–8. 53. Powers CM, Ward SR, Fredericson M, et al. Patellofemoral kinematics during weightbearing and

17 non-weightbearing knee extension in persons with patellar subluxation: A preliminary study. J Orthop Sports Phys Ther. 2003;33:677–85. 54. Souza RB, Draper CE, Fredericson M, et al. Femur rotation and patellofemoral joint kinematics: A weight-bearing MRI analysis. J Orthop Sports Phys Ther. 2010;40:277–85. 55. Lee TQ, Morris G, Csintalan RP. The influence of tibial and femoral rotation on patellofemoral contact area and pressure. J Orthop Sports Phys Ther. 2003;33:686–93. 56. Liao TC, Yang N, Ho KY, et al. Femur rotation increases patella cartilage stress in females with patellofemoral pain. Med Sci Sports Exerc. 2015;47 (9):1775–80.

Pathophysiology of Anterior Knee Pain Vicente Sanchis-Alfonso, Esther Roselló-Sastre, Scott F. Dye, and Robert A. Teitge

1

Introduction

Anterior knee pain (AKP) is the most common reason for adolescents, adults, and physically active people to consult with an orthopedic surgeon who specializes in the knee. Despite the high incidence and prevalence of AKP and an abundance of clinical and basic science research, the etiology of this condition is not well-known. This chapter synthesizes a review of the literature and our research and clinical experience on pathophysiology of AKP in the young patient.

2

Theories on the Genesis of AKP

Until the end of the 1960s, AKP was attributed to chondromalacia patellae, a concept from the early twentieth century [1] that has no clinical

V. Sanchis-Alfonso (&) Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain e-mail: [email protected] E. Roselló-Sastre Department of Pathology, Hospital General de Castellón, Castellón, Spain S. F. Dye University of California San Francisco, San Francisco, CA, USA R. A. Teitge Wayne State University, Detroit, MI, USA

value because it offers no specific diagnostic, therapeutic, or prognostic implications. In fact, many authors have failed to find a clear connection between AKP and chondromalacia patellae [2, 3]. In the 1970s AKP was related to the presence of patellar malalignment (PM) [4–8]. For many years, PM has been widely accepted as an explanation for the genesis of AKP in the young patient. Currently, the PM concept is questioned and is not universally accepted as an underlying factor in AKP. An obvious problem with the PM concept is that not all patellar malalignments, even those of significant proportions, are symptomatic (Fig. 1). A person with PM may not experience pain if the joint is never stressed to the extent that the tissues are irritated. Such individuals probably learn early that “my knee hurts when I do sports” and therefore stop being active. Further, only one knee may be symptomatic, even though the underlying patellar malalignment is entirely symmetrical in both knees (Fig. 1). In addition, patients with normal patellar alignment on computed tomography (CT) can also experience AKP. Therefore, although the patellar malalignment theory is biomechanically appealing, it has failed to explain the presence of AKP in many patients. We must also remember that significant differences have been demonstrated between subchondral bone morphology and the geometry of the articular cartilage surface of the patellofemoral joint (PFJ), in both the axial and sagittal

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_2

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Fig. 1 Disabling AKP and patellar instability of the left knee. The right knee was asymptomatic in spite of the fact that PM was symmetric in both knees. A Preop CT at 0°, B Postop CT at 6 months of proximal realignment surgery, C CT of the right knee, D CT of the left knee at 13 years of follow-up—the patient is completely asymptomatic in spite of the presence of a visible PM.

(A-Reused with permission from Thieme. From: SanchisAlfonso V. American Journal of Knee Surgery. Volume 7, Issue 2. Usefulness of computed tomography in evaluating the patellofemoral joint before and after Insall’s realignment. Thieme: New York. 1994, www. thieme.com)

planes [9]. Therefore, a radiographical PM may not be real, and realignment surgery to correct the nonexistent problem could lead to a worsening of preoperative symptoms. At the end of 1970s, skeletal malalignment of the limb was suggested as the genesis of AKP in some cases [10]. Skeletal malalignment, which is not the same as PM, is the malalignment of the limb measured in the transverse, coronal, and sagittal planes. The presence of excessive femoral anteversion, excessive external tibial torsion, or increased varus or valgus abnormalities has a definite effect on the PFJ [11]. James in 1979 presented a comprehensive review of AKP in which he described the condition of “miserable malalignment”, that is, increased femoral anteversion and increased external tibial torsion [10]. In 1995 he reported on seven patients with miserable malalignment who had been treated with internal rotational tibial osteotomy during an 18-year period [12]. Several years earlier, Cooke and colleagues [13] described internal rotational proximal tibial osteotomy in seven patients presenting with AKP and drew attention to the inwardly pointing knee as an unrecognized cause of AKP. Unlike the concept of PM, however, the concept of skeletal malalignment was almost unnoticed and has had very low influence on orthopedic surgeons. In fact, very few publications refer to skeletal malalignment as a cause of AKP.

In the 1990s, Scott F. Dye and his research group at the University of California, San Francisco, proposed the tissue homeostasis theory [14, 15]. According to this theory, joints are not simply mechanical structures; they are systems that are alive and metabolically active [14]. Pain arises from a physiopathological mosaic of causes, including increased osseous remodeling, increased intraosseous pressure, or peripatellar synovitis leading to a reduced “envelope of function” (or “envelope of load acceptance”) (Fig. 2) [2, 14, 15]. This envelope of function is defined by the range of loading and energy absorption that coexists with normal tissue healing and maintenance (i.e., tissue homeostasis). According to Dye, in the vast majority of AKP cases, the loss of homeostasis of both osseous (Fig. 3) and soft tissue in the peripatellar region is more important than biomechanical/ structural issues in the genesis of AKP. He suggests that AKP patients are often symptomatic because of supraphysiologic loading of anatomically normal knee components [2, 14, 15]. In fact, patients with AKP often lack an easily identifiable structural abnormality to account for their symptoms. According to Dye’s theory of envelope of load acceptance, overuse or cyclical overload of soft tissue or bone areas may explain AKP in many patients. However, it should be noted that this biological perspective is compatible with the biomechanical approach. The

Pathophysiology of Anterior Knee Pain

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Fig. 2 The envelope of function theory. (Reused with permission from SAGE. From Sanchis-Alfonso V, Dye SF. “How to Deal with Anterior Knee Pain in the Active Young Patient” Sports Health. 2017; 9(4):346–351)

Fig. 3 SPECT-CT in a patient with disabling left AKP due to excessive external tibial torsion showing the loss of osseous homeostasis

rotation of the femur [16, 17]. That is to say, the primary contributor to lateral patellar subluxation and patellar tilt is the internal rotation of the femur below the patella. Therefore, control of the rotation of the femur is fundamental to guaranteeing normal patellofemoral kinematics. Thus, a new concept was born. It is the “proximal control” that is currently considered fundamental to understanding the physiotherapeutic treatment of an important subgroup of AKP patients. Lee and colleagues [18] have demonstrated that femoral rotation results in an increase in PFJ contact pressures on the contralateral facet of the patella (i.e., lateral PFJ during internal rotation of the femur and vice versa).

3 diagnostic challenge is to find the cause of the loading which is “in excess of the envelope of function or load acceptance”. Finally, in the 2000s, Chris Powers and his working group conducted weight-bearing studies of the PFJ and suggested that the main factor contributing to patella tilt and lateral displacement during weight-bearing is the internal

A Critical Analysis of Realignment Surgery for PM

After wide usage of certain surgical techniques, surgeons may come to question the basic tenets justifying the procedures and devise clinical research to test the underlying hypotheses. Realignment surgery for treating PM is no exception. In 2005, Sanchis-Alfonso and

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colleagues [19] retrospectively evaluated 40 Insall’s proximal realignments (IPRs) performed on 29 patients, with an average postsurgical follow-up of 8 years (range: 5–13 years). One of the objectives of this study was to analyze whether a relationship existed between the presence of PM and that of AKP. In this study, IPR was found to provide a satisfactory centralization of the patella into the femoral trochlea in the short-term follow-up and the surgery was associated with resolution of AKP [19, 20]. This outcome appears to support the PM theory; however, the success of realignment surgery may have been due to factors independent of the relative patellofemoral position, such as denervation of the patella, extensive postoperative rest (unload), and postoperative physical therapy. Unfortunately, the satisfactory centralization of the patella observed at the short-term follow-up was lost by the long-term follow-up in almost 57% of the cases, based on CT scans [19]. That is, IPR did not provide a permanent correction of patellofemoral congruence in all cases. Nonetheless, this loss of centralization did not correlate with a worsening of clinical results. In short, a relation between the result (satisfactory versus non-satisfactory) and the presence or absence of postoperative PM was not found in the long term [19]. Out of 29 patients in the study, 12 presented with unilateral symptoms. In nine of these patients, the contralateral asymptomatic knee presented a PM, and there was a satisfactory centralization of the patella into the femoral trochlea in only three cases [19]. If the presence of PM is crucial in the genesis of AKP, how can we account for unilateral symptoms in patients with similar morphologic characteristics between both patellofemoral joints? With regard to unilateral pain in the presence of bilateral PM, patients are known to preferentially load one limb more than the other (usually the dominant limb) in highly demanding activities, such as sports. This loading difference could be enough to cause

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unilateral pain, but we did not find a relationship between the lateral dominance and the affected side in cases with unilateral pain [21]. Further, in six patients with bilateral symptoms who received surgery on the knee with the most severe symptoms, the contralateral knee was pain-free at follow-up. Therefore, if the presence of PM is crucial in the genesis of AKP, why do symptoms disappear without any change in the patellofemoral alignment? Loss of both tissue and bone homeostasis may be more important than structural characteristics in the genesis of AKP. Viewing AKP as being necessarily tied to PM is an oversimplification that has impeded progress toward better diagnosis and treatment. The great danger in using PM as a diagnosis is that the unsophisticated or unwary orthopedic surgeon may think that he or she can correct it with surgical procedures. Pursuing this misguided path very often makes the patients’ pain worse. The worst cases of AKP, at least in my series (V. S-A), occur in patients that have had multiple PM-oriented operative procedures for symptoms that initially were only mild and intermittent. We have observed that not all patellofemoral malaligned knees show symptoms, which is not surprising, because asymptomatic anatomic variations are not uncommon. Moreover, we have demonstrated that PM is not a sufficient condition for the onset of symptoms, given that many patients with AKP do not have PM. We can conclude that the pain does not arise from the PM. That is, pain does not arise from the malposition of the patella on the trochlea. Thus, no imaging study should give us an indication for surgery. PM diagnosed with plain x-ray, CT or MRI is only an instant in time and does not describe the dynamics of motion. Moreover, we do not have adequate proof of the definition of normal alignment. History, physical exam, and differential injection must point towards surgery, with imaging only being used to confirm clinical impression.

Pathophysiology of Anterior Knee Pain

4

The Key Question: Is There a Mechanical Overload of the PFJ Behind AKP and What is the Role of Patellofemoral Imbalance in the Genesis of AKP?

Multiple approaches have been taken to determine the genesis of AKP, from the more traditional structural/biomechanical view to the newer tissue homeostasis perspective. Despite their differences, all potential explanations include joint loading as an important factor. This commonality is not surprising because the PFJ is very sensitive to stress. Certain activities that highly load the PFJ, such as going down stairs or inclines or experiencing prolonged flexion while a person is sitting, kneeling, or squatting, are strongly associated with the genesis and persistence of AKP. In addition, a direct blow to the patella in a fall to the ground or with dashboard contact in an automobile accident can also cause pain that may persist for an extended time, even without an overt radiographically identifiable fracture. How can pain be explained in such cases by the tissue homeostasis perspective? The PFJ is one of the most highly loaded joints in the human body [22] as well as one of the most difficult musculoskeletal systems in terms of restoration of functionality after an injury and the subsequent loss of tissue homeostasis [23]. Joint reaction forces that are created within the PFJ with certain activities can be many times the body weight [24]. These high loads have been estimated to be 3.3 times the body weight with activities such as climbing up or down stairs, 7.6 times the body weight with squatting, and in excess of 20 times the body weight with jumping activities [25, 26]. In addition to the load applied to the joint, the actual stresses generated within the PFJ also depend on the surface areas of the patella and femur that may be in contact at any given moment [19]. Such high forces can easily result in loads that may exceed the safe load acceptance capacity of musculoskeletal tissues, leading to symptomatic damage and inducing a mosaic of pathophysiologic processes causing AKP [2, 15].

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Further, patellofemoral overload could be secondary to inappropriate physiotherapy in some cases of AKP. Attempting to strengthen the quadriceps through open kinetic chain exercises will unacceptably overload the PFJ if the exercises are performed between 0 and 45 degrees of flexion [27]. Likewise, closed kinetic chain exercises performed between 45 and 90 degrees of flexion will also overload the PFJ [27]. Although there may be no obvious structural alteration, the PFJ can be overloaded and AKP can be triggered. In some cases, PFJ overloading is secondary to structural anomalies, such as trochlear dysplasia [28]. Patients with AKP are more likely to have trochlear dysplasia compared to pain-free individuals [29]. Moreover, in patients with a trochlear bump (severe trochlear dysplasia) and AKP, both hydrostatic pressure and water content increase in the patella [30]. Such increases potentially provoke episodes of tissular ischemia and mechanical stimulation of nociceptors, which are both associated with pain [31]. Along these lines, Barton and colleagues [32] have demonstrated that the patella contains an intraosseous nerve network that is the densest in the medial and central portions of the patella and significantly sparser laterally. Moreover, growing evidence shows that in the subgroup of patients with patellofemoral chondral lesions, some of their pain is related to such lesions due to the overload of the richly innervated subchondral bone interface [31]. Such subchondral bone overload is secondary to damaged cartilage and the loss of its capacity as a shock absorber. However, of all the structural factors that can cause an overload of the PFJ, the most powerful is the skeletal malalignment of the lower limb (limb alignment in the three planes), specifically torsional alterations (femoral anteversion and/or external tibial torsion) [33, 34]. With regard to malalignment, Albert van Kampen [35] has demonstrated that patellar tracking is highly susceptible to tibial rotations. Therefore, patellar tracking biomechanical studies must take tibial rotation into account. However, the classic PM theory does not take tibial and femoral torsion

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into consideration, which represents another weak point in the PM theory. Limb alignment appears to very strongly influence the quadriceps vector [33, 34]. An abnormal quadriceps vector is an important contributor to AKP, and abnormal limb alignment is the underlying cause of the incorrect quadriceps vector [33, 34]. The direction of the quadriceps vector is likely more important than its magnitude [33, 34]. It should be noted that skeletal malalignment is not an abnormal Qangle or an increased TT-TG distance, nor is it an increased tilt or increased shift of the patella. It instead involves the alignment of the limb in all three spatial planes—coronal, sagittal, and transverse. During a normal gait, the knee joint axis moves straight forward with minimal amounts of internal or external rotation, and the quadriceps force is directed posteriorly, compressing the patella into the trochlea. With abnormal limb torsion, the knee joint axis often moves forward in a manner that is oblique to the direction of motion. Such movement generates abnormal shear forces between the patella and the femur that will eventually cause tissue failure. If the force is not perfectly aligned, it can lead to an unbalanced distortion of the soft tissues surrounding the patella. It is very likely that one of the sources of AKP is in the peripatellar soft tissues due to the stress that the soft tissues undergo. However, we do not know the strain levels that must be reached to trigger the pain. Some patients with torsional deformities have unilateral AKP, despite the deformity being symmetric. Why one side is symptomatic and the other is not remains an enigma. It is probable that most people limit their activity to avoid overuse or injury to the PFJ and thus AKP. Many of these patients are symptomatic only when they attempt an activity that causes increased loading; therefore, many select their activities based on what is comfortable. Once an injury (soft tissue lesion) or overuse (soft tissue strain) develops, quick recovery does not occur because of the underlying mechanical inefficiency. This situation may explain why disabling pain may occur on one side, while the opposite side remains

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asymptomatic. Moreover, the lack of symptoms on one side may be relative. In some cases, patients have asked for surgery on the asymptomatic side after the symptomatic side has been corrected because “they never knew what it was like to feel normal”. In short, according to Robert A. Teitge, it is the excess of force in the PFJ that exceeds tissue homeostasis which is responsible for AKP. However, the problem is not a question of leaving the load acceptance envelope, but rather knowing what the envelope size limits are and why the excess force is excessive. If this is true, then the problem in diagnosing AKP is determining the source of the excess force. Robert A. Teitge puts forward a simile to understand the etiopathogenesis of AKP. To build a bridge, one must be knowledgeable of several factors. They include: (a) the required load limit, meaning the envelope; (b) the design of the bridge parts, which is the skeletal alignment; and (c) what materials the bridge is made of, connoting the response of those materials to the load. In the following sections, we will look at the biological response to a mechanical stimulus. The question we must ask ourselves is whether it is possible that all the neuroanatomical factors that we are going to discuss below are secondary to an excess of force. In other words, is the excess force the precipitating event? We do not have an answer to these questions.

5

Neuroanatomical Bases for AKP in the Young Patient: Neural Model

Sanchis-Alfonso and colleagues have developed the neural model as an explanation for the genesis of AKP in young patients [36]. The origin of AKP can be in the lateral retinaculum (LR), medial retinaculum, infrapatellar fat pad, synovium, or subchondral bone [37–39]. Studies by Sanchis-Alfonso and colleagues on AKP pathophysiology have mainly focused on the LR retrieved during patellofemoral realignment surgery in patients with a diagnosis of PM [40–43].

Pathophysiology of Anterior Knee Pain

5.1 Morphologic Neural Changes in the Lateral Retinaculum Some studies have implicated neural damage in the LR as a possible source of AKP in the young patient. In 1985, Fulkerson and colleagues described for the first time, nerve damage (demyelination and fibrosis) in the LR of patients with intractable patellofemoral pain requiring lateral retinacular release or realignment of the PFJ [44]. The changes in the retinacular nerves observed by these authors resembled the histopathologic picture of Morton's interdigital neuroma. Later, in 1991, Mori and colleagues found degenerative neuropathy in the LR in AKP patients [45]. Sanchis-Alfonso and colleagues have also observed nonspecific, chronic degenerative changes in nerve fibers, including myxoid degeneration of the endoneurium, retraction of the axonal component, and perineural fibrosis, in the LR in many cases (Fig. 4A) [42, 43]. Moreover, Sanchis-Alfonso and colleagues have found that a smaller group of specimens presented nerve fibers mimicking amputation neuromas seen elsewhere in the body (Fig. 4B) [42, 43]. A clear relationship has been demonstrated between the presence of neuromas and AKP; however, a similar relationship between neural

Fig. 4 A Myxoid degeneration in the nerve fibers. No inflammatory cells are seen, B Microneuroma next to a rich vascular area (HE). (B-Reused with permission from SAGE. From: “Quantitative analysis of nerve changes in

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myxoid degeneration and pain has not been found [43]. Nerve damage occurs diffusely in the affected LR, and one must therefore consider the possibility of multiple neurologic sequelae in the peripatellar region. A possible consequence of such damage could be an altered proprioceptive innervation [43]. For example, Baker and colleagues observed an abnormal sense of the knee joint position (proprioception) in subjects with AKP [46]. Current research shows the importance of proprioceptive information from joint mechanoreceptors for proper knee function. Connective tissues, in addition to their mechanical function, play an important role in transmitting specific somatosensory afferent signals to the spinal and cerebral regulatory systems. Thus, the giving-way in AKP patients can be explained, at least in part, by the alteration or loss of joint afferent information with regard to proprioception due to nerve damage in the ascendant proprioception pathway or a decrease of healthy nerve fibers capable of transmitting proprioceptory stimuli. It seems likely that, to a certain degree, the instability of the PFJ in patients with AKP arises not only from mechanical factors but also neural factors [47, 48]. Such factors center on a proprioceptive deficit both in the sense of position and in the slowing or diminution of

the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment” Am J Sports Med. 1998; 26:703–709)

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stabilizing and protective reflexes. In addition, Jensen and colleagues reported abnormal sensory function in the painful and nonpainful knee in some subjects with long-term unilateral AKP [49].

5.2 Hyperinnervation into the Lateral Retinaculum and AKP Several studies have implicated hyperinnervation of the LR as a possible source of AKP in the young patient, with higher innervation in those with severe pain compared with those with moderate or mild pain [43]. Moreover, the LR of patients with pain as the predominant symptom has been shown to have a higher innervation pattern than the medial retinaculum or the LR of patients with patellar instability [43]. This nerve ingrowth consisted of myelinated and

Fig. 5 A Free nerve endings immersed in the connective tissue, B Hot spot of free nerve endings forming a microneuroma, C Nerve endings entering the arterial wall. (Neurofilament NF). (Reused with permission from SAGE. From: “Immunohistochemical analysis for neural markers of the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment” Am J Sports Med. 2000; 28: 725–731)

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unmyelinated nerve fibers with a predominant nociceptive component (Fig. 5) [40]. The nociceptive properties of at least some of these nerves were shown by their substance P (SP) immunoreactivity (Fig. 6) [40]. SP, which is found in primary sensory neurons and C fibers (slow-chronic pain pathway), is involved in the neurotransmission pathways of nociceptive signals [50–62]. SP was detected in the axons of big nerve fibers, in free nerve endings, and in the vessel walls in some patients with pain as the predominant symptom [40]. Nociceptive fibers (i.e., neural fibers with intraaxonal SP) were fewer in number than NF fibers, indicating that not all the tiny perivascular or interstitial nerves were nociceptive [40]. Interestingly, the finding that SP fibers are more abundant in the LR than in its medial counterpart reinforces the role of the LR as the main source of pain in some AKP patients. Moreover, the number of these

Pathophysiology of Anterior Knee Pain

Fig. 6 A Substance P, a marker of sensory fibers, is expressed in the nerve fibers in a granular pattern, B Neuromas are rich in nociceptive axons, as can be demonstrated studying substance P. (Reused with permission from SAGE. From: “Immunohistochemical analysis for neural markers of the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment” Am J Sports Med. 2000; 28: 725–731)

nociceptive fibers has been observed to be higher in patients experiencing pain as the main symptom relative to those with instability as the predominant symptom (with little or no pain between instability episodes) [40]. Nerve ingrowth, is mostly located within and around blood vessels (Fig. 7) [40, 43]. Thus, within the LR of AKP patients, S-100 positive fibers in the adventitia and within the muscular layer of medium and small arteries resemble a necklace. S-100 protein is a good marker of nerves because it permits identification of the Schwann cells in the myelinated parts of axons. Myelinated fibers typically lose their myelin sheath before they enter the muscular arterial wall, but this was found to not be the case in AKP patients. In a study of myelinated fibers by S-100 immunostaining, we were surprised by the identification of S-100positive fibers within the muscular layer of medium and small arteries given that the myelin sheath

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was expected to be lost before the nerve entered the muscular arterial wall [43]. Vascular innervation has been demonstrated to be more prominent (94%) in patients with severe pain, whereas this type of hyperinnervation has been found in only 30% of the patients with light or moderate pain [42]. These findings are in agreement with the statement of Byers, who postulated in 1968 that pain in an osteoid osteoma could be generated and transmitted by vascular pressure-sensitive autonomic nerves [63]. In reviewing the literature, we have seen that hyperinnervation is also a factor implicated in the pathophysiology of pain in other orthopedic abnormalities, such as chronic back pain and jumper’s knee [54, 55, 64, 65]. On the other hand, pain has also been related with vascular innervation in some pathologies, as is the case in osteoid osteoma, in which an increase in perivascular innervations has been found in all the cases, leading the authors to postulate that pain was more closely related to this innervation than to the release of prostaglandin E2 [66]. Grönblad and colleagues have reported similar findings in the lumbar pain of facet syndrome [67]. Finally, Alfredson and colleagues related pain in Achilles tendinosis with vasculo-neural ingrowth [64]. Hyperinnervation has been demonstrated to be associated with the release of neural growth factor (NGF), a polypeptide that stimulates axonogenesis [41]. NGF has two biologically active precursors: a long form with a molecular weight of approximately 34 kD and a short form of 27 kD [68]. The 34 kD precursor has been found in the LR of AKP patients [41]. Since some of the nerve fibers of the LR express NGF, these nerve fibers must still be in a proliferative phase. As expected, NGF expression is higher in PM patients with pain that in those with instability as the main symptom (Fig. 8) [41]. Gigante and colleagues [69] have also found NGF and TrkA (the NGF receptor) expression in the LR of patients with PM, but not in patients with jumper’s knee or meniscal tears. Interestingly, NGF is related not only to neural proliferation in vessels and perivascular tissue but also to the release of neuroceptive transmitters, such as SP [70].

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Fig. 7 Lateral retinaculum vessels are richly innervated in some of our patients. The myelinated innervation enters the muscular wall from the adventitial tissue, forming a necklace. (S-100). (Reused with permission from SAGE.

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From: “Quantitative analysis of nerve changes in the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment” Am J Sports Med. 1998; 26:703–709)

Fig. 8 Immunoblotting detection of NGF showing a thicker band in cases with AKP (4,5,6,7) compared with cases of instability without pain (1,2,3)

In short, in symptomatic PM patients with pain as the main symptom, there are detectable levels of NGF that cause hyperinnervation and stimulate SP release, whereas in patients with instability as the predominant symptom, there are lower levels of local NGF release, less neural proliferation, and less nociceptive stimulus [41].

Consequently, there must be some factors acting on a PM that make the patient has pain or instability as the main symptom. PM may in fact not have anything to do with the presence of pain. In other words, symptoms appear to be related to multiple factors with variable clinical expression, and our imperfect understanding of

Pathophysiology of Anterior Knee Pain

these factors may explain the all-too-frequent failure to achieve adequate symptom relief with the use of realignment procedures. The question is, what are the mechanisms that stimulate NGF release in these patients? We hypothesize that periodic short episodes of ischemia could be the primary mechanism of NGF release and hyperinnervation, and therefore could be implicated in pain, at least in a subgroup of AKP patients.

5.3 Role of Ischemia in the Genesis of AKP: Loss of Vascular Homeostasis Despite numerous publications on AKP, the mechanism underlying the pain is controversial. The loss of vascular homeostasis has been proposed as an intrinsic pain mechanism in a subgroup of AKP patients.

5.3.1 Basic Science According to some authors, ischemia can induce NGF synthesis [70–72]. Moreover, NGF has been shown to stimulate neural sprouting and hasten neural proliferation in blood vessel walls [73, 74], which is the same pattern of hyperinnervation that is seen in the LR of some AKP patients [40, 42, 43]. Similar changes have been studied in animal models and are present in the coronary innervation of patients with myocardial infarcts and brain ischemia [71, 72, 74]. Thus, short episodes of tissular ischemia due to vascular torsion or vascular bending have been hypothesized as the main problem in painful patellofemoral imbalance [40, 42]. Vascular bending could be induced mechanically by medial traction over the retracted LR with knee flexion [38]. Sanchis-Alfonso and colleagues have demonstrated histologic retinacular changes associated with hypoxia in painful PM [42]. They have found lesions that can lead to tissular anoxia, such as arterial vessels with obliterated lumina and thick muscular walls, and other lesions that can arise from ischemia, such as infarcted foci of the connective tissue, myxoid stromal degeneration, and ultrastructural findings

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related with anoxia (degenerated fibroblasts with autophagic intracytoplasmic vacuoles, endothelial cells with reduplication of the basal lamina, young vessels with endothelial cells containing active nuclei and conspicuous nucleoli, and neural sprouting) (Fig. 9) [75]. Another phenomenon related to ischemia is angiogenesis. Chronic ischemia leads to release of vascular endothelial growth factor (VEGF), a potent hypoxia-inducible angiogenic factor that causes hypervascularization [76]. This hypervascularization creates blood vessels to supply the nutrient needs of the tissue. Sanchis-Alfonso and colleagues have performed a quantitative analysis of vascularization in the LR excised during surgical patellofemoral realignments, using a pan-vascular marker, anti-Factor VIIIrelated antigen [42]. They have found an increase in the number of blood vessels in the LR of patients with painful PM, with the severe pain group having greater numbers compared with those of moderate or mild pain group [42]. Moreover, as expected, they found a positive linear correlation between the number of blood vessels and number of nerves [42]. Tissular ischemia induces VEGF release by fibroblasts, synovial cells, mast cells, or even endothelial cells [77–80]. Based on these principles, Sanchis-Alfonso and colleagues performed a study of VEGF expression in the LR of patients with PM, using immunohistochemistry and immunoblot analysis [42]. VEGF release begins 8 h after hypoxia, and the peptide disappears in 24 h if the ischemic crisis has ended [42]. Therefore, VEGF positivity reflects the presence of an ischemic process, or better said, 8–24 h has elapsed since the onset of the transitory ischemic episode. However, given that the average duration of VEGF is very short, its absence has no significance regarding whether a transitory ischemic process is occurring. Although this process has been well documented in joints affected by rheumatoid arthritis and osteoarthritis [79–81], it has never been documented in AKP until the study by Sanchis-Alfonso and colleagues [42]. They have shown VEGF production in stromal fibroblasts, vessel walls, certain endothelial cells, and even nerve fibers, including

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A

B

C

E

D

F

G

Fig. 9 A Arterial vessel in the retinacular tissue can show a prominent and irregular endothelium and thick muscular walls or even an irregular reduction of the vascular lumen. (Hematoxylin–Eosin stain). B Infarcted foci in the connective tissue showing a degenerative pattern of the collagen fibers, with loss of the fibrillar component and accumulation of myxoid material in the interstitium, (Masson’s Trichrome stain). C Myxoid stromal

degeneration in the middle of the fibrous retinacular tissue (Hematoxylin–Eosin stain). D Degenerative changes in fibroblasts (increased autophagic vacuoles— asterisk–) secondary to hypoxia (TEM). E Young vessels with endothelial cells containing active nuclei and conspicuous nucleoli. F Neural sprouting is detected ultrastructurally as a bunch of tiny axons immersed in the Schwann cell cytoplasm. G Neural sprouting detail

similar levels in axons as in perineurium (Fig. 10) [42]. Their immunohistochemical findings were confirmed by immunoblot analysis. VEGF levels were higher in patients with severe

pain than in those with mild to moderate pain; the protein was barely detectable in two cases with mild pain (Fig. 11) [42]. VEGF expression is absent in normal joints, although inflammatory

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Fig. 10 A VEGF, the factor promoting vascular proliferation, is present in smalls vessels (wall and endothelium) and in perivascular fibroblasts. B Some cases have VEGF expression in the perineural shift and inside the axons (VEGF)

Fig. 11 Immunoblotting detection of VEGF showing a thicker band in cases with severe AKP (2,3,10) compared with cases with moderate pain (1,5,8) or light pain (4,6,7,9)

processes can stimulate its release [81, 82]. In such cases, synovial hypoxia secondary to articular inflammation is assumed to trigger VEGF production [82]. However, inflammatory changes have not been observed in the LR of AKP patients [42, 43]. Furthermore, peripheral nervous system hypoxia has been reported to be able to simultaneously trigger VEGF and NGF synthesis via neurons [83], or inflammatory or stromal cells [71, 72]. VEGF induces hypervascularization, and NGF induces hyperinnervation. Both occurrences have been observed in AKP patients [42, 43]. In conclusion, ischemia could be the main trigger for pain in at least a subgroup of AKP patients.

5.3.2 Clinical Studies The role of vascular insufficiency in AKP has not been studied extensively from a clinical point of view. In fact, only a few clinical papers have

alluded to the possibility of hypoxia as a factor in the pathogenesis of AKP. Sandow and Goodfellow [84] investigated the natural history of AKP in adolescents. In a study sample of 54 adolescent girls, the researchers observed that 9 out of 54 (16.7%) had pain that was aggravated by cold weather. According to Selfe and colleagues [85] the proximal part of the rete patellae is very superficial and is therefore vulnerable to thermal environmental stress, resulting in greater hypoxia during cold weather. More recently, Selfe and colleagues [86] studied clinical outcomes in a sample of AKP patients categorized as hypoxic, that is to say, with “cold knees” (his or her legs felt cold even in warm surroundings). Fourteen out of 77 (18.2%) of the patients were categorized as “cold sufferers,” a percentage very similar to that reported by Sandow and Goodfellow [84]. Selfe and colleagues [86] studied local hypothermia by means of infrared thermography and concluded that patients categorized as hypoxic reported greater pain levels and had poorer response to an exercise-based treatment than non-hypoxic patients. Gelfer and colleagues [87], using single photon emission computed tomography (SPECT), also found a relationship between transient patellar ischemia after total knee replacement and the clinical symptoms of AKP. Similarly, using photoplethysmography, which is a reliable technique for estimating blood flow in bone tissue, Naslund also observed that an ischemic mechanism (decreased

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blood flow in the patellar bone) is involved in the pathogenesis of AKP [88]. Moreover, in half of the AKP studied patients, Naslund observed accelerated bone remodeling in bony compartments of the knee joint, which may have been due to a dysfunctioning sympathetic nervous system and caused intermittent ischemia and pain. Selfe and colleagues [85] classified AKP patients into three groups: hypoxic, inflammatory, and mechanical. However, ischemia may be the painprovoking factor in all three groups, given that inflammatory changes can develop not only after ischemia but also after mechanical damage to the vascular system. Ischemia could be caused by higher intraosseous pressure, redundant axial loading, or decreased arterial blood flow.

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The Role of the Peripheral and/or Central Nervous System in the Pathophysiology of AKP—“Central Sensitization”—“The Neuromatrix Model”

AKP is a paradigm of chronic pain. Chronic pain is a multidimensional phenomenon composed of sensitive, cognitive-evaluative and affectivemotivational domains. The central nervous system, both the brain and spinal cord, is where pain is produced and modulated. Several brain and spinal cord areas work together (the pain neuromatrix) in response to corporal stimuli to create the multidimensional experience of pain. Interestingly, Damasio and colleagues [89] observed an overlap between the cerebral activity areas related to chronic pain and those related to cognition and emotions. This finding suggests that chronic pain, cognition, and emotions are interrelated. Moreover, it has been shown that AKP is not only related to structural anomalies but also to altered central neural processes along with alterations in central nociceptive processing [90, 91]. Slutsky-Ganesh and colleagues [92] indicate that the posterior cerebellum could be a key modulator in cognitive assessment of pain in patellofemoral pain across the cortico-cerebellar loops, possibly leading to consequences on motor function downstream.

As we will see in chapter “Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat these Patients”, AKP patients have a high incidence of anxiety, depression, kinesiophobia (the belief that movement will create additional injury or re-injury and pain) and catastrophizing (the belief that pain will worsen, and one is helpless to deal with it) [93–95]. Psychological factors play an important role as pain modulators. Even in cases with clear structural findings that justify pain, psychological factors influence and modify pain sensation as well as subsequent impairment. Therefore, they can be barriers to recovery after the appropriate surgical treatment. Catastrophizing is not only responsible for the chronification of pain due to a psychological mechanism but may also influence the neurophysiology of pain modulation. In a functional MRI study of patients with chronic pain, Gracely and colleagues [96] showed that catastrophizing ideas were associated with a higher degree of brain activity not only in the pain regions but also in the cortical regions associated with attention, anticipation of pain and emotional aspects of pain. Catastrophizing may play a role as a facilitator of the pain perception process. It also has been suggested that pain catastrophizing interfere with descending paininhibitory systems and may facilitate neuroplastic changes in the spinal cord during repeated painful stimulation, thereby promoting sensitization in the central nervous system. Impaired “conditioned pain modulation,” defined as the endogenous pain inhibition ability of a subject, has been demonstrated in young women with long-standing AKP [97]. Central sensitization (CS) has been defined by the International Association for the Study of Pain (IASP) as “increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold input” [98]. In other words, there is ineffective pain modulationinhibition in the central nervous system. That is to say, there is a process of amplification of the afferent signal that arrives from the periphery. For all that, the malfunctioning of the descending pain-inhibiting mechanisms is another of the

Pathophysiology of Anterior Knee Pain

mechanisms involved in CS. From a clinical standpoint, we can suspect that there is CS when the patient presents with allodynia or hyperalgesia. A significant number AKP patients present more signs of CS when compared to healthy pain-free individuals. Interestingly, it has been demonstrated that pain sensitization may be amenable to treatment through exercises, pharmacological therapy, and surgery [99]. In AKP patients, there is “central sensitization,” meaning an increased responsiveness of the central nervous system to a variety of stimuli [100–102]. Rathleff and colleagues [101] suggested that adolescent females with AKP have both localized and distal hyperalgesia (a reduced pressure pain threshold), which can be determined through pressure algometry. This hyperalgesia may signal altered central processing of nociceptive information. Jensen and colleagues [49] have shown that some patients with unilateral AKP have neuropathic pain, which suggests damage in the peripheral and/or central nervous system that causes pain signals without a specific cause. In this way, many AKP patients have alterations in the central nervous system that might play an important role both in the magnitude and persistence of pain after suitable conservative or surgical treatment. Lefaucheur and colleagues [103] found a link between chronic neuropathic pain and motor cortex disinhibition. The current data suggest that repetitive transcranial magnetic stimulation of the motor cortex corresponding to the patient’s site of pain may be a complementary treatment modality for patients with chronic neuropathic AKP [104]. Motor cortex stimulation may produce analgesic effects by restoring missing or impaired intracortical inhibitory processes [103]. As we can see in chapter “Brain Network Functional Connectivity Clinical Relevance and Predictive Diagnostic Models in Anterior Knee Pain Patients”, AKP patients have brain functional connectivity changes compared to healthy controls. That is especially the case between the brain areas involved in cognitive stimulus processing and the regions involved in pain

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modulation. This widespread impact on overall brain function could play an important role in explaining the magnitude, experience and persistence of pain after suitable conservative or surgical treatment.

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Authors’ Proposed AKP Pathophysiology

A subgroup of patients with AKP have a skeletal malalignment of the limb, especially in the transverse plane (femoral and/or tibial rotational malalignment) [33, 34]. This malalignment of the lower limb could provoke pain due to the abnormal stress on tissue which is not of sufficient magnitude or direction to result in instability. It is likely that nerve changes or ischemia may be due to chronic repetitive stretch of soft tissue (retinaculum). Moreover, skeletal malalignment could provoke patellofemoral instability due to a failure of the ligaments that stabilize the PFJ, and it will also lead to the development of patellofemoral cartilage lesions due to the increased patellofemoral compression forces (Fig. 12). However, in most cases, the abnormal femoral rotation is functional due to a deficit of the proximal control [105]. This situation will lead to a patellofemoral imbalance as it occurs in the structural skeletal malalignment of the lower limb. We hypothesize that short and repetitive episodes of tissular ischemia, potentially due vascular torsion or vascular bending induced by a patellofemoral imbalance, could trigger release of NGF and VEGF in the peripatellar soft tissues. Once NGF is present in the tissues, it induces hyperinnervation, attracts mastocytes, and triggers substance P release by free nerve endings (Fig. 13) [70]. In addition, VEGF induces hypervascularization and plays a role in increasing neural proliferation. Free nerve endings, slowly adapting receptors that mediate nociception, are activated in response to deformation of tissues. In the knee, such deformation results from abnormal tensile and compressive forces generated during flexo-

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Fig. 12 Pathways to pain in patients with torsional abnormalities. Force out of balance is the culprit, and force out of the balance is due to the limb out of alignment

Fig. 13 Pathophysiology of AKP

extension of the joint or in response to chemical agents such as histamine, bradykinin, prostaglandins, and leukotrienes [57, 106, 107]. Therefore, SP is released from peripheral endings of nociceptive afferents as a result of noxious chemical or mechanical stimulation. The nociceptive information relayed by these free nerve endings is responsible, at least in part, for the pain. Once SP is liberated in the connective tissue, it induces the release of prostaglandin E2, one of the biochemical agents known to stimulate nociceptors (Fig. 13) [50]. The activation of nociceptive pathways by prostaglandins could be one of the many mechanisms involved in the transmission of pain in AKP patients. Moreover, SP stimulates mast cells, facilitating a

degranulation process that can liberate histamine, another non-neurogenic pain mediator (Fig. 14) [56]. Numerous mast cells have been identified in the LR of AKP patients [19]. Mast cells are also associated with the release of NGF [40, 108], contributing to the hyperinnervation and indirectly provoking more pain. Furthermore, SP has been shown to induce the release of collagenase, interleukin-1, and tumor necrosis factor-alpha (TNF-a) from synoviocytes, fibroblasts, and macrophages [50, 52]. These factors could contribute to the genesis of patellar instability through degradation of soft tissues. SP, NGF and mast cells have also recently been implicated in bone resorption in both in vitro and in vivo experiments, which could explain, at least in part, the osteoporosis found in many cases of AKP

Pathophysiology of Anterior Knee Pain

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A

B

Fig. 14 Mast cells are abundant in the stroma (arrow), mainly in a perivascular disposition. Some of them show a degranulation process (activated mast cells) (A), (Giemsa stain). Ultrastructural image of a mast cell of the lateral retinaculum with its cytoplasm full of chemotactic

granules, (TEM) (B). (A)-(Reused with permission from SAGE. From: “Immunohistochemical analysis for neural markers of the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment” Am J Sports Med. 2000; 28: 725–731)

[109]. Finally, SP and VEGF stimulate endothelial cell proliferation and migration [53], which are essential to the development of a new vascular network that may promote tissue repair, but indirectly maintain a vicious cycle. Woolf [110] described four types of pain from a clinical point of view: (1) nociceptive pain, which is transient pain in response to noxious stimulus; (2) homeostatic pain, which is pain that promotes the healing of injured tissue (i.e., the cascade of events toward re-establishing homeostasis); (3) neuropathic pain, which is spontaneous pain and hypersensitivity to stimulus in association with damage to the nervous system; and (4) functional pain, which is pain resulting from abnormal central processing of normal input. All these mechanisms appear to be involved in the pathophysiology of pain in AKP patients.

orthopedic pathologies from a clinical point of view. AKP obliges us to “think out of the box”, to look deeper into the anatomy, biomechanics, biology, anatomic pathology, physiopathology, and psychology. AKP is a great stimulus for orthopedic intellectual development. Chondromalacia patellae is not synonymous with AKP. It is not the underlying problem. Very often, patellofemoral malalignment (patellar tilt/lateral patellar subluxation) is not the problem. In a subgroup of AKP patients, skeletal malalignment of the limb is responsible for disabling AKP due to both patellofemoral overload and patellofemoral imbalance. Understanding the biomechanics is crucial— orthopedic surgery is very much a mechanical engineering discipline. At this time, from the biomechanical viewpoint, the most powerful treatment effect in treating AKP comes from limb re-alignment. In the vast majority of AKP cases, the loss of both soft tissue (peripatellar synovitis and others soft tissue impingements such as synovial hypertrophy around the inferior pole of

8

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– – –

Take Home Messagess

– Currently, much remains to be learned about the cause of AKP. Our understanding is limited. AKP is one of the most intriguing

–

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–

–

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the patella) and osseous (intraosseous edema, osseous hypertension) homeostasis is more important in the genesis of AKP than local structural anomalies (patellar till, lateral patellar displacement, and patellofemoral chondropathy). However, we do not know how often is AKP present in a structurally perfect limb, except for overtraining. It is likely that the loss of homeostasis can be mechanical with an as yet unrecognized structural anomaly. There is a neuroanatomical basis for AKP in the young patient. A dysfunction of the peripheral and/or the central nervous system may cause neuropathic pain in some individuals with AKP. Periodic short episodes of ischemia, secondary to a mechanical stimulus, could be implicated in the pathogenesis of AKP by triggering neural proliferation of nociceptive axons (SP-positive nerves), mainly in a perivascular location. These findings are in line with the homeostasis perspective. Loss of vascular homeostasis in the knee region (e.g., hypervascularity, ischemia, osseous hypertension) may be associated with AKP. It is possible that all of the neuroanatomical factors involved in the genesis of AKP and the loss of vascular homeostasis are due to an excess of force that would be the precipitating event. Chronic pain is a multidimensional phenomenon composed by sensitive, cognitiveevaluative and affective-motivational domains. The neuromatrix model can explain the multidimensional pain experience in AKP patients.

Key Message

– We hypothesize that it is the force (magnitude or direction) which determines whether one is in or out of Dye’s envelope. In short, the diagnostic challenge is determining the source of excess force which overcomes tissue homeostasis. We are a long way from determining why excess force is excess.

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Femoral and Tibial Rotational Abnormalities Are the Most Ignored Factors in the Diagnosis and Treatment of Anterior Knee Pain Patients. A Critical Analysis Review Vicente Sanchis-Alfonso and Robert A. Teitge

1

Introduction

At the end of 1970s, skeletal malalignment of the limb was suggested as one of the causes of anterior knee pain (AKP) in some young patients [1]. It must be acknowledged that skeletal malalignment is not an abnormal Q-angle or an increased TT-TG distance. Skeletal malalignment is also not the position of the patella on the trochlea. Neither is it its increased shift (subluxation) or increased tilt. Skeletal malalignment is malalignment of the limb measured on the transverse, coronal, and sagittal planes. The presence of excessive femoral anteversion, excessive external tibial torsion, or increased varus or valgus abnormalities has a great impact on the patellofemoral joint (PFJ) biomechanics. In particular, rotational abnormalities are important [2, 3]. In 1979, Stan James presented a comprehensive review of AKP in which the

Supplementary Information The online version contains supplementary material available at https://doi. org/10.1007/978-3-031-09767-6_3. V. Sanchis-Alfonso (&) Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain e-mail: [email protected] R. A. Teitge Wayne State University, Detroit, MI, USA

condition of “miserable malalignment” was described, being increased femoral anteversion and increased external tibial torsion [1]. In 1995, he reported on seven patients with “miserable malalignment” who had been treated with internal tibial rotational osteotomy over an 18-year period [4]. Several years earlier, Cooke and colleagues [5] described internal proximal tibial rotational osteotomy in seven patients presenting with AKP and drew attention to the inwardly pointing knee as an unrecognized cause of AKP. However, the concept of skeletal malalignment was almost unnoticed and has had extremely little influence on orthopedic surgeons even until today. In fact, very few publications refer to skeletal malalignment as a cause of AKP. From 1990 to June of 2021, only 22 published papers in English in which the association between patellofemoral disorders in young patients and in which torsional abnormalities of the femur and/or tibia are analyzed from a clinical point of view could be found [6]. This scarcity of published papers may be indicative that symptomatic torsional abnormalities are a rare condition. However, in our daily clinical practice, surgery to correct torsional abnormalities in young AKP patients is frequent. Obviously, this elevated incidence in our clinical practice may be biased by the fact that numerous patients are referred to both of us for many patellofemoral disorders. The aim of this chapter is to analyze why so little importance is given to

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_3

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this problem in the specialized medical literature. Why do we ignore torsional abnormalities in the diagnosis and especially in the treatment of the AKP patient? It is a fundamental question to delve into. We will attempt to answer it.

2

There is no Agreement on How to Measure Torsion

We fully understand the scarce interest knee surgeons have in rotational osteotomies. The main reason is the diagnostic uncertainty. Limb alignment on the transverse plane is hard to see and difficult to measure. Currently, there is no consensus on how to measure torsion [7–9]. Obviously, accurate measurement of torsion is essential to diagnosing, correct surgical decisionmaking and the preoperative planning of a rotational osteotomy (i.e., the amount of correction needed). The first problem that is faced when we see a patient with a torsional abnormality is to objectify and quantify the magnitude of the torsion and therefore determine whether it is pathological or not. Many times, the values the radiologist provides do not match with the clinical findings. This mismatch generates doubt and uncertainty

Fig. 1 Evaluation in prone position in a patient with excessive left femoral anteversion

in the orthopedic surgeon who is going to treat those patients. This is especially true when it comes to femoral anteversion or femoral torsion. Currently, there are 28 methods to measure femoral neck anteversion [7]. Figure 1 shows the case of a patient with a pathological left femoral anteversion in which the CT study using the Jeanmart's method [10] (classic method), which is the most widespread, reveals a value of 20° that can be considered as normal. Therefore, there is a contradiction between the physical examination and the image in this case. How is it possible that the imaging shows a normal value? Without a doubt, something does not work here. This something is the fact that the radiological method used to evaluate femoral anteversion is not adequate. Murphy and colleagues have shown that the traditional methods may underestimate the actual femoral anteversion by a mean 13° and as much as 18° [11]. In the same way, Kaiser and colleagues have shown a significant difference in measurement techniques of even up to 11° [12]. Unfortunately, the current tendency is to trust the images more and more and devalue or mistrust the physical examination. It is a big mistake. The CT method that we use to evaluate femoral anteversion is the one described by

Femoral and Tibial Rotational Abnormalities …

A

C

43

B

D

Fig. 2 A, B Measurement of femoral anteversion using the Jeanmart's method (classic method). C, D Measurement of femoral anteversion according to the technique described by Murphy. Draw a circle on the femoral head (red circle) and another circle centered in the femoral shaft below the lesser trochanter (green circle). Then, draw a line connecting the center of these two circles. This line

defines the femoral neck axis on the transverse plane. Next, draw a line tangent to the posterior aspect of the femoral condyles (posterior condylar line). The angle between these two lines represents the femoral anteversion. The line that is used as the axis of the femoral neck in the method described by Jeanmart is not the true axis of the femoral neck

Murphy in 1987 (Fig. 2) [11]. Murphy’s method comes closest to defining the reality as it started with the physical measurement of anatomic specimens. His method of anteversion measurement correlates well with the physical examination. In the patient in Fig. 1, the measurement of femoral anteversion with Murphy’s method reveals a value of 39°, which is clearly pathological and coincides with what the physical examination reveals.

Interestingly, Schmaranzer and colleagues [13] have observed that the differences between the classic and Murphy’s method become more evident in patients with a clinical diagnosis of femoral torsional abnormality. It has been shown that the difference in femoral torsion between the classic method and Murphy’s method increased from 3° in a patient with normal femoral torsion to 17° in a patient with excessive femoral torsion upon physical examination [14]. Furthermore,

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the more significant the increase in femoral torsion, the greater the differences between the two methods was also observed [14]. In other words, the differences between the two methods increase progressively with the increase in femoral torsion, the relationship between the two methods being trigonometric and not linear [14]. This must be considered especially when planning a rotational osteotomy in patients with severe femoral torsional abnormalities to avoid mistakes in preoperative planning. Once it is known that there is a pathological torsional abnormality that must be corrected, the next step is to determine at what level the correction must be made. It may be at the proximal, mid-diaphysis or distal level. In theory, the ideal would be to perform the osteotomy at the site where the deformity originates. If we do it at another level, we can create a new deformity on the coronal or sagittal plane even though the total angle is going to be corrected adequately [15]. Some authors [16–18] have used conventional imaging studies in an attempt to define where the torsion occurs along the length of the femur. Femoral anteversion is defined by the angle formed by the intersection of 2 reference lines: one proximal that represents the axis of the femoral neck, and one distal that is tangential to the posterior aspect of the femoral condyles and approximates the knee joint axis. Since this angle of torsion is defined between these 2 lines, it is not possible to specify the level of this torsional alteration. Defining the location of a torsional abnormality between these 2 primary lines will require creation of an additional 3 or 4 references lines. Herzberg and colleagues [19] measured the anteversion angle of the femoral neck and the “retrotorsion” angle of the lesser trochanter in 52 female and 34 male femora taken from 46 human cadavers (age at death 80.3 ± 8.67 years). These authors showed that the lesser trochanter is a well-defined landmark between the proximal and distal femur, and its location follows a linear correlation with femoral anteversion. Therefore, the lesser trochanter is a landmark for separating proximal version and distal femoral torsion. Archibald and colleagues [15] evaluated 1210 paired adult femora from a well-preserved

V. Sanchis-Alfonso and R. A. Teitge

osteological collection. They have shown that both the femoral neck and femoral shaft substantially contribute to femoral version. Kim and colleagues [16] showed that femoral torsion could occur in the supratrochanteric, infratrochanteric region, or in both sites. Seitlinger and colleagues [17] have demonstrated that the neck, mid and distal femur contribute to the total femoral torsion. Sanchis-Alfonso and colleagues [20] have shown that pathological FAV in the AKP patient depends on both the neck and the shaft. However, Waisbrod and colleagues [18] have proposed that femoral torsion is a subtrochanteric deformity. Ferràs-Tarragó and colleagues [21, 22] have used three-dimensional (3D) technology and advanced techniques to assess similarities between volumetric structures in order to evaluate the site where the deformity originates. It might be a good method for planning rotational femoral osteotomy in patients with unilateral torsional femur abnormalities (Fig. 3) (See Videos 1 and 2). In short, there is no universally accepted method that allows us to determine the origin of the deformity. Therefore, it is difficult to decide at what level to perform the rotational osteotomy. In summary, the fact that there is no consensus as to how to measure torsion leaves the orthopedic surgeon in doubt about the confirmation of the diagnosis and, more importantly, in doubt about the surgical planning. The easiest thing to do in this situation is not to recommend surgical treatment. If we do not correct the torsion enough, the pain will persist and the pain will persist if we correct more than necessary. It has been shown that a difference of 10° during rotational osteotomy causes a considerable increase in PFJ pressure (Fig. 4) [23]. In the same way, Karaman and colleagues [24] showed that both external and internal rotational malalignment greater than or equal to 10° after closed intramedullary nailing of femoral shaft fractures provoked AKP while climbing stairs. Finally, Yildirim and colleagues [25] observed that an external rotation deformity of the femur greater than 10° could cause a deterioration in the patellofemoral scores and provoke AKP. Considering the possible iatrogenesis that we can

Femoral and Tibial Rotational Abnormalities …

Fig. 3 3D technology and advanced techniques to assess similarities between volumetric structures in order to evaluate the site where the deformity originates. In this case, the right femur (yellow femur) has an excessive femoral anteversion (39°). However, the left femur (blue femur) has a normal femoral anteversion. In this patient, there is severe right hip pain and disabling right AKP. However, the lower left limb is completely asymptomatic. The left femur is reverted as it was a mirror vision. Then we place the blue femur over the yellow femur to see

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the degree of similarity between them. That is, we overlap both femurs. The differences between both femurs are represented in a color code. The intensity of the blue and red colors represents the magnitude of the positive and negative differences between both femurs. The green color represents the absence of differences. In this case, there is a high similarity in all the femur except in the proximal part. Thus, we can conclude that the torsional deformity in this particular case originates in the proximal part of the femur

Fig. 4 Finite elements analysis in the preop and after intertrochanteric external rotational femoral osteotomy of 5° and 15° (From reference 23). (Courtesy of M.A. Perez, PhD)

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cause in a young patient if we make a hypercorrection of the torsion along with the scarce literature that supports this technique, it is understandable why it is not a common technique among orthopedic surgeons.

3

Not All Torsional Abnormalities are Symptomatic

Another reason for the scarce interest knee surgeons have shown in rotational osteotomies would be the fact that there are patients with clear torsional anomalies that are completely asymptomatic. There are patients with bilateral torsional abnormalities who are completely asymptomatic (Fig. 5). The only explanation is that their level of activity is low enough not to apply sufficient stress to bone and or peripatellar soft tissues. In other cases, the maltorsion is symmetrical but only one side is symptomatic and the other one is completely asymptomatic. This fact increases uncertainty and discourages the surgeons from recommending a rotational osteotomy. We must take note that an abnormal anatomy is only a risk factor for developing AKP [26]. However, the length of time and magnitude of stress on bone and/or soft tissues that are

necessary to initialize the physio-pathological mechanisms that lead to pain and makes for a patient are not known. In AKP patients with torsional abnormalities, knee pain and disability are highly variable. Furthermore, the incidence of psychological affectation is high in AKP patients, and the AKP patient with a torsional abnormality is not an exception. The prevalence of anxiety and depression in AKP patients is higher than those found in the general population [27, 28]. The fact that there are patients with a lot of pain and others with less as well as patients with a lot of pain and little disability with the same magnitude of pathological torsion, makes the importance of the torsional anomaly doubtful with regard to the symptoms. It is understandable that many orthopedic surgeons may think that the main problem is psychological. According to Robert A. Teitge, the main player in patellofemoral disease is the force which traumatizes the PFJ tissues. That force may act on the cartilage and bone, being responsible for cartilage breakdown and pain. It may also place excess tension in the patellar ligaments, being responsible for instability and pain. Of all the structural factors causing overload of the PFJ, the most powerful is the skeletal

Fig. 5 Asymptomatic bilateral torsional abnormality (Courtesy of R. Teitge, MD)

Femoral and Tibial Rotational Abnormalities …

malalignment, especially the torsional [3]. When the skeleton is not normal, the quadriceps force acting on the PFJ is not normal either. A change in the quadriceps lateral vector may result from an increase in femoral anteversion or an increase in limb valgus. Additionally, it may just as well be due to an increase in the external rotation of the tibia on the femur or an actual lateral placement of the tibial tuberosity (TT) on the proximal tibia that will provoke an increment of the TTTG distance. Of all the factors influencing the lateral vector, the most important is femoral anteversion. For example, the lateral vector increases more than 112% if a person has an internal torsion of the femur of 30° above the normal value. Maltorsion may cause a maldistribution of force on the PFJ which probably acts on both the subchondral bone and all surrounding ligaments. Bone overload is detectable using SPECT-CT. In some patients with torsional abnormalities, the SPECT-CT study reveals an uptake increment in the lateral aspect of the PFJ that allows us to justify the pain in these patients. Therefore, SPECT-CT helps to make a correct surgical indication. But in other cases, the SPECT-CT is negative in spite of the presence of a symptomatic torsional abnormality. This raises uncertainty when it comes to blaming torsional abnormality for the pain. This fact discourages the surgeons from putting forward a rotational osteotomy.

4

Lack of Agreement Regarding Surgical Technique. Fear of Internal Fixation Failure and Other Complications

Another reason for the scarce interest knee surgeons have shown in rotational osteotomies is the lack of agreement when it comes to the choice of surgical technique. This means that if five different surgeons were asked about the best way to proceed, it is highly probable each of them would come up with a totally different solution (osteotomy level, open vs percutaneous osteotomy, type of osteotomy fixation, combined procedures: release of the peroneal nerve vs. non-

47

release, fibular osteotomy vs non-osteotomy). This would leave an inexperienced surgeon rather confused. There are a few unanswered questions in osteotomy surgery. One is about knowing how much to correct. From a practical point of view, we always prefer undercorrecting to overcorrecting when performing rotational osteotomy. Another debatable issue is the level of osteotomy. For example, our proposal in rotational tibial osteotomy is an osteotomy distal to the TT. However, other orthopedic surgeons suggest a supra-tuberosity osteotomy. Then again, there are others who are inclined toward a mid-shaft or distal (supramalleolar) osteotomy. Recently, Winkler and colleagues [29] have shown that increased external tibial torsion is an infratuberositary deformity and is not correlated with a lateralized position of the tibial tuberosity. Regarding the surgical technique, take note that it is difficult to achieve a highly precise osteotomy and keep it perfectly in place during healing. With a fracture or an osteotomy, the stress of moving the limb does not reach the bone ends but it does concentrate at the fracture/osteotomy site as strain (displacement) [30]. Relative to a fracture, the more comminuted it is, the less strain is concentrated at the fracture line. This is because it is divided between the number of fracture segments and the length of the fracture. On the contrary, a straight transverse osteotomy causes the greatest strain concentration. Thus, the internal fixation must be more rigid to share the stress and reduce strain to an acceptable level. Greater stability results from the increased compression of fragments. If there is no motion at the osteotomy site and the gap between fragments is less than 0.5 mm, then bone cutting cones pass across the gap and new osteons are produced without the need for a callus. If the gap is
0.5 mm and there is motion, the motion of the bone ends up crushes the cutting cones and primary bone healing will not occur. It is well known that if you see a callus developing after internal fixation, you know the fixation is unstable. IM nails do not normally provide sufficient rigid fixation. Therefore, they are classified as “internal splints”. Inadequate

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stabilization by means of internal fixation results in failure when the strain is too great: plates break, screws bend or pull out or delayed healing. Without a doubt, the fear of internal fixation failure might be another reason for the scarce interest knee surgeons have shown in rotational osteotomies. A more widespread surgical technique for treating AKP patients is the TT osteotomy, which has undoubtedly overshadowed the rotational osteotomy. We do not intend to deny the validity of this technique, but rather to broaden our horizon in order to treat AKP patients. At this point, it would be interesting to make some observations on the surgery of the TT in the patient with torsional abnormality. Mani and colleagues [31] have demonstrated that TT medialization increases tibial external rotation. Therefore, greater AKP could triggered if we perform a medialization of the TT in a patient with excessive external tibial torsion. Moreover, Tensho and colleagues [32] have shown that TTTG distance is affected more by knee rotation than by tubercle malposition. For that reason, the measurement of the TT-TG distance in patients with torsional abnormalities is not reliable. Franciozi and colleagues [33] have seen diminished results from TT osteotomies in patients with increased femoral anteversion. In the same way, Zhang and colleagues [34] evaluated 144 consecutive patients with recurrent patellar instability. Patients were assigned into three groups: group A (femoral anteversion 30°). They have demonstrated that patients with an increased femoral anteversion angle (>30°) had inferior postoperative clinical outcomes and a higher rate of residual J-sign after medial patellofemoral ligament reconstruction combined with TT osteotomy. That is, the TT osteotomy does not prevent the negative effect of femoral anteversion on PFJ. Therefore, the best available evidence supports not performing TT osteotomy in patients with torsional abnormalities. On the other hand, the frequency and types of complications seen in rotational osteotomy surgery are similar to those of the TT osteotomy. We have

V. Sanchis-Alfonso and R. A. Teitge

followed the same definition as Payne and colleagues [35] to compare the total percentage of major complications in rotational osteotomy surgery and TT osteotomy surgery. Major complications were defined as non-union, fracture, infections and wound complications requiring return to the operating room, and DVT or PE. Payne and colleagues [35], in a systematic review, found an overall risk of major complications after TT osteotomy of 3.0%. In our systematic review, the overall risk of major complications after rotational osteotomy was of 3.3% [6].

5

“Orthopedics is All About Anatomy … Plus A Little Bit of Common Sense”

We believe that a logical approach to surgical treatment should be based on restoring native anatomy and repairing what is damaged. This was clearly reflected by Jack Hughston in his well-known sentence: “Orthopedics is all about anatomy … plus a little bit of common sense”. Therefore, it would be logical to correct them surgically if we observe an obvious pathological torsional alteration in the femur or tibia. You should strive to restore normal anatomy, because that will create a better biomechanical environment for the tissue. If you repair a failed tissue that can be bone, ligament or cartilage and ignore the mechanics that caused the tissue failure, you will usually have a failed result. In cases of combined femoral anteversion and excessive external tibial torsion, there is a question. What is more important in the genesis of AKP, femoral anteversion or external tibial torsion? From an anatomical standpoint, the best option to treat a patient with combined excessive femoral internal torsion and excessive external tibial torsion would be a combination of a rotational femoral and a tibial osteotomy. Another option would be to operate on the bone with the greatest variance from normal, the femoral anteversion in the case of Fig. 6. In the case of Fig. 6, we performed a 25° proximal femoral external rotational osteotomy with a good result

Femoral and Tibial Rotational Abnormalities …

Fig. 6 Intra-operative x-Rays. Preoperative (left). The patella is well centered on the distal femur after an external rotational femoral osteotomy of 25°. Mechanical axis (MA)

but there was a recurrence of the symptoms at 9 months. For that reason, a rotational tibial osteotomy was performed that gave a good clinical result. This case highlights the importance of restoring completely the normal anatomy. In short, we must understand biomechanics because orthopedic surgery is a mechanical engineering discipline. A complete physical examination attempts to uncover all of the anatomic abnormalities, of which there are often many. When you uncover any abnormal anatomy you must then answer the question: how does this change the normal biomechanics? This is the key question.

6

The Keys to Increasing Adherence to Rotational Osteotomy by a Knee Surgeon. Future Studies

The first step in attracting orthopedic surgeons to the field of rotational osteotomy is to give them the means to arrive at diagnostic certainty. In this aspect, the SPECT-CT to objectify the origin of pain can help. The SPECT-CT reveals the

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metabolic and geographic pattern of bone homeostasis (Fig. 7). It can evidence overloaded osseous areas. However, the most important contribution to rotational osteotomy being definitively incorporated into daily clinical practice by the knee surgeon is the implementation of a methodology that simplifies preoperative surgical planning and allows for the pre-visualization of the results of surgical interventions on our computers. For this, the working group of the first author of this chapter (V.S-A) uses 3D technology (see Video Case # 1). The imaging dataset used for surgical planning is based on a CT of the patient. Our 3D method, is open Access, that is, it is accessible to any orthopedic surgeon at no economic cost. Furthermore, it not only allows for the quantification of the femoral torsion (Fig. 8) but also carrying out virtual surgical planning. Interestingly, with 3D technology, we have shown that the magnitude of the intertrochanteric rotational femoral osteotomy does not present a 1:1 relationship with the effect on the correction of the deformity (see Video Case # 1). Moreover, rotational osteotomy surgery using 3D printed surgical guides might improve surgical accuracy. In the long run, surgeons will perform rotational osteotomies if they obtain good results. To that end, the selection of the appropriate patient is essential. To obtain a satisfactory result, it is important to analyze patient expectations with regard to the results of the surgery. Moreover, whether it is really feasible to achieve a “Minimal Clinically Important Difference” (MCID) after surgery should be considered. Despite a statistically significant improvement in functional scores after rotational osteotomy in a torsional abnormality, not all patients perceive a MCID in every functional domain of the score. Defining a MCID value for Patient-Reported Outcome Measures (PROMs) is crucial to determining the effectiveness of a surgical procedure and therefore the indication for surgery. It would be interesting to determine the best scores to evaluate patients with torsional abnormalities and ascertain the MCID for this pathology.

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V. Sanchis-Alfonso and R. A. Teitge

Fig. 7 SPECT/CT in an AKP patient with right external tibial torsion. The scintigraphic uptake is markedly high in the right patella. Disabling right AKP. The left knee

was asymptomatic in spite of the fact that external tibial torsion was symmetric in both knees

Fig. 8 Femoral anteversion measurement. Left: Transparency has been added to the proximal femur to identify landmarks for the center of the femoral head and the base of the femoral neck. The junction of the center of the ball of the femoral head and the center of the circumference at the base of the neck define the plane of inclination of the

neck (red). The plane tangent to the posterior condyles and posterior region of the greater trochanter is the femoral bearing plane (purple). Right: Femoral anteversion measurement based on Murphy’s method, between the neck inclination plane (red) and the femoral support plane (purple)

7

Take Home Messages

– Skeletal torsional abnormalities, especially abnormal femoral torsion, are the most ignored factors not only in the diagnosis but

even more so in the treatment of AKP patients. – The “collective consciousness”, that is the beliefs shared by the majority of orthopedic surgeons, conveys the idea that rotational osteotomy is a complex procedure with a high

Femoral and Tibial Rotational Abnormalities …

risk of severe complications. It seems overly aggressive to cut the femur or the tibia of a young “healthy” person that only “complains of pain”. Nothing could be further from the truth. Rotational osteotomy is a very welltolerated surgery with a low complication rate and, in many cases, the results are immediate relative to eliminating pain. – Changing the limb alignment by means of osteotomy is the single most powerful and underutilized treatment available. The quadriceps is responsible for the force acting on the patella. Osteotomy changes the quadriceps direction and therefore the force acting on the patella. If one operates on the traumatized tissue (bone, ligament or cartilage) without changing the force which produced the trauma, one should expect a failed result.

References 1. James SL. Chondromalacia of the Patella in the Adolescent. In: Kennedy JC. editor. The Injured Adolescent Knee. Baltimore: The Williams & Wilkins Company, 1979. 2. Teitge RA. Does lower limb torsion matter? Tech Knee Surg. 2012;11:137–46. 3. Teitge RA. The power of transverse plane limb malalignment in the genesis of anterior knee pain— clinical relevance. Ann Joint. 2018;3:70. 4. Meister K, James SL. Proximal tibial derotation osteotomy for anterior knee pain in the miserably malaligned extremity. Am J Orthop (Belle Mead NJ). 1995;24:149–55. 5. Cooke TD, Price N, Fisher B. The inwardly pointing knee. An unrecognized problem of external rotational malalignment. Clin Orthop 1990;56–60. 6. Sanchis-Alfonso V, Domenech-Fernández J, FerrasTarrago J, et al. The incidence of complications after derotational femoral and/or tibial osteotomies in patellofemoral disorders in adolescents and active adult patients. A Systematic Review with MetaAnalysis. (In press). 7. Scorcelletti M, Reeves ND, Rittweger J, et al. Femoral anteversion: significance and measurement. J Anat. 2020;237(5):811–26. https://doi.org/10.1111/ joa.13249. 8. Stephen JM, Teitge RA, Williams A, et al. A validated, automated, 3-Dimensional method to reliably measure tibial torsion. Am J Sports Med. 2021;49 (3):747–56.

51 9. Snow M. Tibial torsion and patellofemoral pain and instability in the adult population: current concept review. Curr Rev Musculoskelet Med. 2021;14 (1):67–75. 10. Jeanmart L, Baert AL, Wackenheim A. Computer tomography of neck, chest, spine and limbs. Atlas of pathologic computer tomography, vol 3. Springer, Berlin Heidelberg New York, 1983; pp 171–177. 11. Murphy SB, Simon SR, Kijewski PK, et al. Femoral anteversion. J Bone Joint Surg Am. 1987;69 (8):1169–76. 12. Kaiser P, Attal R, Kammerer M, et al. Significant differences in femoral torsion values depending on the CT measurement technique. Arch Orthop Trauma Surg. 2016;136(9):1259–64. 13. Schmaranzer F, Lerch TD, Siebenrock KA. Differences in femoral torsion among various measurement methods increase in hips with excessive femoral torsion. Clin Orthop Relat Res. 2019;477(5): 1073–83. 14. Ferràs-Tarragó J. Planificación quirúrgica tridimensional de las osteotomías femorales en el dolor anterior de rodilla. Doctoral Thesis. University of Valencia, 2021. 15. Archibald HD, Petro KF, Liu RW. An anatomic study on whether femoral version originates in the neck or the shaft. J Pediatr Orthop. 2019;39:e50–3. 16. Kim HY, Lee SK, Lee NK, et al. An anatomical measurement of medial femoral torsion. J Pediatr Orthop B. 2012;21(6):552–7. 17. Seitlinger G, Moroder P, Scheurecker G, et al. The contribution of different femur segments to overall femoral torsion. Am J Sports Med. 2016;44(7):1796– 800. 18. Waisbrod G, Schiebel F, Beck M. Abnormal femoral antetorsion—a subtrochanteric deformity. J Hip Preserv Surg. 2017;4(2):153–8. 19. Herzberg W, Meitz R, Halata Z. Antetorsion of the femur neck. A variable of the trochanter minor? Unfallchirurg 1991;94:168–171. 20. Sanchis-Alfonso V, Domenech-Fernández J, BeserRobles M, et al. Pathological femoral anteversion in the anterior knee pain patient depends on both the neck and the shaft (Submitted). 21. Ferràs-Tarragó J, Sanchis-Alfonso V, RamírezFuentes C, et al. A 3D-CT analysis of femoral symmetry—surgical implications. J Clin Med. 2020;9:3546. 22. Ferràs-Tarragó J, Sanchis-Alfonso V, RamírezFuentes C, et al. Locating the origin of femoral maltorsion using 3D volumetric technology—the hockey stick theory. J Clin Med. 2020;9:3835. 23. Gracia-Costa C. Análisis por elementos finitos de las presiones femoropatelares previas y posteriores a osteotomía desrrotadora. Trabajo de Fin de Grado. Escuela de Ingeniería y Arquitectura: University of Zaragoza; 2019. 24. Karaman O, Ayhan E, Kesmezacar H, et al. Rotational malalignment after closed intramedullary

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V. Sanchis-Alfonso and R. A. Teitge nailing of femoral shaft fractures and its influence on daily life. Eur J Orthop Surg Traumatol. 2013;24 (7):1243–7. Yildirim AO, Aksahin E, Sakman B. The effect of rotational deformity on patellofemoral parameters following the treatment of femoral shaft fracture. Arch Orthop Trauma Surg. 2013;133(5):641–8. Erkocak OF, Altan E, Altintas M, et al. Lower extremity rotational deformities and patellofemoral alignment parameters in patients with anterior knee pain. Knee Surg Sports Traumatol Arthrosc. 2016;24 (9):3011–20. Wride J, Bannigan K. Investigating the prevalence of anxiety and depression in people living with patellofemoral pain in the UK: the Dep-Pf Study. Scand J Pain. 2019;19(2):375–82. Domenech J, Sanchis-Alfonso V, Lopez L, et al. Influence of kinesiophobia and catastrophizing on pain and disability in anterior knee pain patients. Knee Surg Sports Traumatol Arthrosc. 2013;21 (7):1562–8. Winkler PhW, Lutz PM, Rupp MC, et al. Increased external tibial torsion is an infratuberositary deformity and is not correlated with a lateralized position of the tibial tuberosity. Knee Surg, Sports Traumatol, Arthroscopy. 2021;29:1678–85.

30. Muller ME, Allgower M, Schneider R, et al. Manual of internal fixation. Third Edition. Springer. 1991. 31. Mani S, Kirkpatrick MS, Saranathan A, et al. Tibial tuberosity osteotomy for patellofemoral realignment alters tibiofemoral kinematics. Am J Sports Med. 2011;39(5):1024–31. 32. Tensho K, Akaoka Y, Shimodaira H, et al. What components comprise the measurement of the tibial tuberosity-trochlear groove distance in a patellar dislocation population? J Bone Joint Surg Am. 2015;97(17):1441–8. 33. Franciozi CE, Ambra LF, Albertoni LJ, et al. Increased femoral anteversion influence over surgically treated recurrent patellar instability patients. Arthroscopy. 2017;33(3):633–40. 34. Zhang ZZ, Zhang H, Song GY, et al. Increased femoral anteversion is associated with inferior clinical outcomes after MPFL reconstruction and combined tibial tubercle osteotomy for the treatment of recurrent patellar instability. Knee Surg Sports Traumatol Arthrosc. 2020;28(7):2261–9. 35. Payne J, Rimmke N, Schmitt LC, et al. The incidence of complications of tibial tubercle osteotomy: a systematic review. Arthroscopy. 2015;31(9):1819–25.

Why is Torsion Important in the Genesis of Anterior Knee Pain? Robert A. Teitge

Femoral Anteversion and Tibial Torsion are listed in many of the patellofemoral publications over the past 60–80 years as risk factors or associated factors for anterior knee pain, but discussion stops after making the list and is almost never to be reconsidered. Why? I believe this is because we don’t know why torsion should matter, we don’t know why it there, we don’t know how to measure it, we don’t know how to fix it and even those intrepid surgeons who are willing to operate to alter it, have really no guide as where they are starting and where they are going. It is a daunting challenge to know nothing. I wish here to present how interest in these questions grew and propose a rationale for why it matters to anterior knee pain. A challenge to me came from Robert Kerlan MD in 1976 who said to me “Bob, no one has studied foot problems in professional athletes, why don’t you see what you can learn.” The podiatrists were known to be providing “orthotics” but that was almost the limit of studies. I stumbled across The Running Foot Doctor [1] by Steven Subotnick D.P.M. and in it I discovered a drawing of a limb with Chondromalacia of the Knee which was said to result from a pronated foot which was increasing the Q-Angle from 15°

R. A. Teitge (&) Department of Orthopaedic Surgery, Wayne State University, Detroit, MI, USA e-mail: [email protected]

to 30° and creating an abnormal quadriceps pull. I left Dr. Kerlan and moved to Seattle where Sigvard (Ted) Hansen, Jr. M.D. said “Bob, You have to get to know Stan Newell, D.P.M.” Stan Newell was the artist who had produced all of the drawings for The Running Foot Doctor. Stan was making all the orthotics for the professional athletes in Seattle skirting around the orthopaedic community. Stan told me “Bob, I can cure more than 50% of all athletic knee pain with orthotics, even though I have no idea why.” An interesting thought. The recreational running craze was just beginning, Nike was just starting and Stan Newell and Stan James, M.D. in Eugene, Oregon became the consultants to Nike Shoes as the orthopaedic world became interested in running and anterior knee pain. Stan James was working with many world-class runners in Eugene and being asked to lecture on “Runner’s Knee” at various professional society meetings. In 1979 he contributed a chapter “Chondromalacia of the Patella in the Adolescent” to Jack Kennedy’s book The Injured Adolescent Knee [2]. This chapter almost summarizes what we know today and contains the brilliant description of Miserable Malalignment. So, beginning in 1980 and using what I learned from the two Stans, I have examined every knee patient with both the standard knee examination and the runner’s exam and concluded torsion is important. The correlation of physical examination with clinical assessment of femoral or tibial torsion is modest to poor. Consequently, awareness of

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_4

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R. A. Teitge

torsional excess is often overlooked. Special imaging is mandatory. To understand lower extremity kinematics requires knowing where the axis of motion is for all the joints in the chain including hip, knee, ankle and subtalar joint. Variations in joint geometry will change the axis of a particular joint, which will change the kinematics of that limb. Correlating anatomic landmarks with imaging is not standardized and despite modern imaging there is still controversy in locating with precision the axes of these 4 joints. It may not be possible to define an axis of joint motion by studying a single bone. Two points near the ends of the bones are selected and lines between the two points are used to define the axis. Different investigators have selected different points, thus different lines are proposed to reflect the same axes. It is common that axes from different investigators may vary by 100% for the hip, knee, ankle and subtalar joint. Kaiser et al. [3] found the difference between the mean of 2 commonly used measurement techniques was 97% and in one single specimen the difference was 140%. These variations in measurement technique makes comparing studies difficult Fig. 1 A The maximum quadriceps efficiency is with knee joint facing forward in the direction the body is moving (Joint axes are red lines). 1 B With normal femoral anteversion the greater trochanter is posterior when the knee faces straight forward

A

and even these selected lines may have nothing to do with joint motion. The action of a muscle in moving a joint is most efficient when it’s line of action is perpendicular to the joint axis. The quadriceps controls knee flexion. It is most efficient when working in the sagittal plane with the knee axis ⊥ to the sagittal plane and with the knee joint moving straight forward in the direction the body mass is moving. Levens et al. [4] as long ago as 1948, reported the knee joint axis normally moves directly forward during gait in line of the body motion with only a minimal amount of rotation in the transverse plane (Fig. 1). Anterior knee pain is usually the result of an abnormal force. A knee joint in which no force is acting is seldom painful. The abnormal force may be an excessive force or a mal-directed force. A reduction in force generally results in reduction of pain, but usually with some associated loss of function. Most of the quadriceps muscle force is exerted as a vector in the sagittal plane pushing the patella against the trochlea to maintain of control knee flexion–extension. (Fig. 2).

B

Why is Torsion Important in the Genesis … Fig. 2 A The resultant of the quadriceps force vector and the patellar tendon force vector creates the patellofemoral joint reaction force. It is this force which keeps the knee from collapsing and controls its position of flexion–extension. B This force is maximum when it is perpendicular to the knee joint axis and is in the sagittal plane with the knee axis in the coronal plane

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B

A

But the knee joint is unusual because it must have a tibio-femoral valgus. The tibio-femoral valgus is needed to move the knee joint closer to the midline under the center of mass. Placing the knee joint closer to the center of body mass reduces bending forces in the femur and tibia and allows us to balance on one foot, a requirement for bipedal gait. The tibiofemoral angle, however, means the quadriceps does not act perpendicular to the knee joint axis, but is deviated in the lateral direction, thus in addition to the major posterior vector component, there is a lateral component (Fig. 3). It is assumed that the lateral vector is counterbalanced by the lateral trochlear inclination. As the knee internally rotates during flexion the tibial tuberosity moves medially so the direction of the quadriceps force is more medial and the lateral vector of this quadriceps force decreases.

The femur and tibia are both normally twisted. The biomechanical purpose of the twist is unclear. It is an assumption that “normal” twist is optimal for “normal” function such as walking. Femoral twist is measured as the angle in the transverse plane between the axis of the hip and knee. If there is an abnormal inward twist in femur so the knee joint points medially, the knee joint can be placed facing forward only by external rotation of the hip joint. The acetabulum may limit the degree of external rotation needed to place the knee axis forward, or it may place the external rotators of the hip in such a shortened position they cannot provide stability. It is common in such cases, that fatigue of the hip rotators allows the femur to rotate inward so the knee joint axis faces medially. If the patella is pointing medially the quadriceps force will be more in the lateral direction and the lateral

56 Fig. 3 The valgus tibiofemoral angle acts to move the knee joint closer to the center of mass of the body. This tibiofemoral angle deviates the quadriceps insertion laterally which produces a lateral quadriceps vector in addition to the major posterior vector

quadriceps vector increases at the expense of the posterior vector which decreases (Fig. 4). To maintain knee flexion stability, the total force must increase to prevent knee collapse. One cause of anterior knee pain is thought to be this excess lateral quadriceps vector. As the knee joint rotates out of the sagittal plane the posterior vector becomes less effective so the total quadriceps force must increase to maintain stability. As the posterior vector decreases the lateral vector increases so articular shear is increased which shifts the center of force in the PFJ as well as altering tension in the retinacular ligaments. Altering the direction of the quadriceps vector may also alter the tibiofemoral rotation orientation. This is probably best measured today with weight-bearing CT scanning for transverse plane alignment.

R. A. Teitge

If there is an abnormal outward twist of the femur, femoral retroversion, the opposite effect occurs, the quadriceps medial vector will increase obviously shifting the center of force medially in the PFJ (Fig. 5). If there is an increase in external tibial torsion and the knee joint is facing forward the foot will face more laterally. The body weight vector will push on the side of the outward pointing foot resulting in excess pronation, stretch of the medial arch, bunions, posterior tibial tendon strain, shortening of the Achilles tendon and lateral ankle impingement. Landing from a jump requires the ankle joint axis to be perpendicular to the direction of landing so dorsiflexion can absorb excess energy. Since gait on an outward facing foot can be uncomfortable or fatiguing the limb is often internally rotated placing the foot its optimal functional position but causing the knee joint axis to face medially which again increases the lateral quadriceps vector and requiring more total quadriceps force required to stabilizing knee flexion. An increase in internal tibial torsion has the opposite effect with the primary complaint being of increased tripping, lateral ankle sprains and increased loading of the medial plafond. The normal angular relationship of the hip joint, knee joint, ankle joint and subtalar joint axes when viewed in the transverse plane allows for normal kinematics and with normal distribution of forces transferring the body weight to the ground. Precise location of these axes is necessary for limb kinematic and gait studies. Torsional abnormalities in the femur or tibia obviously can only be corrected by transverse plane osteotomy. A simple coronal plane vector diagram of the Q angle including its lateral component vector in a normal aligned limb suggests a 5 mm medial transfer of the tibial tuberosity may reduce the lateral quadriceps vector by 27%, but a reduction

Why is Torsion Important in the Genesis …

A

57

B

Fig. 4 The Quadriceps direction is changed with a change in limb torsion. The quadriceps force is generally in line with the femur. A with normal anteversion the knee joint faces forward and the majority of the quadriceps is posterior which produces the PF Joint reaction force. B If the knee points inward, the quadriceps pulls more laterally so the lateral vector is increased while the posterior vector is decreased. The reduction in posterior force means the total quadriceps force must increase to control knee

stability. The black arrows represent the quadriceps force and its posterior and lateral vectors. The quadriceps force is normally in line with the femur, the posterior force vector is indicated on the left and the lateral force vector is indicated on the right. A medial pointing knee may occur if there is increased femoral anteversion, if there is more internal rotation of the hip joint or if there is more external tibial torsion and the foot is then placed facing forward

of 30° excess femoral anteversion may reduce the lateral quadriceps vector by 112%. Precise biomechanical studies investigating the effect of changing skeletal geometry on force transmission are needed to estimate when pathologic values are reached. These studies

must include the changing of force provided by altered skeletal geometry, contracting muscles, body weight, limb length, hip, and foot and ankle positions. Until then we can only assume that the population normal is a reasonable goal for torsion correction.

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References 1. The Running Foot Doctor by Steven I. Subotnick, D. P.M, World Publications, Mt View, California © 1977. 2. James SL. Chondromalacia of the Patella in the Adolescent, p205–251 in The Injured Adolescent Knee Ed. J.C. Kennedy, Williams & Wilkins Co. Baltimore, © 1979. 3. Kaiser P, et al. Significant differences in femoral torsion values depending on the CT measurement technique. Arch Orthop Trauma Surg. 2016;136 (9):1259–64. 4. Levens AS, et al. Transverse rotation of the segments of the lower extremity in locomotion. J Bone Joint Surg. 1948;30(4):859–72.

Fig. 5 Computer simulation of the skeleton in a patient landing from a jump. Both knees are equally flexed. She has 50° of femoral anteversion on the right and has had an external rotation proximal femoral osteotomy of 35° on the left. The right knee is pointed inward so the quadriceps is not acting in the sagittal plane. She does not have a valgus alignment, the apparent valgus is due to the combination of knee flexion and an inward pointing knee. This produces a very large lateral component to the quadriceps force. On the left, the knee is flexing in the sagittal plane, the patella is facing forward and because the tibia internally rotates in flexioin there is no lateral vector to the left quadriceps

Clinical and Radiological Assessment of the Anterior Knee Pain Patient Vicente Sanchis-Alfonso, Cristina Ramírez-Fuentes, Laura López-Company, and Pablo Sopena-Novales

1

Introduction

Anterior knee pain (AKP), which is pain behind or around the patella, is one of the most common reasons for consultation with an orthopedic surgeon specializing in the knee among teenagers and young adults. Although it typically occurs in physically active people less than 40 years of age, it does indeed affect people of all activity levels and ages [1]. A careful clinical history and physical examination along with imaging studies are crucial to obtaining an accurate diagnosis. They will be the cornerstone for a correct treatment. The objective of this chapter is to come to an understanding of how AKP patients should be evaluated during consultation to obtain a whole picture for each patient. Doing so will aid in

V. Sanchis-Alfonso (&) Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain e-mail: [email protected] C. Ramírez-Fuentes Medical Imaging Department, Hospital Universitario y Politecnico La Fe, Valencia, Spain L. López-Company Department of Rehabilitation and Physical Therapy, Hospital Arnau de Vilanova, Valencia, Spain P. Sopena-Novales Department of Nuclear Medicine, Hospital Vithas 9 Octubre, Valencia, Spain

identifying potentially modifiable factors to personalize treatment and achieve better outcomes. We want to emphasize that the physical examination must not be limited to the knee. The entire limb must be evaluated. Moreover, we must always assess the psychological status and central sensitization of all patients with AKP, including those with severe structural anomalies that may justify the pain.

2

Clinical History—“Listen to the Patient”

Talking with the patient is fundamental but is too often neglected. We must listen very carefully to our patients as they will usually tell us, in their own words, what is wrong. It is our mistake if we fail to truly understand them and assume we know better. The first diagnostic step is a thorough clinical history. This is where we uncover the main clue for an exact diagnosis. For instance, the absence of a traumatic episode or presence of bilateral symptoms should lead towards a patellofemoral pathology and away from a meniscal pathology in the young patient. It is common to have symptoms in both knees that may change from one knee to the other over time. This is a tip-off for a patellofemoral problem. On the contrary, the presence of effusion, more than patellofemoral pain, suggests an intra-articular pathology (e.g., meniscal rupture, pathologic plicae,

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_5

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osteochondral or chondral lesions or synovial pathology). Nevertheless, a small effusion may be present in AKP patients. However, polyarthralgia is not a part of the pathology we are now dealing with. Generally, the onset of symptoms is insidious. It reflects an overuse condition or an underlying malalignment. Overuse can be the result of a new activity or of the increase in the time, frequency or intensity of a previous work or sports activity. In these cases, getting the history should be oriented to determining which supraphysiologic loading activity or activities are of importance in the origin of AKP. The identification and rigorous control of the activities associated with the initiation and persistence of symptoms is crucial for treatment success. For example, patients with left AKP should avoid driving a car with a clutch for prolonged periods of time because it aggravates the symptoms. In these cases, patient education is crucial to preventing recurrence. In other cases, the symptoms can be secondary to a direct knee trauma (e.g., automobile accident in which the anterior knee strikes the dashboard [“dashboard knee”]) or an indirect knee trauma. One must not forget the possibility of AKP secondary to a posterior cruciate ligament (PCL) deficiency when there has been a knee trauma. This is a well-known cause for AKP given that PCL tears increase patellofemoral joint (PFJ) reaction force through posterior displacement of the tibial tuberosity [2]. It is also important to examine the integrity of the anterior cruciate ligament (ACL) as AKP is present in 20–27% of patients with a chronic ACL insufficiency [2]. The main symptom AKP patients experience is pain. That pain can be retropatellar or peripatellar. The pain is often described as dull with occasional sudden episodes of sharp pain. When asked to locate the pain, it is often difficult for the patient to pinpoint the area of pain while placing his or her hand over the anterior aspect of the knee. However, the pain can also be medial, lateral or popliteal. Generally, patients have multiple painful sites with different degrees of pain intensity. Pain related to the extensor mechanism is typically aggravated by activities

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like climbing and descending stairs, squatting, using the clutch when driving a vehicle with manual transmission (left AKP), wearing highheeled shoes. It is also worsened after prolonged sitting with knee flexion, for instance during a long trip by car or prolonged sitting in a cinema (“movie sign” or “theater sign”). It improves by extending the knee. A constant and severe pain way out of proportion to physical findings that has a sudden onset after a knee injury or surgery should make us think of psychological issues or Reflex sympathetic dystrophy (RSD) or Complex regional pain syndrome (CRPS). This is true even when the classic vasomotor findings are absent. It is classified as neuropathic pain. Finally, constant burning pain indicates a neuromatous origin. To quantify the pain, we use the Visual analogue scale (VAS). It is a sensitive outcome measure for AKP, with a difference of 2 cm being considered clinically relevant [3]. To screen for neuropathic pain, we advocate for the use of the Douleur Neuropathique 4 scale (DN4) [4]. The sensitivity and specificity of the DN4 stands at around 95% and 97% [4]. Other symptoms of AKP are a giving-way sensation and crepitus. Determining whether the patient’s pain is associated with a lateral patellar instability is very important because both the treatment and the prognosis are very different in patients with AKP secondary to patellar instability when compared to those without patellar instability. “Giving-way” episodes due to ACL deficiency are brought on by rotational activities. On the other hand, “giving-way” episodes related to patellofemoral problems are associated with activities that do not imply rotational strains. It is a consequence of a sudden reflex inhibition and/or atrophy of the quadriceps muscle. Patients sometimes report locking of the knee, which is usually only a catching sensation. However, they can actively unlock the knee. Therefore, this type of locking should not be confused with the one experienced by patients with meniscal lesions. Finally, another symptom is crepitus. It should not be mistaken for the snapping sensation more consistent with a pathological plica. Crepitus is common but is clinically irrelevant in most cases. However, crepitus creates negative emotions,

Clinical and Radiological Assessment …

inaccurate etiological beliefs and finally leads to fear-avoidance behavior and lower functional performance [5]. Apart from pain, AKP patients present disability to a great or lesser degree. The World Health Organization defines disability as “a limitation of function that compromises an individual’s ability to perform an activity within the range considered normal”. Regardless of how intense the pain is, AKP patients show different degrees of disability in their everyday life. A way to objectify and quantifying disability is by means of self-administered scales like the International Knee Documentation Committee evaluation (IKDC) and the Kujala score. It is also important to know the patient’s activity level prior to the treatment and what he or she wants to achieve through treatment to be able to offer realistic goals. Patients with AKP have a high incidence of anxiety, depression, kinesiophobia (the fear that physical activity will cause more injury or a reinjury and subsequent pain) and catastrophizing (the belief that pain will worsen and cannot be relieved) [6]. Over half of people living with AKP experience anxiety and/or depressive symptoms. The levels of anxiety and depressive symptoms in AKP patients are much higher than those found in the general population (anxiety symptoms: 49.5% vs. 5.9–7.8%, respectively; depressive symptoms: 20.8 vs. 3.3–7.8%, respectively) [7, 8]. Therefore, recognizing and quantifying the presence of these psychological factors are important to getting a whole picture of the patient and to planning the best treatment. Self-administered screening tests for anxiety and depression (Hospital Anxiety and Depression Scale), catastrophizing (Pain Catastrophizing Scale), and kinesiophobia (Tampa Scale for Kinesiophobia) should be incorporated into the clinical history in all the cases [6]. Moreover, signs of central sensitization are present in AKP patients in a high percentage of cases [9]. Therefore, it would be very interesting to recognize and quantify it using a self-administered Central sensitization score. Finally, we must ask about previous knee surgeries. For example, one of the causes of

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disabling AKP after surgery is iatrogenic medial patellar instability (IMPI) secondary to an “extensive” lateral retinacular release. Inappropriate physiotherapy could also be responsible for iatrogenic AKP. Therefore, it is essential that the patient describe exercises that are being or have been done with the physiotherapist or in the gym.

3

Physical Examination

The second diagnostic step is a thorough and careful physical examination. It is essential. Its primary goal is to locate the painful zone and to reproduce the symptoms. The location of the pain can indicate which structure is injured. This is extremely helpful to making the diagnosis and to planning the treatment. The most important diagnostic tool is the “finger”.

3.1 Tests to Locate the Painful Zone and Reproduce the Pain The lateral retinaculum should be felt and assessed carefully. Tenderness anywhere over the lateral retinaculum, especially where the retinaculum inserts into the patella, is a very frequent finding (90%) in AKP patients [10]. We perform the patellar glide test to evaluate lateral retinacular tightness. This test is performed with the knee flexed at 30º and the quadriceps relaxed. The patella is divided into four longitudinal quadrants and is displaced medially (Fig. 1). A medial translation of one quadrant or less is suggestive of excessive lateral tightness [2]. With this test, pain is elicited over the lateral retinaculum. The patellar tilt test can also detect a tight lateral retinaculum. It should always be done. In a normal knee, the patella can be lifted from its lateral edge farther than the transepicondylar axis, with a fully extended knee. On the contrary, a patellar tilt of 0º or less indicates a tight lateral retinaculum. Lateral retinacular tightness is very common in AKP patients. Furthermore, it is the hallmark of the excessive lateral pressure syndrome described by Ficat [11]. In those cases with AKP after ACL reconstruction, we

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Fig. 1 Patellar glide test. The patellofemoral joint is mentally divided into quadrants and patellar mobility is assessed in both directions

passively “tilt” the inferior pole of the patella away from the anterior tibial cortex to rule out pretibial patellar tendon adhesions. The axial compression test of the patella (or patellar grind test) should be part of the systematic examination as it elicits AKP originating in the patellofemoral articular surfaces (patellar and/or trochlear subchondral bone). To perform the axial compression test, we compress the patella against the trochlea with the palm of the hand at various angles of knee flexion (Fig. 2). In addition, this test makes for determining the location of the lesion in the patellar articular cartilage. With knee flexion, the patellofemoral contact zone is displaced proximally in the

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patella and distally in the femur. Thus, proximal lesions will yield pain and crepitation at approximately 90º of knee flexion. On the contrary, distal lesions are tender in the early degrees of knee flexion. We also perform the sustained knee flexion test. When it is positive (the appearance of pain), it means that the patella is the origin of the pain. It is caused by an increase in intraosseous pressure [12]. For the sustained knee flexion test, the patient lies supine on an examination table with his or her knee extended and relaxed. The knee is then flexed fully and kept firmly in a sustained flexion for up to 45s. The test is positive if the patient complains of increasing pain after a pain-free interlude of 15 to 30s. Allen and colleagues [13] found a significant association between proximal patellar tendinosis and abnormal patellar tracking in AKP patients. Therefore, palpation of the inferior pole of the patella ought to be carried out in all cases to rule-out patellar tendinopathy. To perform this test, press downward on the proximal patella. In this way, the inferior pole of the patella tilts anteriorly. This maneuver permits palpation of the proximal patellar tendon attachment (Fig. 3). However, there is quite often mild tenderness at the attachment of the patellar tendon at the inferior pole of the patella in individuals who play sports. Thus, only moderate and severe pain should be considered pathological. Moreover, Hoffa’s fat pad should always be felt as it can be a source of pain as well (Hoffa’s test) (Fig. 4). Finally, existing scars should be palpated and Tinel’s sign performed to detect neuromas. Pain improvement after an infiltration of the painful area with local anesthesia or after unloading the area with functional taping provides evidence for the origin of pain.

3.2 Pressure Algometry

Fig. 2 Axial compression patellar test

The clinical examination is crucial to identifying the neuropathic AKP subgroup. This is important to know the prognosis of the patient that is to undergo treatment. A patient with CRPS presents with skin changes like erythema and edema with

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Fig. 3 Palpation on the distal pole of the patella and the proximal patellar tendon

3.3 Range of Motion and Muscle Length Testing

Fig. 4 In patients with impingement of the Hoffa fat pad, pain is dramatically exacerbated by quadriceps contraction or passive knee extension while applying pressure of the fat pad with the fingers. This happens because this movement causes a small posterior tilt of the inferior pole of the patella, which impinges on an inflamed and sensitized infrapatellar fat pad

an allodynic or a hyperalgesic pain response to palpation on the anterior aspect of the knee and restriction in the mobility of the patella. Hyperalgesia can be demonstrated with pressure algometry [14]. In these cases, we found reduced pain thresholds. However, pressure algometry should be used to quantify the pain at baseline and to monitor an improvement in terms of hyperalgesia with the treatment rather than as a diagnostic method as there is no specific value that serves as a threshold value for hyperalgesia.

The range-of-motion of the knee as well as hip and ankle should be evaluated. Both legs should be examined. Exploring knee extension in both knees is mandatory because even small degrees of extension loss can cause AKP. To evaluate knee extension, the patient lies prone on the examining table with the lower extremity supported by the thighs. The difference in heel height is measured [15]. The conversion of heel height difference to degrees of extension loss is presented in the table of Fig. 5. Limited ankle dorsiflexion range of motion has been related to AKP. Therefore, it should be evaluated in all AKP patients [16]. It is very important to assess the flexibility of anterior hip structures (iliopsoas) (Fig. 6), the quadriceps, hamstring, soleus, gastrocnemius muscles and the iliotibial band as the pathology under scrutiny is often associated with a decreased flexibility of these structures [17, 18]. Tightness of these structures indicates the need for specific stretching exercises and possible training modification. However, only a shortened quadriceps muscle has been shown to predict AKP development [19]. Flexibility tests can be measured with different reproducible tools like the standard or digital goniometer.

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Fig. 5 Evaluation of knee extension. (Table from Dale Daniel et al. Raven Press, 1990) [15]

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Fig. 6 Evaluation of the flexibility of anterior hip structures. A, B Normal subject. C Shortening of the iliopsoas

Clinical and Radiological Assessment …

To test quadriceps flexibility, the patient lies prone, and the knee is passively flexed with one hand while stabilizing the pelvis with the other hand to prevent compensatory hip flexion (Fig. 7). We can measure quadriceps tightness as degrees of prone knee flexion. Suggestions for quadriceps retraction are: (1) asymmetry, a different flexion of one knee compared to the other, (2) the feeling of tightness in the anterior aspect of the thigh, and (3) elevation of the pelvis due to flexion of the hip. It is important to assess quadriceps contracture as this can increase the contact pressure between patella and femur in a direct way. To test hamstring flexibility, the patient lies supine with the hip at 90º of flexion. The patient is then asked to straighten his or her knee (Fig. 8). If complete extension is not possible, there is a hamstring contracture, and its amount is measured by the popliteal angle. Most young athletic individuals have popliteal angles between 160º and 180º [2]. Hamstring tightness implies an increase in the quadriceps force necessary to extend the knee, which augments the PFJ reaction force. Gastrocnemius and soleus flexibility is evaluated by measuring the amount of active ankle dorsiflexion while the physical therapist stabilizes the subtalar joint. Gastrocnemius flexibility is evaluated with the knee extended and we evaluate soleus flexibility with the knee flexed at 90º (Fig. 9). Tightness of the

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gastrocnemius, in the same way as hamstrings tightness, increases the PFJ reaction force, keeping the knee in a flexed position. Moreover, limited ankle dorsiflexion results in increased subtalar joint pronation. It causes an increment of tibial internal rotation with deleterious effects on PFJ biomechanics [2]. The iliotibial band (ITB) is often tight in AKP patients. This causes lateral patellar displacement and tilt as well as weakness of the medial patellar retinaculum. We use Ober’s test to assess ITB flexibility. To perform this test, the patient lies on the side opposite the affected leg with the hip and knee of the bottom leg fully flexed to eliminate the lumbar lordosis. Then, the examiner flexes the affected knee and hip at 90º. After that, he/she passively abducts the affected hip as far as possible and extends the thigh so that it is in line with the rest of the body (neutral position), which places the ITB on maximal stretch. Palpation of the ITB just proximal to the lateral femoral condyle during maximal stretch will cause severe pain in patients who have excessive ITB tightness. At this position, the patient is told to relax, and then the thigh is adducted passively. If the thigh remains suspended off the table, the test is positive (shortened ITB). If the thigh drops into an adducted position, the test is negative (normal ITB). Finally, Thomas’s test (Figs. 10 and 11) is a good method to evaluate both the iliopsoas and iliotibial band tightness. The patient holds the non-test limb with the hip at 90° of flexion while the physician stabilizes the pelvis of the test limb from the anterior superior iliac spine. The free leg is allowed to fall in the extension direction to the point where the pelvis begins to move.

3.4 Assessment of Muscle Strength

Fig. 7 Evaluation of quadriceps flexibility

It has been demonstrated that hip abductors and external rotation weakness are associated with AKP [20, 21]. Therefore, it is crucial to evaluate the strength of these muscles in AKP patients to address muscle imbalances. Traditional manual muscle testing or a handheld dynamometer could be used depending on availability (Fig. 12).

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Fig. 8 Evaluation of hamstrings flexibility. (Republished with permission of AME Publishing Company. From Sanchis-Alfonso V, et al. Evaluation of anterior knee pain

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patient: clinical and radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

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Fig. 9 Evaluation of grastrocnemius (A) and soleus (B) flexibility. (Republished with permission of AME Publishing Company. From Sanchis-Alfonso V, et al. Evaluation of anterior knee pain patient: clinical and

radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

3.5 It is Mandatory to Look Beyond the Patellofemoral Joint

between torsional abnormalities [excessive external tibial torsion (Fig. 13) and femoral anteversion (Fig. 14)] and AKP. It is very important to evaluate skeletal malalignment, the malalignment of the limb on the transverse, coronal, and sagittal planes. With the patient standing, barefoot, with their feet together, we assess (Fig. 13): (1) the alignment

Many orthopedic surgeons focus only on the knee when evaluating an AKP patient. This approach is a great mistake because there are other causes of AKP that are at a distance from the knee. For example, a clear relation exists

Clinical and Radiological Assessment …

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Fig. 10 Thomas’s test in a normal subject

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Fig. 11 Thomas’s test in a pathological case. A Shortening of the iliotibial band. Hip abduction occurs when the hip goes in extension. B Shortening of the iliopsoas. C Shortening of the rectus femoris

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Fig. 12 A Hip abductor strength measurement. B Hip external rotator strength measurement. (Republished with permission of AME Publishing Company. From SanchisAlfonso V, et al. Evaluation of anterior knee pain patient:

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clinical and radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

Fig. 13 External tibial torsion (right limb). Pseudo-varus (right limb). Squinting patella (right knee)

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Fig. 14 Femoral anteversion

on the coronal plane (valgus/varus), (2) patella orientation (neutral, squinting patella), and (3) the morphology of the forefeet (pronatus, hallux valgus). From the back, we evaluate: (1) the varus or valgus alignment of the knee and (2) a varus or valgus alignment of the calcaneus. Finally, we evaluate genu recurvatum or flexum of the knees from the side. When the patient stands with the feet parallel, the patella should be facing forward. In patients with excessive external tibial torsion, a squinting patella and a genu varum can be seen. The varus in patients with external tibial rotation may be real, or it may be a reflection of the tibial torsion (thus pseudovarus). The combination of increased femoral anteversion and increased external tibial torsion has been termed miserable malalignment syndrome that includes the squinting patella, genu varum, genu recurvatum and the pronated foot. In the prone position, the proportion of internal to external rotation of the hips in extension must be measured. If internal rotation exceeds external rotation by more than 30º, there is increased femoral anteversion (Fig. 14). In cases with isolated excessive external tibial torsion, internal and external rotation are similar. In a previous study, we observed that there is an association between Cam femoroacetabular

impingement (FAI) and AKP [22]. Therefore, an evaluation of Cam FAI should be performed during the physical examination of AKP patients, especially in patients with normal knee imaging studies when the pain continues after appropriate conservative treatment. In this case, AKP is secondary to functional femoral external rotation as a defense mechanism to avoid hip pain. Finally, examination of the feet is essential as pronated feet play an important role in the origin of AKP. A functional hallux limitus may be a predisposing factor for AKP [23]. Functional hallux limitus consists of a loss of dorsal flexion of the first metatarsophalangeal joint with the ankle in dorsal flexion. Limited ankle dorsiflexion range-of-motion has been linked with AKP and has also been related to altered kinematics of the knee. The implication is that this may be involved in the pathogenesis of AKP. Therefore, ankle dorsiflexion should be evaluated in all AKP patients (Fig. 15) [24].

3.6 Functional Tests The current trend in evaluating AKP patients is using functional tests to detect inapt body movement patterns that might be responsible for

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Fig. 15 Measurement of ankle joint dorsiflexion range. (Republished with permission of AME Publishing Company. From Sanchis-Alfonso V, et al. Evaluation of anterior knee pain patient: clinical and radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

the pain symptomatology. The final objective would be to retrain these inapt movements and thereby reduce the pain. Fig. 16 Single-leg squat test. A Correct neuromuscular control. B Poor neuromuscular control

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The most frequently used functional tests are: (1) the single-leg squat (Fig. 16); (2) the stepdown test (Fig. 17) and (3) the hop down test (Fig. 18). The three tests explore the same thing but with different levels of demand. Therefore, we will use the most appropriate for each patient, which depends on the disability that the patient has. During these tests, many AKP patients have excessive functional knee valgus. This functional knee valgus is mainly secondary to femoral adduction. Some AKP patients show lower limb abnormalities secondary to muscle weakness with the subsequent lack of dynamic control of the lower extremity. It may have an influence on the normal patellofemoral tracking and bring on patellofemoral imbalance. This has important implications for patient rehabilitation. The malalignment of the patella is secondary to functional knee valgus and abnormal movements of the femur. Such abnormalities are (1) femoral adduction (secondary to weakness of hip abductors—gluteus medius, upper fibers of gluteus maximus and tensor fascia latae), (2) internal rotation of the femur secondary to weakness of

B

Clinical and Radiological Assessment …

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B

Fig. 17 Step-down test. During this test, the limb going down only brushes the floor with the heel and then goes back to full knee extension. A Correct neuromuscular control. B Poor neuromuscular control

the hip external rotators, (3) internal rotation of the tibia, and (4) tibial abduction secondary to (5) excessive pronation of the foot. We must note that a lack of dynamic control of the lower limb does not depend on the degree of physical activity of the patient [25]. That is, most physically active adolescents do not necessarily have better lower limb control [25].

other knee conditions that could simulate patellofemoral pathology. There are three categories of imaging studies in patellofemoral pathology: (1) structural imaging (radiographs, computed tomography [CT], magnetic resonance imaging [MRI]), (2) metabolic imaging (technetium scintigraphy), and (3) a combination of both.

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4.1 Standard Radiography

Imaging Studies

Imaging studies are the second diagnostic step and cannot replace the first step. Overlooking this rule can lead to diagnostic errors that is followed by failed treatment and iatrogenic morbidity. A surgical indication should never be based solely on imaging techniques since the correlation between clinical and image data is not good. The history and physical examination are the fundamental elements in the evaluation of the AKP patient. Nothing can replace the history and clinical examination. The aim of the imaging studies is to quantify the pathology and rule out

The majority of patients with patellofemoral pain will only require standard radiography (standing anteroposterior view, a true lateral view, and the low flexion angle axial view [Merchant]). Generally, imaging studies beyond standard radiography are not indicated. The weight-bearing whole-limb anteroposterior view radiograph allow us to evaluate limb alignment on the coronal plane (varus, valgus), and joint space narrowing (Fig. 19). The lateral view allows one to evaluate the recurvatum and flexion contracture. It also aids in evaluating the

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Fig. 18 A, B, C Hop down test. B Correct neuromuscular control. C Poor neuromuscular control. Excessive knee valgus when landing from a drop. Femoral

adduction and tibial abduction are contributing to this knee position. Knee valgus increases lateral compressive forces in the PFJ

Fig. 19 Weightbearing whole-limb anteroposterior view radiograph in a patient with external tibial torsion. Bilateral varus alignment and squinting patella

patellar height. Is there a high-riding patella or patella alta or a low-riding patella or patella baja? Moreover, a true lateral X-ray (overlapping of the posterior borders of the femoral condyles) allows one to assess trochlear dysplasia (defined by the crossing sign and quantitatively expressed by the trochlear bump and the trochlear depth), and patellar tilt (Fig. 20). Axial views can demonstrate patellofemoral maltracking (i.e., tilt, shift, or both) when this happens beyond 30º of knee flexion, the sulcus angle, loss of joint space, subchondral sclerosis, and the shape of the patella. In addition to this, an axial view can detect secondary clues of earlier dislocation episodes. For example, medial retinacular calcification is sometimes observed in axial views and may occur in association with recurrent subluxation. Finally, a standard X-ray allows one to rule out associated and potentially serious bony conditions like tumors or infections. In cases in

Clinical and Radiological Assessment …

Fig. 20 Lateral X-ray. Patellar tilt

which medial patellar instability is suspected, the stress axial radiography is essential to identifying and quantifying medial patellar instability [26]. When the patient response to conservative treatment is not adequate, other imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI) and singlephoton emission computed tomography (SPECT)-CT are indicated.

4.2 Computed Tomography The CT allows for the measurement of knee parameters like the tibial tubercle-trochlear groove (TT-TG) distance, which is widely used to indicate and plan distal realignment surgeries. However, it must be noted that the value of the TT-TG distance is a controversial issue [16]. The TT-TG distance is influenced by multiple factors like tibial torsion, knee joint rotation, the slices selected, and the landmarks of the distal femur and tibial tuberosity established by the radiologist. However, no pathological distance or index should be interpreted in isolation. Clinical correlation is requisite in all cases. Moreover, the CT allows for the evaluation of torsional abnormalities (Fig. 21). In our clinical practice, we use the technique described by Murphy and colleagues in 1987 to measure femoral torsion [27]. This is the most anatomic, accurate and reproducible method for evaluating

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femoral anteversion (high intra- [ICC: 0.95–0.98] and inter-observer agreement [ICC: 0.93]) [28]. Murphy and colleagues reported that the common method of running a line along the femoral neck on a CT image underestimated the actual anteversion by a mean 13º [27]. Moreover, the line that is used in the most common method, like the axis of the femoral neck, is not the true axis of the femoral neck. External tibial torsion is measured as the angle between the posterior aspect of the tibial metaphysis and the ankle joint line. Our normal reference values are femoral anterversion of 13° for both sexes and external tibial torsion of 21° in males and 27° in females [29, 30].

4.3 Magnetic Resonance Imaging MRI is useful for evaluating intraosseous edema (Fig. 22), soft tissue impingement (Figs. 23 and 24), Hoffa fat pad edema (Fig. 25), and patellar cartilage damage even though this structural damage may not necessarily be the cause of AKP. In addition, it also detects possible concomitant lesions. Moreover, MRI often shows low-grade effusions associated with symptomatic peripatellar synovitis, which is an underdiagnosed pathological condition of the knee.

4.4 Technetium Scintigraphy and Single-Photon Emission Computed Tomography (SPECT)—CT Bone scintigraphy using 99mTc hydroxyl ethylene diphosphonate (99mTc-HDP) may be useful in selected cases. The bone scintigraphy in the three-dimensional and the conventional CT can be fused in a single (SPECT/CT) hybrid imaging procedure which overcomes the limitations of the CT and SPECT as separate techniques (Fig. 26). The intensity and distribution of the tracer uptake correlate with the etiological mechanism and has been accepted as an effective diagnostic tool in the orthopedic field [31–34]. If the patella is hot, this suggests that it is the source of pain, but it does not provide a diagnosis

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Fig. 21 CT evaluation of femoral anteversion (A, B, C, D) and external tibial torsion (E). Measurement of femoral anteversion. Technique described by Murphy (A, B, C). Draw a circle on the femoral head (B) and another circle centered in the femoral shaft below the lesser trochanter (C). Then, draw a line connecting the center of these two circles (A). This line defines the femoral neck axis on the transverse plane. Next, draw a line tangent to the posterior

Fig. 22 Intraosseous edema in a patient with AKP

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aspect of the femoral condyles (posterior condylar line) (A). The angle between these two lines represents the femoral anteversion. (D) Commonly used method described by Jeanmart (classic method). The line that is used as the axis of the femoral neck (yellow line) is not the true axis of the femoral neck connection to the femoral shaft

Clinical and Radiological Assessment …

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Fig. 23 A Peripatellar synovitis in a patient with AKP (white arrow). B Quadriceps fat pad impingement syndrome in a patient with AKP (white arrow). (“Republished with permission of Springer Nature BV, from

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Holistic approach to understanding anterior knee pain, Sanchis-Alfonso V, Knee Surg Sports Traumatol Arthrosc, 22, 2275–2285, 2014; permission conveyed through Copyright Clearance Center, Inc.”)

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Fig. 24 A, B 25-year-old woman with AKP. Morphologic changes of the fat pad observed frequently in patients with Hoffa’s fat pad impingement: edema localized in the superior and posterior part of the fat pad, deep infrapatellar bursitis (directly posterior to the distal part of the patellar tendon, just proximal to its insertion on the tibial tubercle) and non-visualization of intrahoffatic

clefts. Moreover, we can see a patellar intraosseous edema. C Normal knee. (“Republished with permission of Springer Nature BV, from Holistic approach to understanding anterior knee pain, Sanchis-Alfonso V, Knee Surg Sports Traumatol Arthrosc, 22, 2275–2285, 2014; permission conveyed through Copyright Clearance Center, Inc.”)

(Figs. 26, 27 and 28). Dye and Boll [35] observed that about one-half of their patients with AKP presented increased patellar uptake in comparison with 4% of the control group. Biopsy demonstrated that this increased patellar uptake was secondary to the increased remodelling activity of the bone. Bone scintigraphy can detect loss of osseous homeostasis, and often correlates well with the presence of patellar pain and its resolution. According to Dye and Boll [35] the

bone scan commonly reverted to normal at an average time of 6.2 months (range, 3– 14 months), which is interpreted as restoration of osseous homeostasis. Naslund and colleagues [36] showed that nearly 50% of AKP patients show diffuse bone uptake in one or more compartments of the knee (Fig. 28). Not only has a relationship between hyper-uptake and pain been demonstrated, but also between pain intensity and greater uptake (Fig. 28) [37, 38]. Ro and

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and colleagues [40], SPECT bone scintigraphy is highly sensitive in the diagnosis of patellofemoral abnormalities. For those authors, SPECT significantly improves the detection of maltracking of the patella and the ensuing increased lateral patellar compression syndrome. They conclude that this information could be used to treat patellofemoral problems more effectively. SPECT bone scans may be overlaid onto an MRI or CT (fusion) to correlate bone activity with the specifics of anatomy (Figs. 26, 27 and 28). It reveals the metabolic and geographic pattern of bone homeostasis, which is the normal osseous metabolic status of the joint.

5

Fig. 25 Post-traumatic Hoffa fat pad edema. (“Republished with permission of Springer Nature BV, from Holistic approach to understanding anterior knee pain, Sanchis-Alfonso V, Knee Surg Sports Traumatol Arthrosc, 22, 2275–2285, 2014; permission conveyed through Copyright Clearance Center, Inc.”)

colleagues [39] have seen a higher degree of uptake in the patella in cases with a poorer response to conservative management. Scintigraphy may be especially useful in cases of difficult diagnosis (Fig. 29) and in patients with injuries related to workers’ compensation cases in which the physician wishes to establish objective findings. According to Lorberboym

Take Home Messages

– There is no substitute for a thorough history and a complete and careful physical examination. The history and physical examination remain the first step, more than any diagnostic imaging technique, to come to an accurate diagnosis of AKP. – Most orthopedic surgeons only focus on the knee when they explore a patient with AKP. This approach is a great mistake because other important etiological factors that are at a distance from the knee may be responsible for the pain. We should examine the entire lower extremity. – Imaging studies are a second step and can never replace the former.

Fig. 26 SPECT-CT overcomes the limitations of the CT and SPECT as separate techniques. It reveals the metabolic and geographic pattern of bone homeostasis. That is, it correlates bone activity with the specifics of anatomy

Clinical and Radiological Assessment …

A

B

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C

Fig. 27 SPECT/CT in an AKP patient with right femoral anteversion and external tibial torsion. A Fused SPECT/CT MIP, B, C fused axials. The scintigraphic uptake is markedly high in the patella’s articular face

Fig. 28 SPECT-CT in a symptomatic patient with bilateral AKP with much more pain in the left knee. (Republished with permission of AME Publishing Company. From Sanchis-Alfonso V, et al. Evaluation of

anterior knee pain patient: clinical and radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

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Fig. 29 Value of SPECT-CT in the differential diagnosis of knee pain. This patient came to our office with severe AKP. In this case, the patient presented a type I epiphysiolysis of the distal femoral physis that was responsible for pain (Courtesy of A. Darder, MD). (Republished with permission of AME Publishing

Company. From Sanchis-Alfonso V, et al. Evaluation of anterior knee pain patient: clinical and radiological assessment including psychological factors. Ann Joint, 3:26, 2018; permission conveyed through Copyright Clearance Center, Inc.)

– Surgical indications should not be based only on methods of image diagnosis as there is a poor correlation between the clinical and imaging data.

patellofemoral pain: which are reliable and valid? Arch Phys Med Rehabil. 2004;85:815–22. Bouhassira D, Attal N, Alchaar H, et al. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4). Pain. 2005;114(1–2):29–36. Robertson CJ, Hurley M, Jones F. People’s beliefs about the meaning of crepitus in patellofemoral pain and the impact of these beliefs on their behaviour: a qualitative study. Musculoskelet Sci Pract. 2017;28:59–64. Domenech J, Sanchis-Alfonso V, Lopez L, et al. Influence of kinesiophobia and catastrophizing on pain and disability in anterior knee pain patients. Knee Surg Sports Traumatol Arthrosc. 2013;21 (7):1562–8. Wride J, Bannigan K. Investigating the prevalence of anxiety and depression in people living with patellofemoral pain in the UK: the Dep-Pf study. Scand J Pain. 2019;24;19(2):375–382.

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Clinical and Radiological Assessment … 8. McManus S, Bebbington P, Jenkins R, Brugha T, editors. Mental health and well-being in England: Adult psychiatric morbidity survey 2014. Leeds: NHS Digital, 2016. 9. Sigmund KJ, Hoeger Bement MK, Earl-Boehm JE. Exploring the pain in patellofemoral pain: a systematic review and meta-analysis examining signs of central sensitization. J Athl Train. 2021;56(8):887–901. 10. Fulkerson JP. The etiology of patellofemoral pain in young, active patients: a prospective study. Clin Orthop. 1983;179:129–33. 11. Ficat P, Ficat C, Bailleux A. [External hypertension syndrome of the patella. Its significance in the recognition of arthrosis] Rev Chir Orthop Reparatrice Appar. 1975;Mot 61:39–59. 12. Hejgaard N, Arnoldi CC. Osteotomy of the patella in the patellofemoral pain syndrome. The significance of increased intraosseous pressure during sustained knee flexion. Int Orthop. 1987;8:189–194. 13. Allen GM, Tauro PG, Ostlere SJ. Proximal patellar tendinosis and abnormalities of patellar tracking. Skeletal Radiol. 1999;28:220–3. 14. Rathleff MS, Roos EM, Olesen JL, et al. Lower mechanical pressure pain thresholds in female adolescents with patellofemoral pain syndrome. J Orthop Sports Phys Ther. 2013;43(6):414–21. 15. Daniel D, Akeson W, O’Connor J. Knee Ligaments. Structure, Function, Injury and Repair. Raven Press, 1990. 16. Sanchis-Alfonso V, Coloma-Saiz J, Herrero-Herrero M, et al. Evaluation of anterior knee pain patient: clinical and radiological assessment including psychological factors. Ann Joint. 2018;3:26. 17. Sanchis-Alfonso V, McConnell J, Monllau JC, et al. Diagnosis and treatment of anterior knee pain. JISAKOS, 2016. https://doi.org/10.1136/jisakos2015-000033. 18. Piva SR, Goodnite EA, Childs JD. Strength around the hip and flexibility of soft tissues in individuals with and without patellofemoral pain syndrome. J Orthop Sports Phys Ther. 2005;35(12):793–801. 19. Witvrouw E, Lysens R, Bellemans J, et al. Intrinsic risk factors for the development of anterior knee pain in an athletic population. A 2-year prospective study. Am J Sports Med 2000;28(4):480–489. 20. Rathleff MS, Rathleff CR, Crossley KM, et al. Is hip strength a risk factor for patellofemoral pain? A systematic review and meta-analysis. Br J Sports Med. 2014;48:1088. 21. Giles LS, Webster KE, McClelland JA, et al. Does quadriceps atrophy exist in individuals with patellofemoral pain? A systematic literature review with meta-analysis. J Orthop Sports Phys Ther. 2013;43:766–76. 22. Sanchis-Alfonso V, Tey M, Monllau JC. A Novel Association between Femoroacetabular Impingement

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Evaluation of Psychological Factors Affecting Anterior Knee Pain Patients: The Implications for Clinicians Who Treat These Patients Vicente Sanchis-Alfonso, Julio Doménech-Fernández, Benjamin E. Smith, and James Selfe

1

Introduction

Anterior knee pain (AKP) is one of the most common reasons why physically active people consult an orthopedic surgeon specializing in the knee. It can be challenging to manage. Despite its high prevalence and the abundance of research the etiopathogenesis of AKP is not well known. Therefore, there are many myths surrounding this condition, false collective beliefs that are transmitted from generation to generation. One of these myths is that the AKP patient is a person with peculiar psychological traits that are responsible for the genesis of pain. It could not be further from the truth. Many AKP patients have insignificant clinical and radiological findings. However, they have severe pain and an important disability. Moreover, some AKP patients have allodynia (pain in

V. Sanchis-Alfonso (&)
J. Doménech-Fernández Department of Orthopaedic Surgery, Hospital Arnau de Vilanova, Valencia, Spain e-mail: [email protected] B. E. Smith Physiotherapy Outpatients, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, UK J. Selfe Department of Health Professions, Faculty of Health and Education, Manchester Metropolitan University, Manchester, UK

the presence of a non-noxious stimulus), primary hyperalgesia, (pain hypersensitivity in the knee) or secondary hyperalgesia (pain hypersensitivity in uninjured tissues beyond the affected area). We can thus understand that many orthopedic surgeons, who do not know this condition well, may think that the main problem is psychological. Furthermore, the absence of structural pathology leads to cataloging these patients as somatizers in many cases even though there is no evidence to justify this. It is important to note that acute pain does not have anything to do with chronic pain. Chronic pain can have significant psychological effects on the sufferers, and we must note that AKP is a paradigm of chronic pain. Chronic pain is a multidimensional experience with sensitive, cognitive and affective domains [1]. Functional Magnetic Resonance Imaging (MRI) has identified many pain centres in the brain that work together as a network. This pain neuromatrix can account for the multidimensional experience of pain [2]. Interestingly, Damasio and colleagues [3] observed an overlap between the cerebral activity areas related to chronic pain and those related to cognition and emotion. This finding suggests that chronic pain, cognition, and emotion are interrelated [3]. Patients with AKP have a high incidence of anxiety, depression, kinesiophobia (the fear that physical activity will cause more injury or a re-injury and subsequent pain) and catastrophizing (the belief that pain

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_6

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will worsen and cannot be relieved) [4]. However, ascribing AKP only to psychological problems is a crude excuse to hide our ignorance as to the cause of pain in these patients. What it is true is that psychological disorders are the result of the pain severity but not the cause of the pain and disability. We have all seen AKP patients that have been operated on several times with completely inappropriate surgical indications and that were obviously quite affected with painrelated fear. AKP is usually considered a biomechanical paradigm hence the literature is dominated by biomechanical studies that overlook social and psychological factors. Until recently, the role of psychological factors involved in AKP have received little attention. Even so, psychological factors are increasingly recognized for their role in chronic pain conditions. Most of the papers in which AKP is analyzed from a psychological perspective (the human side of the patellofemoral pain) have been published in the last 5 years. The objective of this chapter in to analyze the psychological factors affecting AKP patients in depth. Moreover, we are going to review the experience of living with AKP. This chapter is about expanding our horizons, that is, the options for treating AKP patients. What this chapter is not about is negating any other existing paradigm (the homeostasis paradigm and structural/ anatomic/biomechanical paradigm). From a biopsychosocial perspective, psychological factors are not an isolated cause of pain, but rather interact with biological and structural factors. The key message of this chapter is that psychological factors are modulators of pain and disability. Throughout this chapter, we will work to justify this statement.

a direct and sequential relation between tissue damage and pain, and between pain and disability. Therefore, the doctor’s task would be to repair the damaged tissue and eradicate the pain, making the functional impairment and disability disappear. This model has worked well for some conditions (e.g., meniscal tears). However, for some conditions that develop with chronic pain such as AKP, which is a paradigm of chronic pain, this classic biomedical model is not enough to understand the pathophysiology of the pain and determine adequate treatment. Regardless of how intense the pain is, patients with AKP show different degrees of disability in their everyday life. Furthermore, no significant correlation between structural alterations of the patellofemoral joint and disability have been observed. In fact, some cases with important anatomic alterations (patellar subluxation, patellar tilt, pathologic external tibial torsion, and severe patellar and/or trochlear chondropathy) are painless [5– 8]. Therefore, not only must we consider anatomic, biological and biomechanical factors to understand AKP, but also the psychological and social ones. This approach was proposed by the American pathologist and psychiatrist George Engel. In 1977, the Journal “Science” published his paper “The need for a new medical model: A challenge for biomedicine”, introducing the term “Biopsychosocial Model” (Fig. 1) [9]. This model allows for the development of more adequate therapeutic strategies than the biomedical model. However, very few studies currently focus on the patient with AKP from a psychological and social perspective in comparison with other conditions such as low back pain (LBP), knee osteoarthritis, fibromyalgia or rheumatoid arthritis.

2

3

Biopsychosocial Model in Anterior Knee Pain—An Alternative to the Classic Biomedical Disease Model

Currently, the biomedical disease model is the dominant one used by physicians in the diagnosis and treatment of diseases. This model establishes

Fear-Avoidance Model in Anterior Knee Pain. Kinesiophobia

To try to explain how and why some individuals with musculoskeletal pain develop chronic pain, Lethem and colleagues [11] introduced the socalled “fear-avoidance” model in 1983 (Fig. 2). The central concept of their model is fear of pain.

Evaluation of Psychological Factors …

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Fig. 1 The Biopsychosocial model of chronic pain and disability. International Classification of Functioning Disability and Health, World Health Organization (Modified from Waddell [10])

“Confrontation” and “avoidance” are the two opposite responses to this fear. The former response leads to a reduction of fear over time with the patient being able to cope with it satisfactorily, continue their usual activities and achieve full recovery. On the other hand, patients who interpret pain in an exaggerated or catastrophic way, develop fear of pain and associated behaviors like hypervigilance and avoidance in search of security. Although these behaviors can be adaptive when coping with acute pain, they can worsen the patient’s condition if the pain is chronic, because they favor disuse, depression and increased disability. The fear-avoidance model is framed within the biopsychosocial disease model, the patient being trapped in a vicious circle of pain, disability and suffering (Fig. 2). Asmudson and colleagues [12] added the pain anxiety component to this model as an aggravating factor in the avoidance behavior generating circuit (Fig. 2). Avoidance behavior not only includes limiting one’s movements, but also avoiding social interactions and recreational activities, which increase the pain and suffering in these patients. Crombez and colleagues [13] have even stated that “the fear of pain is more disabling that pain itself”. In many studies, fear and avoidance behaviors have been strongly associated with the disability present in patients with low back pain

(LBP) [15–18]. Also, in LBP longitudinal studies, changes in fear-avoidance beliefs were good predictors of disability [19–24]. The fear of pain and the catastrophic vision of pain also occur in pain free people. Therefore, these beliefs can play an important role in the development of new episodes of pain. In studies performed on subjects without LBP [25–28], it was observed that fear of pain increased the risk of suffering episodes of LBP, and so the risk of disability was increased. Picavet and colleagues [29], in 2002, studied whether pain catastrophizing and fear of movement/(re)injury (kinesiophobia) are important in the etiology of chronic LBP and the associated disability. For patients with LBP at baseline, a high level of catastrophizing predicted chronic LBP, in particular severe LBP and LBP with disability. Moreover, a high level of kinesiophobia showed similar associations. For those subjects without LBP at baseline, a high level of catastrophizing or kinesiophobia predicted LBP with disability during follow-up. They concluded that catastrophizing and kinesiophobia were good predictors for the chronification of pain and disability. In another study, Carragee and colleagues [19] performed a five-year follow-up study on a group of 100 subjects with mild LBP by means of MRI and a discography, measuring their fear-avoidance beliefs with a FABQ (FearAvoidance Beliefs Questionnaire). Surprisingly,

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Fig. 2 The fear-avoidance model of chronic pain based on the fear-avoidance model of Vlaeyen and Linton [14] and the fear-anxiety-avoidance model of Asmudson and colleagues [12]

the severe LBP cases and disabilities had no relation with structural anomalies found in the MRI or discography. It was the presence of fear and avoidance behaviors that turned out to be the strongest predictor in LBP and disability. AKP shares with non-specific LBP a low correlation between the symptoms and structural anomalies found in imaging studies. Moreover, both conditions tend to become chronic and cause disability. The World Health Organization defines disability as “a limitation of function that compromises an individual’s ability to perform an activity within the range considered normal”. AKP patients show different degrees of disability in their everyday life, regardless of how intense the pain is. In some cases, there is severe pain and little disability. In other cases, the pain is severe and the disability, too. Piva and colleagues [30] studied whether changes in fearavoidance behaviors (measured with the FABQ modified for the knee) influenced disability in a group of patients with AKP undergoing conventional physical therapy treatment. They found that those patients who lowered their levels of

fear and avoidance of physical activity and work saw decreased levels of pain and disability at the end of the treatment. Jensen and colleagues [31] studied a group of AKP patients by measuring the degree of pain with the VAS scale and disability with the Cincinnati Knee Rating System (CKRS) questionnaire and found a weak correlation between the level of pain and disability, one that was not statistically significant. Therefore, we can reason that AKP causes pain on one hand and disability on the other, being both independent dimensions with a poor correlation. Domenech and colleagues [4] evaluated the ideas of fear and avoidance with the Tampa Kinesiophobia Scale (TSK) and have found a moderate statistically significant correlation with the patient’s referred disability measured with the Lysholm Score (Table 1) [4]. The greater the fear and avoidance beliefs, the greater the disability perceived by the patient. It is interesting to highlight that the correlation between kinesiophobia and disability was higher than the one between pain and disability (Table 1) [4]. Obviously, not all the AKP patients have

Evaluation of Psychological Factors … Table 1 Spearman correlation between pain, disability and the psychological variables. (“Republished with permission of Springer Nature BV, from Influence of kinesiophobia and catastrophizing on pain and disability in anterior knee pain patients, Domenech J et al., Knee Surg Sports Traumatol Arthrosc, 21, 1562–1568, 2013; permission conveyed through Copyright Clearance Center, Inc.”)

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Pain (VAS) Pain (VAS)

a

Disability (Lysholm) 0.49**

Coping Strategies (CSQ) 0.21

−0.01

Reinterpreting pain sensation

0.18

−0.16

Ignoring pain sensations

0.08

0.06

Coping self-statements

0.08

−0.01

Praying or hoping

0.35*

−0.38**

Catastrophizing

0.48**

−0.59**

Increasing activity level

0.01

Anxiety (HAD)

0.46**

0.57**

Depression (HAD)

0.44**

−0.61**

Kinesiophobia (TSK)

0.26*

−0.53**

Catastrophizing (PCS)

0.43**

−0.53**

Diverting attention

0.15

Subscale PCS rumination

0.39**

−0.49**

Subscale PCS magnification

0.41**

−0.47**

Subscale PCS hopelessness

0.46**

−0.56**

VAS (Visual Analogue Scale), CSQ (Coping Strategies Questionnaire), HAD (Hospital Anxiety and Depression inventory), TSK (Tampa Scale for Kinesiophobia), and PCS (Pain Catastrophizing Scale) * p < 0.01; ** p < 0.001 a Correlation between pain and disability was performed after deleting the subscale pain of the Lysholm questionnaire to avoid colinearity

kinesiophobia. However, its presence is very important because it has clinical relevance. If kinesiophobia is present, then the levels of the pain and the disability soar (Table 2). In many cases, AKP patients also exhibit catastrophizing. Domenech and colleagues [4] evaluated catastrophizing through the Catastrophizing Coping Scale Questionnaire (CSQ) and through the Pain Catastrophizing Scale (PCS) and found a moderate statistically significant correlation with the patient’s disability (Table 1). When the perception of pain is more catastrophic, the patients perceive greater disability. Moreover, pain and disability show a moderate but significant correlation even though it is lower than that observed with catastrophizing or kinesiophobia [4]. Therefore, there are other factors besides pain that contribute to disability. It has been shown that what is mainly responsible for disability is not the pain, but the associated psychological factors. Pain explains only 24% of the variance in disability whereas catastrophizing

and depression account for 56% of the variance in disability [4]. There are other factors besides pain that contribute to disability. It seems plausible that psychological factors contribute to it. There are complex cultural beliefs about many aspects of health including the potential iatrogenic effect of healthcare itself. The pain experience is a good example where there is great cultural complexity for example the fearavoidance model of pain cautions against exercise and activity, which in an acute injury state may be helpful and common sense but in a chronic pain state has a negative impact on outcomes [32]. Crepitus is another example where painless noises from the knee can create negative emotions, inaccurate etiological beliefs and finally leads to fear-avoidance behavior and lower functional performance [33]. Maclachlan and colleagues [34] showed that there were no significant differences in TSK, PCS or HADS between less-severe pain patients and controls. However, more severe AKP

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Table 2 T test comparison of mean values in pain and disability between patients with high or low levels of anxiety, depression, kinesiophobia and catastrophizing. (“Republished with permission of Springer Nature BV, from Influence of kinesiophobia and catastrophizing on pain and disability in anterior knee pain patients, Domenech J et al., Knee Surg Sports Traumatol Arthrosc, 21, 1562–1568, 2013; permission conveyed through Copyright Clearance Center, Inc.”) Pain

Disability

Anxiety High level (  11) n = 29

8.2 (1.1)

Low level (8 degrees valgus or >5 degrees of valgus requires alternate intervention, as does

Robotic-Assisted Patellofemoral Arthroplasty

patella baja [27]. Obesity, although not an absolute contraindication, does portend poorer results and is, at times, utilized as a relative contraindication [28]. Utilizing robotics is up to the discretion of the surgeon. Generally, indications and contraindications do not vary significantly from manual techniques, though consideration of longer operative time should be included in decision-making.

3

Preoperative Planning

A standard series of X-rays should first be obtained. These include standing AP, flexion PA (Rosenberg), lateral, and sunrise views of the knee in addition to full-length standing radiographs (Fig. 1). The sunrise view may be taken at various degrees of flexion in order to evaluate for patellar subluxation tilt, or femoral trochlear dysplasia. Typically, 30 degrees of flexion is sufficient [29]. The lateral view affords investigation for patellofemoral joint space, alignment, and patellar size. The full-length standing radiographs allow for evaluation of complete lower limb alignment. If desired, this can be further investigated with CT scan or Magnetic Resonance Imaging for formal measurement of the tibial tubercle-trochlear groove (TT-TG) distance may assist in operative decision-making as it relates to the need for tubercle osteotomy. In order to create a preoperative template for use in the robotic system, a CT scan must be obtained in order to identify bony landmarks that can be later referenced to ensure reproducible intraoperative findings.

4

Surgical Technique

4.1 Patient Positioning The patient should be placed supine on the operative table. A post of the surgeon’s preference is placed on the operative side to assist in maintaining leg positioning while allowing for

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full knee range of motion. The authors prefer to utilize a nonsterile tourniquet and the limb is prepped and draped in standard sterile fashion. For robot positioning, the robotic arm is typically positioned on the operative side to allow for optimized and independent use by the surgeon. The computer referencing monitor and stand is placed on the opposing side. The monitor is ideally placed at a comfortable and easily visible location for the surgeon. It is imperative that the nonoperative side of the patient is free of any obstructions as a clear line of sight is required for robotic tracking. The camera is angled toward the operative knee, using laser alignment if available. Lastly, the guidance module should be placed where a robotic representative can easily maintain visibility of the surgeon.

4.2 Operative Technique After induction of anesthesia, an examination under anesthesia is performed to assess for range of motion, patellar tracking, crepitation, and knee stability. Prior to incision for arthroplasty, a diagnostic arthroscopy (DA) should be performed. Standard anteromedial and anterolateral portals are utilized to arthroscopically assess each of the three knee compartments with a special focus on evaluating the cartilage integrity. This scrutinization ensures that cartilage integrity reflects that of preoperative imaging and ensures that cartilage to the tibiofemoral articulation is preserved, thus not contraindicating PFA. Additionally, diagnostic arthroscopy allows for assessment of the soft tissues of the knee, including the cruciate and collateral ligaments. Again, confirmation of isolated PFOA is required prior to proceeding with PFA. Upon completion of the diagnostic arthroscopy, a medial parapatellar approach to the joint is initiated. This is started approximately 3 cm above the superior pole of the patella and extends distally to the tibial tubercle. In the MAKO (Stryker, Kalamazoo, MI) system, two reference pins are then inserted into the anterior femur

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A

B

C

Fig. 1 Isolated patellofemoral osteoarthritis plain radiographs as demonstrated on sunrise (A), lateral (B), and anteroposterior (C) radiographs

Robotic-Assisted Patellofemoral Arthroplasty

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Fig. 2 Mako guide pins attached through right femur with receiver in place

proximal to the incision percutaneously (Fig. 2). Registering the femur may then be performed utilizing the reference pins, allowing the robotic system to overlay the intraoperative data with the preoperative CT. Arthrotomy then allows further visualization of the articular surface. Care is taken to avoid disrupting the menisci, intermeniscal ligaments, and articular cartilage. The infrapatellar and suprapatellar fat pads can be partially removed to allow for lateral patellar subluxation. Care should be taken to avoid removing soft tissue medial to the patella in anticipation of eventual soft tissue balancing. Next, a rongeur can be utilized to remove any visible osteophytes, soft tissue adhesions, or chondral defects. Mapping is started at the trochlea. Mapping is achieved using both a blunt- and a sharp-tipped probe and Knee End Effector Array (Fig. 3). Calibration of these systems to ensure accurate triangulation of the position of the probe is vital for adequate intraoperative mapping of the joint.

Articular surfaces are mapped by marking points with the sharp-tipped probe. Two points are marked on the superior edge of the trochlea, one medial and one lateral. Five points are marked along the trochlear groove. Finally, three points are marked on each side of the medial and lateral transition zones. These points are matched with preoperative CT. The sharp probe can be used to push through the cartilage for accurate mapping, as cartilage is not detected on the preoperative CT scan. Preoperative templating may then be adjusted according to the intraoperative mapping that has been performed. The robotic arm may then be advanced into position over the operative field, with centering of the robotic base at the patient’s hip, located one to two meters away from the operative table. The cutting handle is also brought in and placed approximately 10 cm directly above the knee joint. Once in position, beginning with the burring arm, bone over the trochlear surface is removed in accordance with

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Fig. 3 Intraoperative mapping of the patellofemoral joint. Mako Registration to sync to preoperative computed tomography as seen from the navigation console

the future trochlear implant (Fig. 4). Of note, the robotic burr does not allow removal of bone outside of the templated plan. Implant lug holes are created using the burr with special attention

to only plunge once to create lug holes in order to avoid creating excessively large lug holes. The trochlear implant may then be trialed to ensure adequate sizing and smooth patellar tracking.

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Fig. 4 The robotic arm guides preparation of the joint. A Robotic arm in position for trochlear resection view from professional representative’s monitor; B Trochlea status

Once the trochlear implant is appropriately in place, attention is turned to the undersurface of the patella. The everted patella should be measured for maximal thickness utilizing a caliper at the lateral and medial aspects. For patellar sizing, size is estimated by measuring the proximal– distal height of the patellar articular surface. The ideal patellar size is one that does not exceed the inferior or superior margins. Patellar resurfacing is then performed using a reamer or saw, depending on surgeon preference. A patellar reaming guide can be clamped in order to ensure the spikes are fully seated and that the guide sits flush. For optimized patellar tracking, the drill guide should be placed medially on the patella. In doing so, this will lateralize the remaining patellar surface to avoid over-tightening of the vastus lateralis and thereby decrease the risk of a lateral subluxation force. Once in an acceptable position, the peg holes are then drilled followed by placement of the trial patellar component (Fig. 5). Remeasurement of the patellar thickness is performed to ensure appropriate remaining thickness. Additionally, the knee can be taken through range of motion with special attention to

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postresection with retractors in soft tissue to allow for visualization. Three peg hole burr cuts visible

Fig. 5 Final components in position

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patellar tracking and transitioning through flexion and extension. Once the trials are deemed acceptable, they are removed to allow for irrigation of the bony surfaces. Cement can then be mixed and applied to the trochlear implant and resected trochlear notch. The trochlear implant is then placed and impacted, followed by removal of excess cement. The implant is manually held in place until the cement is fully cured, as can be deemed by manufacturing time or the hardening time of an additional sample of cement. Cementation is then performed of the resurfaced patella, peg holes, and patellar implant. The patellar component is then positioned and held in place by clamping to allow for an adequate compression force of the patellar implant. Again, excess cement is resected followed by clamp removal once fully cured. The joint is then irrigated and taken through another manual range of motion check. There should be no patellar tilt or subluxation as the knee is put through flexion and extension. Arthrotomy closure is made using ethibond figure-of-eight sutures followed by an additional

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layer of #0 vicryl suture in a running locking fashion. Again, soft tissue balancing and patellar tracking is confirmed with range of motion. Layered closure is then performed, with the authors’ preference for #0 vicryl followed by #2– 0 vicryl sutures. Skin closure is typically performed with staples. A soft dressing is placed in accordance with the surgeon’s preference.

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Postoperative Course

Rehabilitation following robotic-assisted PFA should follow the same protocol as manual PFA. Weight-bearing as tolerated with an emphasis on range of motion exercises may be initiated in the immediate postoperative period, with gradual increase in activity. Physical therapy may be initiated based on surgeon preference within the first 1–2 weeks. Patients are generally permitted to stationary bike at 4 weeks, with gradual return to full activity within 6–8 weeks. During follow up, postoperative radiographs should include standard anteroposterior, lateral, and merchant

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Fig. 6 Postoperative A lateral and B anteroposterior plain radiographs

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view imaging (Fig. 6). Alignment can be assessed with patellar symmetry, patellar tilt, and subluxation distance [16].

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Discussion

Robotic-assisted patellofemoral arthroplasty is a viable approach to operative management of isolated patellofemoral osteoarthritis. It offers several unique advantages when compared to manual PFS (Table 1). Pre-operative planning using 3-dimensional reconstructed images allows for more accurate appreciation of joint condition, alignment, and eventual implant sizing. Intraoperative cartilage mapping then affords reproducible joint alignment and positioning. These advantages may avoid sources of inconsistency or error that could cause ongoing symptoms in patients that undergo PFA. Owing to the recency of the robotic application to PFA, outcome studies are few. Turktas et al. examined 30 RA-PFA knees with a follow up of 15.9 months. In this series, there were no patients with patellar mal-tracking or misalignment. Additionally, there was a significant increase in post-operative Oxford Knee Score when compared preoperatively. Similar increases in outcome scores were also demonstrated in a study by Ackroyd et al. These studies suggest that RA-PFA offers a reliable procedure that affords patients predictable benefit in functional outcomes. However, its associated limitations should also be acknowledged. Longer term follow up studies are still needed in order to fully

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assess the outcomes, survivability, and issues not appreciable in shorter term follow up. Additionally, RA-PFA requires a significant financial investment into the robot itself as well as preoperative CT scanning. This financial cost is further increased at institutions that prefer to always undergo arthroscopic evaluation of the knee prior to PFA. Together, these capital costs may limit its availability to all institutions.

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Conclusion

Robotic-assisted patellofemoral arthroplasty is an emerging treatment for isolated patellofemoral arthritis. It has the potential to allow for more accurate and anatomic implant sizing and positioning. Although further studies are required to determine its long-term outcomes, it appears to have favorable short-term survivability, outcomes, and joint alignment. Comparable studies to non-robotic PFA will afford data that can be utilized in cost–benefit analyses and to better inform its future role.

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Take Home Messages

• Patellofemoral arthritis is common and can be a debilitating condition for which treatment options typically include total or isolated patellofemoral knee arthroplasty. • Standard patellofemoral arthroplasty is associated with several issues including patellar mal-tracking and inconsistent alignment.

Table 1 Advantages and Disadvantages of Robotic-Assisted Patellofemoral Arthroplasty Advantages Implant design and fixation more anatomical than previous systems Reduced malalignment and mal-tracking Short-term follow-up positive Disadvantages Long-term follow-up not yet available Capital investment and operating costs for robot are significant Preoperative CT scan required Note CT: Computed tomography

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• Robotic-assisted patellofemoral arthroplasty was recently developed in order to address issues with standard arthroplasty and allows for patient-specific templating for implant size, alignment, and positioning. • Outcomes of robotic patellofemoral arthroplasty are promising and demonstrate low rates of malalignment and mal-tracking in addition to encouraging outcome scores • Several operative pearls including avoiding oblique reference pins, achieving appropriate soft tissue balancing, and checking for lateral facet deficiency are key to reliable outcomes. • Further longer-term studies will assist in full analysis of the outcomes, results, and cost– benefit nature of robotic patellofemoral arthroplasty.

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Key Message

• Robotic patellofemoral arthroplasty appears to be a reproducible, beneficial, and feasible treatment for isolated patellofemoral arthritis.

Acknowledgements Figures adapted from Elsevier Inc. https://doi.org/10.1016/j.eats.2019.11.013.

References 1. Davies AP, Vince AS, Shepstone L, Donell ST, Glasgow MM. The radiologic prevalence of patellofemoral osteoarthritis. Clin Orthop Relat Res. 2002;402:206–12. 2. Grelsamer RP, Stein DA. Patellofemoral arthritis. J Bone Joint Surg Am. 2006;88(8):1849–60. 3. Sisk D, Fredericson M. Taping, bracing, and injection treatment for patellofemoral pain and patellar tendinopathy. Curr Rev Musculoskelet Med. 2020;13 (4):537–44. 4. Strickland SM, Bird ML, Christ AB. Advances in patellofemoral arthroplasty. Curr Rev Musculoskelet Med. 2018;11(2):221–30. 5. Mckeever DC. Patellar prosthesis. J Bone Joint Surg Am. 1955 (5):1074–84. 6. Lubinus HH. Patella glide bearing total replacement. Orthopedics. 1979;2(2):119–27.

7. Blazina ME, Fox JM, Del Pizzo W, Broukhim B, Ivey FM. Patellofemoral replacement. Clin Orthop Relat Res. 1979;144:98–102. 8. Tauro B, Ackroyd CE, Newman JH, Shah NA. The Lubinus patellofemoral arthroplasty. A five- to tenyear prospective study. J Bone Joint Surg Br. 2001;83(5):696–701. 9. Kooijman HJ, Driessen APPM, van Horn JR. Longterm results of patellofemoral arthroplasty. A report of 56 arthroplasties with 17 years of follow-up. J Bone Joint Surg Br. 2003;85(6):836–40. 10. Krajca-Radcliffe JB, Coker TP. Patellofemoral arthroplasty. A 2- to 18-year followup study. Clin Orthop Relat Res. 1996 Sep;(330):143–51. 11. van der List JP, Chawla H, Zuiderbaan HA, Pearle AD. Survivorship and functional outcomes of patellofemoral arthroplasty: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2017;25 (8):2622–31. 12. Deckey DG, Rosenow CS, Verhey JT, Brinkman JC, Mayfield CK, Clarke HD, et al. Robotic-assisted total knee arthroplasty improves accuracy and precision compared to conventional techniques. Bone Joint J. 2021;103-B(6 Supple A):74–80. 13. Cobb J, Henckel J, Gomes P, Harris S, Jakopec M, Rodriguez F, et al. Hands-on robotic unicompartmental knee replacement: a prospective, randomised controlled study of the acrobot system. J Bone Joint Surg Br. 2006;88(2):188–97. 14. Law J, Hofmann A, Stevens B, Myers A. Patellofemoral arthroplasty technique: Mako. In: Lonner JH, editor. Robotics in Knee and Hip Arthroplasty: Current Concepts, Techniques and Emerging Uses [Internet]. Cham: Springer International Publishing; 2019 [cited 2021 Nov 13]. p. 115–22. Available from: https://doi.org/10.1007/978-3-030-16593-2_12 . 15. Turktas U, Piskin A, Poehling GG. Short-term outcomes of robotically assisted patello-femoral arthroplasty. Int Orthopaedics (SICOT). 2016;40 (5):919–24. 16. Dahm DL, Al-Rayashi W, Dajani K, Shah JP, Levy BA, Stuart MJ. Patellofemoral arthroplasty versus total knee arthroplasty in patients with isolated patellofemoral osteoarthritis. Am J Orthop (Belle Mead NJ). 2010;39(10):487–91. 17. Laskin RS, van Steijn M. Total knee replacement for patients with patellofemoral arthritis. Clin Orthop Relat Res. 1999;367:89–95. 18. Odumenya M, McGuinness K, Achten J, Parsons N, Spalding T, Costa M. The Warwick patellofemoral arthroplasty trial: a randomised clinical trial of total knee arthroplasty versus patellofemoral arthroplasty in patients with severe arthritis of the patellofemoral joint. BMC Musculoskelet Disord. 2011;12(1):265. 19. Leadbetter WB, Ragland PS, Mont MA. The appropriate use of patellofemoral arthroplasty: an analysis of reported indications, contraindications, and failures. Clin Orthop Relat Res. 2005;436:91–9.

Robotic-Assisted Patellofemoral Arthroplasty 20. Woon CYL, Christ AB, Goto R, Shanaghan K, Shubin Stein BE, Gonzalez Della Valle A. Return to the operating room after patellofemoral arthroplasty versus total knee arthroplasty for isolated patellofemoral arthritis-a systematic review. Int Orthop. 2019;43(7):1611–20. 21. Begum FA, Kayani B, Morgan SDJ, Ahmed SS, Singh S, Haddad FS. Robotic technology: current concepts, operative techniques and emerging uses in unicompartmental knee arthroplasty. EFORT Open Rev. 2020;5(5):312–8. 22. Kayani B, Konan S, Huq SS, Tahmassebi J, Haddad FS. Robotic-arm assisted total knee arthroplasty has a learning curve of seven cases for integration into the surgical workflow but no learning curve effect for accuracy of implant positioning. Knee Surg Sports Traumatol Arthrosc. 2019;27(4):1132–41. 23. Mahure SA, Teo GM, Kissin YD, Stulberg BN, Kreuzer S, Long WJ. Learning curve for active robotic total knee arthroplasty. Knee Surg Sports Traumatol Arthrosc. 2021. 24. Walker T, Perkinson B, Mihalko WM. Patellofemoral arthroplasty: the other unicompartmental knee replacement. J Bone Joint Surg Am. 2012;94 (18):1712–20.

755 25. Lonner JH. Patellofemoral arthroplasty. J Am Acad Orthop Surg. 2007;15(8):495–506. 26. Delanois RE, McGrath MS, Ulrich SD, Marker DR, Seyler TM, Bonutti PM, et al. Results of total knee replacement for isolated patellofemoral arthritis: when not to perform a patellofemoral arthroplasty. Orthop Clin North Am. 2008;39(3):381–8, vii. 27. Leadbetter WB, Seyler TM, Ragland PS, Mont MA. Indications, Contraindications, and Pitfalls of Patellofemoral Arthroplasty. JBJS. 2006;88(suppl_4): 122–37. 28. Sabatini L, Schirò M, Atzori F, Ferrero G, Massè A. Patellofemoral joint arthroplasty: our experience in isolated patellofemoral and bicompartmental arthritic knees. Clin Med Insights Arthritis Musculoskelet Disord. 2016;9:189–93. 29. Iwano T, Kurosawa H, Tokuyama H, Hoshikawa Y. Roentgenographic and clinical findings of patellofemoral osteoarthrosis. With special reference to its relationship to femorotibial osteoarthrosis and etiologic factors. Clin Orthop Relat Res. 1990; (252):190–7.

Modern Patellofemoral Inlay Arthroplasty—A Silver Lining in the Treatment of Isolated Patellofemoral Arthritis Marco-Christopher Rupp, Jonas Pogorzelski, and Andreas B. Imhoff

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Key Notes

• Contemporary patellofemoral inlay arthroplasty demonstrates high patient satisfaction with significant improvements in knee function and pain relief while avoiding progression of tibiofemoral arthritis at mid-term follow-up. • Patient selection is the key to success. • In patients with significant trochlea dysplasia or with (minor) rotational malalignment, an onlay prosthesis might be beneficial as its design addresses those factors better than an inlay design.

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Introduction

Isolated patellofemoral osteoarthritis (PFOA) is a complex and multifactorial pathology. Primary OA of the patellofemoral joint is a relatively rare entity and is defined as isolated OA to the patellofemoral joint without concomitant or underlying pathologies in the sense of tibiofemoral malalignment or patellofemoral instability. Secondary OA however is much more common

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J. Pogorzelski
A. B. Imhoff (&) Department of Orthopaedic Sports Medicine, Hospital Rechts der Isar, Technical University of Munich, Munich, Germany e-mail: [email protected]

and is the result of non-physiologic patellofemoral biomechanics, e.g. due to trochlear dysplasia or axial/torsional malalignment of the femur and tibia with subsequent maltracking of the patella or patellofemoral instability. With multiple etiological factors exhibiting a combined effect on the biomechanical and clinical outcome following PFIA, the surgical management for PFOA is part of a nuanced therapeutical concept and should be viewed in the context of concomitant pathologies. Patellofemoral inlay arthroplasty (PFIA) as a design variant of patellofemoral arthoplasty was first described in the literature in 1979 [1]. In principle, the idea behind the PFIA design was to retain the anatomy of the trochlea and replace only the degenerated part of the cartilage without having to perform a more invasive resection of the subchondral bone. The trochlear component was inserted flush with the surrounding cartilage of the trochlea (“inlay”). However, the first results of these arthroplasty models led to high failure rates due to the suboptimal geometry of these models [2, 3] A trochlear groove that was, by design, non-physiologically deep and an insufficient mediolateral coverage of the trochlea in the first arthroplasty models often resulted in patellofemoral maltracking with persistent pain and additional patellofemoral instability [2, 3]. Based on these experiences, novel surgical techniques and a new generation of inlay arthroplasty models have been developed in recent years (Fig. 1).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_59

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Fig. 1 Modern patellofemoral inlay prosthesis (Kahuna Prosthesis, Arthrosurface, Franklin, MA, USA)

However, as PFOA is a multifactorial pathology, concomitant soft-tissue and bone-based reconstructive procedures have to be considered during conception of the surgical plan. In the case of accompanying malalignment of the femur, surgical procedures such as alignment corrective osteotomies to optimize mechnical leg alignment and patellofemoral tracking [4] may be indicated, since performing an isolated PFIA may not be fully able to restore physiological alignment. Compared to total knee arthroplasty (TKA) in the treatment of isolated PFOA, the procedure is relatively minimal invasive and the tibiofemoral joint compartments can be preserved during the PFIA procedure [5–7]. Lower intraoperative morbidity, shorter intraoperative tourniquet times and a shorter rehabilitation time in young patients postoperatively [8–10] typically result in improved mobility and extension strength of the knee joint with a comparable postoperative satisfaction compared with TKA [7, 8, 11, 12]. Since the PFIA can also be converted to a TKA in cases where the tibiofemoral OA progresses [9], the implantation of a modern PFIA is a viable therapeutic alternative to TKA, especially in younger patients. This chapter aims to provide an overview of the indications and contraindications for PFIA and recommendations for clinical practice.

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Indication

PFIA is indicated in patients suffering from isolated disabling PFOA with minimum grade III– IV (Kellgren-Lawrence classification) or chondral defects grade III–IV (Outerbridge classification) that refractory to conservative treatment and/or failed prior surgery. Performing an isolated PFIA is generally reserved for patients without patellofemoral instability. High-grade patellofemoral or tibiofemoral malalignment as defined by a mechanical valgus or varus of more than 5°; a femoral anteversion of more than 30°; a tibial torsion of more than 40°; a tibial tuberosity trochlear groove distance of more than 20 mm or less than 8 mm; a Caton-Deschamps Index of more than 1.2 or less than 0.8; or a lateral patellar tilt of more than 5° should be managed according to a previously published algorithm [4] additionally to the implantation of a PFIA.

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Contraindication

Contraindications for PFIA implantation are symptomatic tibiofemoral OAwith pain at the joint line during activities of daily living, chronic

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regional pain syndrome, active infection, inflammatory arthropathy, chondrocalcinosis, and a fixed loss of knee range of motion.

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Surgical Technique

Contemporary inlay arthoplasty models typically consist of a cobalt chrome trochlear component that is connected to a titanium taper post via a taper interlock and an (optional) additional allpolyethylene patella component. Most systems are distributed with multiple implant sizes with varying offsets to facilitate a patient-specific geometry match. All inlay prostheses are designed to be implanted flush with the surrounding cartilage into a bone bed within the native trochlea sparing the femoral bone stock (Fig. 2). Typically, inlay arthroplasty models include a trochlear groove that narrows distally to allow for sufficient patella tracking without causing lateral hypercompression of the patella. Compared to an onlay design, the more anatomic principle of the inlay design closely reproduces the complex patellofemoral kinematics. By desing, this avoids soft tissue irritation due to patellofemoral overstuffing, which is an accepted risk factor for the development and progression of tibiofemoral OA due to secretion of proinflammatory cytokines [13]. The arthroplasty procedure is performed according to the specific manufacturers instructions. Typically, the PFIA procedure is performed via a minimally invasive lateral parapatellar approach to spare the medial patellastabilizing soft tissue structures. A further advantage of the lateral approach is that overhanging patellar osteophytes, that are typically located laterally, can be resected without compromising the approach to the trochlea for the implantation of the PFIA. An offset drill guide is used to correctly localize the center for the reamer with the knee in full extension. In principle, the correct placement for the drill guide is located at the center of the trochlear articular surface to confirm trochlear defect coverage (Fig. 3). A guide pin is advanced into the bone,

Fig. 2 Second-Generation patellofemoral inlay arthroplasty model (WAVE Prosthesis, Arthrosurface, Franklin, MA, USA) implanted flush with the surrounding cartilage after creation of a bone bed within the native trochlea

Fig. 3 An offset drill guide is used to establish a working axis prependicular to the central trochlear articular surface and to confirm trochlear defect coverage

once the superior and inferior drill guide feet are optimally aligned with the trochlear orientation. In order determine the adequate implant size, the

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fixation stud. Finally, the trochlear component is positioned using an impactor. Subsequently, debridement of patellar osteophytes, circumpatellar denervation and resurfacing of the patella are performed. To replace the patellar surface, a drill guide is inserted emplyoing an alignment guide. The medial/lateral and superior/inferior offsets are measured and an implant bed is reamed. The patellar component is then mounted onto the implant holder and cemented into the bone bed. Postoperative radiographs in three planes are obtained routinely to confirm optimal implant positioning. (Fig. 6).

6 Fig. 4 The implant bed is reamed employing a guide block

medial/lateral as well as superior/inferior offsets are measured using specific measurement instrumentation. Next, the implant bed is reamed three-dimensionally using a guide block (Figs. 4 and 5). Subsequently, the screw fixation stud is advanced into the bone. The trochlear component is then aligned with the appropriate offsets of the implant holder and placed onto the taper of the

Rehabilitation

All patients are discharged once they are able to flex the knee joint to a minimum of 90° and can climb stairs on crutches safely. All patients are limited to partial weight bearing with 20 kg for two weeks until the healing process of the soft tissue is consolidated. Early rehabilitation includes lymphatic drainage and continuous passive motion for the first two weeks as tolerated. Patients are then allowed to increase weight bearing in a step-wise fashion until full weight

Fig. 5 The correct positioning of the implant is confirmed by positioning of a trial implant that will be used for positioning the tape post

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Fig. 6 Postoperative radiographs of the inlay implant in three planes routinely obtained to confirm implant positioning

bearing is achieved approximately six weeks after surgery. Full active range of motion is typically allowed two weeks after surgery.

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Clinical Outcome

The results after PFIA are mainly influenced by the patient selection, the surgical technique and the arthroplasty design. Early complications are common and mainly caused by implant misplacement and/or postoperative patella maltracking or patellofemoral instability, while longterm failures are mainly the result of progression of tibiofemoral osteoarthritis. An adequate patient selection may be the key factor in achieving favorable outcomes following PFIA. As such—according to the current state of knowledge—risk factors for inferior clinical outcome include an increased body mass index (BMI) prior surgery, an etiology of primary PFOA as compared to secondary PFOA, presence of degenerative changes in the tibiofemoral joint compartments, lack of retropatellar resurfacing during the PFIA procedure as well persistent

patellofemoral instability and malalignment following the PFIA procedure [14–17]. As of biomechanical studies, peak pressure following patellofemoral arthroplasty significantly increases compared to the native joint [5, 18]. As such, if patellar resurfacing is not performed at index surgery, non-physiological pressure conditions may predispose for an abrasion of the native patellar cartilage in contact with the inlay arthroplasty [5]. This may consequently lead to a progression of retropatellar cartilage degeneration resulting in pain as wells as poor postoperative results and may require revision surgery. This finding was confirmed by a multi-center case series, in which the lack of patellofemoral resurfacing at the index surgery was significantly correlated with failure [16]. Interestingly, the presence of primary OA of the patellofemoral joint also seems to be a risk factor for inferior outcome after implantation of a PFIA as compared to patients with secondary PFOA. In this regard, a prospective case series reported that there is a significant progression of tibiofemoral OA in patients with primary PFOA while the tibiofemoral compartments remains

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relatively unchanged in patients undergoing PFIA for secondary PFOA [15]. Patients with secondary PFOA due to patellofemoral instability, in which the anatomical risk factors predisposing for patellofemoral instability were addressed during PFIA implantation, were shown to benefit significantly more from undergoing PFIA than patients with primary PFOA [15]. Potentially patients with primary OA are more prone to degenerative changes in the tibiofemoral joint compartments as part of the inflammatory reactions that occurs within the joint during primary OA [13]. This is in accordance with subsequent outcome studies that reported significantly better results following PFIA in the presence of secondary OA due to trochlear dysplasia with concomitant patellofemoral instability [19–21]. An increased BMI was identified as a further independent factor in PFIA predictive of unfavorable clinical outcome postoperatively [16, 22]. As such, obesity may lead to rapid progression of tibifemoral OA and predispose for an early conversion to TKA. According to the current literature, this is still the main reason for the failure of PFIA [14, 17, 23]. When respecting these risk factors during patient selection, the PFIA procedure is a viable, minimally invasive alternative to the traditional TKA procedure for isolated PFOA. In a study regarding the midterm outcome following PFIA [24], the patient reported outcome scores improved significantly both at short- and midterm follow up with no significant difference between the two time points. In this case series, 17.1% of the patients failed leaving a survival rate of 83% after five years, reflecting the early experiences with modern generation PFIA. In patients who did not fail, no changes in the vertical patellar alignment or significant progression of tibiofemoral OA were observed until final follow up. The main mode of failure reported in this case series was persistent knee pain. An independent case series on the early experiences of modern generation PFIA, who evaluated the outcome after a mean follow-up of 35 months following PFIA, confirmed the promising clinical outcome. Significant

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improvements were observed across all patient reported outcome measures and similarly, no radiological progression of tibiofemoral OA was noted. Around 10% of the patients were converted to TKA, again with persistent pain being the main reason for failure. In the largest series to date, including a total of 263 patients (49 ± 12 years) at mid-term follow-up, 93% of the patients included in the final analysis were satisfied with the procedure with a mean transformed WOMAC Score of 84.5 ± 14.5 points, a mean KOOS Score of 73.3 ± 17.1 points, a mean Tegner Score of 3.4 ± 1.4 points and a mean VAS pain of 2.4 ± 2.0 points. With an overall failure rate was 11% (28 patients), the authors concluded that PFIA shows high patient satisfaction with good functional outcomes at short- to mid-term followup. However, the outcomes reported following isolated PFIA are heterogenous throughout the literature. In a prospective case series of 18 patients [25], a significant progression of OA in the medial tibiofemoral compartment caused a total of 5 implants (28%) to fail within six years. However, even when acknowledging for this high failure rate, clinically significant improvements were observed for clinical and functional outcomes; with an improvement in the the American Knee Society Subjective Score (AKSS) of more than 20 points in 91% of the patients. The relatively high revision rate reported in this case series [25] highlights the necessity for careful preoperative patient selection. A recent review article analyzing the clinical outcome following patellofemoral arthroplasty depending on the size of the respective center proposed found that the outcome in specialized centers with substantial cumulative experience with the procedure may be superior, highlighting the multifactorial complexity of the management of PFOA [26]. This notion is highlighted retrospective cohort of 20 patients who underwent PFIA. 55% of the patients with an increased patellofemoral congruence angle and an elevated Insall–Salvati index and showed an initial satisfactory result, but failed due to pain during follow-up after a

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median time of 25 months. Beckmann et al. concluded that patients with craniolateral types of PFOA as well as a patella alta should be treated with an patellofemoral onlay arthroplasty, as this type of implant is superior in covering the proximal part of the patellar track as compared to the PFIA design [27]. Accordingly, Feucht et al. [28] found that preoperative patellofemoral anatomy is significantly associated with clinical improvement and failure rate after isolated inlay PFA. It was demonstrated that less clinical improvement and a higher failure rate must be expected in patients with patella alta (ISI > 1.2 and PTI < 0.28), absence of trochlear dysplasia, and a lateralized position of the tibial tuberosity (TT-PCL distance > 21 mm), further highlighting the necessity for an adequate patient selection for the PFIA procedure [28]. Overall, when respecting risk factors associated with inferior outcomes during a concise diagnostic work-up and careful patient selection process, PFIA implantation has been shown to be a viable, minimally invasive alternative to TKA in the treatment of PFOA. Yet, future studies reporting on the the long-term outcome following PFIA are required and further research is necessary to define risk factors for failure or insufficient clinical improvement following PFIA.

References 1. Blazina ME, et al. Patellofemoral replacement. Clin Orthop Relat Res. 1979;144:98–102. 2. Borus T, et al. Patellofemoral joint replacement, an evolving concept. Knee. 2014;21(Suppl 1):S47-50. 3. Cartier P, Sanouiller JL, Khefacha A. Long-term results with the first patellofemoral prosthesis. Clin Orthop Relat Res. 2005;436:47–54. 4. Imhoff AB, et al. Prospective evaluation of anatomic patellofemoral inlay resurfacing: clinical, radiographic, and sports-related results after 24 months. Knee Surg Sports Traumatol Arthrosc. 2015;23 (5):1299–307. 5. Vandenneucker H, et al. Isolated patellofemoral arthroplasty reproduces natural patellofemoral joint kinematics when the patella is resurfaced. Knee Surg Sports Traumatol Arthrosc. 2016;24(11):3668–77.

763 6. Tanikawa H, et al. Influence of total knee arthroplasty on patellar kinematics and patellofemoral pressure. J Arthroplasty. 2017;32(1):280–5. 7. Odgaard A, et al. The mark coventry award: patellofemoral arthroplasty results in better range of movement and early patient-reported outcomes than TKA. Clin Orthop Relat Res. 2018;476(1):87–100. 8. Dahm DL, et al. Patellofemoral arthroplasty versus total knee arthroplasty in patients with isolated patellofemoral osteoarthritis. Am J Orthop (Belle Mead NJ). 2010;39(10):487–91. 9. van Jonbergen HP, Werkman DM, van Kampen A. Conversion of patellofemoral arthroplasty to total knee arthroplasty: a matched case-control study of 13 patients. Acta Orthop. 2009;80(1):62–6. 10. Kamikovski I, Dobransky J, Dervin GF. The clinical outcome of patellofemoral arthroplasty vs total knee arthroplasty in patients younger than 55 years. J Arthroplasty. 2019;34(12):2914–7. 11. Walker T, Perkinson B, Mihalko WM. Patellofemoral arthroplasty: the other unicompartmental knee replacement. J Bone Joint Surg Am. 2012;94 (18):1712–20. 12. Dy CJ, et al. Complications after patello-femoral versus total knee replacement in the treatment of isolated patello-femoral osteoarthritis. A metaanalysis. Knee Surg Sports Traumatol Arthrosc, 2012;20(11):2174–90. 13. Kapoor M, et al. Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nat Rev Rheumatol. 2011;7(1):33–42. 14. van der List JP, et al. Survivorship and functional outcomes of patellofemoral arthroplasty: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2622–31. 15. Beitzel K, et al. Prospective clinical and radiological two-year results after patellofemoral arthroplasty using an implant with an asymmetric trochlea design. Knee Surg Sports Traumatol Arthrosc. 2013;21 (2):332–9. 16. Imhoff AB, et al. The lack of retropatellar resurfacing at index surgery is significantly associated with failure in patients following patellofemoral inlay arthroplasty: a multi-center study of more than 260 patients. Knee Surg Sports Traumatol Arthrosc, 2021. 17. Bendixen NB, Eskelund PW, Odgaard A, Failure modes of patellofemoral arthroplasty-registries vs. clinical studies: a systematic review. Acta Orthop, 2019;90(5):473–478. 18. Calliess T, et al. Patella tracking and patella contact pressure in modular patellofemoral arthroplasty: a biomechanical in vitro analysis. Arch Orthop Trauma Surg. 2016;136(6):849–55. 19. Dahm DL, et al. Patellofemoral arthroplasty: outcomes and factors associated with early progression of tibiofemoral arthritis. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2554–9. 20. Nicol SG, et al. Arthritis progression after patellofemoral joint replacement. Knee. 2006;13(4):290–5.

764 21. Feucht MJ, et al. Preoperative patellofemoral anatomy affects failure rate after isolated patellofemoral inlay arthroplasty. Arch Orthop Trauma Surg, 2020. 22. Liow MH, et al. Obesity and the absence of trochlear dysplasia increase the risk of revision in patellofemoral arthroplasty. Knee. 2016;23(2):331–7. 23. van Jonbergen HP, et al. Long-term outcomes of patellofemoral arthroplasty. J Arthroplasty. 2010;25 (7):1066–71. 24. Imhoff AB, et al. High patient satisfaction with significant improvement in knee function and pain relief after mid-term follow-up in patients with isolated patellofemoral inlay arthroplasty. Knee Surg Sports Traumatol Arthrosc, 2018. 25. Laursen JO. High mid-term revision rate after treatment of large, full-thickness cartilage lesions

M.-C. Rupp et al. and OA in the patellofemoral joint using a large inlay resurfacing prosthesis: HemiCAP-Wave(R). Knee Surg Sports Traumatol Arthrosc. 2017;25 (12):3856–61. 26. Benignus C, et al. When nothing else works: patellofemoral joint arthroplasty. Sportverletz Sportschaden. 2021;35(4):227–33. 27. Beckmann J, et al. Patella alta and patellar subluxation might lead to early failure with inlay patellofemoral joint arthroplasty. Knee Surg Sports Traumatol Arthrosc. 2019;27(3):685–91. 28. Feucht MJ, et al. Preoperative patellofemoral anatomy affects failure rate after isolated patellofemoral inlay arthroplasty. Arch Orthop Trauma Surg. 2020;140(12):2029–39.

Virtual Orthopaedic Examination in Patellofemoral Disorders Casey L. Wright and Miho J. Tanaka

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Introduction

Telehealth (also referred to as telemedicine or virtual care) is a rapidly emerging field encompassing a wide range of care paradigms utilizing electronic platforms to provide healthcare services. Telehealth models include triage, radiographic assessment, remote monitoring devices, “store-and-forward” telehealth, asynchronous care, an “at-home” model, and a “regional-hub” model [1]. Virtual musculoskeletal care has primarily been provided through the latter two models. In the “at-home” model, physicians connect directly with patients via a virtual platform to provide healthcare services. Studies comparing at-home telehealth and in-person care demonstrate the success of telehealth in diagnosing and treating a variety of musculoskeletal problems. A study of face-to-face and telehealth visits conducted on the same day for 42 patients with chronic shoulder, knee, or lumbar spine issues demonstrated 83.3% diagnostic and management agreement with an 89% patient satisfaction rating [2]. Despite such encouraging results, prior to the COVID-19 pandemic, telehealth historically

C. L. Wright
M. J. Tanaka (&) Department of Orthopaedic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA e-mail: [email protected]

played only a small role in orthopaedic practices. The unanticipated global spread of severe acute respiratory syndrome coronavirus 2 (SARSCoV2), however, accelerated reliance on telehealth within orthopaedic surgery to enable surgeons to continue providing routine musculoskeletal care during a period in which inperson evaluation was limited to urgent or emergent issues [3]. King and colleagues, who detailed their department’s telehealth implementation process during the pandemic-enforced restrictions, expanded the use of telehealth from 0.4 to 76% of their daily encounters [4]. Early studies evaluating the ability of virtual visits to develop appropriate surgical plans validate the quality of telehealth care. Within sports medicine surgeries, only 4% of surgical plans formulated during telemedicine visits subsequently changed during in-person re-evaluation [5]. In the evaluation of patellofemoral disorders, the diagnoses rely heavily on history and physical examination. When converting the patellofemoral evaluation to a virtual encounter over telemedicine, adaptations to known examination techniques can be considered. Several orthopaedic departments who have published their experience with the rapid implementation of telehealth have advocated for a consistent, structured approach to promote the efficiency and success of the virtual encounter, with instructions for patients to review prior to the visit [1, 4, 6]. Virtual assessments can be augmented with the use of digital measurements or goniometers

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 V. Sanchis-Alfonso (ed.), Anterior Knee Pain and Patellar Instability, https://doi.org/10.1007/978-3-031-09767-6_60

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and can be performed either within a telemedicine platform or through a screen capture process. Virtual goniometers are an effective tool to standardize measurements across patients and are available in a variety of formats. They are available as browser extensions (Protractor, ben. builingham), smartphone applications (DrGoniometer, CDM s.r.l., Milano, Italy [7]), and through the use of a standard goniometer during a virtual visit, including to assess a screen-captured image [8]. Virtual goniometers demonstrate compatibility with multiple telehealth platforms utilized as a browser extension [6]. Several studies have demonstrated high reliability in range of motion measurements obtained virtually [7–10]. Dent and colleagues reported success with the use of a standard clinical goniometer to assess individuals during virtual encounters, which is applicable regardless of telemedicine platform [8]. They noted high agreement between elbow flexion and extension measurements taken during an in-person encounter and when using the same goniometer during a teleconference (Pearson coefficient in flexion: 0.93, in extension: 0.86). Some studies suggest digital knee range of motion assessments using still images have equivalent accuracy and increased precision compared to both visual assessment and standard goniometry [11, 12]. The goals of this chapter are to highlight the considerations when performing evaluation of the patellofemoral joint through a telemedicine visit. We discuss the examination workflow, modifications of standard examination maneuvers, benefits and limitations of the virtual visit, as well as guidelines for optimizing the efficiency and efficacy of the virtual examination.

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Preparation for the Telemedicine Visit

Preparation for the telemedicine visit by both the patient and physician are integral to ensuring a successful and efficient visit. Protocols for the virtual visit, including payment policies, consent, technology requirements, and instructions for the

visit, should be discussed at the time of scheduling. X-rays performed in advance of the visit should be made available for review prior to or at the time of the visit. If images are performed at a facility outside of one’s institution, those images should be submitted in advance so they may be uploaded for review prior to the start of the encounter. Adequate audiovisual capabilities on the part of the patient can significantly improve the quality and flow of the examination. Patients can be instructed to visit a remote verification site to confirm they have the appropriate software and audiovisual capabilities to participate in the appointment. Educational materials sent to the patient in anticipation of the virtual visit should set appropriate expectations and include written, photographic, or video instructions of the physical examination maneuvers to be performed (Tables 1 and 2) Instructions provided in advance of the visit allows patients to familiarize themselves with the upcoming examination, advises of the expectations of the patient during the visit, and allows the patient to prepare for the visit. A standardized protocol for both the preparation for and performance of the virtual visit can improve the diagnostic accuracy and efficiency of the evaluation.

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Inspection

Similar to in an in-person evaluation, the virtual examination begins with inspection, which can be easily performed with the patient standing and facing the camera. Thorough inspection should note skin changes, erythema, incisions, scars, and the presence of an effusion. Asymmetries in patellar position, or muscle bulk and tone may be noted. As with other musculoskeletal assessments, it is helpful to utilize the contralateral leg as a control throughout the examination. However, physicians should be mindful that many patients with patellofemoral disorders may have bilateral involvement, which may influence examination findings [13, 14]. In a recent randomized control trial of 112 patients with patellofemoral pain syndrome, Hott and colleagues

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Table 1 Example of patient instructions to prepare for a virtual visit (Adapted from Tanaka et al. JBJS 2020 [6]) How to prepare for a virtual visit After speaking with a physician or provider regarding your symptoms, he or she will guide you through a physical examination. To improve the success of the visit, please ensure you conduct the virtual appointment in a space that allows for the following: Privacy: Please conduct the visit in a quiet space with minimal background noise in which you are able to speak privately with your physician regarding your health concerns Space: The visit should be conducted in a space that allows for the camera to be positioned 6 feet (1.8 m) in front of you on a low surface (2–3 feet off the ground), such as a chair or low table. This allows for appropriate visualization of your knees during the examination. Sufficient floor space for 6–8 strides should be available for assessment of your gait Camera: The camera should be positioned on a table top or chair such that it does not need to be held during the encounter, yet can be repositioned as needed throughout the examination Lighting: Adequate lighting is crucial to ensure your provider is able to visualize the necessary details of the physical examination. Please minimize backlighting by facing the camera away from windows and light sources Seating: It is best to utilize a swivel chair or easily moveable chair during the examination that will allow you to transition from facing the camera to having your side facing the camera. The physician will also need to evaluate you while you are lying down, so it is necessary to either have a couch or adequate floor space available for you to lie down Clothing: For appropriate visualization, please wear shorts that end 3″ above your knees and remove your shoes and socks

Table 2 Summary and workflow for the virtual patellofemoral examination The virtual examination Seated in chair

Inspection (frontal view) • Skin changes, erythema, incisions, scars, effusion • Asymmetries in patellar position, muscle bulk, tone Palpation (frontal view) • Tibial tubercle, patellar tendon, quadriceps tendon insertion, medial and lateral patellar facets, medial and lateral joint lines, medial and lateral femoral condyles, medial and lateral collateral ligaments • Adductor tubercle (“Bassett’s sign”) Patellar Instability (frontal view) • J sign • Patellar apprehension • Patellar glide Range of Motion • Hip internal and external rotation (frontal view) • Hip flexion with upper extremity assistance (lateral view) • Knee flexion and extension (lateral view) Muscle Strength (lateral view) • Knee extension • Extensor lag • Hip extension – rise from seated without upper extremity support Foot Pronation (lateral view)

Standing

Gait Hypermobility (Beighton scale) (frontal view) Lower Extremity Alignment (frontal view) • Leg lengths, muscular atrophy • Q angle • Genu valgum, tibial tubercle lateralization, tibial torsion, femoral anteversion (continued)

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Table 2 (continued) The virtual examination Range of Motion • Hip abduction and adduction (frontal view) • Hip flexion and extension (lateral view) • Knee flexion and extension (lateral view) Muscle Strength (frontal and lateral view) • Single-leg knee bend Seated or laying on ground

Range of Motion (lateral view) • Hip flexion and extension (side-lying or supine) • Hip abduction and adduction (side-lying) Muscle Strength (lateral view) • Hip abduction (side-lying) • Hip flexion (straight leg raise) (supine) • Knee flexion (prone)

found 72% of included patients had bilateral symptoms [13]. Muscular atrophy is an important finding to identify in patellofemoral disorders. This can be assessed virtually by assessing for side-to-side differences between the symptomatic and contralateral leg. Atrophy can be assessed in the seated, standing, or supine position. The use of digital pixel measurements, aided by a browser extension such as Page Ruler Redux (rocha.codes) can be incorporated to detect subtle differences as a percentage relative to the contralateral side (Fig. 1). Vastus medialis oblique (VMO) atrophy has been associated with a variety of patellofemoral disorders [15, 16], and discordant atrophy between the VMO and vastus lateralis has been shown contribute to lateral patellar instability [17]. In patients with patellar maltracking, patellar tilt has been correlated with the differential activation of the vastus lateralis and medialis [18]. VMO inhibition has been noted to occur at smaller volumes than for other quadriceps muscles, resulting in a dynamic quadriceps imbalance [19]. Identification of muscular atrophy can serve as the basis for a targeted rehabilitation protocol. Assessment for hypermobility should be performed using the Beighton scale [20]. During scoring, one point per side is assigned for the ability to extend each fifth metacarpophalangeal joint beyond 90°, to touch each thumb to the forearm with the wrist flexed, to hyperextend each elbow beyond −10°, and to hyperextend

each knee beyond −10°, as well as one point for the ability to place both palms flat on the floor while standing with the knees extended. A score of four or greater indicates hypermobility, which may contribute to instability. A recent study comparing 82 individuals with recurrent patellar dislocation to age- and sex-matched controls found those with a history of patellar dislocations were more likely to have generalized joint laxity (24% vs 10% of controls, P = 0.013) [21]. Among 174 patients who underwent isolated MPFL reconstruction, 55.1% had a positive Beighton score, although this was not found to influence post-operative outcomes [22].

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Lower Extremity Alignment

Assessment of lower extremity alignment is an integral aspect of the patellofemoral exam, as the presence of malalignment can contribute to instability and pain [23]. For assessment of limb alignment and symmetry, the patient should assume a bipedal stance facing the camera with equal distribution of weight between each foot and toes pointing forward (Fig. 2). The presence of “squinting patellae”, where the patellae appear to be internally rotated, can indicate the presence of excessive femoral anteversion or tibial torsion [24]. The Q angle is the angle formed by the intersection of two lines drawn from the anterior

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A Fig. 1 Pixel measurements can aid in side-to-side comparison of muscle bulk and can be described as a percentage. In this image, the patient’s right thigh

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B measures 73 pixels (A) and the left thigh measures 69 pixels, indicating 95% symmetry (B)

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Fig. 2 Standing alignment is assessed from both the frontal (A) and lateral (B) views

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superior iliac spine (ASIS) to the center of the patella and from the center of the patella to the tibial tubercle. Genu valgum, lateralization of the tibial tubercle, increased external tibial torsion, and increased femoral anteversion can increase the Q angle. The relationship between the Q angle and patellofemoral disorders remains controversial [25–31] as it may be influenced by the lack of standardization in how the Q angle is measured. Consequently, Merchant and colleagues proposed a validated protocol for the assessment of a “Standard Q Angle” to improve inter- and intra-observer reliability [32]. During the virtual examination, adaptation of this technique consists of measuring the Q angle using a web-based goniometer with the patient in the standing position facing the camera and the patellae pointing forward. (Fig. 3). The patient

Fig. 3 The Q angle can be measured on the frontal standing view as the angle between a line connecting the anterior superior iliac spine (ASIS) to the midpoint of the patella and another connecting the midpoint of the patella to the tibial tubercle. Asking the patient to place their thumb or index finger on the ASIS enables its identification

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can be asked to place their thumb or index finger on their anterior superior iliac spine to aid in obtaining this measurement. The patient should be instructed to relax their quadriceps muscles prior to measurements being taken. It should be noted that lateral subluxation of the patella may falsely decrease the Q angle measurement. Assessment of hip range of motion can be helpful in detecting rotational abnormalities. Hip internal and external rotation can be measured with the patient seated in a chair facing the camera and the knees flexed to 90° (Fig. 4). The addition of digital lines overlying the image may assist in comparison of leg lengths, while muscular atrophy may again be assessed using comparison of pixel measurements. Careful attention should be paid to noting modifiable asymmetries, which may be addressed through treatment options such as orthotics or tailored rehabilitation programs [6]. An assessment of patellar height, while commonly performed on radiographs, has also been described clinically by noting whether the patella faces superiorly (alta) or inferiorly (baja) while viewing the knees of a seated patient from the front with the knees in 90° of flexion [33] (Fig. 5). Patella alta is an important risk factor for instability as it hinders engagement of the patella in the trochlear groove during early flexion (0–30°), predisposing to lateral subluxation and tilt in extension [34]. While the severity of patella alta is confirmed using radiographic measurements, the presence of patella alta on examination can help identify patients in whom lower extremity malalignment may be contributing to their symptoms [35, 36]. Foot pronation, resulting in internal tibial rotation, can affect dynamic patellofemoral alignment [37] and has been shown to correlate with patellofemoral pain [16, 38, 39]. Barton and colleagues found individuals with PFPS demonstrated significantly greater foot pronation as detected by longitudinal arch angle (effect size, 0.90) and foot posture index (effect size, 0.71) [38]. Foot pronation may be assessed using standing heel position or navicular drop, which are adaptable to the virtual visit. Foot pronation may be quickly assessed using hindfoot valgus

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Fig. 4 During seated range of motion testing, hip internal and external rotation can be measured with the knee at 90° of flexion

with the patient facing away from the camera in the bipedal standing position. To assess navicular drop, the patient can mark the proximal aspect of the navicular tuberosity on the symptomatic leg (Fig. 6). The distance from the mark to the floor should then be measured while the patient is seated in a relaxed position with the foot resting on the floor [39]. For adequate visualization, the chair should be oriented 90° from the camera with the medial aspect of the examined foot facing the camera. The measurement is then repeated in a weightbearing single leg stance, using a chair or wall for balance only. While a ruler or calibrated sheet of paper may serve as a reference to enable more accurate measurements, the proportion of navicular drop may provide an estimate of foot pronation. Assessment of foot pronation utilizing the navicular drop test has been shown to have good inter- and intraobserver reliabilities (ICCs 0.73–0.91 [40];

ICCs > 0.86 [39]) and can identify a modifiable risk factor that can be addressed through the use of an orthotic support.

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Gait

Assessment of gait from the front and back allows for evaluation of antalgia, asymmetry, stride length, patellar orientation, alignment, and pelvic tilt. Assessing 6–8 stride lengths is generally sufficient and can be performed during the virtual encounter, provided the encounter is conducted in an area with adequate floor space [6]. A shortened stance is suggestive of ipsilateral leg pain. Circumduction, which can be assessed on either the frontal or posterior view, may indicate difficulty with knee flexion. Pelvic tilt, on the other hand, suggests contralateral hip abductor weakness, which often results in

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condyles, quadriceps tendon insertion, medial and lateral patellar facets, and the medial and lateral collateral ligaments. Tenderness over the adductor tubercle (“Bassett’s sign”) is suggestive of MPFL disruption at its femoral attachment [43], which can be associated with patellar instability. In their prospective observational study of 23 patients with acute patellar dislocations, Sallay and colleagues noted a sensitivity of 70% for Bassett’s sign [44]. Tenderness may guide providers in prognostication, as well. In their randomized control trial of 112 patients with PFPS, Hott and colleagues found an increased number of pain locations correlated with inferior 1-year outcomes [13].

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Fig. 5 Digital markers placed at the proximal and distal aspects of the patella, as well as at the proximal aspect of the tibial tubercle, can aid in approximation of patellar height

increased IT band tension [16]. In-toeing is suggestive of femoral anteversion, which can contribute to a lateralizing force on the patella due to an external rotation moment at the knee [41].

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Palpation

Physician-guided palpation can be a useful aspect of the virtual examination. Palpation is ideally performed with the patient seated facing the camera with their feet hanging freely [42]. As in the in-person examination, physicians should begin by asking patients to point to the area of their pain with one finger before guiding them through a series of palpation points. Instructions mailed to the patient prior to the visit can provide a helpful visual reference of where to identify such points. Areas to be palpated include the tibial tubercle and patellar tendon, medial and lateral joint lines, medial and lateral femoral

Range of Motion

Virtual range of motion assessments can be performed in either the standing, seated, or supine position. With the patient in the standing position facing the camera, the physician can note hip range of motion in abduction and adduction. From the lateral view, with the patient facing 90° from the camera, the physician can assess the flexion/extension arc of the hip and knee. Knee hyperextension may be assessed by asking the patient to push their knees posteriorly while maintaining a bipedal stance. Patients who have difficulty maintaining their balance may hold on to a chair for stability. Alternatively, the assessment may be performed in both the seated and supine positions. The seated position allows assessment of hip internal and external rotation, hip flexion with upper extremity assistance, knee flexion and extension and evaluation of the presence of an extensor lag. While oriented 90° from the camera, the lateral view may be utilized to visualize knee extension, antigravity strength, and the presence or absence of an extensor lag. Asking the patient to bring the heel in toward the buttock allows for flexion assessment. The lateral supine position allows near full assessment of hip range of motion as the patient ranges the superior hip from maximal flexion sequentially to abduction, extension, and adduction [16].

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A Fig. 6 Navicular drop, a measure of foot pronation, can be assessed by measuring the height of the navicular tuberosity in the unloaded and loaded positions. In these

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Muscle Strength and Functional Testing

Assessment of strength remains a vital aspect of the patellofemoral exam, as quadriceps weakness [15, 45] and hip abduction, external rotation, and extension weakness [46–49] have been demonstrated to be prevalent in patellofemoral disorders. While the virtual exam may be limited in the ability to detect subtle weakness or side-toside differences in strength, particularly in patients whose habitus or range of motion limitations limit participation, antigravity strength remains an important aspect of the physical exam. While knee extension is readily assessed in the seated position, knee flexion (prone), hip flexion (supine straight leg raise), and hip abduction (lateral supine) are best assessed with the patient lying on a couch or bed. Hip

images, navicular height measures 30 pixels in the unloaded position and 23 pixels in the loaded position, indicating a 23% change

extension strength may be assessed by asking the patient to stand from the seated position without utilizing upper extremity support [6] (Fig. 7). Functional assessments of strength, which may lend themselves to the virtual examination, may be more predictive of patellofemoral disorders than manual strength testing [50]. When assessing functional strength, Nunes and colleagues found patients with PFPS climbed stairs more slowly and performed fewer consecutive chair stands (by 12%), which can be assessed during the virtual encounter. Stair climbing may be simulated with step-up-step-down testing. The utility of functional strength assessments is further supported by their high intra-rater reliability and association with variations in pain scales [51]. Numerous specialized tests for the evaluation of functional strength, dynamic alignment/ tracking, and severity of symptoms are easily

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latency in gluteus medius activation, decreased hip abduction torque, and decreased lateral flexion force [52], which may contribute to symptomatology among patients with patellofemoral symptoms [53].

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Fig. 7 Hip extension strength can be tested by having the patient transition from seated to standing without using his or her upper extremities

adaptable to the virtual examination. A simple squat and single-leg knee bend viewed from anteriorly and laterally provide an assessment of functional strength, lower extremity support (core, hip, and quad strength and foot pronation), dynamic patellar tracking, pain, and subjective crepitus. Dynamic valgus alignment of the knee and pelvic tilt can be identified during during this maneuver (Fig. 8). The step-down test, which simulates a single-leg squat similarly allows assessment of balance, eccentric quadriceps strength, dynamic alignment, and support. To perform, the patient can be observed stepping down off a small step first with one leg and then the other. Crossley and colleagues demonstrated good inter- and intra-rater reliability (k = 0.800– 0.600 and k = 0.800–0.613, respectively) when utilizing the step-down test to evaluate hip muscle dysfunction [52]. Providers assessed overall functional movement with respect to

Patellar Tracking

Assessment of patellar tracking is an integral component of any patellofemoral assessment. The J sign represents lateralization of the patella in knee extension, which reduces into the trochlear groove during early knee flexion (Fig. 9). Tanaka and colleagues evaluated the correlation between patellar maltracking identified on dynamic kinematic computed tomography (DKCT) with symptoms of patellar instability among 76 knees [14]. They identified a J sign pattern, with increased lateral translation of the patella in knee extension, among 82% of individuals with patellar instability symptoms, with a sensitivity of 93% among individuals who demonstrated greater than three quadrants of lateral patellar motion in extension. Several studies have evaluated the ability to use video assessment of knee flexion and extension to assess patellar tracking with variable results. Fujita and colleagues utilized video analysis to quantify patellar tracking among 23 knees with prior patellar dislocation, 23 asymptomatic contralateral knees, and 23 healthy controls [54]. Video-based measurements were able to successfully quantify patellar tracking, which was noted to be similar between affected and unaffected knees, as well as significantly different than healthy controls at low flexion angles. Best and colleagues, on the other hand, found orthopaedic surgeons correctly identified patellar maltracking in web-based video assessment of the J sign in only 68% of cases (k = 0.45) when compared with 4DCT [55]. Future advances to improve the precision of J sign assessment may help better identify risk factors and prognoses in the evaluation and treatment of patellar instability [35, 56–58].

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Fig. 8 Frontal and lateral views of the patient performing a single-leg squat can provide information regarding lower extremity strength by evaluating for changes in coronal and sagittal alignment

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Fig. 9 Patellar tracking can be assessed in the frontal plane by having the patient extend (A) and flex (B and C) the knee. The J sign is observed when the patellar

C displaces laterally in extension and can be quantified by quadrants of patellar motion

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Patellar Apprehension

The patellar apprehension test was first described by Fairbank in 1937, in which patients exhibited apprehension when a laterally-directed force was applied to the patella [59]. A positive result occurs when there is verbal or non-verbal (e.g. quadriceps contraction) expression of apprehension. Notably, expression of pain does not constitute a positive test. Although the test has been shown to have limited sensitivity (