Clinical-MRI Correlations of Anterior Knee Pain: Common and Uncommon Causes 3031399587, 9783031399589

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Clinical-MRI Correlations of Anterior Knee Pain Common and Uncommon Causes Ioan I. Codorean Ion Bogdan Codorean

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Clinical-MRI Correlations of Anterior Knee Pain

Ioan I. Codorean • Ion Bogdan Codorean

Clinical-MRI Correlations of Anterior Knee Pain Common and Uncommon Causes

Ioan I. Codorean Hyperclinica Medlife Grivita Bucharest, Romania

Ion Bogdan Codorean Artro Sport Clinic Bucharest, Romania

ISBN 978-3-031-39958-9    ISBN 978-3-031-39959-6 (eBook) https://doi.org/10.1007/978-3-031-39959-6 © 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 translation, 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 Paper in this product is recyclable.

We dedicate this book to the late Romanian-American Professor Emeritus Gheorghe Mateescu (1928–2021) from Case Western Reserve University, Cleveland, Ohio, USA for his significant contribution to the promoting and developing magnetic resonance imaging in Romania. Professor Gheorghe Mateescu initiated the 5-day international Magnetic Resonance Course The Summer School of Magnetic Resonance Imaging and Spectroscopy – from Principles to Advanced Application, which took place in Romania for an extended period (1995–2008). At these annual international courses, 84 World Magnetic Resonance personalities from the most renowned universities have been part of the teaching team, including two Nobel Prize laureates, Paul C. Lauterbur and Richard Ernst.

Preface

The book Clinical-MRI Correlations of Anterior Knee Pain—Common and Uncommon Causes is the result of a collaboration between a radiologist and an orthopedic surgeon who have worked closely together in this field for over 15 years, accumulating a wealth of clinical and imaging studies, materially focused on MRI.  The book’s title reflects the challenge in diagnosing and managing anterior knee pain, which can affect individuals of all age groups and presents a nonspecific clinical picture. MRI is widely recognized as the gold standard for investigating such cases, as it allows visualization of the normal or pathological appearance of every anatomical structure in the knee joint that could be the source of pain. Each MRI image presented in the book corresponds to a patient who underwent a clinical and imaging examination performed by the two authors. For a good organization of the book, we chose to present the anatomical structures of the anterior compartment from superficial to deep, respectively, vii

Preface

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from the pre-patellar extracapsular soft tissues to profound articular structures, which include the synovial lining and the patellar and trochlear cartilage. Thus, we have structured the book in the following nine chapters, from the pre-patellar soft tissues—Chap. 3 to the deep articular structures—Chap. 8. Chapter 1 presents the clinical examination of the patient with anterior knee pain and Chap. 2 covers clinical conditions causing anterior knee pain. Chapter 4 presents the pathology of the quadriceps tendon, Chap. 5patella, and Chap. 6—patellar tendon and tibial tubercle. All these three chapters present and illustrate by MRI a broad spectrum of diseases developed from the components of the extensor mechanism of the knee. Chapter 7 presents and shows MRI pathological conditions that develop from intracapsular and extrasynovial peripatellar fat pads. Chapter 8 looks at the deep intra-­ articular structures, associated with anterior knee pain, such as the synovial lining, patellar and trochlear cartilage. This chapter illustrates MRI in some 103 figures with 181 magnetic resonance images. In Chapter 9, we selected representative clinical cases for each age group related to the unique pathological substrate or associated with other conditions, which were clinically expressed by anterior knee pain. The cases are divided into four age groups, with 20 cases for each: children and adolescents 10–18 years, early adulthood 18–30 years, adulthood 30–50 years, and older adulthood > 50 years (80 cases with 375 MR images). The book has approx. 455 pages, 500 figures, and over 1000 MR images. We acquired all published MR images with 3T equipment at the Hyperclinica MedLife Grivita Bucharest, Romania. The authors’ primary aim is to benefit resident radiologists, specialists in MRI, orthopedic surgeons, sports medicine specialists, physiotherapists, and clinicians interested in knee joint pathology with this richly illustrated book on MRI. Bucharest, Romania Bucharest, Romania 

Ioan I. Codorean Ion Bogdan Codorean

Acknowledgments

We would like to thank and express our deep gratitude to Emeritus Professor and Chairman of Radiology Radu Manoliu, Amsterdam Medical Center, for his constant encouragement and attention to detail, from the initiation of our project to its completion. His advice and suggestions were truly beneficial for scientific support. As authors of our first book published by Springer, with no prior experience at this level, we extend our special thanks and heartfelt gratitude to the editorial team who published our book—Antonella Cerri, NandiniPriya Mohanasundaram, Joshi Raja Rathnam, and Vera Deuerling. It was a productive collaboration between the editorial team and the authors. Finally, we would like to thank our families for their support and patience throughout the process of writing this book.

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Contents

1 Clinical  Examination of the Patient with Anterior Knee Pain����   1 1.1 Introduction������������������������������������������������������������������������������   1 1.2 Patient’s History������������������������������������������������������������������������   1 1.3 Physical Examination of the Knee��������������������������������������������   3 1.3.1 Inspection����������������������������������������������������������������������   3 1.3.2 Palpation ����������������������������������������������������������������������   8 1.4 Specific Stress Tests������������������������������������������������������������������   9 1.4.1 Tests for the Medial and Lateral Collateral Ligaments (MLCL)������������������������������������������������������  10 1.4.2 Tests for Meniscal Injuries��������������������������������������������  11 1.4.3 Tests for Patellofemoral Disorders��������������������������������  12 References������������������������������������������������������������������������������������������  16 2 Condition  Causing Anterior Knee Pain ����������������������������������������  21 2.1 Patellofemoral Pain ������������������������������������������������������������������  21 2.1.1 Introduction Patellofemoral Pain����������������������������������  21 2.1.2 Terminology and Defining of PFP��������������������������������  21 2.1.3 Clinical Presentation ����������������������������������������������������  22 2.1.4 Physical Performance Measures ����������������������������������  23 2.2 Patellar Instability ��������������������������������������������������������������������  24 2.2.1 Introduction������������������������������������������������������������������  24 2.2.2 Anatomic Structures and Abnormal Biomechanics of the Patellofemoral Joint Involved in Patellar Instability��������������������������������������  24 2.2.3 Classification of Patellar Instability������������������������������  26 2.2.4 Clinical Evaluation��������������������������������������������������������  26 2.3 Patellofemoral Osteoarthritis (PFOA)��������������������������������������  27 2.3.1 Introduction������������������������������������������������������������������  27 2.3.2 Risk Factors Associated with Patellofemoral OA��������  28 2.3.3 Patellofemoral Pain and Patellofemoral Osteoarthritis����������������������������������������������������������������  28 2.3.4 Clinical Presentation of PFOA��������������������������������������  29 2.4 Patellar Tendinopathy “Jumper’s Knee” ����������������������������������  30 2.4.1 Introduction������������������������������������������������������������������  30 2.4.2 History and Physical Examination��������������������������������  30 2.4.3 Differential Diagnosis ��������������������������������������������������  32

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2.5 Lateral Patellar Compression Syndrome����������������������������������  32 2.5.1 Introduction������������������������������������������������������������������  32 2.5.2 Anatomic and Biomechanical Abnormalities ��������������  32 2.5.3 Clinical Presentation ����������������������������������������������������  33 2.6 Synovial Plica Syndrome����������������������������������������������������������  33 2.6.1 Introduction������������������������������������������������������������������  33 2.6.2 Pathophysiology������������������������������������������������������������  34 2.6.3 Clinical Presentation ����������������������������������������������������  34 2.7 Sinding-Larsen-Johansson Syndrome��������������������������������������  35 2.7.1 Introduction������������������������������������������������������������������  35 2.7.2 Pathophysiology������������������������������������������������������������  35 2.7.3 Risk Factors������������������������������������������������������������������  35 2.7.4 Clinical Presentation ����������������������������������������������������  36 2.7.5 Differential Diagnosis ��������������������������������������������������  36 2.8 Osgood–Schlatter’s Disease (OSD)������������������������������������������  36 2.8.1 Introduction������������������������������������������������������������������  36 2.8.2 Pathophysiology������������������������������������������������������������  37 2.8.3 Risk Factors������������������������������������������������������������������  37 2.8.4 Clinical Presentation ����������������������������������������������������  37 2.8.5 Differential Diagnosis ��������������������������������������������������  38 2.9 Juvenile Osteochondritis Dissecans (JOCD)����������������������������  38 2.9.1 Introduction������������������������������������������������������������������  38 2.9.2 Etiology������������������������������������������������������������������������  38 2.9.3 Clinical Presentation ����������������������������������������������������  39 2.10 Hoffa Syndrome������������������������������������������������������������������������  40 2.10.1 Introduction������������������������������������������������������������������  40 2.10.2 Anatomic and Biological Characteristics of IPFP��������  40 2.10.3 Pathophysiology������������������������������������������������������������  41 2.10.4 Physical Examination���������������������������������������������������  41 2.10.5 Clinical Diagnosis��������������������������������������������������������  41 2.11 Superficial Patellar Bursitis������������������������������������������������������  42 2.11.1 Introduction������������������������������������������������������������������  42 2.11.2 Normal Anatomy����������������������������������������������������������  42 2.11.3 Pathophysiology������������������������������������������������������������  42 2.11.4 Clinical Presentation ����������������������������������������������������  43 2.12 Patellar Fractures����������������������������������������������������������������������  44 2.12.1 Introduction������������������������������������������������������������������  44 2.12.2 Anatomy and Biomechanics ����������������������������������������  44 2.12.3 Mechanism of Injury and Classification of Patellar Fractures������������������������������������������������������  44 2.12.4 Clinical Presentation ����������������������������������������������������  45 2.13 Symptomatic Bipartite��������������������������������������������������������������  46 2.13.1 Introduction������������������������������������������������������������������  46 2.13.2 Classification����������������������������������������������������������������  46 2.13.3 Pathophysiology������������������������������������������������������������  46 2.13.4 Causes of Pain��������������������������������������������������������������  46 2.13.5 Clinical Presentation ����������������������������������������������������  47

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2.14 Idiopathic Anterior Knee Pain��������������������������������������������������  47 2.14.1 Introduction������������������������������������������������������������������  47 2.14.2 Clinical Presentation ����������������������������������������������������  47 References������������������������������������������������������������������������������������������  48 3 MRI  Findings of Superficial Prepatellar Soft Tissues������������������  59 3.1 Introduction������������������������������������������������������������������������������  59 3.2 Superficial Prepatellar Bursae��������������������������������������������������  59 3.2.1 Superficial Prepatellar Bursitis ������������������������������������  59 3.2.2 Superficial Infrapatellar Bursitis ����������������������������������  61 3.3 Prepatellar Morel-Lavallée Lesion��������������������������������������������  67 3.3.1 Pathologic and Anatomic Features��������������������������������  67 3.3.2 Clinical Presentation ����������������������������������������������������  68 3.3.3 Diagnostic Imaging������������������������������������������������������  69 3.3.4 MRI Classification of MLL������������������������������������������  70 3.3.5 Differential Diagnoses��������������������������������������������������  72 3.4 Prepatellar Subcutaneous Fat����������������������������������������������������  72 3.4.1 Pseudo-Bursitis ������������������������������������������������������������  73 References������������������������������������������������������������������������������������������  75 4 Quadriceps Tendon��������������������������������������������������������������������������  77 4.1 Introduction������������������������������������������������������������������������������  77 4.2 Normal MRI Anatomy of the Quadriceps Tendon��������������������  77 4.3 MRI Pathological Findings of Quadriceps Tendon Injuries ����  83 4.3.1 Complete Ruptures of the Quadriceps Tendon ������������  84 4.4 Incomplete Ruptures of the Quadriceps Tendon����������������������  86 4.5 Quadriceps Tendinopathy ��������������������������������������������������������  89 4.5.1 Summary ����������������������������������������������������������������������  89 References������������������������������������������������������������������������������������������  90 5 Patella������������������������������������������������������������������������������������������������  93 5.1 Introduction������������������������������������������������������������������������������  93 5.2 MRI Anatomy Normal Appearance������������������������������������������  93 5.2.1 Osseous Anatomy���������������������������������������������������������  93 5.2.2 Soft Tissue Anatomy����������������������������������������������������  98 5.3 MRI Patellar Measurements ���������������������������������������������������� 102 5.3.1 MRI Measurements of Patellar Height in the Sagittal Plane������������������������������������������������������ 102 5.3.2 MRI Measurements of Patellar Position in the Axial Plane���������������������������������������������������������� 110 5.4 Acute Patellar Dislocation/Subluxation, MRI Findings ���������� 115 5.4.1 Introduction������������������������������������������������������������������ 115 5.4.2 Patellofemoral Stabilizers �������������������������������������������� 116 5.4.3 Specific Anatomical Risk Factors for Knee Instability/Dislocation�������������������������������������������������� 117 5.4.4 Injury Mechanism of APD�������������������������������������������� 121 5.4.5 Clinical Examination of APD �������������������������������������� 121 5.4.6 MRI Findings After Acute Patellar Dislocation������������ 121

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5.5 Recurrent Lateral Patellar Dislocation�������������������������������������� 132 5.5.1 Predisposing Factors of Recurrent Patellar Dislocation�������������������������������������������������������������������� 132 5.5.2 MR Imaging Findings After Recurrent Patellar Dislocation������������������������������������������������������ 134 5.6 Patellar Contusion and Fracture������������������������������������������������ 143 5.6.1 Mechanism of Injury of Patellar Fractures ������������������ 143 5.6.2 Clinical and Imagistic Evaluation�������������������������������� 144 5.6.3 Types of Patellar Fractures: MRI Illustration �������������� 144 5.7 Bipartite Patella������������������������������������������������������������������������ 157 5.7.1 Clinical Features and Classification of Bipartite���������� 157 5.7.2 MR Findings Associated with an Asymptomatic Bipartite Patella������������������������������������������������������������ 158 5.8 Dorsal Defect of the Patella������������������������������������������������������ 159 References������������������������������������������������������������������������������������������ 162 6 Patellar  Tendon and Tibial Tubercle���������������������������������������������� 169 6.1 Introduction������������������������������������������������������������������������������ 169 6.2 Normal MRI Anatomy of Patellar Tendon�������������������������������� 169 6.3 MRI Pathological Findings of Patellar Tendon������������������������ 170 6.3.1 Patellar Tendinopathy �������������������������������������������������� 170 6.3.2 Sinding-Larsen-Johansson Syndrome and Patellar Sleeve Fractures���������������������������������������� 175 6.4 Patellar Tendon Rupture������������������������������������������������������������ 184 6.4.1 Classification and MRI Appearance����������������������������� 184 6.5 Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures�������������������������������������������������������������������� 190 6.5.1 Pathophysiology and MRI Findings ���������������������������� 190 References������������������������������������������������������������������������������������������ 200 7 Intracapsular  and Extra Synovial Peripatellar Fat Pads������������ 203 7.1 Introduction������������������������������������������������������������������������������ 203 7.2 Normal MRI Anatomy and Physiology of Peripatellar Fat Pad�������������������������������������������������������������������������������������� 204 7.2.1 Infrapatellar Fat Pad (Hoffa’s Fat Pad—HFP)�������������� 204 7.2.2 Suprapatellar Fat Pad���������������������������������������������������� 207 7.3 MRI Pathological Findings of Infrapatellar Fat Pad ���������������� 208 7.3.1 Intrinsic Pathology of Infrapatellar Fat Pad������������������ 208 7.3.2 Extrinsic Pathology of Infrapatellar Fat Pad���������������� 222 7.4 MRI Pathological Findings of Suprapatellar Fat Pad �������������� 234 7.4.1 MRI Pathological Findings of Anterior (Quadriceps) Suprapatellar Fat Pad Quadriceps Fat Pad Lesion�������������������������������������������������������������� 235 7.4.2 MRI Pathological Findings of Suprapatellar Posterior Prefemoral Fat Pad���������������������������������������� 238 References������������������������������������������������������������������������������������������ 241

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8 Intra-articular  Structures, the Synovial Lining, Patellofemoral Osteoarthritis �������������������������������������������������������� 245 8.1 Introduction������������������������������������������������������������������������������ 245 8.2 MRI Compartments������������������������������������������������������������������ 245 8.2.1 Central Compartment���������������������������������������������������� 245 8.2.2 Suprapatellar Pouch������������������������������������������������������ 247 8.2.3 Posterior Femoral Recesses������������������������������������������ 247 8.3 Synovial Plicae of the Knee������������������������������������������������������ 253 8.3.1 Embryology and Anatomy�������������������������������������������� 253 8.3.2 Classification and Imaging Appearance of Synovial Plicae of the Knee Joint���������������������������� 253 8.4 Pigmented Villonodular Synovitis�������������������������������������������� 281 8.4.1 Clinical Characteristics ������������������������������������������������ 282 8.4.2 Diagnosis of PVNS ������������������������������������������������������ 283 8.5 MRI of Synovial Chondromatosis�������������������������������������������� 288 8.5.1 Epidemiology and Pathogenesis ���������������������������������� 289 8.5.2 Clinical Characteristics ������������������������������������������������ 292 8.5.3 MRI Imaging Characteristics���������������������������������������� 293 8.6 Patellofemoral Joint Osteoarthritis ������������������������������������������ 293 8.6.1 Biomechanics of the PFJOA ���������������������������������������� 294 8.6.2 Clinical Manifestation�������������������������������������������������� 302 8.6.3 MRI Assessment of Patellofemoral Joint Osteoarthritis���������������������������������������������������������������� 302 References������������������������������������������������������������������������������������������ 307 9 Clinical-MRI  Cases Selected by Age Group���������������������������������� 313 9.1 Children and Adolescents (10–18 Years)—20 Cases���������������� 313 9.2 Early Adulthood (18–30 Years)—20 Cases������������������������������ 330 9.3 Adulthood (30–50 Years)—20 Cases���������������������������������������� 344 9.4 Older Adult Hood (>50 Years)—20 Cases�������������������������������� 357

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Clinical Examination of the Patient with Anterior Knee Pain

1.1 Introduction

1.2 Patient’s History

Anterior knee pain (AKP) may result from a single traumatic event or, more commonly, repetitive overuse. Potential pain sources include a wide range of knee pain etiologies, ranging from the acute pain of a patellar dislocation to the more chronic, indolent pain of OsgoodSchlatter’s disease, or can be transmitted from structures located at a distance from the knee nerve-­ mediated abnormalities, of the lumbar spine or hip [1, 2]. Profound knowledge of anatomy, painful structures, and patellofemoral biomechanics is essential to finding the underlying pathology within heterogeneous and diverse etiologies. Patients with anterior knee pain often report pain during weight-bearing activities that involve significant knee flexion, such as squatting, running, jumping, and walking up stairs. A detailed history and a meticulous and precise clinical examination are key to detecting the painful and deficient structures, the associated anatomical risk factors, and functional deficits to make the correct diagnosis and decide on the ideal treatment. This chapter will describe some of the tests commonly used to diagnose AKP. The goal is to accurately diagnose and treat this common orthopedic, rehabilitation, and sports medicine disorder.

Patients may complain of anterior knee pain and patellar instability. Pain related to extensor mechanism (patellofemoral) problems are typically exacerbated by climbing or descending stairs and other activities requiring strong quadriceps contraction [3]. Descending stairs requiring a coordinated eccentric contraction to lower one’s body weight to the next stair is particularly painful for many patients with patellofemoral disorders and quadriceps insufficiency [4]. Stair climbing requires more concentric quadriceps contraction to provide knee extension lifting the body up and forward. A strenuous eccentric or concentric extensor mechanism challenge can produce musculotendinous overload and pain in an otherwise “normal” knee if adequate flexibility and strength are not present [5, 6]. Prolonged periods of knee flexion, such as long car rides or watching a movie, can also cause pain in the anterior knee area. The reason prolonged flexion causes pain is uncertain but may be related to additional tension in sensitive peripatellar soft tissues and onto deficient patellofemoral cartilage when the knee is held in flexion [5]. Important elements of the history include distinguishing between acute and chronic knee pain, identifying any trauma that may have caused the knee pain, learning the mechanism of injury if trauma was involved, and understanding what

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_1

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1  Clinical Examination of the Patient with Anterior Knee Pain

activities the patient participates in that may contribute to their symptom [1, 7]. Acute highenergy injuries disrupt normal soft-tissue restraints and musculotendinous units or cause bony injury. Acute injuries generally fall into two categories: those involving indirect trauma and those involving blunt trauma [7]. Highenergy indirect forces can cause acute patellar dislocation/subluxation in athletes during valgus/external rotation injuries. A typical example of high-energy blunt trauma is an automobile accident in which the anterior knee strikes the dashboard [7]. Patients with insidious onset of symptoms or low-energy injuries should be considered especially likely to have overuse injury or underlying patellar malalignment, and the examination should focus on bony and soft tissue malalignment factors [8]. Tissue overload may occur in peripatellar soft tissues or in the patella itself, depending on the type of activity and the areas of relative weakness or inflexibility. Although anatomic malalignment may be present in overuse patients and might even predispose some knees to overload, even normally aligned knees can be plagued by overuse pain syndromes [5]. Although the examiner can rely on physical examination to differentiate involved structures and alignment and make an accurate diagnosis, the history must be probed for correctable causes of overuse injury [7]. The center of the patella, as a reference point, the anterior region of the knee can be divided into several locations corresponding to the peripatellar structures for a more precise source of pain [9] (Fig. 1.1). The bony patella, the underlying cartilage, and the overlying skin comprise the first region. The superior structures, such as the superior pole of the patella and the quadriceps tendon, form the second region. The inferior structures, such as the inferior pole of the patella, patellar tendon, and tibial tubercle, form the third. The medial structures, including the medial retinaculum, pes anserinus (hamstring tendon insertion), and medial patellofemoral ligament, comprise the fourth. Lastly, the lateral structures, such as the

Fig. 1.1  Key points of palpation around the knee include (1) quadriceps tendon [QT]. (2) superior pole of the patella [SPP]. (3) Patellar body [PB]. (4) Inferior pole of the patella [IPP]. (5) Patellar tendon [PT]. (6) Tibial tubercle [TT]. (7) Medial joint line [ML]. (8) Medial retinaculum [MR]. (9) Lateral joint line [LJL], and (10) Lateral retinaculum

lateral retinaculum, lateral patellar facet, and iliotibial band, form the fifth region [1]. When asked to localize the pain, patients often place their entire hand over the front of the knee. In these cases, it may help to have the patient point to one area that bothers him or her most. The patient should be asked to characterize the pain in simple terms. Constant, dull pain can be a sign of referred or sympathetic-mediated pain [10]. Referred pain from the hip may be suspected if there is decreased hip range of motion (ROM) and difficulty performing tasks such as putting on and taking off one’s shoes. Referred pain from the lumbar spine should be suspected if back pain radiates into the buttocks/posterior thigh region or is accompanied by lower extremity numbness or weakness [1]. Sharp, intermittent pain may be due to loose bodies or cartilage flaps in the joint, which can also be associated with locking and catching. Locking episodes

1.3 Physical Examination of the Knee

may be associated with swelling and severe pain; however, patients may be entirely asymptomatic between episodes [11]. Activity-related pain is usually caused by soft tissue/bone overload exacerbated by increased activity. Pain caused specifically by kneeling, crawling, going up and down stairs, and prolonged knee flexion can signify patellofemoral overload or malalignment. This pain is generally relieved with periods of rest and inactivity [3]. Also, ask about previous operations, which can lead to malalignment or patella Baja due to infrapatellar scarring [12]. Furthermore, pain-­ triggering factors need to be enquired about [13]. Postural AKP, while in a flexed position for a longer period and having to extend the knee from time to time for pain relief, is suspicious for pathology to the extensor mechanism and not to the femorotibial joint [14]. Pain while jumping, running, ascending, and descending steps may indicate tendinopathy [9, 15]. Ask for “giving-­ way” sensations [16]. This is a sudden feeling of subjective instability of the knee, which can be associated with pain. Painless “giving-way” can be associated with a transient patellar malposition or subluxation, a trapped synovial plica, an unstable cartilage flap, or any other ligamentous or meniscal instability of the femorotibial joint [17, 18]. Rotational movements leading to “giving way” is more common with ACL insufficiency or meniscal injuries than with patellofemoral issues. Therefore, investigating AKP always requires an understanding of potential underlying femorotibial pathologies [7]. Before assuming a mechanical patellofemoral diagnosis, the clinician will ensure that the patient does not have a fever, chills, redness, or swelling that could represent an infection [12]. The patient should be asked about other joint involvement that might represent systemic or rheumatologic disease. Pain that is worst at night or when the patient wakes can be a sign of infection, neoplasm, or prepatellar bursitis and warrants further evaluation [1]. Night pain is a classic red-flag symptom that should alert the clinician to the possible diagnosis of a tumor [9].

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1.3 Physical Examination of the Knee When the knee is evaluated, the sequence should involve inspection, active and passive range of motion (ROM) assessment, palpation, and special tests. The uninvolved knee should be evaluated first to establish a baseline “normal” for the patient before the involved extremity is examined.

1.3.1 Inspection The clinician begins the inspection by looking for obvious deformities, discoloration, swelling, or scars. Abnormal protuberances, ecchymosis, joint effusion, or edema should be noted in or around the knee [19]. Scars may be from a history of trauma or surgery. The examination will progress from standing to seated to supine.

1.3.1.1 Standing Examination The upright portion of the patellofemoral examination consists of static observation in addition to dynamic observation during squats and gait [9]. The subject must change into shorts that do not cover the knees and remove socks and shoes to aid in the examination. The latter is key to assessing foot alignment (particularly looking for pes planus), which has been directly related to knee pain in some patients. The knee should be inspected for a prepatellar or intra-articular effusion. An effusion of the prepatellar bursa is anterior to the patella; with an intra-articular effusion, the patella remains palpable subcutaneously. On inspection, a true knee joint effusion is often best appreciated in the suprapatellar pouch. The effusion can be “milked” from the supra-patellar pouch with one hand while the other hand palpates the effusion (Fig. 1.2). Compared with the contralateral knee, the injured knee may fail to reach full passive extension, indicating a mechanical block or hamstring spasm. Limited ROM is expected with large knee effusions or pain. Although full ROM is required for a complete knee examination, it is not always possible at the first visit and should not be forced.

1  Clinical Examination of the Patient with Anterior Knee Pain

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A short course of physical therapy with reexamination in several days to 1 week can be helpful [20]. The medial and lateral patellar facets can be

palpated while assessing for the apprehension sign. Then the medial and lateral joint lines should be palpated and the remainder of the examination performed, including specific tests for ligaments and menisci. Any test that is expected to cause pain should be done last [20]. Finally, it is important to remember that pain felt in the knee may be referred from other locations, including the spine and the hip. A careful history can help differentiate referred spinal pain. Routine examination of the hip and spine is recommended when evaluating knee pain, with particular attention paid to the loss of hip rotation. A general standing examination should be evaluated in the three basic cardinal planes. Each plane has certain unique aspects that should be examined to ensure the clinician has a good understanding of structural or functional adaptations or compensations that may be a source of AKP symptoms. Postural Anterior/Posterior Frontal Plane Alignment. A varus or valgus knee posture can Fig. 1.2  The effusion can be “milked” from the supra-­ patellar pouch with one hand while the other hand pal- usually be seen clearly in the anterior coronal plane view (Fig. 1.3a, b). pates the effusion a

b

Fig. 1.3  An anterior view assesses a varus angulation of the right knee (image a) and valgus angulation (image b)

1.3 Physical Examination of the Knee

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A reduction of the normal inclination of the femoral neck and femoral shaft (coxa vara) will create a genu valgus at the knee, while an increase in the normal angle (coxa valga) will create a genu varus at the knee. The patella position should also be evaluated to determine its position relative to internal or external rotation. The patellar position relative to the proximal tibia should be assessed for a bayonet sign or excessive external tibial torsion. The tibial alignment for the tibia varum should also be assessed, realizing that some distal tibia varum is normal. Traditionally, alignment at the knee is quantified by the Q-angle, which is the angle formed between a line from the anterosuperior iliac spine (ASIS) to the patella and another from the patella to the middle of the anterior tibial tuberosity. The foot should be evaluated from the anterior view to check for forefoot dysfunction, midtarsal joint position (using the Navicular Drop test, Feiss’ Line, or Medial longitudinal arch angle) and from the posterior view to check the weight-­ bearing subtalar joint position [19] (Fig. 1.4).

The lateral view is best to observe for either genu recurvatum or flexion contracture. Excessive genu recurvatum can create Hoffa’s syndrome due to impingement of the infrapatellar fat pad and the inferior pole of the patella. Quadriceps weakness due to either strength loss or inhibition may present as knee hyperextension. Flexion contracture results from loss of knee extension range of motion and can be caused by motion limitations post-surgery, trauma, injury, or excessive hamstring tightness [9]. This view also allows a clinical assessment of a patella Alta or Baja (Fig. 1.5). Additionally, this view permits an assessment of a camel sign of the knee, which may be normal or contribute to Hoffa’s syndrome [19]. After completing the static assessment, the patellofemoral joint must be observed dynamically. This evaluation is usually accomplished with single and double-leg squats in addition to observation of gait. Malalignment during squats can indicate weakness in the gluteus (core) or quadriceps (particularly vastus medialis obliquus) muscles and may be exacerbated by poor motor control in the ankle. Previous studies have shown that patients with poor dynamic muscle control

Fig. 1.4  Posterior view can be used to assess valgus/ varus angulation of the knee and to assess forefoot, mid-­ tarsal, andsubtalar joint

Fig. 1.5  A lateral view can be used to assess for genu recurvatum, knee flexion contracture, and patella Alta or Baja

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1  Clinical Examination of the Patient with Anterior Knee Pain

tend to have a pelvic drop, hip adduction, hip internal rotation, knee abduction, external tibial rotation, and ankle hyperpronation, which in turn has been associated with patellofemoral syndrome (PTFS) [21, 22]. Although quadriceps weakness has traditionally been associated with PTFS, weakness of the hip abductors and external rotators may play an even more important role [23]. Hamstring tightness has also been implicated [24]. While observing the patella itself, close attention should be paid to actual patellar tracking, looking specifically for the presence of a J-sign. This finding exemplifies that when the knee is flexed, the patella is forced centrally to track the trochlea from the femur. As the knee approaches full extension, the centralizing forces have a less mechanical advantage, and a patella prone to track laterally will jump out of the groove and move laterally nearer full extension [25]. Palpation of the patella during dynamic squatting may reveal crepitus and grinding, indicating the underlying patellofemoral arthrosis or chondromalacia. Gait analysis is the final phase of dynamic patellofemoral assessment in the upright patient. An assessment of gait should be performed, looking for varus or valgus, quadriceps avoidance, and antalgic gaits. Substantial primary varus or valgus deformity may be the result of single-­ compartment osteoarthritis. With quadriceps avoidance, the patient bears weight with a knee locked in extension because of either a weakened extensor mechanism or pain. An antalgic gait can result from any condition causing knee pain. Next, an assessment of standing limb alignment should be performed, taking note of specifics, such as pes planus and excessive femoral anteversion, which can contribute to patellofemoral tracking problems. Excessive femoral anteversion may be identified by an inward-pointing or squinting (or winking) patella [20]. Also, the patient should be inspected from both anterior and posterior views while walking forward, backward, on the heels, and the toes along a stable flat surface. The latter two portions of the gait analysis are a simple assessment of general lower extremity function. Assessing gait

while walking backward is an effective way to assess patient compliance because it is difficult to fake a limp walking backward. The most important part of the gait analysis is inspecting the gait while looking from the front and back of the patient [9].

1.3.1.2 Seated Examination The patient is then examined in a seated position with the knees flexed over the table. The knee should again be observed for any abnormalities. Any skin changes and significant swelling compared to the asymptomatic limb should be noted. Differences in quadriceps muscle bulk, the vastus medialis (VMO) in particular, can often be seen at this point. The VMO has been shown to play an important role in patellar stabilization [26, 27]. It is important to observe the position of the patella in the seated position. If the patella is tilted laterally, giving it a “grasshopper-eye” appearance may indicate laterally directed forces on the patella [9, 19, 20]. Patellar height may be best observed from the side. Normally, the proximal aspect of the patella should line up with the anterior cortex of the distal femur in a seated position. An abnormally low patella, or patella Baja, may represent a quadriceps tendon rupture [28]. In addition, patients with congenital patella Alta may be at increased risk of patellar subluxation, owing to the increased time necessary for the patella to engage with the trochlea in knee flexion. The angle between the tibial tubercle and the patella (bent knee Q-angle) should also be observed. In normal individuals, this angle averages 4°, but larger angles suggest external tibial torsion, which can contribute to patellar maltracking [29]. During the next step of the physical examination, the knee’s passive and active range of motion should be measured and compared with that on the contralateral side. A decrease in the passive range of motion may be related to an intra-articular abnormality or may be due to tightness of any muscle groups that cross the knee joint [20]. A decrease in active extension compared to passive extension, also known as an extensor lag, may represent the disruption of the extensor mechanism or motor weakness. Often

1.3 Physical Examination of the Knee

any significant injury to the knee may cause a decrease in active extension secondary to pain. In this situation, an intra-articular anesthetic injection may assist in clarifying the true cause of the lack of full active extension [9]. During the active range of motion, the patella should again be observed for any sudden lateral movement as it exits the trochlea, also known as the J-sign. It is suggested that the examiner place a hand over the patella during active range of motion to assess for patellofemoral crepitus or a grinding sensation. Johnson and colleagues found that 40% of asymptomatic female patients had patellofemoral crepitus with range of motion [29]. Quadriceps and hamstring strength may be tested by having the patient extend and flex the knee against resistance, and this should be compared with the contralateral side.

1.3.1.3 Supine Examination The uninjured knee should be examined first because it relaxes the patient and helps the examination not cause pain while accounting for individual variations between the uninjured and the contralateral knee. Relaxation of the hip and the knee facilitates the examinations of passive movement and instability. All joints proximal and distal to the knee that can refer to or influence functioning at the knee should be assessed. The lumbar spine, sacroiliac joint, hip joint, proximal tibiofibular joint, ankle, and subtalar joints should be checked. Various methods to clear the joints can be used, such as active range of motion (AROM), passive range of motion (PROM), resistive range of motion (RROM), or special tests of the respective areas. The musculature, particularly the quadriceps, should be inspected for atrophy. In addition, the patella should be assessed for malalignment, which may predispose the patient to maltracking or patellar dislocation. Any localized swelling and masses, including swelling of the prepatellar bursa, a meniscal cyst, and Osgood-Schlatter disease of the tibial tubercle, should be noted. Swelling of the distal femur or proximal tibia may indicate a neoplasm or infection [20]. ROM should be assessed, first with active motion and then with gentle passive motion if

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necessary. Compared with the contralateral knee, the injured knee may fail to reach full passive extension, indicating a mechanical block or hamstring spasm. Limited ROM is expected with large knee effusions or pain. Although full ROM is required for a complete knee examination, it is not always possible at the first visit and should not be forced. A short course of physical therapy with reexamination in several days to 1 week can be helpful [20]. An effusion combined with joint line tenderness (JLT) is one of the most sensitive and reliable signs of a meniscal tear [30]. Evaluate the knee joint for effusion by milking the suprapatellar pouch with one hand and checking to see if the patella is ballotable with the other hand (Fig. 1.6). Peripatellar tissues should not be touched during compression. Compress the patella at various flexion angles from full extension to full flexion. Beware of patients with prepatellar bursitis that may cause pain with this test. Hold the hand over each patella during active and passive knee flexion observing for crepitus and pain. In patients with patellofemoral pathology, effusion suggests

Fig. 1.6  Effusion test

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1  Clinical Examination of the Patient with Anterior Knee Pain

moderate to severe patellofemoral arthrosis, osteochondral or chondral loose bodies, or severe plica inflammation. Joint effusion causes reflex quadriceps inhibition [20]. As little as 15 ccs of fluid injected into normal knees has been shown to produce marked reflex inhibition [31]. The threshold for VMO inhibition is approximately 20–30 cc of intra-articular fluid compared to the 50–60  cc required to inhibit the rectus femoris and the vastus lateralis [31]. Thus, asymmetrical inhibition may result in some dynamic malalignment effusion. With the patient relaxed, the range of motion should again be assessed with special attention to patella tracking during flexion and extension. When the patella tracks laterally during terminal knee extension, this is referred to as a “J-sign” and is indicative of patellar malalignment [32]. The Q-angle can be measured in full extension, with slight flexion, and at 90° of flexion.

1.3.1.4 Side-Lying Examination In the side-lying position, with the knee flexed at 20°, the lateral retinaculum can be evaluated for excessive tightness by passively moving the patella in a medial direction [33]. The superficial retinacular fibers are considered tight if the femoral condyle is not easily exposed. To test the deep fibers, the hand is placed on the middle of the patella, the slack of any lateral glide is removed, and an anteroposterior pressure on the medial border of the patella is applied. The lateral border of the patella should move freely away from the femur, and on palpation, the tension in the retinacular fibers should be similar. In this position, ITB tightness can be evaluated with Ober’s test and the gluteus medius can be tested for strength deficits [34]. Strength testing (Hip Abductors, Adductors) of the hip is performed on side lying. With the bottom leg slightly flexed for stability, the top hip is brought into slight abduction. Resistance is given toward the table with the clinician’s hand on the distal thigh near the knee joint [19]. Replicating the same resistance placement is important for reassessment later to ensure the

same moment arm is placed on the extremity. The patient is asked to adduct the tested hip with the top leg in front of the bottom. Pressure is given on the distal thigh toward the table [35]. The flexibility of the quadriceps is tested in the prone position. Because the rectus femoris crosses both the hip and the knee joint it can easily become passively insufficient. Ely’s test is performed prone by placing the hip in neutral or extension which places the rectus femoris on stretch proximally at the hip and again distally as the knee is further flexed [35].

1.3.2 Palpation The primary goal of the examination is to reproduce and localize the patient’s pain. Tenderness on palpation and knowledge of knee anatomy is especially useful for diagnosis. Palpation should be done systematically, altering the approach depending on the area of discomfort and examining the area of reported pain last. A suggested approach is to begin anteriorly and work posteriorly, starting with the quadriceps tendon and then palpating the patella, patellar tendon, and tibial tuberosity [20]. Any localized swelling and masses, including swelling of the prepatellar bursa, a meniscal cyst, and Osgood-Schlatter disease of the tibial tubercle, should be noted [19]. Innervated tissues of the patellofemoral joint, which could generate anterior knee pain, include the subchondral bone of the patella and trochlea, synovium (including plicae), patellar and quadriceps tendons, and retinacular soft tissue restraints medially and laterally [36]. The patella can be palpated for grating or crepitus, in both closed kinetic and open kinetic chain movements, which may indicate articular cartilage damage. If the crepitus correlates with the patient’s symptoms at a particular point in the range of motion (ROM), it assists in clinical reasoning and forming guidelines for designing the therapeutic exercise program. Likewise, palpating the peri patellar soft tissue in a weight-bearing position may also produce symptoms in a non-weight-bearing position

1.4 Specific Stress Tests

[19]. Next, the medial and lateral patellar facets can be palpated while assessing for the apprehension sign (Fig. 1.7). Then palpate the medial and lateral retinacular tissues, the medial femoral condyle in the region of the medial parapatellar plica, each of the quadriceps tendon insertions and the patellar tendon in each patient. Palpate deep to the patellar tendon for evidence of increased density and/or reproduction of the patient’s pain. Palpation of the quadriceps muscle bellies can occasionally reveal tenderness. Palpate all scars for neuromata, especially if the history suggests this diagnosis. In acutely injured knees, palpation of the medial parapatellar structures helps differentiate acute lateral patellar instability and medial collateral ligament sprain. Sallay et al. reported 70% of their patients were maximally tender over the adductor tubercle after acute lateral dislocation [37]. Acute evaluation of possible extensor injuries must include palpation for defects in the quadriceps and patellar tendons. Palpation of the medial femoral condyle in the

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region of the medial parapatellar plica, each of the quadriceps tendon insertions, and the patellar tendon. Palpate deep to the patellar tendon for evidence of increased density and/or reproduction of the patient’s pain. Tenderness is very common in the medial and lateral patellar retinacula and the patellar tendon, all of which rank high among the knee’s most densely innervated soft tissues [36]. Tenderness is common in the peripatellar tissues that are overly tight and have been chronically overloaded. This tenderness may result from the neuromatous degeneration found in such retinacular tissues excised at lateral release [38, 39]. Precise diagnoses in acute injuries and chronic pain are often made by careful mental visualization of the specific structures that are most tender. Particular attention should be paid to the medial femoral condyle area where the medial parapatellar plica can often be readily palpated. Tenderness, as the plica is rolled underneath a finger, is diagnostic medial plica irritation and medial plica syndrome [40]. Patients with soft tissue pain secondary to excessive lateral patellar tilt commonly have tenderness in the vastus lateralis insertion, the lateral retinacular insertion, and the inferior portion of the medial retinaculum [41]. The bony and soft tissue palpation areas around the knee should be consistently and methodically palpated, rather than randomly during the physical examination [19].

1.4 Specific Stress Tests

Fig. 1.7  Patellar apprehension test. With the knee fully extended and the quadriceps relaxed the examiner passively translates the patient’s patella in a lateral direction. The test is positive if a feeling of apprehension or impending dislocation is experienced

A thorough examination of all knee structures should be a part of every evaluation. To ensure the most accurate diagnosis possible, it is crucial that testing stress maneuvers be performed correctly and that the examiner is aware of each maneuver’s sensitivity, specificity, and limitations [42]. Many of the tests currently used to help diagnose the injured structures of the knee were developed before the availability of advanced imaging. However, several of these examinations are as accurate or, in some cases, more accurate than state-of-the-art imaging studies [20].

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1  Clinical Examination of the Patient with Anterior Knee Pain

1.4.1 Tests for the Medial and Lateral Collateral Ligaments (MLCL) The MCL is among the most frequently injured ligaments in the knee. Valgus stress testing is the primary method used to diagnose MCL injury, although few studies have evaluated its accuracy or interexaminer reliability. Injuries of the lateral collateral ligament (LCL) are less common, and even fewer studies have evaluated the accuracy of the varus stress test in diagnosing this injury. The patient is supine on the examination table. Flex the knee to 30° over the side of the table, place one hand on the lateral aspect of the knee, and grasp the ankle with the other hand. Apply abduction (valgus) stress to the knee. The test must also be performed in full extension [42]. Valgus Stress Tests performance in 0° of flexion (Fig. 1.8a). Hold the knee in full extension, secure the ankle with one hand, and place the other hand around the knee, so the thenar is against the fibular head. Then push medially against the knee and laterally against the ankle to a

open the knee joint on the inside. Also, try to palpate the medial joint line for gapping and pain. Valgus test in 30° of knee flexion (Fig. 1.8b). The execution here is the same but can use a cushion to place the knee in 30° of flexion or place the knee on your thigh. Then again, secure the ankle with one hand and place the other hand around the knee so that the thenar is against the fibular head. Then push medially against the knee and laterally against the ankle to open the knee joint on the inside. Also, try to palpate the medial joint line for gapping and pain [43]. Varus stress test (Fig. 1.9). The patient is supine on the examination table. Flex the knee to 30° over the side of the table, place one hand on the medial aspect of the knee, and grasp the ankle with the other hand. Apply adduction (varus) stress to the knee. The test must also be performed in full extension [42]. Varus stress test for LCL injuries. The patient is supine. Take the leg and bring it in 30° Flexion (MLPP) à use a cushion or edge of the bed so the patient can relax. With one hand, fixate the femur. Apply slight lateral rotation and perform passive

b

Fig. 1.8  Valgus test in 0° of knee flexion (a), and Valgus test in 30° of knee flexion (b)

1.4 Specific Stress Tests

Fig. 1.9  Varus stress test

adduction at the knee joint and thus put stress on the LCL. Check for excessive gapping and if you can reproduce the patient’s pain.

1.4.2 Tests for Meniscal Injuries Meniscal tears occur commonly; however, their clinical diagnosis is often difficult, even for an experienced clinician. Because the menisci are avascular and have no nerve supply in their inner two-thirds, an injury to the meniscus can result in little or no pain or swelling, which makes accurate diagnosis even more challenging [42]. In 1803, Hey described “internal derangement of the knee,” Since then, significant literature on the clinical diagnosis of meniscal tears has evolved [44].

1.4.2.1 Joint Line Tenderness The Joint Line Tenderness (JLT) test is a physical examination test commonly used to screen for sensitivity related to meniscal injuries [45, 46]. The test can be used if the pain is localized to the joint’s medial or lateral aspect and is suggested to correlate with degenerative pathology of the articular joint cartilage or compromised integrity of the medial or lateral meniscus [47]. Joint line palpation is among the most basic maneuvers, yet it often provides more helpful information than provocative maneuvers designed to detect meniscal tears. Flexion of the knee enhances palpation of the anterior half of each meniscus. The medial edge of the medial meniscus becomes more

11

prominent with internal rotation of the tibia, allowing for easier palpation. Alternatively, the external rotation allows improved palpation of the lateral meniscus. The literature notes a sensitivity for joint line tenderness of 55–85%, with a specificity range of 29–67% [48, 49]. The specificity and sensitivity of the JLT test are generally considered high; thus, the diagnostic accuracy of the test is high. However, the test scores for the lateral meniscus are suggested to be significantly higher than the test for the medial meniscus. In a study by Osman [46], the medial sensitivity was 86% and the specificity 67%, in contrast to the lateral sensitivity of 92% and specificity of 97%, confirmed by other authors [45]. Similarly, the LR for the lateral test scores is higher than the medial test [50]. Therefore, a positive correlation has been found between JLT and meniscal lesions with a high sensitivity but relatively lower specificity, i.e., patients with JLT may not exclusively have meniscal tears, especially medial meniscus tears [45]. The accuracy of JLT predicting meniscal pathology also decreases in the presence of an anterior cruciate ligament tear [45].

1.4.2.2 McMurray Test Technique. With the patient supine, the examiner holds the knee and palpates the joint line with one hand, thumb on one side, and fingers on the other, while the other hand holds the sole and supports the limb, and provides the required movement through the range. From a position of maximal flexion, extend the knee with internal rotation (IR) of the tibia and a VARUS stress, then return to maximal flexion and extend the knee with external rotation (ER) of the tibia and a VALGUS stress [35, 51, 52]. The IR of the tibia followed by extension, the examiner can test the entire posterior horn to the middle segment of the meniscus. The anterior portion of the meniscus is not easily tested because the pressure on that part of the meniscus is not as great.IR of the tibia + Varus stress = lateral meniscus.ER of the tibia + Valgus stress = medial meniscus. Positive findings: Pain, snapping, audible clicking, or locking can indicate a compromised meniscus. Studies of specificity and sensitivity have demon-

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1  Clinical Examination of the Patient with Anterior Knee Pain

strated varied values due to poor methodological quality [53]. A recent meta-analysis reports sensitivity and specificity to be 70% and 71% [54]. The test has, therefore, often been reported to be of limited value in current clinical practice. However, if positive findings are grouped with positive findings from other tests, such as joint line tenderness and Apley’s test, the test may be more valid. There are several different reported methods of performing McMurray’s Test (Fig.  1.10). The Apley grind test was described by Apley in 1947 [55]. This test is named after Alan Graham Appley (1914–1996), a British orthopedic surgeon who discovered this assessment technique [56]. The test is performed in conjunction with Apley’s distraction test. The Apley grind test has a reported sensitivity of 97% and a specificity of 87% [57]. Technique: With the patient in the prone position, the knee being tested is flexed to 90 degrees while the other leg is fully extended, resting on the exam table. The

examiner should apply a downward axial loading force to compress the patient’s knee’; this occurs by compressing down on the sole while using the other hand to hold down the posterior thigh for stabilization. Internal and external rotations should be applied along with compression. This is a positive test if there is pain or restriction with compression and internal or external rotation. If the patient experiences pain over the medial aspect of the knee, this is indicative of a medial meniscus injury. Alternatively, if the patient experiences pain over the lateral aspect of the knee, this is indicative of a lateral meniscus injury. Commonly this is performed with Apley’s distraction test, which tests for ligamentous injury rather than meniscal injury. In the same prone position, the examiner will now pull up on the patient’s affected leg instead of providing a downward loading force. This force places a strain on the ligaments of the knee. A positive result is when the patient experiences pain (Fig.  1.11). Pain with knee distraction significantly decreases the likelihood of meniscal pathology. By the nature of the distraction force, the force applied to the meniscus becomes reduced considerably [58, 59]. Diagnosis of a meniscal injury is by physical/ orthopedic examination and provocative tests, like Apley’s grind test and Apley’s distraction test, in tandem with advanced imaging like MRI, which can guide a physician to provide proper treatment [60].

1.4.3 Tests for Patellofemoral Disorders

Fig. 1.10  Mc Murray test for lateral meniscus. With the patient’s knee fully flexed, the tibia is internally rotated, engaging the posterior horn of the lateral meniscus under the lateral femoral condyle. The knee is then extended, entrapping the meniscus. With the patient’s knee fully flexed, the tibia is externally rotated engaging the posterior horn of the medial meniscus under the medial femoral condyle. The knee is then extended entrapping the meniscus

The patellar compression or grinding test and the patella apprehension test are two of the most common tests used in evaluating patellofemoral disorders.

1.4.3.1 Patellar Tilt and Glide Patellar tilt and glide are often cited together and are often considered synonyms. The patellar tilt indicates tightness of lateral restraints; it is performed with the patient supine with the knee in full extension. If the lateral side of the patella

1.4 Specific Stress Tests

a

13

b

Fig. 1.11  Apley’s grind test, like Apley’s distraction test (a) and Apley’s grind test (b) in tandem

Fig. 1.12  Patellar tilt test

Fig. 1.13  Patellar Glide at 30 degrees of flexion

cannot be elevated above the horizontal, the test is positive (Fig. 1.12). The glide test (Fig.  1.13) is performed with the knee flexed at 30°: if the patella glides laterally over 75% of its width, a medial restraints laxity is diagnosed; when it glides less than 25%, lateral restraints tightness is predicted [61].

The main restraint to the lateral dislocation is the medial patellar femoral ligament (MPFL). As in the glide test, the MPFL can be evaluated with the knee in full extension and the patella medially subluxated with the thumb. This maneuver tightens the MPFL; if an area of tenderness is palpated, this usually identifies the location of the

14

1  Clinical Examination of the Patient with Anterior Knee Pain

tear. A lateral glide greater than 75% of the patellar width is abnormal and indicates MPFL insufficiency [61].

1.4.3.2 Patellofemoral Grinding Test The term chondromalacia patellae did not appear in published form until 1924 [62]. Aleman is credited with using this term as early as 1917 [63], although the first mentioned chondromalacia in the English language in 1933 Kulowski [64]. In 1936, Owre published the results of a clinical and pathologic investigation of the patella [65]. His description of the patellofemoral grinding test follows: Pressure pain over the patella is tested by clasping the patella with each hand’s thumb and index finger, with the remaining fingers resting against the thigh and leg. The patient is positioned in supine or long sitting with the involved knee extended. The examiner places the web space of his hand just superior to the patella while applying pressure (Fig. 1.14). The patient is instructed to gently and gradually contract the quadriceps muscle. A positive sign on this test is a pain in the patellofemoral joint [66]. While the patient lies with the leg relaxed and extended, the patella is pressed against the medial and lateral femoral condyles. Moving the patella in an upward and downward direction, the greater part of the surface cartilage may be examined in this manner. In some cases, pain is elicited by the

Fig. 1.14  Patellar grind test

slightest pressure of the patella against the condyle; at other times, considerable pressure must be exerted to obtain a positive response to an unpleasant sensation. Owre considered a positive test indicated by pain predictive of pathologic changes to the retropatellar cartilage or chondromalacia patella [65]. Currently, a positive test may or may not be associated with the pathologic diagnosis of chondromalacia patella, as determined by direct arthroscopic visualization and probing. Solomon et al. provide a more contemporary description of the test: “The subject is lying supine with the knees extended. The examiner stands next to the involved side and places the thumb’s web space on the patella’s superior border. The subject is asked to contract the quadriceps muscle while the examiner applies downward and inferior pressure on the patella [67]. Pain with movement of the patella, or an inability to complete the test, is indicative of patellofemoral dysfunction”. These two descriptions vary significantly. In the first (or passive grind) test, the potentially pathologic and painful patella is compressed against the patellofemoral joint to reproduce pain from pathologic chondral changes on the patella. The latter description involves an active contraction of the quadriceps with external compression on the patella, presumably resulting in a more dynamic compression of the patella against the femur. Neither test replicates how the patella normally moves within the patellofemoral joint. No studies documented the patellofemoral grinding test’s sensitivity or specificity in diagnosing patellofemoral syndrome. However, several studies in the last 20  years have shown a generally poor correlation between retropatellar pain and articular cartilage damage [68–72]. We caution against using the active grind test because we have found it to cause pain in normal asymptomatic subjects while teaching this maneuver to students and residents [42]. O’Shea et al. reported on the diagnostic accuracy of clinical knee examination in patients with arthroscopically documented knee pathology, including chondromalacia patella [73]. They reported that only 11 of 29 patients were correctly diagnosed with the pathologic findings of chondromalacia patella

1.4 Specific Stress Tests

based on history, physical examination, and standard radiographs for a sensitivity of 37%.

1.4.3.3 Clarke Sign or Test A more contemporary and common version of the patellar grind test is known as the Clarke sign or test, although to our knowledge, there is no record of its origin in the literature [74]. It incorporates active contraction of the quadriceps while the examiner braces the patella in the web space of the thumb, exerting compressive and inferior pressure. These two patella compression tests are sometimes differentiated as passive versus active, but neither accurately reproduces normal patellofemoral mechanics [42]. In summary, the correlation between the clinical history and examination and the diagnosis of chondromalacia patella is poor. An explanation for the disparity between clinical signs and pathologic findings is not simple and reflects the continuing question of what ultimately causes pain in patients with patellofemoral syndrome [42]. 1.4.3.4 Apprehension Test for Patellar Dislocation This test was first described by Fairbank in 1936 [75]. The test, often referred to as the Fairbank’s Apprehension Test, has been described by Fairbank as such: While examining cases of suspected recurrent dislocation of the patella, I have been struck by the marked apprehension often displayed by the patient when the patella is pushed outwards in testing the stability of this bone. Not uncommonly, the patient will seize the examiner’s hands to check the manipulation, which she finds uncomfortable and regards as distinctly dangerous. This sign, when present, I regard as strong evidence in favor of a diagnosis of slipping patella [75]. A more detailed and more recent description of the apprehension test for subluxation of the patella was given by Hughston [76]. His description is as follows: This test is carried out by pressing on the medial side of the patella with the knee flexed about 30 degrees and with the quadriceps relaxed. It requires the thumbs of both hands to press on the medial side of the patella to exert the laterally directed pressure. Accordingly, the leg with

15

relaxed muscles is allowed to project over the side of the examining table and is supported with the knee at 30 degrees of flexion by resting the leg on the thigh of the examiner, who is sitting on a stool. In this position, the examiner can almost dislocate the patella over the lateral femoral condyle. Often the finding is surprising to the patient and he becomes uncomfortable and apprehensive as the patella reaches the point of maximum passive displacement, with the result that he begins to resist and attempts to straighten the knee, thus pulling the affected patella back into a relatively normal position [76]. Sallay et  al. [37], in their 1996 study, reported on the characteristic clinical and arthroscopically determined pathologic findings associated with patellar dislocations. Only 39% of patients with a history of dislocation were found to have a positive apprehension sign. In contrast, 83% had a moderate to large effusion, and 70% had significant tenderness over the posterior medial soft tissues. MRI revealed a moderate to large effusion on all scans. Increased signal adjacent to the adductor tubercle was seen in 96% of patients, tearing of the medial patellofemoral ligament was found in 87%, and an increased signal was noted in the vastus medialis oblique muscle in 78%. On arthroscopic evaluation, gross lateral laxity of all subjects’ patellofemoral articulation was most prominent at 70–80° of flexion. This degree of flexion is significantly higher than the 30° classically recommended for the apprehension sign and may explain the low sensitivity of this test in the diagnosis of patella dislocation [37].

1.4.3.5 Patellar Instability Patellar instability is common, affecting young, active persons and females more than males, and can be debilitating [77]. Patients with true patellar instability report either patella dislocation requiring reduction or lateral subluxation with a spontaneous reduction [10]. The cause is multifactorial; contributing factors include the bony structure of the patella and femoral trochlea, integrity and/or laxity of the surrounding tissues, including the medial patellofemoral ligament, muscle tone, balance, and overall limb alignment [77–79].

16

1  Clinical Examination of the Patient with Anterior Knee Pain

1.4.3.6 Wilson Sign In 1967, Wilson observed that patients with OCD of the medial femoral condyle often had a specific antalgic gait with external rotation of the foot, which he proposed relieves the pressure of the tibial spine on the medial femoral condyle [80]. The test has to be performed: Ask the patient to sit on a table with his legs dangling over the edge. Bend the patient’s knee, which is flexed at a 90° angle. Grasp the patient’s foot and bring the tibia in internal rotation. Instruct the patient to extend his leg until he/she feels pain. The test is positive when the patient reports pain in the knee about 30° from full extension and then by rotating the foot back (external rotation of the tibia) in its normal position, the pain disappears [66].

Examination of the extensor mechanism, like other anatomic features of the knee, is guided by the patient history. A quadriceps or patellar tendon tear is diagnosed by the inability to extend the knee against gravity and a palpable defect directly proximal or distal to the patella, combined with a history of an acute injury [20]. In larger patients, it may be difficult to palpate the defect, particularly a quadriceps tendon rupture. Advanced imaging can be helpful when a quadriceps or patellar tendon rupture is suspected and the defect cannot be palpated. Radiographs may also reveal patella Alta or Baja (i.e., an Insall-­Salvati ratio of 1.2 or 0.8, respectively) [84].

1.4.3.7 Q Angle The quadriceps angle, or Q angle, is a measure of the direction of pull of the quadriceps relative to the line of action of the patella; this angle is theoretically important because it relates to the lateral displacement force on the patella. The Q angle is defined as the acute angle formed by lines drawn from the anterior superior iliac spine to the center of the reduced patella and from the center of the patella to the tibial tuberosity [81]. The average Q angle for males is 14°, and the average for females is 17°. An increase in this angle can indicate abnormal patellar tracking [61].

References

1.4.3.8 J-Sign The J-sign indicates pathologic patellar tracking and refers to the inverted “J” course of the patella as it subluxate laterally in full extension and then reduces into the femoral trochlea in early flexion, observable with both active and passive motion [9, 82]. It is considered a sign of severe instability that is difficult to treat [79] and has been associated with vastus medialis obliquus insufficiency; however, recent evidence shows it more likely indicates a ligamentous problem or trochlear dysplasia [83]. However, its clinical validity is questioned because one study found that the subjective J-sign did not correlate with lateral patellar subluxation [83].

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out associated anterior cruciate ligament tears. Acta Orthop Traumatol Turc. 2003;37:193–8. 46. Osman TE.  The accuracy of joint line tenderness by physical examination in the diagnosis of meniscal tears. Arthroscopy J Arthrosc Relat Surg. 2003;19(8):850–4. 47. Lerew S, Stoker S, Nallamothu S. The rules of four: a systematic approach to diagnosing common musculoskeletal conditions of the knee. SMRJ. 2020;4(2) 48. Kurosaka M, Yagi M, Yoshiya S, Muratsu H, Mizuno K, Efficacy of the axially loaded pivot shift test for the diagnosis of a meniscal tear. Int Orthop. 1999;23:271–475. 49. Fowler PJ, Lubliner JA. The predictive value of five clinical signs in the evaluation of meniscal pathology. Arthroscopy. 1989;5:184–6. 50. Horn A.  Diagnostic accuracy of orthopedic special tests for meniscal injury. Oregon: Pacific University Research Repository; 2011. 51. Piantanida AN, Yedlinsky NT.  Physical examination of the knee. In: Seidenberg PH, Beutler AI, editors. The sports medicine resource manual. Saunders; 2008. https://doi.org/10.1016/B978-­1-­4160-­3197-­0. X1000-­2. 52. Waldman SD.  Painful conditions of the knee. In: Pain management, vol. 1. Saunders; 2007. https://doi. org/10.1016/C2009-­1-­59662-­1. 53. Meserve BB, Cleland JA, Boucher TR.  A meta-­ analysis examining clinical test utilities for assessing the meniscal injury. Clin Rehabil. 2008;22(2):143–61. 54. Hegedus EJ, Cook C, Hasselblad V, Goode A, McCrory DC. Physical examination tests for assessing a torn meniscus in the knee: a systematic review with meta-analysis. J Orthop Sports Phys Ther. 2007;37(9):541–50. 55. Gillis L.  Diagnosis in orthopaedics. Toronto: Butterworth; 1969. 56. Who Named It? Alan Graham Apley. Available from: http://www.whonamedit.com/doctor.cfm/203.html 57. Eltorai AE, Eberson CP, Daniels AH.  Orthopedic surgery clerkship: a quick reference guide for senior medical students. Springer; 2017. p.  307. ISBN 9783319525679. 58. Mordecai SC, Al-Hadithy N, Ware HE, Gupte CM. Treatment of meniscal tears: an evidence-based approach. World J Orthop. 2014;5(3):233–41. 59. Doral MN, Bilge O, Huri G, Turhan E, Verdonk R.  Modern treatment of meniscal tears. Efort Open Rev. 2018;3(5):260–8. 60. Hashemi SA, Ranjbar MR, Tahami M, Shahriarirad R, Erfani A. Comparison of accuracy in expert clinical examination versus magnetic resonance imaging and arthroscopic exam in diagnosis of meniscal tear. Adv Orthop. 2020;2020:1895852. 61. Katchburian MV, Bull AMJ, Shih Y-F, Heatley FW, Amis AA. Measurement of patellar tracking: assessment and analysis of the literature. In: Review article,

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19 83. Sheehan FT, Derasari A, Fine KM, Brindle TJ, Alter KE.  Q-angle and J-sign: indicative of maltracking subgroups in patellofemoral pain. Clin Orthop Relat Res. 2010;468(1):266–75. 84. Insall J, Salvati E. Patella position in the normal knee joint. Radiology. 1971;101(1):101–4.

2

Condition Causing Anterior Knee Pain

2.1 Patellofemoral Pain 2.1.1 Introduction Patellofemoral Pain Patellofemoral Pain (PFP) is a common musculoskeletal condition characterized by diffuse anterior knee pain, typically behind the patella. It is traditionally aggravated during knee-loading activities such as squats, stair climbing, and running. Patellofemoral pain occurs across the lifespan, from young children to older individuals [1]. The highest prevalence of PFP is observed in those aged between 12 and 19 years [2] but may depend on activity level and environmental context [3]. However, this prevalence peak contrasts with the Pearl Diver data analysis, which reported the highest percentage of PFP diagnosis in the 50–59 age group [4]. The discrepancy in prevalence related to age may be due to environmental contexts, such as treatment in a sports clinic versus a general practice office. However, 50–56% of adolescents report persistent knee pain two years after their initial diagnosis [5].

2.1.2 Terminology and Defining of PFP Terminology. Two terms are proposed for this condition [6]: (1) PFP and (2) patellofemoral arthropathy. PFP has been used as the preferred

term over recent years. However, it does not consider how nonpainful joint conditions could precede pain development, nor include symptoms such as crepitus, and principally focus on the “pain” aspect of the condition. The term “patellofemoral pain” is the preferred term and is a synonym for other terms, including (1) PFP syndrome, (2) chondromalacia patellae, (3) anterior knee pain and/ or syndrome, and runner’s knee [4]. Defining PFP: The main criterion required to define PFP is the pain around or behind the patella, aggravated by at least one activity that loads the patellofemoral joint during weight bearing on a flexed knee (e.g., squatting, stair ambulation, jogging/ running, and hopping/ jumping). Additional criteria (not essential) are (A) Crepitus or grinding sensation emanating from the patellofemoral joint during knee flexion movements. (B) Tenderness on patellar facet palpation. (C) Small effusion. (D) Pain on sitting, rising from sitting, or straightening the knee following sitting [4]. 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. Currently, such patients are considered a subgroup of people with patellofemoral disorders and/or pain, who may have distinct presentations, and biomechanical risk factors, and require different treatment approaches. Despite being commonly

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_2

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diagnosed, its exact pathophysiology is unknown, but it is believed to be related to a combination of anatomical, biomechanical, behavioral, and psychological factors [7].

2.1.3 Clinical Presentation Patellofemoral pain is a common musculoskeletal-­ related condition characterized by the insidious onset of poorly defined pain quality localized to the knee’s anterior retropatellar and/or peripatellar region. The onset of symptoms can be slow or acutely developed, with a worsening of pain with lower-limb loading (e.g., squatting, prolonged sitting, ascending/descending stairs, jumping, or running, especially with hills) [6, 8]. Therefore, diagnosis is based on a cluster of signs and symptoms after ruling out other pathoanatomic diagnoses [5]. Diagnosis is often delayed and describes the typical clinical course because symptoms are typically progressive, insidious onset [9].

2.1.3.1 History Pain might worsen in intensity, duration, and rapid onset of the aggravating activity repeatedly. Pain may be exacerbated by sitting with the knee flexed for a protracted time, such as watching a movie. Patients with this condition often prefer to sit in an aisle seat, where they may more frequently keep the knee extended. Patients should be asked about previous knee injuries and surgeries, current activity levels, and recent changes in their activity. PFP is a common form of knee overuse injury. Less commonly, patients may experience knee buckling due to weakness or pain in the quadriceps, resulting in a brief loss of muscle tone, not the intrinsic knee joint. A physical examination of the knee should be performed in all patients presenting with a chief symptom of knee pain. Diagnosis of PFP can be difficult and must integrate both clinical history and physical exam as positive; signs are often vague and clinical history may not always correlate with biomechanical findings [10]. Assessing patients for potential risk factors of PFP can help

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guide physical exams and exclude other conditions from the differential [11]. Start by observing the patient in a static standing position looking at knee alignment, especially with concern for the genu valgum or varum. One should be sure to take time to assess the entire kinetic chain from pelvic drop to excessive dynamic adduction or internal rotation of the femur down to excessive pronation of the feet. Once the patient has been assessed at rest, one should move on to functional tasks. The step-down test or single-leg squat can be done quickly and easily. Ask the patient to stand on one leg with hands on their hips and bend their knee to around 60° [12]. Observe the patient for hip abductor weakness, increased femoral internal rotation/adduction, and dynamic knee valgus. In a recent study, this test was more predictive of PFP than the single-hop test, gait, or stairs [13, 14]. Large joint effusion, erythema, and increased warmth are not features of PFP and should prompt consideration of an alternative diagnosis such as infection, acute trauma, and inflammatory arthropathy. In a meta-analysis, the presence of pain with squatting was the most sensitive physical examination finding for PFP, and a positive result on the patellar tilt test carried the highest positive likelihood ratio [15]. Physical examination of a patient with patellofemoral syndrome should include the following [16]: The upper and lower body should be examined to exclude generalized diseases that make up the differential diagnoses (e.g., osteoarthritis). The usual physical findings are localized around the knee. Tenderness often is present along with the facets of the patella. The facets are most accessible to palpation by manipulating the patella while the knee is fully extended and the quadriceps muscle is relaxed. Manual positioning of the patella medially, laterally, superiorly, and inferiorly allows for palpation of the respective facets. An apprehension sign may be elicited by manually fixing the position of the patella

2.1 Patellofemoral Pain

against the femur and having the patient contract the ­ipsilateral quadriceps. Crepitus may be present, but a single symptom does not make a definitive diagnosis. Determine the Q-angle by measuring the angle between the tibia and femur. Use the attachment of the patella to the patellar tendon as the intersection point. Repetitive squatting may reproduce knee pain. Use the physical examination and historical details to help exclude other diagnoses. Examination of the contralateral limb is equally important, as the syndrome often is bilateral. However, one side usually manifests more symptoms. Palpation of the tibial tuberosity may detect tenderness, suggesting that other impairments also are present. Determining the bulk of the vastus medialis is possible because it is situated superficially and has little overlying tissue. Bulk may observe by direct visualization during contraction. The vastus medialis believed to be the most active muscle in the last 15° of resisted knee extension, making this the best arc of movement for assessing its strength. Genu recurvatum and hamstring weakness may contribute to the occurrence of patellofemoral syndrome, and therefore, identifying such impairments may aid in the choice of management. Examination of gait and posture help identify contributing causes of PFPS, such as exaggerated lumbar lordosis, asymmetric hip height, atrophic quadriceps, excessive foot pronation, excessive knee valgus, or an antalgic gait pattern. A literature review by Arazpour found that compared with healthy subjects, persons with patellofemoral syndrome tend to have the following [17]: Reduced gait velocity. Reduced cadence. Decreased knee extensor moment in association with the loading response and terminal stance. Delayed peak rearfoot eversion in association with gait. Increased hip adduction. The reports used in the review differed as to whether hip rotation in patellofemoral syndrome increased, decreased, or remained the same.

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2.1.4 Physical Performance Measures The most accurate diagnostic clinical test for PFP is the reproduction of pain with squatting [9, 18]. The squatting maneuvers are performed in a manner that feels normal to the individual. The test has a high–LR (negative likelihood ratio); of 0.10–0.20 (95% CI: 0.1, 0.4), indicating that the probability of PFP being present when there is a negative test is moderately decreased [13]. Sensitivity, specificity, and likelihood ratios were calculated for pain with stair climbing and pain with kneeling. These tests demonstrated moderate to high sensitivity and – LR (negative likelihood ratio), suggesting that the probability of PFP is moderately decreased when there is a negative test [19]. Collins et al. [20] conducted a retrospective review of 4 separate studies of persons with PFP, including 459 total participants, and found that 54.4% of persons with PFP reported increased knee pain with prolonged sitting. Pain with prolonged sittings was found to have low to moderate diagnostic accuracy in an earlier systematic review suggesting that its presence may be a diagnostic indicator for PFP [21]. The eccentric step-down test demonstrates moderate specificity (0.82; 95% CI: 0.62, 0.93) and +LR (positive likelihood ratio), (2,3; 95% CI: 1.9, 2.9), suggesting that the probability of PFP being present when there is a positive test is moderately increased [9]. Reproduction of AKP during the test is considered a positive test result [11]. The FPPA has acceptable between-day reliability for healthy men (ICC  =  0.88; 95% CI: 0.82, 0.93) and women (ICC  =  0.72; 95% CI: 0.56, 0.82) as a test for increased knee valgus during the SLS [22]. Harris-Hayes et al. [23] performed a cross-sectional study of 30 athletes to determine the reliability of video assessments of lower extremity movement patterns (FPPA) and the construct validity of the measurement. Observers classified lower extremity movement patterns as dynamic valgus (greater than 10° in the positive direction), dynamic varus (greater than 10° in the negative direction), or no change (less than 10° in either direction). They reported

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kappa values ranging from 0.80 to 0.90 for intratester reliability and 0.75–0.90 for intertester reliability. Piva et al. [24] developed an assessment of the quality of movement during a lateral step-­ down test to assess lower extremity biomechanics during a dynamic task in individuals with PFP.

2.2 Patellar Instability 2.2.1 Introduction Patellofemoral instability can be defined as a patella movement out of its normal position and divided into dislocation and subluxation. Patellar subluxation is a partial movement of the patella out of the trochlea, but some articular contact remains. Patellar tracking refers to the dynamic relationship between the patella and trochlea during knee motion. Patellar maltracking occurs due to an imbalance of this relationship, often secondary to anatomic abnormality. It is a recognized cause of anterior pain and, in extreme cases, presents as acute and often recurrent patellar dislocation, usually transient. Early diagnosis is essential, as chronic maltracking will lead to patellofemoral cartilage damage and osteoarthritis. The term “patellar maltracking” is not used routinely because of the ambiguity of its meaning [25].

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2.2.2 Anatomic Structures and Abnormal Biomechanics of the Patellofemoral Joint Involved in Patellar Instability

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• Advances in understanding the normal anatomy and biomechanics of the patellofemoral joint and the knowledge of static and dynamic factors and the mechanism that contribute to its stability allow us to identify the causes of patellar instability. Thus: • The proper biomechanics of the patellofemoral joint requires an intact and anatomically normal-shaped trochlear groove and inline

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congruent forces acting on the patella so it can glide across the trochlea groove smoothly. Any disruption in this mechanism will dislocate the patella out of the trochlear groove [25]. The bony structures of the patellofemoral joint, patella, and trochlear groove provide inherent stability to the patella, and any defect in the joint surfaces will result in instability. The majority of the patella articulation occurs between the lateral facet and the lateral trochlear groove. The normal trochlear groove has a large depth and steepness that provides inherent stability to the patellofemoral joint [26]. Trochlear dysplasia and flattening of this groove will cause patellar instability. Any osteochondral fracture or defect will lead to pain and instability and requires fixation [25]. Besides bony support, the soft tissue envelope is even more important to the patella’s stability. The quadriceps are inserted at the superior patella and encase the patella until it merges with the patellar tendon. The patellar tendon originates at the inferior aspect of the patella and inserts onto the tibial tubercle. The quadriceps tendon, patella, and patellar tendon combined make up the extensor mechanism of the knee. Disruption of the extensor mechanism along its length will result in significant patellar instability and maltracking [25, 27]. The MPFL contributes 50–60% of resistance to lateral translation of the patella [26]. Any laceration, avulsion, or traumatic disruption of MPFL will lead to lateral patellar instability. Once the patella enters the trochlea at 20–30 degrees of flexion, the bony anatomy becomes the major stabilizer as the patella sits in the trochlear groove. The patella Alta does not engage in the groove until higher-than-normal knee flexion, which predisposes the patella to dislocation [28, 29]. Studies have shown that lateral structures contribute 22% to lateral translation and stability in lateral patellar dislocations [29]. These include the deep lateral transverse retinaculum, epicondylopatellar ligament, and patellotibial band. Dynamic stability is also a contributor to patellar stability. The vastus medialis muscle

2.2 Patellar Instability

confers medial restraint to lateral translation. The vastus lateralis confers a lateral restraint to medial translation [25]. Knee alignment is a key factor in patellar stability. The normal alignment of the knee joint is at 6 degrees of valgus. The mechanical axis of the knee is a line drawn from the center of the hip to the center of the ankle. The line should pass through the center of the patella. The anatomic axis of the knee is a line that goes through the center of the femoral and tibial shaft. In general, the anatomic axis of the femur is 6 degrees from the mechanical axis. Therefore, the knee angle (femorotibial angle) is approximately 6 degrees of valgus (in relation to the mechanical axis). An increased valgus at the knee off normal will later force the patella out of the trochlear groove and contribute to patellar instability [30]. The normal femoral anteversion is 15–20 degrees. Femoral anteversion >20 degrees increases the risk for patellar dislocation laterally because it produces a high laterally directed force across the patella [31, 32] and increases the Q-angle leading to increased lateral force across the patella. External tibial torsion also will contribute to lateral patellar instability. Normal tibial external rotation during childhood is 15 degrees [33]. The indications for derotational tibial osteotomy are poorly defined. Staheli recommends surgical correction for severe rotational deformities >30 degrees [33]. Typically, external tibial torsion requires surgical correction with either a supramalleolar derotational osteotomy or a proximal tibial derotational osteotomy [34]. Increased femoral anteversion, genu valgus, and external tibia torsion is “miserable malalignment syndrome” [35, 36]. These entities increase the Q-angle and subsequently increase the risk for patellar instability. Trochlear dysplasia is a disease characterized by a shallow trochlear groove. It is thought to be caused by either congenital factors or lateral patellar tracking. Lateral patellar tracking will eventually flatten the trochlear groove leading to patellar instability. Regardless of the cause, trochlear dysplasia results in a loss of the inherent stability of the patellofemoral joint [25].

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Disorders that affect collagen include Ehlers-­ Danlos syndrome or Down Syndrome. These diseases cause a chronic progression of ligamentous laxity. When the soft tissue structures around the knee become lax, the patella loses its restraints, and these patients typically complain of habitual dislocations. These patients will have a classic presentation of Ehlers-Danlos with hyperelastic skin, joint hypermobility, and generalized ligamentous laxity. The typical morphotype [37] of the patient with patellar instability characterize as an adolescent female [38], with ligamentous laxity and multiple developmental anomalies [39], including patella Alta [40], trochlear dysplasia [41], and rotational and angular bony malalignment [42]. Trochlear dysplasia and patella Alta, which reduce the “containment” of the patella within the femoral trochlea at any given flexion angle than in the normal knee, directly contribute to the risk of recurrent patellar dislocation by reducing the relative height of the lateral trochlear buttress [43]. A summary of predisposing factors for patellar instability [25, 27, 37, 43]: Femoral trochlea dysplasia (excessively shallow) Patellar dysplasia Combined patellofemoral dysplasia Patella Alta Patella Alta without trochlear dysplasia Inadequate bony restraints of the patellofemoral joint Inadequate medial soft tissue restraints MPFL tear or elongation VMO disruption VMO weakness Lower extremity malalignment Abnormally high Q-angle Excessive femoral anteversion Excessive external tibial torsion Genu valgum Proximal tibia vara Age Familial history of dislocation Training Errors and Overuse Joint hypermobility and generalized ligamentous laxity Foot pronation Pes planus

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2.2.3 Classification of Patellar Instability Various classification systems propose lateral patellar instability based on clinical and imaging characteristics. No single system is considered the gold standard. We present some of the existing classification systems as follows [44]: Dejour et  al. divided patellofemoral disorders into three main groups [45, 46]: Objective patellar instability, Potential patellar instability, and Patellofemoral pain. Objective patellar instability. This group includes patients who have experienced at least one episode of patellar dislocation or subluxation and present at least one of the principal factors of instability. This category also includes patients with severe patellar instability (recurrent or permanent dislocations). Potential patellar instability. Patients in this group have never experienced dislocation or subluxation; their main symptom is pain, presenting one or more of the principal factors of instability. Patellofemoral pain. Pain is the main symptom presented by patients classified in this group, in whom none of the principal factors of instability can identify. In 2015, Frosch and Schmeling recommended a classification system based on instability criteria and clinical and radiologic analyses of maltracking and loss of patellar tracking. They reported five types of patellar instability and maltracking patterns, along with management recommendations [47]: • Type I was traumatic patellar dislocation without maltracking and instability, with a low risk of redislocation. It was rare, and treatment was conservative. • Type II had a high risk of redislocation after primary dislocation but no maltracking. Medial patellofemoral ligament (MPFL) reconstruction would be the treatment of choice.

2  Condition Causing Anterior Knee Pain

• Type III represented both instability and maltracking. Maltracking is caused by (a) soft-­ tissue contracture or a muscle imbalance, (b) patella Alta, (c) pathologic TT-TG distance, (d) valgus deviation, or (e) torsional deformities. Isolated MPFL reconstruction may not suffice to treat patellar instability in the presence of maltracking. Additional osseous corrective surgeries may be required to achieve physiologic patellar tracking and to prevent redislocation. • Type IV featured a highly unstable “floating patella” with a complete loss of tracking caused by severe trochlear dysplasia. The treatment of choice was trochleoplasty, combined with other bony and soft tissue procedures. • Type V represented patellar maltracking without instability; for example, an internally rotated patella secondary to torsional deformity of the lower limb but without frank patellar dislocation would require a corrective derotational osteotomy femur and/or tibia.

2.2.4 Clinical Evaluation 2.2.4.1 History A careful history should include the total number of dislocation events, age at first dislocation, mechanism, amount of swelling present after dislocation, description of sensation at the time of episode(s) and whether the knee cap came out of place, prior treatments (including whether a reduction was necessary), symptomatology between instability episodes, and family history regarding patellar instability and/or systemic hypermobility [43, 48]. The clinician should ascertain whether the primary complaint is pain or instability. Elements of history can influence the treatment plan. A history of contralateral patellar dislocation would increase the risk of recurrence sixfold, as much as a previous dislocation on the index knee [49]. Non-contact and episodic instability are more likely to require ­surgical stabilization than a first-time traumatic dislocation [50].

2.3 Patellofemoral Osteoarthritis (PFOA)

Locking or catching symptoms, in addition to reports of significant swelling, may correlate with osteochondral loose bodies, which may require the removal of small fragments.

2.2.4.2 Physical Examination Every patient should receive a thorough knee examination, including gait evaluation, bilateral hips, knee ligament exam, and alignment in all planes. The objective of the patellofemoral examination is to verify and understand the excessive motion of the patella due to lack of constraint, and the exam starts with ensuring that the patella is currently reduced. After obtaining a thorough history, the patient should easily be classified into one of the following three categories [43]: (I) First-time patellar instability; (II) Recurrent patellar instability; (III) Patients having undergone previous surgery. For an acute dislocation, whether firsttime or recurrent, effusion with tenderness to palpation over the medial retinaculum is a typical finding. If the effusion is large and tense, aspiration can serve as a palliative measure and assist in diagnosing an osteochondral fracture. Other important examination findings for patients with first-time and recurrent patellar dislocations include [27, 38, 41, 44]. Lateral and medial patellar translation at full extension and 30 degrees of flexion: laxity measured by quadrants or millimeters. Pathologic laxity is appreciated when there is apprehension and an absence of an endpoint with lateral translation at 30 degrees of flexion. In full extension, translation in the pathologic knee is asymmetric without a fi endpoint. Tight lateral structures may be encountered in patients with recurrent dislocations, indicating that a lateral lengthening procedure might be a beneficial adjuvant. J sign: the patella abruptly translates laterally as the knee is fully extended, moving in an upside-down “J” pattern. For a patient who has failed non-operative treatment and has recurrent dislocations, a persistent J sign may encounter where the patella reduces into the trochlea at a higher flexion angle. Patellar facet palpation: tenderness may indicate an osteochondral or avulsion injury.

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Hip rotation: In patients with recurrent dislocations, a complete rotational profile should be assessed to determine if additional factors contribute to patellar instability when operative intervention is considered. Excessive hip anteversion is best assessed in the prone position with the knees flexed and hips extended. If internal rotation exceeds external rotation by 45° or more, consider a CT for axial lower extremity rotational alignment. If considering a TTO with distalization for patella Alta, it is particularly important to assess knee flexion in this position. Patellar instability is often associated with a constellation of “miserable malalignment,” which includes increased femoral anteversion, hyperpronation of the foot, and external tibial torsion [35]. Patients with significant valgus when standing should be more closely evaluated for these other anomalies. Hypermobility: an emphasis should be placed on the evaluation of knee hyperextension. The Beighton hypermobility score should assess general ligamentous laxity [47]. The Q-angle is rarely helpful, as it is imprecise and changes with patellar mobility [43]. If a patella is laterally subluxated, the Q-angle measurement is falsely low. On the other hand, femoral and tibial torsion can play a role in patellar instability, with the most significant lateral force placed on the patella when the tibia rotates externally in terminal knee extension [43].

2.3 Patellofemoral Osteoarthritis (PFOA) 2.3.1 Introduction Patellofemoral Osteoarthritis (PFOA) occurs due to the loss of the cartilage of the patella and the trochlear groove in approximately half of the patients diagnosed with degenerative arthritis of the knee. Depending on the source population and definition of OA, isolated patellofemoral PFOA is present in 11–24% of older individuals and occurs in combination with tibiofemoral OA in 4–40% of people [51]. Patellofemoral pain and PFOA have similar presentations, including the

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location of pain, quadriceps, and hip muscle weakness, and reported pain and difficulty with similar activities (e.g., stair climbing and prolonged sitting) [51, 52]. However, long-term prospective data are presently lacking to confirm or refute this link, with a recent consensus statement concluding that insufficient evidence exists to link a history of PFP with PFOA [53].

2.3.2 Risk Factors Associated with Patellofemoral OA A variety of factors may alter the mechanics of the patellofemoral joint and increase joint stress, potentially leading to OA [6]: Abnormal patellofemoral joint alignment and trochlear morphology are associated with patellofemoral OA (radiographic and MRI features). A recent systematic review [54] concluded that there is strong evidence that patellofemoral OA is associated with abnormal trochlear morphology and frontal plane knee alignment. There is also limited evidence that malalignment in the sagittal (patella Alta) and axial (lateral patellar displacement and tilt) planes is associated with patellofemoral OA. However, there remains a knowledge gap regarding optimal measures and thresholds to predict patellofemoral OA best. Muscle weakness: Quadriceps weakness is an important factor in patellofemoral OA. Quadriceps function, such as muscle size, [55] strength [56, 57], and muscle force [58] impaired in people with patellofemoral OA.  Importantly, quadriceps weakness is a risk factor for patellofemoral OA [59]. Weakness of muscle groups above the knee (involving the glutei, often referred to as the ‘proximal muscles’) is well documented in young individuals with non-arthritic PFP [60– 65]. Emerging evidence suggests that those with patellofemoral OA may also demonstrate more proximal muscle dysfunction than controls, including lower gluteus minimus and medius peak muscle force and lower hip abductor strength [66]. These studies found no

2  Condition Causing Anterior Knee Pain

differences in gluteus maximus peak muscle force or hip external rotator strength [67]. In the absence of longitudinal studies, the potential hip muscle weakness to increase the risk of patellofemoral OA remains unknown. Abnormal biomechanics: Recent evidence shows that individuals with patellofemoral OA demonstrate abnormal biomechanics during gait [68–71]. Fok et  al. [58] reported that those with patellofemoral OA had lower knee extension moments, quadriceps forces, and patellofemoral joint reaction forces during stair ascent and descent. In contrast to these findings, Pohl et al. [67] reported that pelvis, hip, and knee kinematics were not different between people with patellofemoral OA and controls. In the only longitudinal study to date, Teng et  al. [72] found that peak knee flexion moment and flexion moment impulse at baseline lead to the progression of patellofemoral cartilage damage over 2  years and increase the risk of patellofemoral OA. Other risk factors include obesity, injury or previous knee surgery, and professional bending and lifting [73].

2.3.3 Patellofemoral Pain and Patellofemoral Osteoarthritis Patellofemoral pain (PFP) and Patellofemoral Osteoarthritis (PFOA) have similar presentations, including the location of pain, quadriceps, and hip muscle weakness, and reported pain and difficulty with similar activities (e.g., stair climbing and prolonged sitting). However, long-term prospective data are presently lacking to confirm or refute this link, with a recent consensus statement concluding that insufficient evidence exists to link a history of PFP with PFOA [51–53]. However, there is retrospective evidence of a relationship between the previous history of PFP and the presence of PFOA later in life [74]. Thomas et  al. conducted a systematic review examining the link between a history of PFP as an adolescent or young adult and subsequent development of PFOA [75]. This systematic

2.3 Patellofemoral Osteoarthritis (PFOA)

review included six prospective studies, follow-­ ups of 5 case series, one randomized controlled trial (RCT), and one retrospective case-control study. The retrospective study aimed to examine the link between PFP and PFOA later in life [76]. The prospective studies were of low quality due to the small sample size, low follow-up rates, the inclusion of PFP due to trauma, and lack of control groups. The evidence for a link between PFP and PFOA development was limited to one retrospective case-control study by Utting et al. [76]. They compare the history of individuals with a patellofemoral arthroplasty PFOA to those with a unicompartmental tibiofemoral arthroplasty. Those undergoing patellofemoral arthroplasty (n  =  118) more frequently recalled a history of PFP (22% versus 6%), patellar instability (14% versus 1%), and patellar trauma (16% versus 6%) compared to those undergoing unicompartmental tibiofemoral arthroplasty (n = 116).

2.3.4 Clinical Presentation of PFOA A diagnosis of PFOA can be made based on history and physical examination.

2.3.4.1 History Patients with patellofemoral arthritis typically present with anterior knee pain. The patient should be asked the following questions [77]: • How long has the pain been present? • What makes it worse? • Is the condition aggravated by prolonged squatting, stair climbing, or other activities? • Is the pain dull and achy, or is it sharp? • Has the patient sought treatment for this condition in the past? • Why seek treatment now? • Is it a recent change in activity? • What type of work? • What other types of activities participate in (e.g., gardening, kneeing at church, yoga, and cycling)? • Has the patient noticed swelling in the knee? • Has the patient had prior knee surgeries?

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Pain from arthritis and malalignment is typically variable, becoming worse with activity. Constant pain that does not vary with activity suggests a referred or nonmechanical origin. Isolated patellofemoral arthritis may cause anterior knee pain that worsens with stair climbing or rising from a seated position and is not present with other activities, such as walking or running on level surfaces.

2.3.4.2 Physical Examination The physical examination comprises observation, measurement, and palpation [77]. Observations of gait and lower-extremity alignment are essential for the physical examination. Leg-length discrepancies, Q angle, and torsional deformities of the femur, tibia, and foot should be noted. Flexion contractures of the limb should be noted. Gait, such as waddling gait, should be observed, with the patient not wearing shoes. Excessive pronation of the feet, patella tracking, and rotation of the lower limb should be observed. Muscle tone and atrophy of the quadriceps and hamstrings should be assessed. Patella tracking with passive flexion, extension, and very careful semi-­squatting should be determined. Crossley et al. found that, compared with normal controls, people with patellofemoral joint osteoarthritis demonstrated the following differences while walking [78]. • Greater anterior pelvic tilt throughout the stance phase. • Greater lateral pelvic tilt (i.e., pelvis lower on the contralateral side). • Greater hip adduction. • Lower hip extension during the late stance phase. Physical findings must be evaluated in the context of patient complaints. A study of 210 adults with asymptomatic knees revealed abnormal radiographic or physical examination findings in 95% of women and 79% of men [79]. Physical findings include patellar crepitus upon flexion and extension of the knee, a hypermobile patella, and lateral position of the patella on the axial radiographs were common in this group of patients.

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Measurements of femoral anteversion, knee valgus, tibial pronation, lower limb length, and Q angle should be taken. Limb lengths were measured from the anterior iliac spine to the medial malleolus. Length discrepancies should be noted. Women typically have larger Q angles than men because of their wider hips. While an association exists between varus knee alignment and the development of osteoarthritis, no study has definitively linked Q angles to knee pathology. Palpation Both the affected and nonaffected knees should be examined. The presence of crepitus is nonspecific. Passive and active range of motion should be recorded. The strength and tightness of the hamstring and quadriceps muscle groups should be determined. Assess for the presence of ligamentous laxity, instability, and patella maltracking and attempt to elucidate the source of pain. The goal of palpating the structures of the anterior knee is to determine whether the patient’s complaints are related to arthritic changes or the underlying soft tissues [80]. Attention should focus on the lateral retinaculum, the quadriceps and patellar tendons, and the quadriceps muscle. The patella is compressed as the patient flexes the knee. Pain often is elicited by this maneuver if arthritis is present. Resisted knee extension also may reproduce the patient’s symptoms in arthritic conditions. Patients with instability contract their quadriceps muscles or complain of pain due to the sensation of subluxation, when moving the patella with the knee in lateral extension.

2.4 Patellar Tendinopathy “Jumper’s Knee” 2.4.1 Introduction Tendinopathy is a broad term encompassing painful conditions in and around the tendon due to overuse. It commonly affects the extensor mechanism (patellar tendon) and is termed a “jumper’s knee” [81]. It is characterized by progressive activity-related anterior knee pain and tenderness in the patellar tendon. It is commonly

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seen in sports that require a high demand of speed and power for leg extensors, thus causing repetitive stress to the patellar tendon [82]. These symptoms may lead to limited activity, reduced sports participation in recreational athletes, and impaired performance among professional players that may even impair their athletic careers [83]. Most athletes with mild or moderate pain continue their practice and competition. A survey conducted by Victorian Institute revealed that one-third of athletes with PT could not continue their training and competition for at least six months despite the treatments applied [84]. Once the symptoms become aggravated, even the activities of daily living, such as stair climbing, squatting, and prolonged sitting, may be affected [85]. Cook et al. reported a higher prevalence of PT in males than females, which was not confirmed in a two-year follow-up study on 138 college students [86, 87]. The higher prevalence of PT among males could be due to the difference in force generation and the ability of athletic movements between males and females [82].

2.4.2 History and Physical Examination The clinical diagnosis of the jumper’s knee is based on the subjective sensation of the pain and restriction of activities: the symptoms are insidious in onset. Usually, they relate to increased frequency or intensity of activity involving rapid repetitive ballistic movements of the knee joint [88]. The first clinical challenge is establishing whether the tendon is the source of the patient’s symptoms [89]. Patellar tendinopathy, as one of many potential diagnoses producing anterior knee pain, has specific clinical features [90, 91] that consist of (1) pain localized to the inferior pole of the patella [92] and (2) load-related pain that increases with the demand on the knee extensors, notably in activities that store and release energy in the patellar tendon [82, 93]. Other signs and symptoms, such as pain with prolonged sitting, squatting, and stairs, may be present but are also features of patellofemoral pain (PFP) and potentially other pathologies. Tendon pain occurs

2.4 Patellar Tendinopathy “Jumper’s Knee”

instantly with loading and usually ceases almost immediately when removed [94]. Pain is rarely experienced in a resting state. Pain may improve with repeated loading (the “warm-up” phenomenon) [91], but there is often increased pain the day after energy-storage activities [94]. Clinically, it is noted that dose-dependent pain is a key feature, and assessment should demonstrate that the pain increases as the magnitude or rate of application of the load on the tendon increases [91]. Assessing pain and irritability is a fundamental part of managing patellar tendinopathy and determines the duration of symptom aggravation (during loading) following energy-storage activities like a training session. Studies have suggested that up to 24 h of pain provocation after energy-­ storage activities may be acceptable during rehabilitation [95, 96], so here we will define “irritable” tendon pain as pain provocation of greater than 24 h and “stable” tendon pain as settling within 24 h after energy-storage activities. Usually, the aggravation of symptoms manifests as pain during loading activities, such as walking downstairs or performing a decline squat. Pain level can rate on an 11-point numeric rating scale, where 0 is no pain, and 10 is the worst pain imaginable. The Victorian Institute of Sport Assessment-patella (VISA-P) questionnaire is a validated pain and function outcome measure that can assess the severity of symptoms and monitor outcomes [97]. The VISA-P is a 100-­ point scale, with higher scores representing better function and less pain. The minimum clinically important difference is a change of 13 points [98]. In the authors’ experience, as progress with patellar tendinopathy is slow and the VISA-P is not sensitive to very small changes in the condition, the VISA-P should be used at intervals of 4 weeks or more. A thorough examination of the entire lower extremity must identify relevant deficits at the hip, knee, and ankle/foot region [89]. A deficit in energy-storage activities can be assessed clinically by observing jumping and hopping. Evidence shows that individuals with a history of patellar tendinopathy may use a stiff vertical jump-landing strategy (reduced knee flexion at peak vertical ground reaction force) [99]. A stiffness strategy and hip extension rather

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than flexion during a horizontal jump landing have also been observed among participants with asymptomatic patellar tendon pathology [100]. A systematic review examining landing strategies in three groups (controls, those with asymptomatic pathology, and those with symptomatic patellar tendinopathy) reported no differences between the controls and those with symptomatic patellar tendinopathy [101]. However, the data from the meta-analysis only included six symptomatic athletes. The clinical experience of the present authors suggests that athletes with patellar tendon pain tend to reduce the amount of knee flexion and appear stiff in their landing. Regardless of the individual strategy, it is optimal to distribute load through the entire kinetic chain. The purpose of evaluating function (including hopping and landing) is to identify deficits that need to be addressed in rehabilitation [89]. Ferretti et  al. classified PT into five stages [94]. Stage 0-No pain. Stage 1-Mild pain without sports restriction. Stage 2-Moderate pain during activity without affecting performance. Stage 3-Pain with slight qualitative and quantitative restrictions in performance. Stage 4-Pain with severe restriction in performance. Stage 5-Pain during daily activities. The Royal London Hospital test and the palpation test are usually used for making a diagnosis: according to Mafulli et al., both tests should be performed together for the proper clinical diagnosis [96]. The Royal London Hospital test demonstrated a lower sensitivity and higher specificity when compared to the palpation test in symptomatic individuals [102]. Single-leg decline squat is also used for the functional testing of PT [103]. The test performs on a 25° decline board. The patient stands on the board with the affected leg squatting up to 90° while keeping the trunk upright. Several scoring systems for knee injuries and pathologies are available in the literature. However, none of them successfully detects the specific inadequacies of athletes with PT [104]. The Victorian Institute of

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Sport Assessment (VISA) was found to be adequate by different researchers and tested for inter-tester and intra-tester reliability [98].

2.4.3 Differential Diagnosis Aside from the inferior pole of the patella, tendinopathy of the extensor mechanism of the knee can occur at the quadriceps tendon or distal insertion of the patellar tendon at the tibial tuberosity. These less common clinical presentations also have specific features. Quadriceps tendinopathy is characterized by pain localized to the quadriceps tendon [90]; in the authors’ experience, quadriceps tendinopathy is often associated with movements requiring deep knee flexions, such as those performed by volleyballers and weight lifters [105]. Distal patellar tendon pain, often seen in distance runners, is localized near the tibial tuberosity [90, 106]. The infrapatellar bursa is an intimate part of the distal patellar tendon attachment, and irritation of the bursa often coexists with distal patellar tendinopathy [107]. Mid or whole-tendon patellar tendinopathy is generally the result of a direct blow. However, careful differential diagnosis is required, as other structures, such as the bursae, fat pad, and patellofemoral joint, can also be injured with this mechanism [108].

2.5 Lateral Patellar Compression Syndrome 2.5.1 Introduction Due to pathologic, lateral soft tissue restraints, chronic anterior knee pain with a stable patella is often associated with overload and increased pressure on the lateral facet. “Lateral pressure in flexion” describes the pathologic process of increasing contact pressure over the lateral patellar facet as knee flexion progresses [109]. Previously described as “patellar compression syndrome” or “excessive lateral pressure syndrome,” the disorder is associated with overload and increased pressure on the lateral facet due to

2  Condition Causing Anterior Knee Pain

pathologic lateral soft-tissue restraints [110– 112]. As the knee is flexed, increased posterolateral compressive forces are exerted on the lateral aspect of the patella [113]. Because contact pressure over the lateral patellar facet increases as knee flexion progresses, a more specific term to identify the pathologic process would be “lateral patellar pressure in flexion” or, more concisely, put, “lateral pressure in flexion” (LPIF) [109].

2.5.2 Anatomic and Biomechanical Abnormalities The normal anatomy and kinematics of the patellofemoral joint should be considered to understand the pathologic process of LPIF. The lateral retinaculum is a richly innervated connective tissue structure located on the lateral aspect of the knee [114]. It is composed of 2 layers [115, 116]. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserted into the lateral margin of the patella and the patellar tendon. The deep layer of the retinaculum consists of several structures, including the transverse and lateral patellofemoral ligaments and the patellotibial band. It is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed [117]. Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this mediolateral equilibrium can lead to pain and instability [118]. The patella lies laterally with the knee extended, but in early flexion, the patella moves medially and engages in the trochlea. The knee continues to flex, and the patella flexes and translates distally [119]. By 45°, the patella is fully engaged in the trochlear groove, resulting in less dramatic changes in total contact area with greater knee flexion angles. With deeper flexion, the patella moves laterally as progressive increases in the patellofemoral joint contact area have been observed from 0° to 60° of knee flexion with greater lateral facet contact area, the medial facet contact area at each knee flexion angle [109].

2.6 Synovial Plica Syndrome

2.5.3 Clinical Presentation Patients with excessive lateral pressure syndrome usually complain of lateral retinaculum pain. The vastus lateralis inserts into the proximal lateral retinaculum and occasionally causes medial peripatellar pain due to soft tissue stretching [120]. Pain is frequently noted with stair climbing, squatting, or stooping down. As the condition worsens and articular cartilage erosion and degeneration occur, crepitation develops with passive and active motion [121]. The most critical finding on physical examination is that the patella is tilted laterally, and the lateral retinacular structures have excessive tightness compared with the medial side. Excessive lateral pressure syndromes may develop due to congenital lateral tilting of the patella, which may be subtle initially [119]. The magnitude of stress on a chronically tilted patella may become substantial [120–122]. When the patella is chronically tilted (laterally), even to a mild degree, adaptive shortening of the lateral retinaculum will occur [123]. Additionally, the medial retinacular structures, which have been placed on constant stretch, can become attenuated. A loss of normal patellar mobility characterizes this condition. In the normal knee, fully extended and relaxed, the patella can be passively displaced medially and laterally approximately 1 cm in each direction or approximately 25% of the width of the patella [124]. Patients with excessive lateral pressure syndrome may or may not exhibit associated patellar subluxation [125]. Frequently, the patient exhibits muscular atrophy of the vastus medialis oblique muscle fibers. Fulkerson et al. have reported that the small nerve branches that innervate the retinaculum may become inflamed and injured in patients with chronic retinaculum tightness [126]. The radiologic examination is extremely helpful in diagnosing this condition [126–128]. The major long-term problem with excessive lateral pressure syndrome is a deleterious effect on the articular cartilage and surrounding soft tissue. Fulkerson and Hungerford [123] stated that excessive lateral pressure syndrome primarily results from chronic lateral patellar tilt [123].

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Lateral patellar compression in flexion must be confirmed by clinical examination. Focal tenderness is present at the inferomedial patella and/ or the anteromedial joint line. There is no effusion or crepitus, and the patella is stable in both flexion and extension. A maneuver to test for LPIF involves manually centering the patella in the trochlea at 45°. The involved knee was examined with the patient in the seated position. The patient with LPIF will have pain at rest and reproduce pain with range of motion. Pain will limit extension and increase as the knee approaches 90° of flexion. Next, the examiner attempts to center the patella in the trochlea by pushing the patella medially. This maneuver will usually immediately relieve the inferomedial patellar and anteromedial joint line pain by reducing tension on the medial patellotibial ligament [109]. Complete extension is usually possible. When this maneuver decreases the patient’s pain and allows a greater pain-free arc of motion, particularly in extension, LPIF is likely.

2.6 Synovial Plica Syndrome 2.6.1 Introduction A plica is a band of thin fibrotic tissue that extends from the synovial capsule. As a result of overuse or injury, plica can become inflamed or irritated due to friction across the patella or the medial femoral condyle. Synovial plicae in the knee are anatomically normal duplications of the synovial membrane and are classified, based on their location, as suprapatellar, mediopatellar, lateropatellar, or infrapatellar (ligamentum mucosum) [129]. When the plica becomes inflamed or irritated, it can cause anterior knee pain. The literature varies widely regarding the estimated prevalence of plica syndrome. Most report a 10% prevalence based on arthroscopic studies [130]. It is estimated that plica syndrome is underdiagnosed because the symptoms are similar to other etiologies of knee pain. A study in Japan looked at 3889 knee joints during arthroscopy and found the incidence of medial plica to be 79.9% [131]. The study did not specify that the plica was the

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etiology of symptoms in all these patients, thus revealing the incidence of plica, not plica syndrome [132]. Other reviews show autopsy results that plica is present in approximately 50% of individuals [142]. Thus, the prevalence of plica on arthroscopy does not correlate with the prevalence of clinical plica syndrome.

2.6.2 Pathophysiology Plicae are normal structures in the knee joint that come together in utero. Plica typically involutes when the fetus is around 12  weeks old, but autopsy results indicate plica is present in 50% of individuals [133]. There are four different normal plicae for approximately 50% of people with a plica. They are thin and pliable and appear almost transparent in their normal state. The suprapatellar plica is found between the knee joint and the suprapatellar bursa. The infrapatellar plica was found between the intercondylar notch and the synovium around the infrapatellar fat pad. The medial plica is found between the infrapatellar fat pad and the medial aspect of the joint. Medial plicae are the most common and most common symptomatic [134]. Proximally, the mediopatellar plica is attached to the articularis genus muscle while it runs distally to the intra-articular synovial lining and blends into the medial patellotibial ligament on the medial aspect of the retropatellar fat pad [135, 136]. Depending on its position, size, and elasticity, the plica may impinge between the quadriceps tendon and femoral trochlea at 70–100 degrees of knee flexion, causing mechanical symptoms [137, 138]. In some individuals, the size and elasticity of the synovial fold can be more developed than in others. Plicae become pathological when their inherent qualities change due to an inflammatory process that alters the pliability of synovial tissue [139]. This inflammatory process makes a pathological synovial plica inelastic, tight, thickened, fibrotic, and sometimes hyalinized. A synovial plica affected by such changes may bowstring across the femoral trochlea, causing impingement between the patella and femur in knee flexion [140–143].

2  Condition Causing Anterior Knee Pain

2.6.3 Clinical Presentation 2.6.3.1 History The spectrum and diversity of symptoms can make plica syndrome challenging to pinpoint. Often, symptoms resemble or overlap with those of other pathologic conditions [139, 144, 145]. • Anterior or anteromedial knee pain • Intermittent or episodic pain • Snapping sensation along the inside of the knee as the knee is bent • Clicking, catching, clunking, grinding, popping • High-pitched snapping • Tender to the touch • Occasional giving way • Locking (really pseudo-locking) and catching • Felt as a tender band underneath the skin • Aggravation of symptoms by activity, stair climbing, or prolonged standing, squatting, or sitting Meniscal tears, patellar tendinitis, Osgood-­ Schlatter’s disease, Sinding-Larsen-Johansson disease, and patellar instability are the most commonly found concomitant conditions [146].

2.6.3.2 Physical Examination Plica syndrome. The inferomedial quadrant is usually the most painful region by physical examination. On physical examination, the patient typically has tender points along the medial and inferior aspect of the patella; in some instances, a painful, hypertrophied membrane is palpable. The inferomedial quadrant is the most consistently painful region. Occasionally, a medial apprehension test of the patella elicits a positive response, but careful evaluation reveals that it is due to direct tenderness to palpation in the region of the plica and is not true patellar instability [Rovere]. Rovere et al. stated that a palpably tender plica without an intra-articular effusion conclusively establishes a diagnosis of plica syndrome, provided that other causes of knee pain are ruled out [147]. Upon palpating the medial peripatellar region, a taut articular band that reproduces the patient’s

2.7 Sinding-Larsen-Johansson Syndrome

pain is virtually pathognomonic for plica syndrome. The pain may refer to as a positive TARP sign, in which TARP stands for the following: T—Taut, A—Articular band, R—Reproduces, P—Pain. Irha and Vrdoljak described two diagnostic tests for medial plica syndrome [148]. The first is the active extension test, where a quick extension of the tibia is performed, such as kicking a ball. The test is positive when painful, caused by the abrupt tension on the plica from the quadriceps femoris muscle. The second test is the flexion test, where the tibia is quickly swung into flexion from a full extension position, stopped between 3° and 60° of flexion [148]. The test is again positive when painful, caused by the plica stretching with eccentric contraction of the quadriceps muscle. Kim et al. also described a test to diagnose medial plica syndrome [149]. The mediopatellar plica test (MPP) was conducted with a supine patient and the knee extension [149]. The test applies manual force to the inferomedial portion of the patellofemoral joint and flexing the knee to 90° [150]. The test is positive when the patient experiences pain with the knee in extension and the pain is eliminated or reduced with the knee in flexion [149, 151]. The sensitivity and specificity of this test compared to arthroscopy were 89.5% and 88.7%, respectively, with a diagnostic accuracy of 89.0% [149].

2.7 Sinding-Larsen-Johansson Syndrome 2.7.1 Introduction In 1921–1922 Sinding-Larsen and Johansson independently described the symptoms of this disease of the inferior pole of the patella accompanied by fragmentation or calcification of the pole [152]. The syndrome is seen in adolescents typically between 10 and 14  years of age but most often in males who play sports (football, running, volleyball, gymnastics) [153, 154]. The

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etiology appears to be traction tendinitis with de novo calcification in the proximal attachment of the patellar tendon, which had been partially avulsed [155].

2.7.2 Pathophysiology The Sinding-Larsen-Johansson Syndrome is caused by increased tension and pressure due to repetitive traction by the patellar tendon on the lower pole of the patella (still partly cartilaginous in adolescents) during contraction of the quadriceps muscle [156] and leads to cartilage damage, swelling, and pain, especially after the exertion of force, and later to tendon thickening and fragmentation of the lower pole of the patella and sometimes to bursitis, i.e., inflammation of a bursa situated between the tendon and the patella [156]. The Sinding-Larsen-Johansson Syndrome (SLJS) has a pathogenesis similar to the Osgood-­ Schlatter’s disease, and the two disorders sometimes occur simultaneously [157]. This pathology is also considered traction apophysitis with symptoms in anterior tibial tuberosity. In both entities, the patient and family must be informed of the self-limiting nature of the symptoms and their approximate duration of 12 months before spontaneous resolution.

2.7.3 Risk Factors • Repetitive running and jumping activities. • Long periods of increase in training. • Sport specialization—Doing the same sport year-round without adequate breaks places stress on the same areas of the body. • Fall on the front of the knee. • Improper training technique, including a poor form for conditioning, running, and/ or jumping. • Improper footwear. • Muscle tightness in the leg. • Weak hip or core muscles.

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2.7.4 Clinical Presentation Clinically it is characterized by pain localized to the lower pole of the patella. Any activity, from normal walking to climbing stairs, may increase the person’s pain depending upon the severity of the condition. In less severe cases, a person may not begin to feel pain until after extended activity, such as running for several miles. The pain occurs when straightening the knee against force: deep knee bends, kneeling, jumping, climbing stairs, squatting, running, or weightlifting [158]. Tenderness to the touch, limping, and a tender bump in the infrapatellar area are common signs. The knee’s lower extremity neurovascular signs or crepitus are rare and may indicate another pathology. During a subjective assessment, a patient often reports localized pain, swelling, or tenderness at the front of the patella’s knee base. Patients are typically young active boys aged 10–13 years. Symptoms are usually: • Worse with exercise, stair climbing, squatting, kneeling, jumping, and running. • May report that they limp after exercise. • May be unilateral or bilateral. • Is relieved by rest. Evolution is usually benign with spontaneous recovery; full recovery usually takes 12–24 months, thanks to physiological regeneration. The pain disappears when the patella is completely ossified, and complications are rare [159].

2.7.5 Differential Diagnosis The differential diagnosis was primarily established with a sleeve fracture in the lower pole of the patella. Other entities to be ruled out include stress fracture of the patella, type I bipartite patella, and patellar tendinitis or “jumper’s knee” [160]. Other diseases (with similar symptoms to the Sinding-Larsen-Johansson Syndrome) are injuries to the infrapatellar fat pad, Hoffa disease,

2  Condition Causing Anterior Knee Pain

patellofemoral joint dysfunction, and mucoid degeneration of the infrapatellar tendon [161]. The clinical presentation of the Sinding-Larsen-­ Johansson Syndrome (SLJD) can be difficult to differentiate from other injuries or diseases like a sleeve fracture, osteochondritis, stress fracture of the patella, tendinopathy of the patella tendon, and Osgood-Schlatter’s disease [162]. Based on the radiographic findings, the difference between a sleeve fracture, osteochondritis, and a stress fracture is difficult. The SLJD results from overuse, while the sleeve fracture is due to trauma (acute) with an explosive acceleration that causes rapid quadriceps contraction while the knee flexes. This mechanism causes an avulsion of the periosteum, retinaculum, and patella cartilage [163]. So with the anamnesis (patient’s account of the mechanism). Likewise, osteochondritis is related to overuse, just like the SLJD. The etiology of these three injuries (SLJD, osteochondritis, and a stress fracture) does not differ sufficiently. Following this, further investigation needs to be performed. Tendinopathy (jumper’s knee) and SLJD can appear at the same time. Further studies must clarify the differences between SLJD and osteochondritis, stress fracture, and tendinopathy [152]. For this purpose, MRI is the method of choice. Research shows that the Osgood-Schlatter’s disease and SLJD incidence is four times greater in sport-­specialized athletes than in multisport athletes. Osgood-­ Schlatter’s disease and S ­ inding-Larsen-­Johansson Syndrome may, in some cases, appear in the same patient at the same time [152, 162].

2.8 Osgood–Schlatter’s Disease (OSD) 2.8.1 Introduction Osgood-Schlatter’s Disease, also known as osteochondrosis or traction apophysitis of the tibial tubercle, is a common cause of anterior knee pain in the skeletally immature athletic population. It was first described in 1903 by Robert Bayley Osgood (1873–1956) and Carl Schlatter

2.8 Osgood–Schlatter’s Disease (OSD)

(1864–1934) [164–166]. Osgood-Schlatter’s Disease is an overuse injury in active adolescent patients. It occurs secondary to repetitive strain and microtrauma from the force applied by the strong patellar tendon at its insertion into the relatively soft apophysis of the tibial tubercle. This force results in irritation and severe cases, partial avulsion of the tibial tubercle apophysis. The force increases with higher activity levels, especially after rapid growth [167]. The incidence is higher in athletes (21%) compared to non-­athletes (4.5%), 21% in athletes compared to 4.5% in non-athletes in one study [168]. Rarely trauma may lead to a full avulsion fracture. Predisposing factors include poor flexibility of quadriceps and hamstrings or other evidence of extensor mechanism misalignment [167].

2.8.2 Pathophysiology The growth plate of the tibial tuberosity does not develop until several months after birth and is structurally different from most growth plates loaded primarily by compression [169]. Histologically, it is particularly different from the juxtaposed proximal tibial growth plate. The physis of the tibial tuberosity is composed primarily of fibrocartilage and fibrous tissue, with bone being added to the anterior portion of the tibial metaphysis by membranous bone formation [169]. Initially, very little of the growth plate comprised columnated cells, but by the time of maturation of the tuberosity, with the exception being the most distal region, the columnar portion has extended distally and is found under most of the tuberosity [169]. These structural features would adapt to the strong tensile forces exerted in this region. The tibial tubercle develops as a secondary ossification center that provides attachment for the patellar tendon [167]. Bone growth exceeds the ability of the muscle-­ tendon unit to stretch sufficiently to maintain previous flexibility leading to increased tension across the apophysis [167]. The physis is the weakest point in the muscle-tendon-bone attachment (as opposed to the tendon in an adult) and is

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at risk of injury from repetitive stress. With the repeated contraction of the quadriceps muscle mass, especially with repeated forced knee extension as seen in sports requiring running and jumping (basketball, football, gymnastics), softening and partial avulsion of the apophyseal ossification center may occur with a resulting osteochondritis. The appearance and closure/ fusion of the tibial tubercle occur in the following sequence pattern [167]: Tibial tubercle is entirely cartilaginous (age  18 years).

2.8.3 Risk Factors The main risk factors for Osgood-Schlatter’s disease are [168]: Age. The Osgood-Schlatter’s disease occurs during puberty’s growth spurts. Age ranges differ by sex because girls experience puberty earlier than boys. The Osgood-Schlatter’s disease typically occurs in boys ages 13–14 years and girls ages 11–12 years. Sex. The Osgood-Schlatter’s disease is more common in boys, but the gender gap is narrowing as more girls become involved with sports. Sports. The condition often happens with sports involving running, jumping, and swift changes in direction.

2.8.4 Clinical Presentation Osgood-Schlatter’s disease causes pain in the front lower part of the knee. This pain is usually at the ligament–bone junction of the patellar ligament and the tibial tuberosity. Intense knee pain is usually the presenting symptom during running, jumping, squatting, direct knee trauma, kneeling, and ascending or descending stairs.

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The pain is worse with acute knee impact. Pain is initially mild and intermittent. In the acute phase, the pain is severe and continuous. The impact on the affected area can be very painful. Pain typically improves with rest and subsides minutes to hours after the inciting activity or sport stops. Pain is exacerbated particularly by running and jumping. An enlarged prominence at the tibial tubercle is present, with tenderness over the site of patellar tendon insertion. Pain may be reproduced by resisted knee extension and active or passive knee flexion. In up to 10% of the refractory cases, symptoms may persist for >1–2 years beyond skeletal maturity [167]. In skeletally mature patients with persistent symptoms, ossicle excision may be performed. Bilateral symptoms were observed in 20–30% of patients [168]. Usually, OSD resolves at the end stages of skeletal growth. Osgood Schlatter Disease is a clinical diagnosis, and radiographic evaluation is usually unnecessary [167]. Plain radiographs may rule out additional diagnoses such as fracture, infection, or bone tumor if the presentation is severe or atypical. The radiographic evaluation may also indicate evaluating for avulsion injury of the apophysis or other injuries after a traumatic event. Classic radiographic findings in Osgood-Schlatter’s disease include an elevated tibial tubercle with soft tissue swelling, fragmentation of the apophysis, or calcification in the distal patellar tendon. It is worth noting that these findings can also be seen as normal variants and do not always represent pathology, so the clinical correlation is of utmost importance [167, 168]. If ordering radiographs, consider comparing bilateral images to delineate normal versus abnormal in the individual patient. In up to 10% of the refractory cases, symptoms may persist for >1–2  years. In addition to a complete medical history and physical examination, diagnostic procedures for Osgood-Schlatter’s disease may include: bone scans—a nuclear imaging method to evaluate any degenerative and/or arthritic changes in the joints to detect bone diseases and tumors; to determine the cause of bone pain or inflammation; ultrasound determines any swelling in the soft tissue, cartilage, bursa, and tendon.

2  Condition Causing Anterior Knee Pain

2.8.5 Differential Diagnosis Some other diseases should be considered in the differential diagnosis of OSD, such as Sinding-­ Larsen-­Johansson syndrome, Hoffa’s syndrome, soft tissue or bone tumors, patellar tendon avulsion or rupture, chondromalacia patellae, patellar tendinitis, infectious apophysitis, accessory ossification centers, osteomyelitis of the proximal tibia, and tibial tubercle fracture [167, 170, 171].

2.9 Juvenile Osteochondritis Dissecans (JOCD) 2.9.1 Introduction Osteochondritis Dissecans (OCD) is an acquired condition of the joint that affects the articular surface and the subchondral bone [172]. The term osteochondritis dissecans was first coined by Konig in the late 1880s; he described it as an inflammation of the bone cartilage interface [173]. The juvenile form of the disease (JOCD) presents in those aged five to 16 years with open growth plates [174]. The causes of OCD are unknown; however, repetitive trauma, inflammation, accessory centers of ossification, ischemia, and genetic factors have been proposed [175– 181]. Osteochondritis dissecans of the knee are frequently located in the medial femoral condyle. The location in the patella is rare (approximately 2%) and is predominantly in the lower portion [182]. It was first described by Rombold in 1936 [183]. Only isolated cases or small series of patients have been reported in the literature. Based on a register of more than 30,000 operated knees, Schwarz et  al. [184] showed a surgical incidence of 0.15%.

2.9.2 Etiology Mechanical, biological, and anatomical factors may all have a role in developing this disease. A great weight has been placed on mechanical factors causing OCD [185]. First proposed in the 1950s, the traumatic theory [186] has evolved

2.9 Juvenile Osteochondritis Dissecans (JOCD)

from a single traumatic event to a repetitive microtrauma theory [187, 188]. Biomechanical factors, including obesity [176], lower-limb alignment abnormalities [177], soft-tissue instability [189], and knee activity-related positioning, have also been implicated [190]. Local ischemia has been proposed as another causative factor for OCD. Enneking demonstrated that the vascular anatomy of subchondral bone is similar to that of bowel mesentery with poor arteriole anastomoses, making it susceptible to any ischemic insult [191]. In cadaveric specimens at OCD predilection sites, novel imaging techniques have demonstrated abnormal vascular architecture [180]. An increased incidence of JOCD in monozygotic twins suggests a genetic etiology to JOCD [174, 192, 193]. Other researchers have described familial cases of OCD lesions associated with short stature and multiple lesion sites [194]. Osteochondritis dissecans of the knee are frequently located in the medial femoral condyle. Only isolated cases or small series of patients have been reported in the literature. Based on a register of more than 30,000 operated knees, Schwarz et  al. [184] showed a surgical incidence of 0.15%. JOCD is a significant cause of knee pain in adolescents, both athletes and non-athletes [172]. The lateral aspect of the medial condyle of the femur is the most common site of JOCD, accounting for 75% of JODC lesions [195]. The term “osteochondritis” suggests an inflammatory etiology; however, histology of the lesion had shown damage to bone and cartilage rather than inflammation [196]. The lesion of JOCD can be either closed or open, and either stable or unstable [197].

2.9.3 Clinical Presentation The clinical presentation of JOCD is highly variable, with some children being completely asymptomatic. Pain can be poorly localized in nature; joint swelling and mechanical symptoms may also be associated. The symptoms caused by JOCD are variable and will depend on the location and severity of the disease. JOCD typically presents with poorly localized, activity-related

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knee pain in sporty patients. Crepitus, catching, or locking of the joint may occur later [172]. Clinical findings and judicious imaging can frequently make the diagnosis. The physical examination should include careful inspection of the knee, palpation for point tenderness, joint effusion, range of motion (ROM), evaluation of limb alignment, and associated injuries (ligaments/ meniscus). Wilson has described a clinical test to identify the presence of JOCD in the medial femoral condyle [198]. It involves eliciting knee pain with internal rotation of the tibia during 30° to 90° of knee flexion and then easing the knee pain with external rotation [172]. Unfortunately, this test has proven to be of limited diagnostic value, although it may be useful for charting clinical progress [199, 200]. There are no pathognomonic symptoms or signs of JOCD. A routine thorough physical examination of the hip should also be performed to rule out hip pathology, which commonly refers to knee pain [172]. JOCD is four times more common in males than females, and the lesion is bilateral in 10–20% of the cases [195]. The highly active athlete presents a history of aching, gradual knee pain for several days to weeks, typically located over the anterior knee, and worse during activity. There may be a history of intermittent knee swelling following a practice or game session. The examination may or may not reveal mild effusion or knee motion limitation. Findings may also vary depending on the stage of the disease [197]. In the early stages, with the articular cartilage over the femoral condyle intact, the signs are non-specific. When the articular cartilage is eroded in the late stages, the fragment may separate and become an intra-­ articular loose body. This fragment can cause pain, effusion, and locking. When the athlete flexes the internally rotated leg, from full extension to about 3° degrees, pain is elicited, relieved upon external rotation (Wilson sign) [198, 199], and it is typically only for the lesion on the medial femoral condyle. X-rays indicated when JOCD is suspected. In addition to the AP and lateral views, a tunnel view is useful to see the lesion, which appears as a well-demarcated radiolucent area [201, 202]. An MRI is often obtained in those who demonstrate significant edema or hemar-

40

throsis, marked discomfort, and inability to bear weight without pain. An MRI can help identify unstable lesions. However, it is important to note that MRI is less specific for identifying lesion stability in skeletally immature adolescents when compared to evaluating the same lesion in adults [203, 204].

2  Condition Causing Anterior Knee Pain

of several synovial recesses separated by fat projections or alae [212]. The deep infrapatellar bursa is interposed inferiorly between the patellar tendon and posteriorly to the proximal tibia [213]. The HFP is a dynamic structure. It alters position, pressure, and volume throughout the knee ROM [214]. When the knee moves into flexion, the superolateral portion of the fat pad becomes 2.10 Hoffa Syndrome relaxed, freely expansive, and moves posteriorly. The HFP lies between the lateral patella facet and 2.10.1 Introduction quadriceps tendon in extension. Therefore, the most commonly observed symptoms are associThe infrapatellar fat pad (IPFP), also known as ated with the extension. However, it could also Hoffa’s fat pad (HFP), is an intracapsular extra-­ see in flexion, where the pain is provoked by the synovial structure in the anterior knee joint. trapped IFP between the patella tendon and anteStructurally it is composed of adipose tissue sim- rior femur [215]. ilar to subcutaneous fat [205]. Its role is to HFP facilitates gliding between the femoral improve the distribution of the lubricant effect of condyles and joint capsule. Knee mechanics can intra-articular joint fluid by increasing the syno- be altered when there is adhesion in the fat pad vial surface [206] and reducing the impact of that changes the position of the patella and patelloading by absorbing forces generated in the lar tendon. Consequently, the effectiveness of the knee joint [207]. Even under extreme starvation extensor mechanism is compromised, decreasing conditions where subcutaneous fat is eliminated, the effective moment arm and placing greater its preservation suggests a central role in knee demands on the quadriceps to produce the same joint homeostasis [208]. Acute or chronic inflam- knee extension force. A shorter patellar tendon mation of the Infrapatellar fat pad (IFP) is a com- length affects patellar mobility and creates resismon source of anterior knee pain, also called tance to lateral translation at full extension [214]. Hoffa’s disease, fat pad syndrome, or hoffitis. The HFP comprises adipocytes and adipose conAlbert Hoffa first reported fat pad syndrome in nective tissues containing collagen embedded in 1904 [209]. an amorphous ground substance encompassing glycosaminoglycans. It can be divided into inner and outer tissues [216]. The inner tissue is the 2.10.2 Anatomic and Biological pad’s core with hard pillow-like adipose tissue Characteristics of IPFP with cushioning properties, whereas the outer tissue is a soft adipose tissue surrounding the inner The infrapatellar fat pad is bordered by the infe- tissue. It described that the inner tissue might rior pole of the patella superiorly, the joint cap- undergo a compressive load, and the outer tissue sule and patellar tendon anteriorly, the proximal may undergo a tensional load. The HFP has tibia and deep infrapatellar bursa inferiorly, and space-filling properties in the joint cavity, which the synovium-lined joint cavity posteriorly [210]. implies an essential role in joint function, such as The fat pad is tethered to the intercondylar notch secreting synovial fluid [217], promoting lubricasuperiorly by the infrapatellar synovial fold or tion [218], and shock absorption. The periphery plica ligamentum mucosum. It also is attached of the IPFP is highly vascularized, but the center directly to the anterior horns of the menisci infe- is poorly vascularized. riorly [211] and the periosteum of the tibia [209]. The blood of HFP is supplied by two vertiThe interface between the posterior aspect of cal arteries connected by two to three horizonthe fat pad and the adjacent joint space consists tal arteries [219]. The primary blood supply

2.10 Hoffa Syndrome

originates from the synovial membrane. The HFP is also richly innervated and contains lymphatic vessels. Bohnsack et  al. [220] and Witoński et al. [221] found a significant distribution of substance-­P (SP) nerves inside the IPFP.  As a neurotransmitter, SP is released from primary afferent nerve endings and exists in the central, autonomous, and peripheral nervous systems. Besides pain mediation, SP also plays an important role in chronic inflammatory conditions [222].

2.10.3 Pathophysiology Little is known about the development of fat pad syndrome. The anatomical location of IFP exposes it to mechanical load, especially during extension [223]. Overuse or repeated microtrauma from sports or falls leads to hypertrophy. If the fat pad fails to recover, it can become chronically inflamed, which, if not properly managed, may result in fibrosis and ossification [211]. Predominantly seen in young women, jumping sports and ligamentous laxity are also risk factors for Hoffa’s disease [215].

2.10.4 Physical Examination The inflamed fat pad is often enlarged, firm in consistency, and easy to palpate. Hoffa’s test can be performed. To avoid pain provocation in adjacent structures and incur false results, Krumar et  al. [224] suggested a modification of Hoffa’s test that involves taking the knee into passive forced hyperextension by lifting the heel and keeping anterior pressure on the tibia. This position stimulates pain exclusively in the fat pad if inflamed [215]. Gliding the patella in all four directions (medially, laterally, superiorly, and inferiorly) is important to detect adhesion or movement restriction during knee movement, particularly in hyperextension. Pain in hyperextension is a strong indicator of the presence of inflamed IFP [214]. The examination should also aim to exclude any other radiating pathologies, particularly from the spine and hip.

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2.10.5 Clinical Diagnosis Fat pad syndrome could be a primary disorder or secondary to other pathologies such as meniscus injuries or ligamentous tears. Prevalence is not widely investigated; however, two studies reported isolated fat pad in 1% [225] of anterior knee pain cases and 6.8% [224] as a secondary disorder. Synovitis and swelling of the fat pad were reported after the anterior cruciate ligament (ACL) rupture [225]. A detailed history and findings on functional assessment are important to discriminate fat pad syndrome from other conditions such as patellar lateral femoral friction syndrome, impingement of the infrapatellar plica, and arthrofibrosis “cyclops syndrome.” Symptoms of fat pad syndrome are anterior knee pain, often retropatellar and infrapatellar. Patellofemoral crepitus might be present with knee loading, such as in stairs negotiation [215], squatting, jumping, and running [214]. Effusion and decreased ROM are often seen with inflamed IFP. Pain and/or discomfort from long walks, flat shoes, and prolonged standing refer mostly to fat pad syndrome. Pain resulting from up or downhill walking is a characteristic of PFPS. Conditions that involve the Hoffa fat pad include intrinsic abnormalities (Hoffa disease, intracapsular chondroma, localized nodular synovitis, postsurgery fibrosis, shear injury, and nonspecific inflammation). Extrinsic abnormalities include articular disorders (joint effusion, intraarticular bodies, meniscal cyst, ganglion cyst, cyclops lesion); synovial abnormalities (pigmented villonodular synovitis; hemophilia; synovial hemangioma; primary synovial chondromatosis; chondrosarcoma; lipoma arborescent; rheumatoid, seronegative, and septic arthritis; synovitis associated with primary osteoarthritis) and anterior extracapsular abnormalities such as Osgood-­ Schlatter’s disease, Jumper’s Knee and Sinding-Larsen-Johanssen syndrome. HFP impingement is a clinical syndrome— manifesting mainly as anterior knee pain [226, 227], which most commonly occurs after repetitive local microtraumas. Impingement is typically located at the superolateral portion of the

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HFP. It is secondary to a repetitive pinch of the external portion of the fat pad between the lateral patellofemoral ligament and the cartilage of the lateral facet of the trochlea. Any conditions associated with a decreased distance between these two structures can facilitate local impingement. A higher position of the patella (patella Alta) is also associated with HFP impingement. The impingement is typically observed during full flexion of the knee [228]. The patient presents lateral parapatellar pain aggravated by physical activity, which slowly disappears with rest. A joint effusion is only rarely detected. The differential diagnosis of chondromalacia of the patellar cartilage is difficult during the physical examination since the symptoms are nearly identical in both conditions. Proximal patellar tendinopathy (jumper’s knee) presents anterior knee pain, and a local pressure of the proximal tendon reproduces the patient’s symptoms. Whereas ultrasound can easily confirm the diagnosis of the jumper’s knee, this technique is useless in diagnosing HFP impingement [228]. Some studies have reported an association between HFP impingement and superolateral, posterior, or diffuse edema [227]. HFP edema characteristically manifests as an area of increased signal intensity on high-contrast MRI images. A careful correlation between MRI data and the clinical findings is necessary to plan the correct treatment.

2.11 Superficial Patellar Bursitis 2.11.1 Introduction A bursa is a fluid-filled structure between the skin and tendon or tendon and bone. The main function of a bursa is to reduce friction between adjacent moving structures. Inflammation of this fluid-filled structure is called bursitis. Trauma, infection, overuse, and hemorrhage are common inflammation causes [229]. Other causes include systemic illnesses like collagen vascular disease and inflammatory arthropathy; in some instances, the cause is unknown [230]. Some cases of bursitis are associated with certain occupations and are named accordingly; for instance, prepatellar

2  Condition Causing Anterior Knee Pain

bursitis is also known as housemaid’s knee, and superficial infrapatellar bursitis is synonymous with clergyman’s knee [231].

2.11.2 Normal Anatomy Bursae are flattened sacs that serve as protective buffers between bones and overlapping muscles (deep bursae) or between bones and tendons or skin (superficial bursae) [232]. The prepatellar bursa is located between the patella and the overlying subcutaneous tissue. The prepatellar bursa allows the patella to slide freely beneath the skin during flexion and knee extension. Infrapatellar bursae can be superficial or deep. The superficial infrapatellar bursa is located between the tibial tubercle and the overlying skin, whereas the deep infrapatellar bursa is located between the posterior aspect of the patellar tendon and the tibia [231].

2.11.3 Pathophysiology The bursa is a synovial lining representing a potential space insofar as it is collapsed upon itself until a resulting trigger causes the bursa to become irritated and fill with synovial fluid [233]. The patient experiences pain when the inflamed bursa is compressed against bone, muscle, tendon, ligaments, or skin. Inflammation of the bursa causes synovial cells to multiply, increasing collagen formation and fluid production [232]. A more permeable capillary membrane allows the entrance of high-protein fluid. The bursal lining may be replaced by granulation tissue, followed by fibrous tissue. The bursa becomes filled with fluid, often rich in fibrin, and the fluid can become hemorrhagic [229]. Bursitis has three phases: acute, recurrent, and chronic [234]. Local inflammation occurs during the acute phase of bursitis, the synovial fluid thickens, and movement becomes painful. Chronic bursitis leads to continual pain and can cause weakening of overlying ligaments and tendons and, ultimately, rupture of the tendons. Because of the possible adverse effects of chronic bursitis

2.11 Superficial Patellar Bursitis

on overlying structures, bursitis, and tendinitis may occur together; the differential diagnosis should include both of these diagnoses [232]. Prepatellar bursitis, also known as housemaid’s knee, is associated with trauma or repetitive kneeling over an extended period. The prepatellar bursa is also a common site for septic (infectious) bursitis, a diagnosis that should be considered when skin injury, erythema, warmth, or severe tenderness over the patella. In patients with prepatellar septic bursitis, the patella is not palpable, and knee flexion is painful. Bursitis has many causes, including autoimmune disorders, crystal deposition (gout and pseudogout), infectious diseases, traumatic events, hemorrhagic disorders, and secondary overuse. Repetitive injury within the bursa results in local vasodilatation and increased vascular permeability, stimulating the inflammatory cascade. The incidence of bursitis is higher in athletes, reaching levels as high as 10% in runners. Approximately 85% of cases of superficial septic bursitis occur in men. A French study assessing the prevalence of knee bursitis in the working population found that most cases occurred in male workers whose occupations involved heavy workloads and frequent kneeling [235].

2.11.4 Clinical Presentation 2.11.4.1 History The patient may give a history of acute or repetitive trauma to the area consistent with nonseptic bursitis (NSB) or prior local cellulitis suggesting septic bursitis (SB). Unfortunately, no physical exam finding is specific or sensitive enough to include or exclude an infectious etiology [236] adequately. Infrapatellar bursitis is inflammation of the superficial or deep infrapatellar bursa. Symptoms may include knee pain, swelling, and redness below the patella. It may be complicated by patellar tendonitis [237]. The emergency provider must distinguish NSB from SB, which is usually a result of direct inoculation into the bursa rather than hematogenous seeding [238]. The most common organism is Staphylococcus aureus. It more commonly affects immunocom-

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promised individuals with risk factors such as alcoholism, diabetes, and patients with repeated steroid exposure [239, 240].

2.11.4.2 Physical Examination On physical examination, patients have tenderness at the site of the inflamed bursa. If the bursa is superficial, physical examination findings are significant for localized tenderness, warmth, edema, and skin erythema. Reduced active range of motion with preserved passive range suggests bursitis, but the differential diagnosis includes tendinitis and muscle injury [232]. A decrease in both active and passive range of motion suggests other musculoskeletal disorders [233]. The affected limb may show disuse atrophy and weakness in patients with chronic bursitis. Tendons may also be weakened and tender. Although septic bursitis is not diagnosed solely based on clinical signs, certain signs tend to favor the diagnosis of septic over sterile inflammatory bursitis. In particular, patients with septic bursitis may have a fever, bursal warmth, tenderness that is more severe than nonseptic bursitis, and associated peribursal cellulitis [240, 241]. Joint motion is typically preserved in septic bursitis, whereas other types of bursitis are associated with a limited range of motion. In prepatellar bursitis, inflammation arises secondary to trauma or constant friction between the skin and the patella, most commonly when performing frequent forward kneeling. Previously referred to as housemaid knee, it is now seen regularly in many other occupations, including carpet laying (carpet-layer knee), coal mining (beat knee), roofing, gardening, and plumbing. Bursitis may develop 7–10  days after a single blow, such as a fall. Prepatellar bursitis is often visualized as fluctuant, well-circumscribed warm edema over the lower pole of the patella. Knee flexion causes increased tension over the bursa and increased pain. The knee joint itself, however, is normal. Superficial infrapatellar bursitis (clergyman’s knee) is located more distally than prepatellar bursitis and is often caused by frequent kneeling in an upright position. It can also be seen in gout

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or syphilis. The differential diagnosis includes Osgood-Schlatter’s disease. The deep infrapatellar bursa is less frequently inflamed [242]. Clinically, the patient exhibits pain with flexion and extension at the extremes of the range of motion. Edema is located on both sides of the patellar tendon and is associated with tenderness.

2.12 Patellar Fractures 2.12.1 Introduction Patellar fractures account for approximately 1% of all skeletal fractures and may result from direct, indirect, or combined injuries [243]. They are most prevalent in individuals between 20 and 50 and occur twice as often in men as in women [244]. Patellar fractures are the most common cause of disruption of the extensor mechanism, six times as frequent as soft tissue injuries such as quadriceps or patellar tendon rupture [245]. Fractures may be caused by excessive force through the extensor mechanism or by a direct blow. Complications include stiffness, extension weakness, and patellofemoral osteoarthritis [246]. Fractures of the patella are rare injuries in children, with an incidence under 1% of all fractures in children [247]. A type of patella fracture, particularly in children, is the sleeve fracture, where the small, eggshell-like bony fragment is dislocated with a larger soft tissue consisting of cartilage, periosteum, and retinaculum [248].

2.12.2 Anatomy and Biomechanics The patella is the largest sesamoid bone of the human body and is embedded in the quadriceps tendon. It is one of the few bones without a periosteal surrounding [244]. The proximal three-­ fourths of the patella is covered by a thick layer of cartilage, whereas the remaining distal pole is not part of the articular congruency. The adjacent quadriceps muscle consists of four muscles: the rectus femoris is the longest and most superficial. The deep layer of the quadriceps tendon inserts at the proximal basis of the patella, whereas the

2  Condition Causing Anterior Knee Pain

superficial fibers extend over the patella itself continuously to the tibial tuberosity. The fascia lata spreads over the anterior surface of the knee and forms the patellar retinaculum in combination with aponeurotic fibers introduced by the lateral and medial vastus muscles. The patellofemoral ligaments—radiating from the patella to the femoral epicondyles—contribute to the patellar retinaculum [249]. These fibers have a crucial function as they allow some degrees of active extension even in a patellar fracture (reserve extensor mechanism) [244]. The crucial function of the extensor mechanism of the knee is to maintain an erect position and realize the unassisted gait. The principal purpose of the patella is linking and displacement [250]. During flexion, it is located in the groove of the femoral trochlea acting primarily as a link between the quadriceps muscle and the proximal tibia. At 45°–60° of flexion, the proximal part of the patella, covered by a thick cartilage layer, can withstand most pressure [251]. Between 45° of flexion and full extension, the patella increases the effective lever arm of the quadriceps by displacing the linkage between the quadriceps and tibia away from the axis of knee rotation. Biomechanical studies have demonstrated that this increases the lever arm of the quadriceps by up to 30% at full extension [250]. The patella also plays an important role in the resistance of knee flexion [252]. It converts tensile forces into compression forces and thus decelerates knee flexion, particularly during walking downstairs or downhill [253, 254], also known as the “patellofemoral joint reaction (PFJR)” [254]. To fulfill its function, the patella has to withstand high forces, which are as high as 3200 N equaling four to five times standard body weight [255].

2.12.3 Mechanism of Injury and Classification of Patellar Fractures Patellar fractures result from direct, indirect, or combined injury. Direct injuries can be secondary to low-energy trauma (fall on the knee from sitting or standing height) or high-energy trauma (dashboard impact in a motor vehicle accident)

2.12 Patellar Fractures

[243]. Most commonly, though, the mechanism of injury combines direct and indirect patterns, i.e., a culmination of a direct blow, quadriceps contraction, and secondary joint collapse [243]. The fracture pattern is not determined solely by the mechanism of injury but also depends on factors such as patient age, bone quality, and degree of knee flexion [244]. Patellar fractures are commonly classified according to their morphologic pattern and degree of displacement. Cramer et al. postulated that fractures with less than 3 mm displacement should be considered non-displaced [256]. With indirect injuries, the fracture mechanism involves failure of the extensor mechanism due to eccentric overload, typically a forceful contraction mechanism of the quadriceps with the knee in the flexed position. When the force of the fall overwhelms the resistance to knee flexion, the extensor mechanism fails, resulting in a patellar fracture [257]. Several primary patellar fractures have been identified, with separate diagnostic, imaging, and management considerations [258]. As seen on plain radiographs, patella fractures are typically classified by the fracture line orientation. The primary types include vertical, transverse, marginal, stellate, osteochondral, and comminuted [244, 245, 259, 260]. Transverse fractures occur horizontally across the patella and are often due to an indirect impact (i.e., falls). Vertical fractures typically run from the inferior to the superior pole and may be stable and treated conservatively. Fractures to the patella’s margins that occur at the patella’s perimeter are commonly due to a direct force to the side of the patella. Comminuted fractures are often seen in multiply injured patients. These cases often present a high degree of soft tissue damage [244]. Patella sleeve fractures are most common in children aged 8–16 years and are more likely to occur during adolescence. More than half of patients in skeletally immature patients are patella sleeve fractures [261].

2.12.4 Clinical Presentation History. An individual who has sustained a patella fracture presents pain in the affected knee. The history reveals a direct blow to the knee, a

45

fall, or a combination of the two. Overlying abrasions, ecchymosis over the anterior aspect of the knee, or both may be present. Physical Examination. Any lacerations must be assumed to communicate with the joint until the saline load test disproves this assumption. Because the retinaculum may have a large tear, injecting a significant amount of saline (up to 100 mL) may be necessary to exclude an open joint [262]. An accompanying intra-articular effusion may be present, revealing fat globules if aspirated [262]. If the fracture is displaced, a defect is palpable at the fracture site. The extensor mechanism must always be evaluated. As a result of the pain associated with the injury and hemarthrosis, the patient may not perform a straight leg raise. Aspiration of the hemarthrosis under sterile conditions and the instillation of lidocaine may relieve the pain sufficiently to perform a reliable examination. Disruption of the extensor mechanism renders the patient unable to extend the knee against gravity and usually implies a tear in the medial and lateral quadriceps expansion [262]. Evaluation of the soft tissue status is crucial as the degree of soft tissue damage determines the further course of the patient. In up to 25% of cases, a skin abrasion is present, interfering with the timing of surgery and the surgical approach [263]. Osteochondral fractures of the patella are usually a result of shear forces caused by a patellar dislocation and occur less frequently by a direct impact trauma of the patella [264, 265]. Patients rarely have an extension deficit, but the affected knee commonly presents with acute hemarthrosis and a positive apprehension sign of the patella, as described by Fairbank [266]. Patients with patella sleeve fractures present with hemarthrosis, the inability to extend the knee and bear weight, and either patella Alta (inferior sleeve) or patella Baja (superior sleeve). These fractures occur without an antecedent direct blow to the patella. A palpable defect is often present superior or inferior to the patella. Diagnosis may be difficult with a minimal fracture displacement as patients can extend their knee without an extension lag with internal rotation of the limb and utilization of the tensor fascia lata [261].

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2  Condition Causing Anterior Knee Pain

2.13 Symptomatic Bipartite

2.13.3 Pathophysiology

2.13.1 Introduction The patella generally develops from a single ossification nucleus, and ossification starts from the center toward the periphery. The primary ossification nucleus appears between 3 and 5 years of age. During the ossification of the patella, secondary ossification centers may appear around 12  years of age [267]. The complete fusion of primary and secondary ossification centers causes the formation of a unique patella. However, bipartite or tripartite patella forms occur when these ossification centers fail to fuse and remain separate. Bipartite patella (BP) is accepted as a normal anatomic variant of the patella and is usually asymptomatic and identified incidentally on knee radiographs taken for other reasons [268].

Tissues interposed between the bipartite fragment and the body of the patella are reportedly fibrous tissue and fibro-cartilage [270], fibrocartilage only [271], or fibrocartilage and hyaline cartilage [272]. Oohashi et al. [270] noted that a striking histopathological feature of the painful bipartite patella’s interposed tissue was fibrous or necrotic fibrocartilage. The bone marrow adjacent to interposed tissue showed numerous small vessels. Additionally, the trabecular bone and fibro-cartilage surfaces adjacent to the bone marrow were scalloped and lined with numerous osteoclasts [270]. Similar observations of areas of increased vascularity [271] and osteoclastic activity have been described [273]. Such findings are consistent with a reparative reaction in the interposed tissue [270].

2.13.2 Classification

2.13.4 Causes of Pain

Saupe (1921) proposed the first classification system for BP by analyzing some cases reported in the literature. This classification system is based only on the location of the fragment, and BP is grouped into three distinct types:

• Movement at the interface. As causes of pain, several authors reported mobility at the interface between the bipartite fragment and the body of the patella in patients who had undergone surgery [271, 273–275]. This movement presumably causes pain in most symptomatic patients [276]. • Articular cartilage of the bipartite fragment. Although many authors have reported that the articular cartilage of the bipartite fragment of the superolateral bipartite patella was intact [271, 277–279], there have been a few cases of abnormal findings relevant to the articular cartilage of the bipartite fragment [270, 280]. Ogata found that the articular surface of the separated fragment had been replaced with fibrocartilage in one type II patella [280]. Oohashi et  al. [270] also reported a patient with lateral bipartite patella in which the proximal one-fourth and distal one-half of the articular surface of the bipartite fragment was replaced by fibrous tissue.

• Type I: inferior pole ~1%. • Type II: lateral margin ~20–25%. • Type III: superolateral portion ~75%. Most recently, Oohashi et al. (2010) reclassified the BP and proposed a new classification system based on the location and number of fragments [269]. They claimed that there is no true secondary ossification center at the patella’s inferior pole and previously reported inferior pole BP (Saupe classification Type I) was the sequel of Sinding-Larsen-Johansson disease (traction apophysitis of the inferior patellar pole). Therefore, they excluded inferior pole BP from classification and included two subtypes of more than two fragments (tripartite patella).

2.14 Idiopathic Anterior Knee Pain

• Traction apophysitis. Several authors have hypothesized that a major cause of pain in patients with a bipartite patella was excessive traction force by the vastus lateralis muscle on the bipartite fragment [271, 277, 279, 280]. This situation is analogous to Sinding-Larsen-­ Johansson disease at the inferior patellar pole or Osgood-Schlatter’s disease in the tibial tuberosity.

2.13.5 Clinical Presentation In 1977, Weaver reported a series of 21 patients with bipartite patellae and described two characteristic modes of symptom onset: (1) gradual onset during activity in athletes and (2) sudden onset after an injury in non-athletes, such as a direct blow to the knee [275]. Since these two reports were published, bipartite patella has been a cause of anterior knee pain in adolescents and young athletes [276]. Symptomatic bipartite patella is occasionally observed in adolescents and young athletes, especially those who regularly participate in strenuous sports [278, 279, 281, 282]. In 58% of patients with symptomatic bipartite patella, the onset of pain is at 12–14 years of age [269]. The most common symptom is pain in the separated fragments during or after strenuous activity [277, 278, 281–283]. Patients sometimes complain of pain during knee bending or when climbing stairs [269]. Localized tenderness over the separated fragments is the most common physical finding [275, 277, 278, 281, 283, 284]. In adults, a bipartite patella becomes symptomatic following a minor injury, such as a blow to the knee [269, 272, 274], or a major injury, such as acutely displaced separation of the bipartite fragment [285]. Rarely, in middle-aged or elderly patients a severe injury such as a fall causes both separations of the bipartite fragment and rupture of the quadriceps tendon [286–289]. Among adults, bipartite patella rarely becomes symptomatic in those with gout tophus in the space between the bipartite fragment and the body of the patella [290, 291].

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2.14 Idiopathic Anterior Knee Pain 2.14.1 Introduction Idiopathic anterior knee pain refers to non-­ specific, vague, mostly activity-related anterior knee pain and is the most common cause of knee pain in adolescents [196, 292–295]. The exact cause is unknown [296]. Most believe that the origin of the problem lies in the patellofemoral joint [297]. Several theories have been proposed, including muscular imbalance, physical overactivity, and extremity malalignment [298, 299]. Sandow and Goodfellow considered it the “headache of the knee” [300]. McNerney and Arendt state that idiopathic anterior knee pain affects around 30% of the adolescent population and is more common in adolescent females, 2–10 times higher than their male counterparts [301].

2.14.2 Clinical Presentation Each patient should take a detailed history of the nature and type of knee pain. The young active athlete presents with either acute or gradual onset anterior knee pain affecting one or both knees, usually seen following a recent increase in physical activity. The pain is increased after prolonged sitting, ascending or descending stairs, and repeated squatting exercises. Usually, the pain is present for a few weeks with intermittent activity-­related exacerbations and improves with a period of rest [302]. The athlete may give a history of knee catching, pseudo locking, or giving away [294]. Clinical examination should ensure that knee pain is not secondary to a structural or pathological abnormality and include assessment of patellar follow-up, knee stability, joint line sensitivity, and radiographic evaluation. The legs and hip joints need to be also examined for any abnormalities and include patellar tracking assessment, knee stability, joint line tenderness, and radiographic evaluation. On examination,

48

look for abnormal gait, increased lumbar lordosis, and any asymmetry of hips or lower extremities; observe atrophy and weakness of the quadriceps muscles by comparing it to the normal side. A decrease in flexibility of the hamstrings and quadriceps is while displacing it medially or laterally. Crepitus may be felt in some athletes. Pain elicited with patellar inhibition or compression test [296]. It is important that before labeling a case as idiopathic AKP, one excludes various physical causes such as trochlear dysplasia, patellar instability, OsgoodSchlatter’s disease, etc. [296].

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56 241. Lieber SB, Fowler ML, Zhu C, Moore A, Robert H. Shmerling & Ziv Paz Clinical characteristics and outcomes of septic bursitis. Infection. 2017;45:781–6. 242. Chatra PS. Bursae around the knee joints. Indian J Radiol Imaging. 2012:22. 243. Melvin JS, Karunakar MA.  Patella fractures and extensor mechanism injuries. In: Court-Brown CB, Heckman JD, McQueen MM, Ricci WM, Tornetta III P, editors. Rockwood and Green’s fractures in adults. Philadelphia: Wolters Kluwer; 2004. p. 2269–302. 244. Gwinner C, Mardian S, Schwabe P, Schaser KD, Krapohl BD, Jung TM.  Current concepts review: fractures of the patella. GMS Interdiscip Plast Reconstr Surg DGPW. 2016;5:Doc01. 245. Pengas IP, Assiotis A, Khan W, Spalding T.  Adult native knee extensor mechanism ruptures. Injury. 2016; https://doi.org/10.1016/j. injury.2016.06.032. 246. Jarraya M, Diaz LE, Arndt WF, Roemer FW, Guermaz A.  Imaging of patellar fractures. Insight Imaging. 2017;8:49–57. https://doi.org/10.1007/ s13244-­016-­0535-­0. 247. Dai LY, Zhang WM.  Fractures of the patella in children. Knee Surg Sports Traumatol Arthrosc. 1999;7:243–5. 248. Wu CD, Huang SC, Liu TK. Sleeve fracture of the patella in children. A report of five cases. Am J Sports Med. 1991;19:525–8. 249. Reider B, Marshall JL, Koslin B, Ring B, Girgis FG.  The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351–6. 250. Kaufer H. Mechanical function of the patella. J Bone Joint Surg Am. 1971;53(8):1551–60. 251. Goldstein SA, Coale E, Weiss AP, Grossnickle M, Meller B, Matthews LS.  Patellar surface strain. J Orthop Res. 1986;4(3):372–7. 252. Hungerford DS, Barry M.  Biomechanics of the patellofemoral joint. Clin Orthop Relat Res. 1979;144:9–15. 253. Benjamin J, Bried J, Dohm M, McMurtry M.  Biomechanical evaluation of various forms of fixation of transverse patellar fractures. J Orthop Trauma. 1987;1(3):219–22. 254. Koval KJ, Kim YH. Patella fractures. Evaluation and treatment. Am J Knee Surg. 1997;10(2):101–8. 255. Huberti HH, Hayes WC, Stone JL, Shybut GT. Force ratios in the quadriceps tendon and ligamentum patellae. J Orthop Res. 1984;2(1):49–54. 256. Cramer KE, Moed BR. Patellar fractures contemporary approach to treatment. J Am Acad Orthop Surg. 1997 Nov;5(6):323–31. 257. Scolaro J, Bernstein J, Ahn J. Patellar fractures. Clin Orthop Relat Res. 2011;469:1213–5. 258. Christine Lamoureux et al. Patella fracture imaging medscape. Updated: Sep 14, 2020. 259. Ali Yousef MA, Rosenfeld S. Acute traumatic rupture of the patellar tendon in pediatric population: Case series and review of the literature. Injury. 2017;48(11):2515–21.

2  Condition Causing Anterior Knee Pain 260. Linjun Xie MS, Hong Xu MS, Lizhi Zhang MD, Rong Xu MS, Guo Y.  Sleeve fracture of the adult patella, case report and review of the literature. Medicine. 2017;96:32(e7096). https://doi. org/10.1097/MD.0000000000007096. 261. Hunt DM, Somashekar N. A review of sleeve fractures of the patella in children. Knee. 2005;12:3–7. 262. Schwartz AK.  Patella fractures. Updated: Aug 19, 2020. 263. Bumbaširević M, Lešić A.  Acute injuries of the extensor mechanism of the knee. Curr Orthop. 2005:1949–58. 264. Hawkins RJ, Bell RH, Anisette G.  Acute patellar dislocations. The natural history. Am J Sports Med. 1986;14(2):117–20. 265. Stanitski CL, Paletta GA Jr. Articular cartilage injury with acute patellar dislocation in adolescents. Arthroscopic and radiographic correlation. Am J Sports Med. 1998;26(1):52–5. 266. Fairbank HA.  Internal derangement of the knee in children and adolescents (section of orthopaedics). Proc R Soc Med. 1937;30(4):427–32. 267. Ogden JA. Radiology of postnatal skeletal development X. Patella and tibial tuberosity. Skelet Radiol. 1984;11:246–57. 268. Kose O, Eraslan A, Ergun A, Egerci OF, Ercan EC. Prevalence of bipartite patella in Turkish population analysis of bilateral knee radiographs in 897 subjects. Int J Morphol. 2015;33(3):1108–13. 269. Oohashi Y, Koshino T, Oohashi Y. Natural history of the superolateral bipartite fragment of the patella in children. J Orthop. 2010;7(4):e5. 270. Oohashi Y, Noriki S, Koshino T, Fukuda M.  Histopathological abnormalities in painful bipartite patellae in adolescents. Knee. 2006;13:189–93. 271. Ogden JA, McCarthy SM, Jokl P. The painful bipartite patella. J Pediatr Orthop. 1982;2:263–9. 272. Canizares GH, Selesnick FH. Bipartite patella fracture. Arthroscopy. 2003;19:215–7. 273. Green WT.  Painful bipartite patellae. Clin Orthop Relat Res. 1975;110:197–200. 274. Iossifidis A, Brueton RN.  Painful bipartite patella following injury. Injury. 1995;26:175–6. 275. Weaver JK. Bipartite patellae as a cause of disability in the athlete. Am J Sports Med. 1977;5:137–43. 276. Oohashi Y.  Developmental anomaly of ossification type patella partita. Knee Surg Sports Traumatol Arthrosc. 2015;23:1071–6. https://doi.org/10.1007/ s00167-­014-­2887-­7. 277. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M.  Vastus lateralis release for the painful bipartite patella. Arthroscopy. 2002;18:404–11. 278. Bourne MH, Bianco AJ.  Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10:69–73. 279. Mori Y, Okumo H, Iketani H, Kuroki Y.  Efficacy of lateral retinacular release for painful bipartite patella. Am J Sports Med. 1995;23:13–8.

References 280. Ogata K. Painful bipartite patella. A new approach to operative treatment. J Bone Joint Surg Am. 1994;76:573–8. 281. Carney J, Thompson D, O’Daniel J, Cassidy J. Arthroscopic excision of a painful bipartite patella fragment. Am J Orthop. 2010;39:40–3. 282. Weckstrom M, Parviainen M, Pihlajamaki HK. Excision of painful bipartite patella. Good long-­ term outcome in young adults. Clin Orthop Relat Res. 2008;466:2848–55. 283. Ishikawa H, Sakurai A, Hirata S, Ohno O, Kita K, Sato T, Kashiwagi D.  Painful bipartite patella in young athletes. Clin Orthop Relat Res. 1994;305:223–8. 284. Felli L, Fiore M, Biglieni L. Arthroscopic treatment of symptomatic bipartite patella. Knee Surg Sports Traumatol Arthrosc. 2011;19:398–9. 285. Ireland ML, Chang JL.  Acute fracture bipartite patella: case report and literature review. Med Sci Sports Exerc. 1995;27:299–302. 286. Carter SR.  Traumatic separation of a bipartite patella. Injury. 1989;20:244. 287. Gorva AD, Siddique I, Mohan R.  An unusual case of bipartite patella fracture with quadriceps rupture. Eur J Trauma. 2006;4:411–3. 288. Woods GW, O’Connor DP, Elkousy HA. Quadriceps tendon rupture through a superolateral bipartite patella. J Knee Surg. 2007;20:293–5. 289. Tonotsuka H, Yamamoto Y. Separation of a bipartite patella combined with quadriceps tendon rupture: a case report. Knee. 2008;15:64–7. 290. Enomoto H, Nagosi N, Okada E, Ota N, Iwabu S, Kamiishi S.  Hemilaterally symptomatic bipartite patella associated with bone erosions arising from a gouty tophus: a case report. Knee. 2006;13:474–7. 291. Kobayashi K, Deie M, Okuhara A, Adachi N, Yasumoto M, Ochi M. Tophaceous gout in the bipartite patella with intra- osseous and intra-articular lesions: a case report. J Orthop Surg (Hong Kong). 2005;13:199–202.

57 292. Dutton RA, Khadavi MJ, Fredericson M.  Patellofemoral Pain. Phys Med Rehabil Clin N Am 2016;27:31–52.9. 293. Rathleff MS, Vicenzino B, Middelkoop M, et  al. Patellofemoral pain in adolescence and adulthood: same, but different? Sports Med. 2015;45:1489–95. 294. Kodali P, Islam A, Andrish J. Anterior knee pain in the young athlete: diagnosis and treatment. Sports Med Arthrosc. 2011;19:27–33. 295. Barber Foss KD, Myer GD, Chen SS, et  al. Expected prevalence from the differential diagnosis of anterior knee pain in adolescent female athletes during preparticipation screening. J Athl Train. 2012;47:519–24. 296. Patil S, White L, Jones A, Anthony CWHUI. Idiopathic anterior knee pain in the young. A prospective controlled trial. Acta Orthop Belg. 2010;76:356–9. 297. Nimon G, Murray D, Sandow M, Goodfellow J. Natural history of anterior knee pain: a 14-20 year follow up of non-operative management. J Pediatr Orthop. 1998;18:118–22. 298. Shea KG, Pfeiffer R, Curtin M. Idiopathic anterior knee pain in adolescents. Orthop Clin North Am. 2003;34:377–83. 299. Witvrouw E, Lysens R, Bellemans J, Cambier D, Vanderstraeten G. Intrinsic risk factors for the development of anterior knee pain in an athletic population. Am J Sports Med. 2000;28:480–9. 300. Sandow MJ, Goodfellow JW. The natural history of anterior knee pain in adolescents. J Bone Joint Surg. 1985;67-B:36–8. 301. Mcnerney ML, Arendt EA. Anterior knee pain in the active and athletic adolescent. Curr Sports Med Rep. 2013;12:404–10. 302. Patel DR, Villalobos A. Evaluation and management of knee pain in young athletes: overuse injuries of the knee. Transl Pediatr. 2017;69(3):190–8. https:// doi.org/10.21037/tp.2017.04.05.

3

MRI Findings of Superficial Prepatellar Soft Tissues

3.1 Introduction Anterior knee pain (AKP) is the most common knee complaint. It has various underlying causes, including the superficial prepatellar soft tissues at the anterior knee, the skin, subcutaneous fat, superficial prepatellar bursae, superficial infrapatellar bursa, and fascia. These extracapsular soft tissues are predisposed to acute injury, repetitive overuse, penetrating trauma, and infection [1]. The most common pathology affecting the superficial layer is symptomatic bursitis of the superficial prepatellar and infrapatellar bursae. The bursae are made up of a synovial membrane. This thin tissue membrane secretes the synovial fluid contained within the bursa sac. Synovial fluid is a lubricant, and this viscous fluid inside the bursa allows structures to glide easily. Bursae can be divided into two types, anatomic and adventitial. Anatomic bursae are true synovial lined sacs that may be fluid-filled and located in expected positions near the joint. In contrast, adventitial bursae are not synovial lined and may occur away from the joint. Bursae are normal, synovial-lined cavities that reduce friction between neighboring moving structures such as tendons, ligaments, and bones [2]. Prepatellar bursae also allow the absorption of shocks and the protection of the structures of the patellofemoral joint [3]. Normally none of these superficial bursae com-

municate with the knee joint. Prepatellar soft tissues are also the second most common location of the Morel-Lavallée lesion is a closed traumatic degloving injury located at the interface between the subcutaneous fat and the fascia. A shearing injury causes a lesion during a fall on the knee or a blow against the playing ground or another player during sports [2].

3.2 Superficial Prepatellar Bursae Usually, superficial prepatellar bursae contain no fluid, so they may not be detectable on MRI. They become visible in imaging studies only when distended due to fluid accumulation, usually traumatic, inflammatory, degenerative, or other pathologic processes. Distended bursae may be symptomatic or asymptomatic and incidentally discovered in imaging studies. When symptomatic, they may present as a palpable mass, painful knee, mechanical dysfunction, or limitation in range of motion [2]. The symptoms may mimic the pathology of adjacent structures, i.e., ligaments, menisci, or bone.

3.2.1 Superficial Prepatellar Bursitis The prepatellar bursa lies superficial to the quadriceps continuation and is centered in the ­midline,

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_3

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and it may not extend medially or laterally relative to the patella [4, 5] (Fig. 3.1). Standard anatomic medical books describe the prepatellar bursa as a unicompartmental bursa situated symmetrically anterior to the patella [6, 7]. Surgical and cadaveric studies have shown the prepatellar bursa to be trilaminar or bilaminar, separated by two thin septa oriented in the coronal plane [4, 8] (Fig. 3.2). The compartments are superficial, compartment, designated the prepatellar subcutaneous bursal space, localized between the subcutaneous tissue and an extension of the fascia lata, called the transverse superficial fascia, which is the structure classically described in the anatomic literature; an intermediate compartment, the prepatellar subfascial bursal space, situated between the transverse superficial fascia and an intermediate oblique fascia formed by fascial extension of the vastus lateralis and vastus medialis muscles; and a deep compartment, the prepatellar subaponeurotic bursal space [4, 8]. In MRI clinical routine, those compartments are often not apparent (Fig. 3.3).

a

Fig. 3.1  Prepatellar bursitis in a 43-year-old woman with anterior knee pain. PD FS image in the sagittal plane (a) shows a distended superficial prepatellar bursa (asterisk), and in the axial plane (b) highlights that the prepatellar

The normal prepatellar bursa is very small and thin. The average diameter in an adult human is about 4 cm and is about 2 mm thick [9]. The bursal membrane is semipermeable, allowing some materials to flow across the membrane into and out of the sac. Any superficial bursa’s acute or repetitive injury results in bursitis, a common condition with fluid accumulation, synovitis, and bursal wall thickening resulting in anterior knee pain and swelling. Chronic overuse can lead to bursal wall thickening, superficial fibers, and fascial thickening rather than bursal fluid accumulation (Fig. 3.4). While bursitis is most common in the middle aged and elderly, young athletes such as wrestlers and football linemen who place excessive compressive or shear loads on the prepatellar tissues, can also develop recalcitrant bursitis [1]. Elite cyclists can develop significant fascial thickening related to repetitive rubbing of the more mobile anterior fiber layers against the fixed deep layer [10]. It usually is little or no fluid visible in the prepatellar tissues in younger patients. However, older patients often show

b

bursa does not extend medially or laterally relative to the patella. Note the presence of a small synovial cyst under the tibial insertion of the anterior cruciate ligament (arrow a)

3.2 Superficial Prepatellar Bursae

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small amounts of asymptomatic ill-defined superficial fluid (Fig.  3.5). Accumulation of ­ superficial bursal fluid results in better-defined focal fluid accumulation producing an arc of coronally oriented fluid over the patella, patellar tendon, or tibial tubercle that is typically unilocular [1] (Fig. 3.6). Occasionally, septa are evident in the fluid collection, presumably representing the various prepatellar fibrous layers. However, it can be challenging to distinguish which bursae are affected.

3.2.2 Superficial Infrapatellar Bursitis

Fig. 3.2  PD FS image in the sagittal plane in a patient with post-traumatic prepatellar bursitis 6 weeks after the accident. The marked resorption of the bursal fluid enables visualization of the fibrous septa: transverse superficial fascia (black arrow), intermediate oblique fascia; (white dotted arrow), and deep longitudinal fibers of rectus femoris tendon (white arrow)

a

Fig. 3.3  Prepatellar bursitis in a 51-year-old woman with anterior knee pain and swelling. PD FS images in the sagittal plane (a) and axial plane (b) show a distended oval

Superficial infrapatellar bursitis, called clergyman’s knee, is inflammation and fluid accumulation. It is a small, thin structure in only 55% of anatomic specimens [11]. The normal bursa is often compartmentalized by a thin, longitudinally oriented septum and rarely exceeds the width of the underlying tendon, and maybe adventitial without a true synovial lining [11]. The superficial infrapatellar or pretibial bursa

b

fluid-signal-intensity lesion between the subcutaneous tissue and the patella (black arrows)

3  MRI Findings of Superficial Prepatellar Soft Tissues

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a

Fig. 3.4  Chronic superficial prepatellar, slightly infrapatellar bursitis in a 57-year-old man tiler with anterior knee pain for about 4 months.T1 SE image (a) and PD FS image (b) in sagittal plane show swelling of the prepatel-

Fig. 3.5  Chronic superficial prepatellar-infrapatellar bursitis in a 31-year-old man cyclist with anterior knee pain for about 2  months. PD FS image in the sagittal plane shows swelling of the prepatellar-upper infrapatellar bursa with no fluid visible and fascial thickening related to repetitive flexions (black arrows). Note a fluid accumulation in the suprapatellar si retropatelat bursa (asterisk)

b

lar- slightly infrapatellar bursa with bursal wall thickening (white arrows image a and black arrows image b) and little fluid visible in the bursa

Fig. 3.6  Unilocular superficial bursitis in a 35-year-old woman athlete. The PD FS image in the sagittal plane shows fluid accumulation with a coronal column (thick black arrows) covering the patella, patellar tendon, and tibial tubercle (black dotted arrows). Note the myxoid-­ inflammatory infiltration at the level of the patellar insertion of the Quadriceps (white dotted arrow) and patellar tendons (white arrow) with an aspect of insertional tendinitis/tendinosis

3.2 Superficial Prepatellar Bursae

usually is located between the tibial tuberosity and the overlying skin. Concerning the triggering factor, infrapatellar bursitis can occur in acute (Fig. 3.7), subacute (Fig. 3.8), or chronic forms. This bursa can be located in the soft tissues slightly inferior to the patella (Fig. 3.9) or the soft tissues superior to the tibial tuberosity. Sometimes, the pretibial bursa can extend along the entire length of the patellar tendon (Fig. 3.10). Cadaveric injection studies suggest that these bursae communicate to varying degrees, resulting in a unilaminar, bilaminar, or trilaminar appearance at imaging when distended [5, 12]. In chronic inflammation, the infrapatellar bursa can communicate with the more superiorly located prepatellar bursae or the pretibial bursa located below the tuberosity [13] (Fig. 3.11). Clinically, there is a palpable swelling inferior to the patella. On MRI, it appears as a loculated collection anterior to the patellar tendon, forming a swelling

a

Fig. 3.7 Acute superficial infrapatellar bursitis in a 50-year-old man with anterior knee pain 3 days ago after a fall on his right knee.T1 SE image (a) and PD FS image (b) in the sagittal plane show swelling of the infrapatellar bursa located between the tibial tuberosity and the overly-

63

(Fig. 3.12). It should be differentiated from subcutaneous edema on imaging: edema is seen as a diffuse fluid collection all over the knee’s anterior aspect, whereas bursitis appears as a localized collection with well-defined borders (Fig.  3.13). Superficial bursitis at the anterior knee is most commonly due to mechanical overuse and is commonly referred to as “housemaid’s knee,” although other occupations requiring ­prolonged kneelings, such as tile or carpet laying, can also lead to this disorder [13]. Non-­ mechanical causes of superficial bursitis include chronic glucocorticoid use, inflammatory arthritis, infection, and gout [3] (Fig.  3.14). Bursae containing fluid may appear simple, demonstrating homogeneous fluid equivalent signal on T1 and T2-weighted images or complex and multiloculated with thin internal septations. Clinical factors determine the significance of fluid found within the bursae on MRI. The MRI observation

b

ing skin, with oval cystic appearance with dimensions of 0.9 / 0.7 cm and fluid content, hyposignal T1 SE (white asterisk) and hypersignal PD FS (black asterisk). A fine blade of perilesional edema suggests recent acute development (short arrows a, b)

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64

a

b

Fig. 3.8  Subacute superficial infrapatellar bursitis in a 31-year-old woman athlete with anterior knee pain four weeks ago. PD FS image in the sagittal plane (a) shows elongated oval distension of the tibial pretuberosity infrapatellar bursa, with relatively homogeneous fluid

a

Fig. 3.9  Superficial infrapatellar bursitis is located in the soft tissues slightly inferior to the patella in a 47-year-old man, a former athlete with anterior knee pain located suprapatellar at the insertion of the quadriceps tendon.

content (black arrow). PD FS image in the axial plane (b) highlights that the prepatellar bursa is not extended medially or laterally (continue arrows) relative to the patellar tendon (dotted arrow)

b

Note that the avulsion of a small cortical bone fragment from the anterosuperior contour of the patella is a possible source of suprapatellar pain (dotted arrows a, b)

3.2 Superficial Prepatellar Bursae

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Fig. 3.10  Superficial infrapatellar bursitis in a 53-year-­ old man with anterior knee pain. It is located in the soft tissues extending along the entire patellar tendon length at the subpatellar level. PD FS image in the sagittal plane shows homogeneous fluid accumulation with a fusiform appearance that distended the infrapatellar bursa along the entire length of the patellar tendon (dotted and continuous white arrows). Note relatively homogeneous fluid accumulation in the suprapatellar bursa (synovial recesses) with its distension (asterisk)

a

b

Fig. 3.12  Subacute exophytic superficial infrapatellar bursa in a 37-year-old woman with anterior knee pain 4 days ago after a car accident. Sagittal T1 image (a), sagittal PD FS image (B), and axial PD FS image (c) show

Fig. 3.11  Chronic superficial infrapatellar bursa with proximal and distal extension in a 61-year-old man with prolonged kneeling and chronic anterior knee pain. The PD FS image in the sagittal plane shows a distended infrapatellar bursa, which communicates with the superior prepatellar bursae and the pretibial bursa below the tuberosity. Multiple fibrous septa are interrupted due to mechanical stress exceeding physiological limits by repeated kneeling (black arrows). Increased fluid accumulation in the suprapatellar bursa (asterisk) is associated with the thickening of the synovial fold (dotted arrows)

c

ovoid distension of the infrapatellar bursa (arrows a–c) with fluid content in hyposignal T1 and hypersignal PD FS

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a

Fig. 3.13  Illustration of differences between prepatellar bursitis fluid accumulation and subpatellar edema. (a) A 57-year-old woman with infrapatellar bursitis. The sagittal PD FS image shows fluid accumulation in the infrapatellar bursa and a good view of the bursal walls (white

Fig. 3.14  Nonmechanical causes of superficial bursitis in a 51-year-old woman with rheumatoid arthritis and chronic knee pain improve after glucocorticoid treatment. PD FS image in the sagittal plane shows fluid accumulation in the infrapatellar bursa (star) with proximal and distal extension in the prepatellar (black continue arrow) and pretuberosity bursa (dotted black arrow). Note fluid accumulation in the suprapatellar bursa (asterisk), and deep infrapatellar bursa (white dotted arrow), with the appearance of reactive bursitis following prolonged treatment with glucocorticoids

b

arrows). (b) A 37-year-old woman demonstrates a diffuse fluid collection seen all over the anterior aspect of the knee (black arrows), compared to bursitis, in which fluid accumulation appears localized with well-defined borders

shows bursal distension, mild circumferential bursal wall thickening, adjacent soft tissue, and reactive marrow edema. Because synovial fluid may be absorbed by the synovial cell lining, whereas fibrin and other debris are not, cyst contents may become inspissated or mineralized. Bursae containing proteinaceous or hemorrhagic material may demonstrate hyperintensity on T1-weighted images, while those containing calcification or hemosiderin will exhibit intrinsic low signal on both T1 and T2-weighted images. Superficial infrapatellar bursitis, also called clergyman’s knee, is due to inflammation and fluid accumulation resulting from chronic stress [14]. Septic bursitis at the anterior knee can be hematogenous but is more often iatrogenic or related to a penetrating injury. A draining sinus tract, intrabursal gas, or foreign bodies in the bursa suggests infection, but aspiration is only recommended when an infection is suspected [15]. Intrabursal hemorrhage can also lead to complex fluid collections with fluid–fluid levels of variable signal intensity related to the state of blood product degradation [15].

3.3 Prepatellar Morel-Lavallée Lesion

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3.3 Prepatellar Morel-Lavallée Lesion

larger and looser in women [4, 5]. Typically, these injuries are manifested as fluid collections at the interface between the subcutaneous fat and A Morel-Lavallee lesion (MLL) is a post-­ underlying fascia, with variable appearances on traumatic soft tissue degloving injury, originally MRI [20]. described by French surgeon Victor Auguste Francois Morel-Lavallee in 1863 [15]. These lesions have been given multiple names, includ- 3.3.1 Pathologic and Anatomic Features ing Morel-Lavallee effusion, Morel-Lavallee hematoma, Morel-Lavallee extravasation, pseudolipoma, pseudocyst, ancient hematoma, orga- The mechanism of injury is a sudden shearing nizing hematoma, chronic expanding hematoma, force that occurs tangentially to the fascial planes, and post-traumatic soft tissue cyst [16]. It is causing the somewhat mobile dermis and subcucaused by a vertical shearing force which causes taneous fat to move abruptly relative to the firmer closed internal degloving where the skin and sub- underlying fascia [17, 21]. The dissecting trauma cutaneous tissue are separated from the underly- can disrupt perforating capillaries, lymphatics, ing fascia. This separation disrupts the blood and nerves. These disrupted capillaries may convessels and lymphatics, accumulating blood in a tinuously drain into the perifascial plane, leading newly formed cavity [16, 17]. The most com- to the accumulation of lymph, blood, debris, and monly involved site is over the greater trochanter, fat in the interfascial plane, which leads to the while less common sites include the pelvis, thigh, formation of a collection in this potential space and knee [18]. More recently, authors have [22]. The rate at which this collection form described cases of MLLs involving the knees of depends on the number of disrupted vessels and football players and the abdominal wall of the flow into the cavity [23]. By the time the patients following liposuction and abdomino- lesion gets a fibrous capsule in its periphery, with plasty [19]. Several authors have noted a gender blood products, necrotic fat tissue, fibrin, and discrepancy in the incidence of MLLs, describing debris centrally [18]. Lesion evolution is generally divided into four the increased incidence in women to differences in the anchorage of skin to underlying fascia and stages [18, 21]. The dermis is separated from the the anatomy of the fat compartments, which are underlying fascia (Fig. 3.15). Next, extravasation

a

b

Fig. 3.15  A 45-year-old man presented with right knee pain after a motor vehicle accident. Clinical examination 2 days after the accident suggested ACL rupture without any skin damage to the knee. MRI examination 3 weeks after the injury—PD FS in axial, coronal, and sagittal (a– c), and T1 SE in the sagittal plane (d), confirmed complete acute rupture of ACL (the images are not shown here). Besides, it stands out, fusiform fluid collections (asterisk,

c

d

b–d) in hypersignal PD FS and hyposignal T1, located in the post-traumatic space created between the subcutaneous fat (dotted arrows a–d) and the underlying vastus medialis oblique muscle (black arrows b, c) and the medial retinaculum inferiorly (white arrows a–d), aspect suggestive for an ML lesion (acute post-traumatic seroma)

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from the lymphatics and the injured subdermal plexus produces a fluid collection mixture of blood, lymph, and fatty debris. After this stage, over time, these components are replaced by serosanguinous fluid as the lesion enlarges. If left untreated during the acute stage, local inflammation leads to the fourth stage of pseudocapsule formation and lesion maturation as the body attempts to sequester the fluid-filled space [21]. Several forms of subcutaneous fluid collections may result, depending on the severity of the injury, ranging from seroma to hematoma (Fig.  3.16). After some time, the blood is reabsorbed and replaced by serosanguineous fluid [24]. This hemolymphatic collection may continue to enlarge, and patients may present with a large mass, usually located over the external aspect of the thigh. Because of this enlarging nature, these collections may be mistaken for soft tissue tumors [18, 25]. This serosanguineous collection may spontaneously resolve or undergo a secondary inflammatory reaction with subsequent fibrous capsule formation [17, 18] (Fig. 3.17).

3.3.2 Clinical Presentation The MLL may present acutely or appear days following injury, and presentation depends on multiple factors. The extent and rate of hemoa

b

Fig. 3.16  A 51-year-old woman presented with right knee pain and lateral swelling to a direct hit. The MRI examination was performed 3 days after the trauma. PD FS images in coronal (a), axial (b), and T1 SE in the sagittal plane, show a fluid biloculated collection in hypersignal PD FS (asterisk) and hyposignal T1 (asterisk c). Fluid

lymphatic accumulation within the cavity and the patient’s body habitus frequently determine the clinical identification of an MLL [21]. The key clinical feature to aid diagnosis and accurate history is the presence of fluctuance within the lesion [18, 26]. Patients may also experience decreased skin sensitivity and increased mobility [18, 27]. Ecchymosis, road rash, and abrasions may give clues to the diagnosis [28]. Superficial skin discoloration may be delayed for several days, so the lesion initially may go unrecognized. Hudson estimated that one-third of MLLs go undiagnosed during acute trauma [29]. The area may become painful and firm as time elapses, indicating fibrous capsule formation. Chronic lesions may mimic other soft tissue masses, including neoplasms [29]. If improper management occurs, the lesion’s late evolution can lead to infection or necrosis of the soft tissue envelope. Potential differential diagnoses include bursitis, necrosis, hematoma, hemangioma, soft tissue sarcoma, and early myositis ossificans [30, 31]. Because these lesions may be slow-growing and clinically silent, they may be ignored and diagnosed after trauma when they become painful and large. To be retained, a patient who presents with pain and palpable mass at a time interval between a few days and even months or years after trauma should be suspected and investigated for MLLs [18]. c

is located in the post-traumatic space created between the subcutaneous fat (dotted arrows a, b) and the distal segment of the iliotibial tract and lateral retinaculum (white arrows a, b), the suggestive appearance of an acute post-­ traumatic seroma

3.3 Prepatellar Morel-Lavallée Lesion

a

69

b

c

d

Fig. 3.17  Type I Morel-Lavallee (ML). Chronic seroma is located anterolateral in the distal left thigh and the anterolateral face of the knee in a 27-year-old man with a swelling that started 2 weeks ago in the distal aspect of the left thigh and the anterolateral face of the knee. The patient gave a history of a road traffic accident 1 month ago. He sustained an injury to his chest but did not complain of trauma in his lower left limbs. On local examination, the swelling was seen over the distal aspect of the left thigh and the anterolateral knee. Neurovascular status was intact.T1 SE image in the sagittal plane (a) and PDF

image (b–d) in the sagittal, coronal, and axial plane shows a multiloculated fluid collection (white arrows a, dotted black arrows b), septate (black arrows c, d), inhomogeneous hyposignal T1 (asterisk a) conferred by the presence of small fatty bodies (black dotted arrow a) and PD FS hypersignal (asterisk b–d) located at the interface between the subcutaneous plane and the underlying fascia at the level of the distal iliotibial tract and lateral retinaculum. History of trauma and MRI features are consistent with a type I ML-chronic seroma

The lesions are usually unilateral but may be bilateral [4, 8]. Patients generally complain of pain and swelling. Physical exam reveals a soft fluctuant area of contour deformity, which may have skin mobility [29]; the decreased cutaneous sensation is often associated with the skin over the area of degloving because of shearing injury to the cutaneous nerves [32].

strates exquisite soft tissue contrast and can delineate the lesion stage and estimate the chronicity of the hematoma. It is the modality of choice when a more global overview of the lesion is required. It provides the clinician with a precise assessment of the lesion’s extent (e.g., underlying muscle contusion) and morphology, particularly in large lesions [22, 24]. The MR signal intensity of the lesion varies according to the degradation of the internal blood products. Each stage has its corresponding MR signal intensity [17]. Several forms of subcutaneous fluid collections may result, depending on the severity of the injury, ranging from seroma to hematoma. After some time, the blood is reabsorbed and replaced by serosanguineous fluid [12]. This hemolymphatic collection may continue to enlarge, and patients may present with a large mass, usually located over the external aspect of the thigh. Because of this enlarging nature, these collections may be mistaken for soft tissue tumors [2, 3]. This serosanguineous collection may ­spontaneously resolve or undergo a secondary inflammatory reaction with subsequent fibrous capsule formation [5, 19, 25, 29].

3.3.3 Diagnostic Imaging The diagnosis of MLL ideally is made via history and physical examination of the patient, but advanced imaging modalities can be used to ­provide additional information. Plain radiography may reveal a noncalcified soft tissue mass and associated fractures. The sonographic appearance is nonspecific and variable, with lesions described as anechoic, hypoechoic, and hyperechoic. Hyperechoic nodules of internal fat may be seen on ultrasound [33]. CT can show fluid–fluid levels related to sedimentation of the hemolymphatic fluid, varying amounts of internal debris, including internal fat lobules, and may indicate a peripheral capsule. MRI demon-

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3.3.4 MRI Classification of MLL Six MLLs have been described based on the chronicity, tissue composition, and lesion appearance MRI [16]. In 2005, Mellado JM and Bencardino JT proposed an extensive six-stage imaging classification based on the lesion’s shape, presence or absence of a capsule, signal intensity on T1- and T2-weighted images, and enhancement pattern [16, 18, 34]. Type I MLL is a seroma that exhibits fluid-like signal characteristics on MRI. This type appears homogeneously hypointense on T1-WI and hyperintense on T2-WI, respective to muscle. This lesion can be found in both chronic (Fig.  3.17) and acute settings and is most often not encapsulated [16] (Fig. 3.18). Type II MLL is a subacute hematoma. These lesions are usually homogeneously hyperintense on both T1WI and T2WI. The typical T1 hyperintensity of type II lesions is methemoglobin, a characteristic of subacute hematomas [18, 20] (Fig. 3.19). The high signal on T1SE is caused by methemoglobin; the methemoglobin is first observed in the periphery of early subacute hematomas and progressively acquires a more homogeneous distribution. Subacute hematomas often have a hemosiderin-rich hypointense cap-

a

b

Fig. 3.18  Type I ML. Acute seroma is located in the distal lateral right thigh and the lateral face of the knee. A 41-year-old man presents knee pain after trauma from overturning an ATV 3 days ago. On local clinical examination, the swelling was present over the distal lateral thigh of the right thigh and the lateral knee face. T1 SE image in the sagittal plane (a) and the PD FS image in the axial (b) and coronal plane (c) shows a large, fluid collection with an oval-shaped pseudocyst appearance, with

sule on T1- and T2-WI. In some subacute hematomas, internal inhomogeneity is caused by entrapped fat globules, internal septations, or fluid-fluid levels (Fig. 3.20). The presence of capillaries within the lesion can lead to patchy internal enhancement, falsely leading to a soft tissue tumor [18]. These subacute hematomas can further be subdivided into early and late subacute hematomas. The early ones tend to be more homogeneous, whereas the latter is more heterogeneous with internal septations and debris and develops a fibrous capsule [18]. Type III MLL Chronic organizing hematomas demonstrate hypointensity on T1WI and heterogeneous hypointensity/iso intensity on T2WI with capsular formation. Type III MLLs may show capsular and internal enhancement secondary to neovascularization and granulation tissue in the organizing hematoma on post-contrast sequences. This can even lead to growth over time [34]. Type IV MLL represents a closed laceration without a capsule. It shows T1 hypointense and T2 hyperintense signals. Type V MLL demonstrates a small, rounded, pseudo-nodular appearance and has variable T1 and T2 signal intensity.

c

irregular contour and homogeneously hyposignal T1 (asterisk a) and hypersignal PD FS (asterisk b, c). The lesion is located in the post-traumatic space created between the subcutaneous plane (dotted arrow b, c) and the deep fascia of the distal segment of the iliotibial tract (continuous arrow c) extending in the posteroanterior direction of the lateral retinaculum fascia (continuous arrow b). The history of trauma and MRI features are consistent with a type I ML-acute seroma

3.3 Prepatellar Morel-Lavallée Lesion

a

71

c

b

Fig. 3.19  Type II Morel-Lavallée Lesion-Subacute bilateral early hematoma located postero-lateral and posteromedial in the distal portion of the right thigh. A 31-year-old woman presented right knee pain after a ski accident and a stinging sensation behind the knee. Clinical examination 2 days after the accident suggested ACL rupture without any skin damage to the knee. MRI examination 3 weeks after injury confirmed complete acute ACL rupture (the images not shown here). PD FS image in coronal (a), axial (b), sagittal (d) planes, and T1 SE image in the sagittal plane (c) show unilocular elongated ovoid fluid collection (asterisk images a and b) located in the post-traumatic space created between the subcutaneous plan (vertical

a

b

Fig. 3.20  Type II Morel-Lavallée lesion-Subacute late hematoma. A 27-year-old man presented with left knee pain after a ski accident. Clinical examination 2 days after the accident suggested ACL rupture without any skin damage to the knee. One week after the accident, an MRI examination reveals a complete acute ACL rupture and a grade 3 lateral meniscus lesion. Three weeks after the accident, ACL arthroscopic reconstruction and suturing of the lateral meniscus are performed without other post-­ traumatic lesions. About 3  weeks after ACL reconstruction, the patient complained of pain on the lateral side of his left thigh. A Control MRI examination is performed 6 weeks after the skiing accident. PD FS images in coronal (a), sagittal (b), and T1 SE image in the sagittal plane

d

dotted line a) and underlying fascia of the myotendinous junction of the femoral biceps muscle and the proximal portion of the fascia of the lateral gastrocnemius muscle (white arrows a). The fluid collection is unencapsulated with diffuse contour and shows T1 hypersignal with multiple septa (white arrows c) and hypersignal PD FS with small lobular images with fatty lobules content (black arrows image d), appearance compatible with a subacute hematoma. A similar lesion (ML type II) of smaller dimensions is also noticed in the posteromedial distal portion of the thigh in the space between the subcutaneous tissue and the fascia of the tendon of the semimembranosus muscle (dotted arrows a and continue arrow b)

c

(c) highlight a collection with a fluid signal on the lateral face in the distal portion of the left thigh, located in the space between the cutaneous plane (dotted arrow a) and the iliotibial tendon (thick white arrow a) with maximum dimensions of 7.2  cm in the caudal cranial plane and 1.3 cm in the transverse plane. The fluid collection presents inhomogeneous hypersignal T1, and PD FS (asterisk a–c) is multiloculated with internal septa (black arrows a–c) and debris (dotted white arrows a–c) fluid-fluid level (black dotted arrows) and has the capsule in hyposignal T1 and PD FS with hemosiderin content. History and MR imaging features suggest ML lesion—late hematoma type II

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Type VI MLL represents a superimposed infection, with a thick enhancing capsule associated with the sinus tract.

3.3.5 Differential Diagnoses Other soft tissue masses can present near the fascial planes and demonstrate imaging findings similar to those in MLLs. Specifically, bursitis, soft tissue sarcomas, and subcutaneous hematomas can appear similar to MLLs when these lesions appear in the appropriate locations [18]. Bursitis is the inflammation of the bursal sacs in joints like the hip and knee. It typically presents as hypointense on T1WI and hyperintense on T2WI, similar to the T1WI hypointense and T2WI hyperintense Type I MLL. Chronic ­hemorrhagic bursitis can resemble Type III MLLs with location and clinical history being helpful distinguishing factors. Acute hematomas typically demonstrate hypointensity on T1 WI and hyperintensity on T2WI.  Subacute hematomas show hyperintensity on both T1 WI and T2 WI due to the presence of methemoglobin within the

a

b

Fig. 3.21  Hemorrhagic infrapatellar bursitis versus Type II Morel-Lavallée lesion (late subacute hematoma). A 57-year-old man presented with left knee pain 3 months after a hard object hit him. He later complained of recurrent pain and swelling of the anterior knee. Clinical examination showed fluctuating swelling in the subpatellar anterior part of the left knee, with surrounding erythema. MRI was performed 4 months after the injury. T1 TSE sagittal (a), PD FS sagittal (b), coronal (c), and axial (d) showed an ovoid fluid collection with maximum dimensions of 4.7/2.3/4.1 cm. In T1(A), it presents an intermediate signal compared to skeletal muscles, suggestive aspect for the presence of methemoglobin and an internal inho-

lesion [18]. Subacute hematomas often have a hemosiderin-­rich hypointense capsule on T1- and T2WI.  In some subacute hematomas, internal inhomogeneity is observed caused by entrapped fat globules, internal septations, or fluid-fluid levels (Fig. 3.21). Hematomas are internal hemorrhages contained within the subcutaneous tissue. The distinguishing feature between a hematoma and an MLL is the location of the MLL in the interfascial plane, but the imaging findings can be similar [18].

3.4 Prepatellar Subcutaneous Fat Subcutaneous fat is the layer of subcutaneous tissue that is most widely distributed. It comprises adipocytes grouped in lobules separated by connective tissue [35]. It acts as padding and an energy reserve, providing minor thermoregulation via insulation and regulating hormone action [32]. The anatomy of anterior knee fat is a complex structure capable of withstanding considerable

c

d

mogeneity conferred by the presence of blood clots (small black arrows a) internal septum (white dotted arrow a–c). In PD FS images (b–d), the collection shows inhomogeneous hypersignal caused by entrapped fat globules (black dotted arrow b, short white arrow c), internal septations (white dotted arrow a), and fluid-fluid levels (black arrows b). The fluid collection has a hemosiderin-rich hypointense capsule on both T1- and PD FS (peripheral short white arrows). Notice that the distension of the bursa exceeds the medial and lateral edges of the patellar tendon (white arrows d), an uncharacteristic appearance in typical bursitis [4, 5]

3.4 Prepatellar Subcutaneous Fat

compressive and shear stress. Specific lesions occur when such mechanical stress exceeds the physiological limits and is little known. Superficial fat can be the site of either acute injury by closed degloving called the MLL or chronic injury when subject to repeat excessive shear forces due to more complex and less well-­defined disruptions that result in pseudo-bursitis [36].

3.4.1 Pseudo-Bursitis It is a repetitive injury secondary to kneeling positions, such as for tillers and construction workers, resulting in anatomical adaptations or skin and subcutaneous fat lesions. Skin and epidermal layer thickening are some of the main changes in forming protective callosities. Changes also occur within the fat, and in many cases, edema of prepatellar fat, at first asymptom-

a

Fig. 3.22  Prebursitis. An overweight 61-year-old woman kneels for half an hour twice weekly to say her prayer. MRI images in the sagittal plane T1 SE (a) and PD FS (b) show overall thickening of the subcutaneous fat (double

73

atic, can be seen on MR images (98% of cases of the series described by Roth et al.) [37]. MRI provides evidence of overall thickening of the subcutaneous fat, thickening of the fibrous septa surrounding the fat lobules, and a prepatellar fluid infiltrate showing high signal intensity on T2 fat sat-weighted images (Fig.  3.22). The mechanical properties of the fat lobules are altered because of their larger size, lesser elasticity, and the changes to the fibrous septa and adjacent vascular plexuses that cause the interlobular prepatellar exudate (Fig. 3.23). The final stage is full-blown pseudo-bursitis (Fig. 3.24). The complete disruption of the fibrous septa causes dissection of the fat when the shearing forces are maximal. Excessive effusion of lymph and blood between the separated lobules leads to a poorly delimited fluid collection or “pseudo-bursitis” (Fig. 3.25). This condition is a “chronic” form of the Morel-Lavallée lesion [36].

b

arrow a), thickening of the fibrous septa (black arrow A and white arrow B) surrounding the large fat lobules (asterisk a, b) and a prepatellar fluid exudate in hyposignal T1 and hypersignal PD FS (star)

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a

b

Fig. 3.23  Pseudo-bursitis initial stage. A 57-year-old man carpenter. Images in the sagittal plane T1 SE (a), PD FS (b), and axial plane (c) show the larger fat lobes (asterisk a–c) by rupture of interlobular septa (arrow a, b) and

Fig. 3.24 Pseudo-­ bursitis prefinal stage. A 53-year-old man tiler with chronic anterior right knee pain. Images in the sagittal plane T1 SE (a), PD FS (b) show the complete disruption of the fibrous septa causing dissection of the fat at the point where the shearing forces are maximal (asterisk), and a compressive fluid exudate in hyposignal T1 and hypersignal PD FS localized prepatellar and tibial pretuberosity (stars)

a

c

adjacent vascular plexuses that cause the interlobular prepatellar exudate (star). Notice a small Baker cyst (black arrow c)

b

References

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a

Fig. 3.25  Complete pseudo-bursitis, the final stage. A 62-year-old man suffers anterior knee pain after repeated kneeling and stress injuries of the anterior left knee. PD FS MRI images in the sagittal plane (a) and axial plane

References 1. Flores DV, Gómez CM, Pathria MN.  Layered approach to the anterior knee: normal anatomy and disorders associated with anterior knee pain. Radio Graphics. 2018;38:2069–101. 2. Costello J, Bursae K. MRI web clinic. 2020. 3. Steinbach LS, Stevens KJ. Imaging of cysts and bursae about the knee. Radiol Clin N Am. 2013;51:433–54. 4. Dye SE, Campagna-Pinto D, Dye CC, Shifflett S, Eiman T.  Soft tissue anatomy anterior to the human patella. J Bone Joint Surg Am. 2003;85:1012–10174. 5. Borrero CG, Maxwell N, Kavanagh E.  MRI findings of prepatellar Morel-Lavallée effusions. Skelet Radiol. 2008;37(5):451–5. 6. Netter FH.  In: Colacino S, editor. Atlas of human anatomy. Summit, NJ: Ciba-Geigy; 1989. 7. Sobotta J.  Sobotta atlas of human anatomy: volume 2, thorax, abdomen, pelvis, lower limbs. 11th ed. Baltimore, MD: Urban and Schwarzenberg; 1990. 8. Aguiar R, Viegas FC, Fernandez RY, Trudell D, Haghighi P, Resnick D. The prepatellar bursa: cadaveric investigation of regional anatomy with MRI after sonographically guided bursography. AJR Am J Roentgenol. 2007;188(4):W355–8. 9. Sears B, Opole IO. The anatomy of the bursa, small fluid-filled sacs that allow your joints to move smoothly. 2020. 10. Claes T, Claes S, De Roeck J, Claes T.  Prepatellar friction syndrome: a common cause of knee pain in the elite cyclist. Acta Orthop Belg. 2015;81(4):614.

b

(b) show a poorly delimited fluid collection (star) through the excessive effusion between the separated fat lobules (arrows)

11. Viegas FC, Aguiar RO, Gasparetto E, Marchiori E, Trudell DJ, Haghighi P, et  al. Deep and superficial infrapatellar bursae: cadaveric investigation of regional anatomy using magnetic resonance after ultrasound-guided bursography. Skelet Radiol. 2007;36:41–6. 12. Hirji Z, Hunjun JS, Choudur HN. Imaging of the bursae. J Clin Imaging Sci. 2011;1:22. 13. Donahue F, Turkel D, Mnaymneh W, Ghandur-­ Mnaymneh L.  Hemorrhagic prepatellar bursitis. Skelet Radiol. 1996;25(3):298–301. 14. Chhabra A, Cerniglia CA. Bursae, cysts, and cyst-like lesions about the knee. J Am Osteopath Coll Radiol. 2013;2(4):2–13. 15. Morel-Lavallée VAL.  Decollements traumatiques de la peau et des couches sous jacentes. Arch Gen Med. 1863;1(20–38):172–200. 16. Mallado JM, Bencardino JT.  Morel-Lavallee lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin N Am. 2005;13:775–82. 17. El-Essawy MT, Vanhoenacker FM.  Half-moon shaped Morel-Lavallée lesion of the knee. J Belgian Soc Radiol. 2015;99:103–4. https://doi.org/10.5334/ jbr-­btr.837. 18. Bonilla-Yoon I, Masih S, Patel DB, et al. The Morel-­ Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol. 2014;21(1):35–43. 19. Tejwani SG, Cohen SB, Bradley JP. Management of Morel-Lavallée lesion of the knee: twenty-seven cases in the national football league. Am J Sports Med. 2007;35:1162–7.

76 20. Mellado JM, Perez del Palomar L, Diaz L, Ramos A, Sauri A.  Long-standing Morel-Lavallée lesions of the trochanteric region and proximal thigh: MRI features in five patients. AJR Am J Roentgenol. 2004;182:1289–94. 21. Scolaro JA, Chao T, Zamorano DP.  The Morel-­ Lavallée lesion: diagnosis and management. J Am Acad Orthop Surg. 2016;24:667–72. https://doi. org/10.5435/JAAOS-­D-­15-­00181. 22. McLean K, Popovic S. Morel-Lavallée lesion: AIRP best cases in radiologic-pathologic correlation. Radiographics. 2017;37:190–6. 23. De Coninck T, et al. Imaging features of Morel-Lavallée lesions. J Belgian Soc Radiol. 2017;101(S2):1–8. https://doi.org/10.5334/jbr-­btr.1401. 24. Qureshi A, Monoot P.  A case review of a Morel Lavallee lesion with delayed presentation. Marshall J Med. 2018;4(1) Article 9 https://doi.org/10.18590/ mjm.2018.vol4.iss1.9. 25. Kalaci A, Karazincir S, Yanat AN.  Long-standing Morel-L-+avallee lesion of the thigh simulating a neoplasm. Clin Imaging. 2007;31:287–91. https://doi. org/10.1016/j.clinimag.2007.01.012. 26. Gummalla K, George M, Dutta R.  Morel-Lavallee lesion: case report of a rare extensive degloving soft tissue injury. Ulus Travma Acil Cerrahi Derg. 2014;20(1):63–5. Imaging. 2007; 31: 287–91. https:// doi.org/10.1016/j.clinimag.2007.01.012. 27. Dodwad S, Niedermeier S, Yu E, Ferguson T, Klineberg KS.  The Morel-Lavallée lesion revisited: management in spinopelvic dissociation. Spine J. 2015;15(6):45–51. 28. Singh R, Rymer B, Youssef B, Lim J.  The Morel-­ Lavallée lesion and its management: a review of the literature. J Orthop. 2018;15:917–21.

3  MRI Findings of Superficial Prepatellar Soft Tissues 29. Hudson DA.  Missed closed degloving injuries: late presentation as a contour deformity. Plast Reconstr Surg. 1996;98(2):334–7. 30. Nair A, Nazar P, Sekhar R, Ramachandran P, Moorthy S.  Morel-Lavallée lesion: a closed degloving injury that requires real attention. Indian J Radiol Imag. 2014;24(3):288–90. 31. Vanhegan I, Dala-Ali B, Verhelst L, Mallucci P, Haddad F. The Morel-Lavallee lesion as a rare differential diagnosis for recalcitrant bursitis of the knee: case report and literature review. Case Rep Orthop. 2012:593193. 32. Jump up to Kenneth, Saladin. Human anatomy. Rex Bookstore, Inc.; 2007. 135, 478, 602. ISBN 978-0071259712 33. Carroll JF. Morel-Lavallee lesions. MRI Web Clinic; 2010. 34. Diviti S, Gupta N, Hooda K, Sharma K, Ncelo LR.  Morel-Lavallee lesions-review of pathophysiology, clinical findings, imaging findings and management. J Clin Diagn Res. 2017;11(4):TE01–4. 35. Jump up to “The hypodermis”. An organ revealed L’Oréal Retrieved 4 June 2013. 36. Lapègue F, Sans N, Brun C, Bakouche S, Brucher N, Cambon Z, Chiavassa H, Larbi A, Faruch M.  Imaging of traumatic injury and impingement of anterior knee fat. Diagn Interv Imaging. 2016;97:789–807. 37. Roth C, Jacobson J, Jamadar D, Caoili E, Morag Y, Housner J.  Quadriceps fat pad signal intensity and enlargement on MRI: prevalence and associated findings. AJR Am J Roentgenol. 2004;182:1383–7.

4

Quadriceps Tendon

4.1 Introduction The extensor apparatus is responsible for knee extension and stabilization of the assessment [1]. This information is needed to determine the prognosis, formulate an appropriate rehabilitation plan, and, in some cases, for planning surgery. Magnetic resonance imaging (MRI) is probably the imaging study of choice when there is doubt about the diagnosis. MRI can depict the laminated structure of the quadriceps tendon. Complete ruptures show the transsection of all of the layers of the tendon. Incomplete ruptures show discontinuities of individual layers, with the remaining layers intact. MRI may demonstrate complications such as scarring, hematoma, and heterotopic ossification for patients with an inadequate response to therapy or chronic symptoms [2]. MRI will likely have a significant and expanding role in evaluating and treating many acute or chronic quadriceps injury patients. This chapter describes the MR imaging anatomy of the quadriceps tendon as a component of the extensor mechanism, the spectrum of injuries that involve these segments, and MR imaging’s role in characterizing such injuries.

4.2 Normal MRI Anatomy of the Quadriceps Tendon Because of the excellent soft tissue contrast and the ability to obtain direct multiplanar images of quadriceps, MRI is the preferred technique for evaluating the extensor mechanism of quadriceps muscle and tendon, patella, and patellar tendon (Fig.  4.1). To maximize image signal to noise, acquire images using a dedicated extremity coil. In specific cases of patellar pathology, limited high-resolution images of the patellofemoral joint can be obtained using a small anterior surface coil [3]. MRI standard protocol for evaluating the extensor mechanism includes the following: Sagittal spin-echo T1-weighted images (T1 SE), sagittal proton density-weighted images with fat suppression (PD FS), or short tau inversion recovery (STIR) images. On sagittal MR images, the quadriceps muscles can be seen converging distally toward the common quadriceps tendon; they demonstrate the typical intermediate signal intensity of skeletal muscles on T1- and T2-weighted images. Axial proton density-­ weighted images with fat suppression (PD FS). The phase encoding direction should be left to right on axial images to prevent pulsation artifacts from the popliteal artery [3]. Coronal

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_4

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Fig. 4.1  The extensor mechanism components of the knee. Image T1 SE in midsagittal plane (a) reveals quadriceps tendon (QT), patella (P), prepatellar tissue (PPT), patellar tendon (PT), tibial tuberculum (TT), and Hoffa pad (HP). PD FS image in the axial plane (b) reveals patella (P), lateral retinaculum (LR), medial retinaculum

(MR), vastus medialis oblique (VMO), femur (F), trochlear groove (TG). PD FS image in the coronal plane (c) reveals: the vastus medialis muscle (VMM), vastus lateralis muscle (VLM), rectus femoris muscle (RFM), patella (P), medial patellofemoral ligament (MPFL), lateral patellofemoral ligament (LPFL), patellar tendon (PT)

sequences are of limited value for patellar tendons due to volume-averaging artifacts and the non-orthogonal slice orientation [4]. All ­examinations included images of sagittal, coronal, and axial planes acquiring T1, PD FS-STIR sequence. The quadriceps tendon is formed by the convergence of all four muscles just proximal to the superior patella. The quadriceps tendon is a multilayered and laminated structure, as shown by anatomical specimens and MRI scans. [5] On MR imaging, the layers of the distal quadriceps tendon are often interspersed with fibrofatty connective tissue. The normal appearance of the multilaminar quadriceps tendon manifests as low-signal tendon fibers with interdigitating longitudinal streaks of intermediate signal on most sequences (Fig. 4.2). Some authors suggest that the three layers of the quadriceps tendon remain distinct in their insertion into the patella [6, 7]. Although the usual description of the quadriceps tendon includes three layers, an MRI study [5, 6] revealed that only 56% of the subjects presented with a trilaminate appearance (Fig. 4.3). Thirty

Fig. 4.2  PD FS image in sagittal plane reveals a multilaminar aspect of the distal quadriceps tendon, manifesting as low-signal tendon fibers with interdigitating longitudinal streaks of high signal (circle and black arrows)

4.2 Normal MRI Anatomy of the Quadriceps Tendon Fig. 4.3 Trilaminar quadriceps tendon. Sagittal PD FS MR image (a) and axial plane (b) show three distinct layers. A superficial layer is formed by the rectus femoris tendon (RFT), the middle layer is formed by the medial and lateral vast tendons (VM + VLT), and the deep layer is formed by the vast intermedius tendon (VIT)

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Fig. 4.4  Bilaminar quadriceps tendon. PD FS image, sagittal (a), and axial plane (b). The superficial layer is formed by the medial and lateral vastus tendons (VM + VLT). The deep layer is formed by the vastus intermedius tendon (VIT). The rectus femoral tendon joint with the medial and lateral vastus tendons in the distal

portion of the quadriceps tendon. The superficial layer is thicker than the deep layer, indicating that the middle layer has merged mostly with the rectus femoris layer. In an athlete’s long jumper, note reactive osteophytes following repetitive tendon traction at the patellar insertion (head arrow image A)

percent presented them with only two different fiber planes (Fig. 4.4). Five percent were shown with a four-layered quadriceps tendon (Fig. 4.5) and 7% were classified as having one layer because no fascial boundaries could be distin-

guished (Fig. 4.6). The rectus femoris becomes tendinous 3–5 cm proximal to the patella and is the most superficial layer inserted onto the patella [8]. Occasionally, the anterior layer (the rectus femoris tendon) can be seen extending

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Fig. 4.5  Normal quadriceps tendon with four layers. The sagittal PD FS image shows four distinct layers. The superficial layer is formed by the rectus femoral tendon (RFT). The middle layer is formed by the separate medial and vast lateral tendons (VMT, VLT). The deep layer is formed by the vast intermedius tendon (VIT)

Fig. 4.6  T1 SE image on sagittal plane reveals one (single) layer of quadriceps tendon (black arrow)

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Fig. 4.7  T1SE image on the sagittal plane reveals the patellar continuation of the rectus femoris tendon (long arrow). Note the articular genu muscle of the knee, an accessory muscle (dotted arrows) separate from the vastus muscle group, which extends from the anterior surface of the femur to insert into the suprapatellar bursa. It lifts the upper synovial membrane on the suprapatellar bursa during knee extension, thus preventing compression of the synovial folds between the femur and the patella

anterior to the patella in direct continuity with the patellar tendon [9, 10] (Fig. 4.7). The middle layer comprises the vastus lateralis and the vastus medialis (VM). The vastus medialis, composed of the vastus medialis obliques (VMO) and the vastus medialis longus (VML), becomes tendinous only a few millimeters from its insertion into the patella. The vastus lateralis becomes tendinous about 3  cm proximal to its insertion into the patella [7, 9, 11] (Fig.  4.8). The deep layer is composed of the vastus intermedius (VI). The quadriceps tendon has an average thickness of 8  mm and an average width of 35  mm [7]. Therefore, the number of layers is determined by whether the vastus medialis and the vastus l­ateralis layers converge with the superficial and deep layers or remain a separated tendinous layer [6]. There are two different types of muscle attachments in the human body: the periosteal–metaph-

4.2 Normal MRI Anatomy of the Quadriceps Tendon

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Fig. 4.8  Successive cranio-caudal images of the left knee. T1 SE sequences, in the axial plane from the upper pole of the patella (a) to the level of the intercondylar fossa (c), show the vastus medialis and its long and oblique portions (VMM), which becomes tendinous only

a few millimeters from its insertion into the patella (dotted arrows a, b). The vastus lateralis muscle (VLM) becomes tendinous about 3  cm proximal to its insertion into the patella (arrow b). Image c shows the medial patellofemoral ligament (MPFL)

yseal type, in which the tendon fibers are inserted directly into a bony crest, and the chondroapophyseal type, in which the tendon is gradually transformed into fibrocartilage as it is attached to the bone [12]. Most of the quadriceps tendon inserts are on the anterosuperior surface of the patella. Continuity of the quadriceps and patellar tendons is accomplished by the distal extension of fibers of the rectus femoris tendon, which inserts into the bone at the anterior surface of the patella. This associate is a chondroapophyseal type of attachment (an enthesis) in which tendon fibers transform into fibrocartilage at the insertion. This layer of fibrocartilage is thickest at the quadriceps tendon insertion on the anterosuperior patellar surface (0.136  mm), thinner at the patellar tendon attachment (0.023  mm), and thinnest at the prepatellar quadriceps continuation attachment to the anterior patellar surface (0.004 mm) [2, 13]. It has been postulated that this layer of fibrocartilage is thin because its function is to diminish friction between the patella and overlying tendinous fibers rather than to anchor the tendon to the patella [13]. Separation of the prepatellar quadriceps continuation from the

anterior patellar surface has been observed on MRI in patients after an acute traumatic event (Fig.  4.9) or by cumulative microtrauma produced by repetitive knee flexion and extension resulting in focal inflammation in athletes [2, 14] (Fig. 4.10). Peterson et al. [15] found that the blood supply to the quadriceps tendon arises from the descending branches of the lateral circumflex femoral artery, branches of the descending geniculate artery, and branches of the medial and lateral superior geniculate arteries. The superficial layers are well vascularized. However, an oval avascular area of 30 × 15 mm in size in the deep layer makes it more susceptible to injury [11] (Fig. 4.11). The quadriceps tendon appears as a laminated structure on MR images, with layers arising from separate muscle groups. Recognition of the various appearances is essential, particularly in evaluations of incomplete rupture, because discontinuities of individual layers may mimic such injuries. MR imaging can be used to diagnose partial rupture and accurately assess the extent of the injury, which is essential in planning effective treatment.

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Fig. 4.9  A 42-year-old athlete reports prepatellar knee pain after a fall to the right knee, cannot fully extend his knee, and has difficulty mobilizing. On physical examination, tenderness to deep palpation at the patella. The Sagittal PD FS image shows the abnormal high-intensity signal in the prepatellar fibrous tissue, suggesting an isolated rupture of the prepatellar continuation of the rectus femoris tendon (thick arrow) and patellar subcortical edema with osteochondritis appearances (dotted arrow). There is also a congestive-edematous process at the level of the superficial prepatellar and infrapatellar soft tissues with the appearance of bursitis (short white arrows). The quadriceps and patellar tendons appear normal. Note a high-intensity signal on the subpatellar Hoffa’s fat pad, and there is a traumatic signal change representing edema and hemorrhage at the superior pole of Hoffa’s fat pad (black star)

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Fig. 4.10  A 31-year-old athlete reports supra and prepatellar right knee pain after a long training period. Clinical examination highlights tenderness to deep palpation at quadriceps tendon insertion at the patella. Sagittal PD FS image reveals edema/fluid signal intensity deep to the prepatellar RF tendon continuation (blackhead arrows), consistent with partial separation from the patella. Note traction osteophytes developed at the upper pole of the patella (white arrow)

4.3 MRI Pathological Findings of Quadriceps Tendon Injuries

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Fig. 4.11  A 33-year-old man, an athlete, has anterior knee pain located suprapatellar, accentuated by compression of the junction of the quadriceps tendon with the upper pole of the patella.T1 SE image in the sagittal plane (a) and PD FS images in the sagittal plane (b, e), coronal plane (c), and axial plane (d) highlight the quadriceps tendon with multilayer architecture. The suprapatellar fat pad appears in hyposignal on the sagittal T1 SE (circle and arrow a) and hypersignal on PD FS in the sagittal, coronal, and axial plane (circle and arrow b, c, and d). The

sagittal PD FS image (b) reveals the edematous infiltration of the posterior portion of the tendon at the patellar insertion and the interruption of some fibers in the intermedius vastus tendon and medial and lateral vastus tendons (circle and arrow b). Zoom image (e) highlights myxoid-edematous infiltration tendons of medial, lateral, and intermedius the vastus and interruption of some fibers consistent with partial rupture of the quadriceps tendon associated with the insertional tendinitis/tendinosis in the avascular area

4.3 MRI Pathological Findings of Quadriceps Tendon Injuries

mechanism include acute traumatic rupture, chronic repetitive/overuse injury, and tendon degeneration [3, 14, 16]. It is generally accepted that rupture of a healthy tendon is rare. Acute traumatic injuries occur secondary to direct blunt trauma or excessive tension applied to the extensor mechanism through quadriceps contraction. Risk factors include age, repetitive micro-trauma, genetic predisposition, systemic diseases, and certain medications [17].

The extensor mechanism of the knee plays an important role in the movements of the lower extremity. Although its main function is to extend the knee, it also stabilizes the patellofemoral joint and resists passive flexion of the knee when landing from jumping [10]. Injuries to the extensor

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In most cases, quadriceps ruptures due to indirect trauma are the end stage of long-standing chronic tendon degeneration by cumulative microtrauma produced by repetitive knee flexion and extension, which results in focal inflammation [14]. Overuse injuries typically are seen in high-performance athletes, most commonly in sports requiring long-distance running or jumping. Magnetic resonance imaging (MRI) is the imaging study of choice when there is doubt about diagnosing a quadriceps injury. MRI can depict the laminated structure of the quadriceps tendon. Complete ruptures show the transsection of all of the layers of the tendon. Incomplete ruptures show discontinuities of individual layers, with the remaining layers intact. Knowledge of characteristic patterns of injury on MR imaging increases injury detection. Radiologists must be aware of common anatomic variants and imaging pitfalls of the extensor mechanism seen in MR imaging [1, 8].

4.3.1 Complete Ruptures of the Quadriceps Tendon Acute injury of the quadriceps tendon is relatively infrequent and commonly occurs during falls or a rapid eccentric contraction of the quadriceps muscle, with the foot planted and the knee partially flexed [8, 18]. Other mechanisms of injury include direct blows or excessive tension applied to the extensor mechanism through quadriceps contraction, lacerations, and iatrogenic causes [3, 19–23]. In athletes, the quadriceps tendon ruptures result from a sudden and strong contraction of the muscles from a jump and landing mechanism or a sudden change in direction while running [18]. Quadriceps tendon ruptures in non-athletes are usually the direct result of a fall or other trauma in individuals with preexistent medical comorbidities, which are thought to cause pathologic tendon degeneration [24]. Mechanism extensor of the knee is a common clinical problem and can be accurately evaluated with MRI. MR imaging is useful in differentiating partial and complete tears in evaluating tissue edema, hemorrhage, and fluid accumulation.

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Often, an associated hematoma is seen with heterogeneous signal intensity on T1-weighted images. It also detects unsuspected patellar fractures. Ruptures occur most frequently at the insertion of the quadriceps on the patella. The broken fragment retracts cranially in the quadriceps, and no fibers are identified inserted on the patella (Fig. 4.12). With complete tears, discontinuity of the tendon with associated retraction of the distal remnant fragment and the low secondary position of the patella, and laxity of the patellar tendon (Fig.  4.13). Although an undulating contour of the patellar tendon can be seen with complete quadriceps tendon tears, it can also result from the knee’s hyperextension and is not a specific indirect sign [18]. Complete quadriceps ruptures are much less common than partial tears. MR imaging findings of complete rupture show a fluid signal within a torn and retracted quadriceps tendon; no fibers are identified or inserted on the patella. There is frequently a large joint effusion with hematoma at the rupture site (Fig.  4.14). Ruptures of the quadriceps tendon most often occur unilaterally. Bilateral ruptures are highly correlated with systemic disease but have been reported in healthy patients who do not have predisposing factors [18, 24–26]. Quadriceps tendon ruptures have a positive correlation with age and multiple medical comorbidities. Medications and medical comorbidities associated with quadriceps tendon ruptures include fluoroquinolones, corticosteroids, anabolic steroids, hyperparathyroidism, gout, diabetes, obesity, chronic kidney disease, hypercholesterolemia, hyperuricemia, rheumatoid arthritis, systemic lupus erythematosus, and osteogenesis imperfecta [27–31]. Historically, this injury is more prevalent in men, with susceptibility increasing proportionally with age after 40 years [2, 18], and usually occurs distally 0–2 cm from the superior pole of the patella through pathologic tissue. It is important to differentiate between complete quadriceps ruptures and partial tears because the treatments differ substantially. Acute quadriceps full-thickness rupture is treated surgically by tunneling the quadriceps tendon into the patella [1]. Clinical patients typically present with acute knee pain, swelling, and functional loss after a stumble, fall,

4.3 MRI Pathological Findings of Quadriceps Tendon Injuries

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Fig. 4.12  A 43-year-old man with anterior knee pain after complete quadriceps tendon rupture of the right knee. The patient reports hearing an audible pop and experiencing a tearing sensation immediately after a fall on stairs, followed by a decreased ability to bear weight and an inability to extend the knee. At the physical examination, the swelling of the anterior aspect of the distal thigh, a palpable defect, was felt at the superior pole of the patella. The knee PD FS images in coronal plane a, b, and axial plane c. Acute patellar tendon rupture at the osteo-­ tendon junction with complete patellar disinsertion and

Fig. 4.13  A 37-year-old man with anterior knee pain after acute complete quadriceps tendon rupture of the left knee. PD FS image in the sagittal plane shows acute rupture of the quadriceps at the muscle–tendon junction (black arrows) with distal retraction and angulation of the lower tendon fragment (white asterisk). Note the low secondary position of the patella (white arrow). Posttraumatic lamellar hemorrhagic fluid and edema delimit the ruptured tendon fragment (white asterisk)

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proximal retractions and angulation. Complete disinsertion of the quadriceps tendon at the level of the patellar junction highlights the suprapatellar gap (double arrow a). Contusive lesions in the vastus lateral oblique muscle (stars b, c) and vastus medialis oblique (asterisk b, c) are characterized by diffuse edema and myofibrillar ruptures. Diagnosis: Complete rupture of the quadriceps tendon at the level of the patellar insertion with proximal retraction. Treatment: The quadriceps tendon was fixed with sutures through holes in the long axis of the patella

or giving away of the knee. There may be no history of prior knee pain. However, younger patients with jumper knees usually have a history of chronic pain above the patella exacerbated by jumping or kneeling [8]. It is necessary to ask the patients about any history of systemic disease, steroid use, infection, tumors, or prior surgeries. There may be a history of an audible pop at the time of injury [18]. Patients with recent ruptures have difficulty ambulating. Usually, obvious suprapatellar swelling, ecchymosis, and tenderness are present. There may be a palpable defect in the suprapatellar area and a low-lying patella, but swelling initially may obscure this finding. Testing for full, active extension against gravity is the most important aspect of the examination [8] and makes the defect more apparent. The patient is unable to perform straight leg raise. Management. Like most musculoskeletal injuries, initial management of suspected quadriceps tendon ruptures includes rest, ice, compression, and elevation [32]. Partial quadriceps tendon ruptures may be managed non-operatively. Early repair and reconstruction are recommended for complete acute ruptures to avoid retraction and

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Fig. 4.14  A 39-year-old woman with anterior knee pain due to known quadriceps tendinosis and Patella Baja has a skiing accident. T1 SE image (a) and PD FS image (b) in the sagittal plane show the complete rupture of the quadriceps tendon at the level of the osteotendinous junction, with an interfragmentary hiatus filled with serosanguine-

ous fluid (circle and star a, b). A large amount of fluid has extravasated from the suprapatellar bursa into the anterior soft tissues. The suprapatellar bursa communicates with the superficial, pre-, and subpatellar bursae. Low secondary position of the patella (thin arrow a, b)

atrophy of the quadriceps muscle [18, 33]. Primary approximation and reconstruction with hamstring grafts have been recommended [34]. The worst results were noted in delayed repairs. Reported complications included heterotopic ossifications in 6.9% of patients, deep venous thrombosis or pulmonary embolism in 2.5%, superficial infection in 1.2%, and deep infection in 1.1% [35]. The type of surgical repair does not influence the clinical results. Despite the specific surgical approach, a delayed recognition or operative intervention results in tendon retraction and reduced tissue quality. These factors both impair surgical success and hinder recovery. Operative repair is advised within 48–72  h after complete tendon ruptures [18]. If there is a delay in treatment, tendon retraction makes surgical repair more technically challenging and may limit functional recovery. Allograph reconstruction may be necessary if significant tendon retraction results in a large tendon gap [18]. The overall rate of re-­ rupture was 2% [35]. The timing of surgical repair has been attributed to optimal recovery and functionality than the specific surgical.

Complete quadriceps tendon ruptures are uncommon injuries, usually resulting from indirect trauma, in middle-aged men more often than women. Early diagnosis and prompt repair are crucial to obtaining optimal results. Good to excellent functional results are usually achieved. Patients with associated comorbidities such as diabetes and chronic kidney disease may be particularly susceptible to complications, including deep vein thrombosis, pulmonary embolism, and re-rupture [35].

4.4 Incomplete Ruptures of the Quadriceps Tendon Clinically, the patient may fully extend the knee from the supine position but not from the flexed position. If only tendinitis is present, no extension lag should be noted with any test position. Pain and swelling decrease over time, and quadriceps function can improve. Patients may be able to ambulate but will do so with a gait demonstrating knee stiffness and elevation of

4.4 Incomplete Ruptures of the Quadriceps Tendon

the hip to accommodate the swing-through phase. Also, patients may have frequent buckling of the knee and difficulty with stair climbing. Neurologic examination results are normal, except for decreased quadriceps motor function and an absent patellar reflex. Full, active knee extension against gravity is the key component of the physical examination [32]. Partial tears of the quadriceps tendon most commonly involve the anterior rectus femoris tendon fibers at the patellar insertion (Fig. 4.15). The pathophysiology mechanism of injury occurs due to repetitive eccentric contractions of the extensor mechanism with microtears of the tendon, most commonly at the bone–tendon interface (Fig. 4.16). Injury may also involve the prepa-

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Fig. 4.15  A 53-year-old man, following a car accident, presents with swelling of the knee, and pain when extending and lifting the left leg. PD FS images in the sagittal plane (a) show a complete interruption of the fibers of the rectus femoris tendon and both vastus medial and vastus lateral tendons, with a hiatus between the broken fibers and the insertion on the upper pole of the patella (yellow

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tellar quadriceps continuation (Fig.  4.17). Chronic avulsion injuries usually result from repetitive minor trauma or chronic overuse, traction forces, or tensile stresses transmitted from the quadriceps tendon to its site of cortical patellar attachment with the separation of a bone fragment from the anterosuperior contour of the patella (Fig. 4.18). Incomplete ruptures of the quadriceps tendon (partial ruptures) are managed by evacuating the hemarthrosis to reduce pain and tenderness, followed by rest, ice, compression, and anti-­ inflammatory medication. The knee is immobilized in full extension for about 6 weeks, followed by progressive knee Range Of Motion (ROM) strengthening, and physical therapy.

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arrows and black double arrow a). The deep layer represented by the tendon of the vastus intermedius muscle is surrounded by hemorrhagic and synovial fluid (asterisk b). Fluid-signal accumulation at the level of the tendon tear extending distally to the prepatellar tissues, with the appearance of supra and prepatellar pseudobursitis (black arrows image a)

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Fig. 4.16  A 52-year-old athlete presents with pre- and suprapatellar pain that worsens with prolonged walking, going up and down stairs with activity, and is associated with swelling, limitation of range of motion, and sensitivity to deep palpation at the insertion of the quadriceps tendon into the patella. PD FS sagittal image shows thickening of the middle layer of the quadriceps tendon, represented by the vastus medialis and vastus lateralis (dotted white arrow), and disruption of continuity at the suprapatellar level with separation of a small tendon fragment (asterisc, circle) consistent with chronic tendinitis and tears parts of the middle layer. Superficial pre and infrapatellar bursitis (black arrows). Note the thin patellar cartilage and cystic image in the adjacent subchondral cancellous bone (dotted circle and white arrow)

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Fig. 4.17  A 50-year-old former sportsman (high jumper) has chronic prepatellar pain exacerbated after a fall to the knee and tenderness to deep palpation at quadriceps tendon insertion on the patella. Sagittal PD FS image highlights interruption of the continuity of the rectus femoris tendon (fused with the vastus medialis and lateralis tendons) at the prepatellar level (white arrow), reactive osteophytes (dotted arrow), and superficial pre and infrapatellar bursitis (stars). Note the degenerative mucoid infiltration at the level of the patellar insertion of the patellar tendon with the aspect of insertional tendinosis (black arrow)

4.5 Quadriceps Tendinopathy

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Fig. 4.18  A 39-year-old woman, a former gymnast with anterior knee pain, accentuated the kneeling movements. Sagittal images, T1 SE (a), and PD FS (b) show a separation of a small cortical bone fragment detached from the

anterosuperior contour of the patella (circle and arrow images a, b). Note a small chronic superficial infrapatellar bursitis (white arrow image a and black arrow image b)

4.5 Quadriceps Tendinopathy

with varying intensity levels. Patients often complain of gradual worsening of activityrelated pain and do not recall or describe an inciting event [38].

Quadriceps tendinopathy is a significant cause of anterior knee pain most commonly seen in athletes due to chronic degenerative tendon changes from repetitive loading, stress, and extension of the knee [36]. Quadriceps tendonitis is a common cause of activity-related anterior knee pain and is typically an overuse injury caused by too much sport, training errors, muscle imbalance, and weightlifting, but it can also affect non-­athletes [37]. The quadriceps tendon is most often injured within a hypovascular zone, 1–2 cm superior to the patella injury, and usually occurs in patients older than 40  years, with a peak incidence in the fifth through seventh decades [2]. At the insertion in the patella, the distal tendon is the most common site of involvement (Fig. 4.19). The main symptom of quadriceps tendinopathy is anterior knee pain,

4.5.1 Summary Quadriceps tendinopathy is an important cause of anterior knee pain. It is a clinical diagnosis characterized by activity-related anterior knee pain and is most commonly seen with overuse activities in athletes. Structural histologic tendon changes in quadriceps tendinopathy have been demonstrated to be more degenerative than inflammatory [37]. Quadriceps tendinopathy is typically an overuse injury from repetitive jumping and sprinting activities. It causes activity-­ related anterior knee pain with localized tenderness on the superior border of the kneecap.

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older than 40  years. A strong association exists with numerous systemic diseases and prior degenerative changes in the knee extensor mechanism. Ruptures most often occur unilaterally. Bilateral ruptures are highly correlated with a systemic disease but have also been reported in healthy patients who did not have predisposing factors [8, 18].

References

Fig. 4.19  A 41-year-old man, a former athlete (runner), presents supra and prepatellar anterior knee pain with varying intensity levels during and after activity. There was no associated swelling and limited range of motion, with tenderness to deep palpation of the distal quadriceps tendon. The sagittal PD FS image highlights the thickening of the deep layer of the quadriceps tendon, represented by the vastus intermedius tendon (white star). Angulation of the distal rectus femoris tendon (black arrow) and myxoid-­degeneration infiltration of the patellar insertion (full and dotted arrows) changes compatible with the diagnosis of insertional tendinosis of the quadriceps tendon

In the acute phase, the main feature of quadriceps tendonitis is inflammation. In chronic cases, the main feature of quadriceps tendinosis is degeneration. Quadriceps tendonitis often coexists with patellar tendonitis. Quadriceps tendonitis is most commonly treated non-operatively with rest, physical therapy, activity modification, and exercises. More severe cases may require injections or surgery. People typically recover from quadriceps tendonitis knee pain and return to their pre-injury sporting level within 2–6 months [37]. Ruptures of the quadriceps tendon are relatively infrequent and usually occur in patients

1. Yablon CM, Pai D, Dong Q, Jacobson JA. Magnetic resonance imaging of the extensor mechanism. Magn Reson Imaging Clin N Am. 2014;22:601–20. https:// doi.org/10.1016/j.mric.2014.07.0041064-­9689. 2. Kerr RM.  MRI Web Clinic  — May 2014 MRI of Rectus Femoris/Quadriceps Injury, MD. 3. Mosher TJ. MRI of knee extensor mechanism injuries overview of the knee extensor mechanism. Updated: Nov 12, 2015. 4. Levey DS.  Jumper’s Knee, MRI Web Clinic. December 2006. 5. Waligora AC, Johanson NA, Hirsch BE.  Clinical anatomy of the quadríceps femoris and extensor apparatus of the knee. Clin Orthop Relat Res. 2009;467(12):3297–306. 6. Zeiss J, Saddemi SR, Ebraheim NA. MR imaging of the quadriceps tendon: normal layered configuration and its importance in cases of tendon rupture. AJR Am J Roentgenol. 1992;159:1031–4. 7. Fulkerson JP.  Disorders of the patellofemoral joint. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004. 8. Lyle JE.  Quadriceps tendon rupture. Updated: May 02, 2019. 9. Sonin AH, Fitzgerald SW, Bresler ME, Kirsch MD, Hoff FL, Friedman H. MR imaging appearance of the extensor mechanism of the knee: functional anatomy and injury patterns. Radio-graphics. 1995;15:367–82. 10. Long JR, Rubin DA.  Postoperative imaging of the knee extensor mechanism. Semin Musculoskelet Radiol. 2018;22(4):424–34. https://doi. org/10.1055/s-­0038-­1653956. 11. Yepes H, Tang M, Morris SF, Stanish WD. Relationship between hypovascular zones and patterns of ruptures of the quadriceps tendon. J Bone Joint Surg Am. 2008;90(10):2135–41. https://doi.org/10.2106/ JBJS.G.01200. 12. Benjamin M, Ralphs JR. Entheses—the bony attachments of tendons and ligaments. Ital J Anat Embryol. 2001;106(2 Suppl 1):151–7. 13. Wangwinyuvirat M, Dirim B, Pastore, et  al. Prepatellar quadriceps continuation: MRI of cadavers with gross anatomic and histologic correlation. AJR. 2009;192:W111–6.

References 14. Ibounig T, Simons TA. Etiology, diagnosis, and treatment of tendinous knee extensor mechanism injuries. Scand J Surg. 2015;105(2):67–72. 15. Petersen W, Stein V.  Tillmann Blood supply of the quadriceps tendon. Unfallchirurg. 1999 Jul;102(7):543–7. 16. Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol. 2004;59(7):543. 17. Fu SC, Rolf C, Cheuk C, et al. Deciphering the pathogenesis of tendinopathy: a three-stage process. Sports Med Arthrosc Rehabil Ther Technol. 2010;2:30. 18. Petrsen W, Stein V, Tillman B. Blood supply of the tibialis anterior tendon. Arch Orthop Ttrauma Surg. 1999;119(7–8):371–5. https://doi.org/10.1007/ s004020050431. 19. Benecke P, Krug F, Wohlschlager C.  A rare cause of rupture of the quadriceps tendon. Lancet. 2000;356(9237):1236. 20. Haas SB, Callaway H.  Disruptions of the extensor mechanism. Orthop Clin North Am. 1992;23(4):687–95. 21. Naver L, Aalberg JR. Rupture of the quadriceps tendon following dislocation of the patella. Case report. J Bone Joint Surg Am. 1985;67(2):324–5. 22. Viola R, Marzano N, Vianello R.  Rupture of the quadriceps tendon after arthroscopic lateral meniscectomy: a postoperative complication? Arthroscopy. 2001;17(1):E4. 23. Pope JD Plexousakis MP. Quadriceps tendon rupture. Last Update: March 27, 2019. 24. Brooks P. Extensor mechanism ruptures. Orthopedics. 2009;32:9. 25. Melvin JS, Mehta S. Patellar fractures in adults. J Am Acad Orthop Surg. 2011;19(4):198–207. 26. Kelly BM, Rao N, Louis SS. Bilateral, simultaneous, spontaneous rupture of quadriceps tendons without trauma in an obese patient: a case report. Arch Phys Med Rehabil. 2001;82(3):415–8. 27. Barge-Caballero G, López-Bargiela P, Pombo-Otero J, Pardo-Martínez P.  Quadriceps tendon rupture in wild-type transthyretin amyloidosis (ATTRwt). Eur Heart J. 2019;40(16):1307.

91 28. Wu W, Wang C, Ruan J, Wang H, Huang Y, Zheng W, Chen F. Simultaneous spontaneous bilateral quadriceps tendon rupture with secondary hyperparathyroidism in a patient receiving hemodialysis: a case report. Medicine (Baltimore). 2019;98(10):e14809. 29. Leciejewski M, Królikowska A, Reichert P.  Polyethylene terephthalate tape augmentation as a solution in recurrent quadriceps tendon ruptures. Polim Med. 2018;48(1):53–6. 30. Hsu D, Chang KV.  StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2019. Biceps Tendon Rupture of the Lower Limb 31. Colombelli A, Polidoro F, Guerra G, Belluati A. Patellar and quadriceps tendons acute repair with suture anchors. Acta Biomed. 2019;90(1-S):209–13. 32. Boublik M, Schlegel TF, Koonce RC, Genuario JW, Kinkartz JD.  Quadriceps tendon injuries in national football league players. Am J Sports Med. 2013;41(8):1841–6. 33. Ramseier LE, Werner CM, Heinzelmann M.  Quadriceps and patellar tendon rupture. Injury. 2006;37:516. 34. Hak DJ, Sanchez A, Trobisch P.  Quadriceps tendon injuries. Orthopedics. 2010;33:40–6. 35. Nori S. Quadriceps tendon rupture. J Family Med Prim Care. 2018;7(1):257–60. https://doi.org/10.4103/ jfmpc.jfmpc_341_16. 36. King D, Yakubek G, Chughtai M, Khlopas A, Saluan P, Mont MA, Genin J.  Quadriceps tendinopathy: a review—part 1: epidemiology and diagnosis. Ann Transl Med. 2019;7(4):71. https://doi.org/10.21037/ atm.2019.01.58. 37. King D, Yakubek G, Chughtai M, Khlopas A, Saluan P, Mon MA.  Jason Genin Quadriceps tendinopathy: a review, part 2—classification, prognosis, and treatment. Ann Transl Med. 2019;7(4):72. https://doi. org/10.21037/atm.2019.01.63. 38. Goldin M, Malanga GA.  Tendinopathy: a review of the pathophysiology and evidence for treatment. Phys Sportsmed. 2013;41:36–49.

5

Patella

5.1 Introduction

5.2.1 Osseous Anatomy

The patella is an integral articulating component of the extensor mechanism of the knee joint. The primary function of the patella is to act as a fulcrum, effectively increasing the lever arm of the quadriceps. The fulcrum action requires a pivot surface for the quadriceps tendon adapted to bearing high compressive loads with minimal friction forces [1, 2]. A detailed description of patella anatomy and MRI normal appearance, MRI pathological findings of the patella, and the biomechanical function are provided in this chapter. Knowledge of the patella’s normal anatomy and biomechanics is necessary for understanding the pathogenesis of disorders involving the anterior knee compartment.

The patella has anterior and posterior surfaces and superior, lateral, and medial borders. The base of the patella is roughened for the attachment of the rectus femoris and vastus intermedius. The paramedian borders of the patella are roughly vertical at the level of the articular surface but then become thinner and run obliquely distally toward the midline to converge at the apex [1]. The medial border is considerably thicker than the lateral border. Both sides receive the attachment of the synovium, the joint capsule, the patellofemoral retinaculum, and the quadriceps expansion (the vastus medialis descending more distally than the lateralis) [3].

5.2 MRI Anatomy Normal Appearance The patella is a large, flat, triangular sesamoid bone anterior to the knee joint. It is situated within the tendon of the quadriceps muscle and provides a central point of attachment for the quadriceps tendon and patellar ligament. The peak dimensions of the average patella are 4–4.5  cm in length, 5–5.5  cm in width, and 2–2.5 cm thick [2].

5.2.1.1 Patellar Facets The posterior surface of the patella articulates with the femur. It is marked by two facets: the medial facet, which articulates with the medial condyle of the femur, and the lateral facet, which articulates with the lateral condyle of the femur. The articular area is divided by a vertical ridge into the lateral and medial facets (Fig. 5.1). Medial Facet The medial facet shows the greatest anatomical variation. It is subdivided into the medial facet proper and a much smaller one called the “odd

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_5

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Fig. 5.1  PD FS image in the axial plane. The posterior surface of the patella articulates with the femoral trochlear groove. Two facets mark it: the medial facet (thin dotted arrow) articulates with the medial condyle of the femur (thick dotted arrow), and the lateral facet (thin continues arrow) articulates with the lateral condyle of the femur (thick continues arrow)

5 Patella

Fig. 5.2  PD FS image in the axial plane. The medial facet shows the most significant anatomical variation. It is subdivided into the medial facet proper (MFP)(continuous line) and a much smaller one called “odd facet” (ODD) (dashed line) along the medial border of the patella, found in about 30% of the population [1]

facet” along the medial border of the patella found in about 30% of the population. The odd facet, the so-called “third facet,” is separated from the remainder of the medial facet by a vertical ridge and is described as a “secondary ridge” because it is less prominent than the medial ridge and is developing after birth in response to load which meets the medial condyle of the femur in extreme flexion [1, 4] (Fig. 5.2). Lateral Facet The lateral portion of the articular surface is concave in both vertical and transverse planes, is longer and more sloped to match the lateral femoral condyle, and usually is 1  cm higher than the medial, which helps maintain the patella in a central position in the trochlea [1]. The average ratio of the lateral facet to medial facet width was 1.3 (range 0.8–1.6) [5] (Fig. 5.3). Wiberg introduced a classification system for the different facet sizes of the patella by comparing the medial and lateral facets of the underlying surface of the patella [4] (Fig. 5.4). In type I (with a prevalence of 10%), the medial and lateral facets are concave and approximately equal in size. The medial facet of a Wiberg type II patella is flat or slightly convex and considerably smaller than

Fig. 5.3  Image in the axial plane. The lateral patellar facet (dotted curved line) is concave in vertical and transverse planes. It is longer than the medial facet (continuous arrow) and more sloped to match the lateral femoral condyle (arrow). Usually, it is higher than the medial (arrow), which helps maintain the patella’s central position in the trochlea. The average ratio between the lateral and medial facets’ width was 1.3 (0.8–1.6) [5]

the lateral facet. This is the most frequent morphology (65%) [1]. A type III patella—representing 25% of all cases—also has a smaller medial

5.2  MRI Anatomy Normal Appearance

a

b

Fig. 5.4  Wiberg classification system for the different facet shapes of the patella. Axial PD FS-weighted images. (a) Type I: the facets are concave, symmetrical, and approximately equal in size. (10%). (b) Type II: the medial facet is smaller than the lateral facet and flat or

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c

only slightly convex. The lateral facet is concave (65%). (c) Type III: the convex medial facet is markedly smaller than the concave lateral facet, and the angle between the medial and lateral facets is nearly 90° (25%)

facet than the lateral facet but has a convex form in contrast to type II [4, 6]. These facets are of importance concerning the functional anatomy of the patellofemoral joint.

5.2.1.2 Patellar Cartilage The posterior surface of the patella is divided into two parts. The superior or articular portion of the posterior surface is entirely covered by hyaline cartilage. It makes up approximately 75% of the height of the patella (Fig. 5.5). The inferior portion forming the apex of the patella is non-­ articulating, represents a complete 25% of the patellar height, and forms a rounded projection that receives the attachment of the patellar ligament [3, 7]. The patellar cartilage, a thickness of 4–5  mm in its central portion, is the thickest in the body [7], although there is progressive thinning after 50 years, presumably a normal aging process. This thick cartilage is thought to dissipate large joint reaction forces created during forceful contractions of the quadriceps muscle [2]. Patella cartilage has much greater congruency in the axial plane than in the sagittal plane, contributing to the gliding capability of the joint itself. MRI has revolutionized the evaluation of articular cartilage abnormalities through the superior contrast of soft tissues and the possibilities of multiplanar facility acquisition. It is the technique of choice in visualizing cartilage structural changes [8]. The availability of high-field strength magnets, dedicated surface coils, and

Fig. 5.5  Sagittal T1 SE image shows the posterior surface of the patella covered by hyaline cartilage and makes up approximately 75% of the patella’s height (dotted line). The inferior portion forming the patella’s apex is non-articulating, represents 25% of the patellar height, and forms a rounded projection that receives the attachment of the patellar ligament (small black arrow). The articularis genus is an accessory muscle (dotted arrows) independent from the vastus muscle group, extending from the femur’s anterior surface to insert into the suprapatellar bursa. Articularis genus muscle prevents impingement of the synovial membrane between the patella and the femur (white arrow)

dedicated pulse sequences has taken articular cartilage imaging to a higher level. Articular hyaline cartilage is a highly specialized tissue com-

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posed of a dense extracellular matrix (ECM) with a sparse distribution of chondrocytes. In lesser amounts, the ECM is composed of water, collagen, proteoglycans, and other noncollagenous proteins and glycoproteins [8, 9]. Together, these components provide a smooth, lubricated surface for low-friction articulation between the patella and the trochlear groove of the femur. The patellofemoral joint is unique because cartilage does not follow the contour of the underlying subchondral bone [6]. The structure of articular cartilage can be divided into four major zones: superficial, middle, deep, and calcified. High-­ resolution MRI frequently shows a trilaminar appearance of normal cartilage [10, 11]. The superficial layer in MRI is believed to represent the superficial histological zone, the middle layer represents the histological middle zone, and the deep layer represents a combination of the deep zone, calcified zone, and subchondral bone [10]. Conventional Pulse Sequences. The most commonly used pulse sequences in clinical practice are T1 SE, T2TSE, and PD SE +/− FS. T1 SE of the articular cartilage has a homogeneous signal, with an intermediate intensity, compared to the muscle signal, with a good delimitation to the bone and a weaker delimitation to the articular fluid. It is helpful in evaluating the subchondral bone cartilage interface (Fig. 5.6). There is a lima

Fig. 5.6  T1 SE images of the patellar articular cartilage in the axial plane (a) and sagittal plane (b) have a homogeneous signal, with the intermediate intensity (dotted

ited role of T1 SE imaging in cartilage evaluation due to the lack of good tissue contrast between the adjacent joint fluid and the articular cartilage surface, making it suboptimal for particular usage [12]. T2TSE pulse sequences are a fast conventional technique with a shorter repetition time than spin echo, which reduces the acquisition time of the images and allows simultaneous evaluation of other structures such as meniscus, ligaments, and tendons. The T2-weighted imaging sequences show excellent contrast difference due to fluid-cartilage interphase but at the expense of slightly reduced signal from the articular cartilage (Fig. 5.7). Fat Suppression Techniques. There are currently many pulse sequences used for the evaluation of patellar cartilage. One of the ideal pulse sequences is proton density (PD FS) fat-­ suppressed which is very valuable in evaluating patellar cartilage as it has a high spatial resolution, suitable contrast-to-noise (CNR) ratio, and good scan time [13]. A fat suppression sequence is implemented in the routine cartilage imaging pulse sequences protocol because it improves the dynamic range of signal intensity and provides better detection of minor signal intensity modifications [14]. PD FS (proton density fat sat) pulse sequences are part of the standard protocol and have the advantages: fast, easy to interpret, do not b

arrow), with a good delimitation to the cortical and subchondral bone (arrow image a), but a weaker delimitation to the articular fluid (arrow image b)

5.2  MRI Anatomy Normal Appearance

require detailed measurements, and allow the complete evaluation of the joint structures (meniscus, ligaments), sensitivity 80–97% (arthroscopy reference standard), specificity 89–96 [12] (Fig.  5.8). A T1-weighted inversion recovery sequence, termed short tau inversion

Fig. 5.7  T2 SE image in axial plane shows good contrast between low-signal intensity of cartilage (arrow) and high signal intensity of synovial fluid (dotted arrow). A disadvantage of this sequence is a lack of contrast between cartilage (asterisk) and the cortex of the subchondral bone (short white arrow)

a

Fig. 5.8  PD FS image in the axial plane (a, b). Normal patellar cartilage (small white arrow image a) with good contrast between low-signal intensity of the cortical and spongy bone of the patella (asterisk) and the high signal of the synovial fluid (dotted arrow a). (b) Cartilage fibrilla-

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recovery (STIR), is another technique that obtains the effect of fat suppression. A combination of fat suppression and a three-dimensional (3D) spoiled gradient-echo sequence only depicts the articular cartilage as a bright structure. The sequence with the best possible potential to assess the articular cartilage accurately is the spoiled gradient-echo sequence (SPGR) [15] (Fig. 5.9). Gradient-echo sequences (GRE) allow volumetric image acquisition with reduced imaging times and improved spatial resolution. Technically, a refocusing pulse separates two or more gradient echoes, eventually combining the echoes to generate an image [16]. Gradient-recalled echo (GRE) sequences suffer from a potential fallacy, as they are unusually sensitive and susceptible to intravoxel dephasing, especially in patients with previous surgical intervention or some hardware placement [16]. There is better detection of minor signal intensity modifications. A T1-weighted inversion recovery sequence termed short tau inversion recovery (STIR), is another technique that obtains the effect of fat suppression. A combination of fat suppression with a three-­ dimensional (3D) spoiled gradient-echo sequence only depicts the articular cartilage as a bright

b

tion (circle) categorizes as a grade 2 cartilage lesion at the medial patellar facet in a patient with repeated patellar dislocations expressed by the partial tear of MPFL in the third posterior portion (black arrow) and femoral disinsertion (star). Trochlear dysplasia Dejour A (dotted line)

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a

b

Fig. 5.9  3D-spoiled gradient echo (3DSPGR) images in the sagittal plane (a) and axial plane (b). The T1-3D sequence with fat suppression has the highest accuracy in detecting chondral changes. In this sequence, the normal articular cartilage shows a high-intensity signal, homogeneous throughout its thickness. Advantages: highlights the

trilaminate structure of the cartilage. Cartilage volume can be calculated. Disadvantages include long acquisition time (>8 min) and difficult assessment of other joint structures. It is sensitive to motion artifacts and magnetic susceptibility

structure. The sequence with the best possible potential to assess the articular cartilage accurately is the spoiled gradient-echo sequence (SPGR) [15]. Standard SE MRI has a lower accuracy as compared to the fat-suppressed ­ SPGR. The sensitivity of the sequence approaches 93%, with articular cartilage appearing bright and the remainder of the structures appearing relatively dark [16]. 3D SPGR is recommended by the International Cartilage Repair Society (ICRS) as a standard sequence in imaging for the evaluation of articular cartilage lesions, especially in post-cartilage repair status [12]. This technique is helpful for cartilage volume and thickness measurements. However, it does not adequately highlight surface defects with fluid and does not allow a thorough evaluation of other joint structures, such as ligaments or menisci [15]. The patellar cartilage is best assessed in the axial plane and trochlear cartilage in the sagittal plane.

5.2.2 Soft Tissue Anatomy The quadriceps tendon and patellar ligament fibers are in continuity over the anterior aspect of the patella. In contrast, the medial and lateral expansions of the quadriceps tendon blend with the medial and lateral patellar retinaculum [17].

5.2.2.1 Patellar Retinaculum The patellar retinaculum consists of aponeurotic expansions from the vastus medialis and lateralis, with contributions from the deep fascia. They insert obliquely into the anterior aspect of the tibia, medial and lateral to the patellar tendon. The tendon of the vastus medialis inserts into the rectus femoris’s tendon, the patella’s superomedial border, and the medial condyle of the tibia as the medial retinaculum of the patella. Similarly, the vastus lateralis tendon inserts into the patella’s superolateral border and the tibia’s lateral condyle as the patella’s lateral retinaculum [18].

5.2  MRI Anatomy Normal Appearance

The Medial Retinaculum and Ligaments The medial retinaculum includes the vastus medialis obliquus (VMO) and three ligaments: the medial patellofemoral ligament (MPFL), medial patellotibial ligament (MPTL), and medial patellomeniscal ligament (MPML) (Fig. 5.10). The main dynamic stabilizer on the medial side, counteracting the pull of the vastus lateralis and the iliotibial band (ITB), is the vastus medialis oblique (VMO). This muscle has a 60-degree force vector to the anatomic femoral axis and is most active at 0–30 degrees of knee

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flexion [19]. In addition to its role as a dynamic stabilizer, the VMO also serves as a static stabilizer, and its sectioning has been shown to produce an increased lateral translation of the patella. The most important static medial stabilizers are the medial patellofemoral ligament (MPFL), which provides 53–60% of the check-rein to lateral displacement patella at 0–30 degrees of knee flexion, and is variable in size, averaging 59 mm in length, 12 mm in width, and 0.44 mm in thickness [20–23]. The medial patellofemoral ligament extends from the medial femoral epicondyle

a

b

c

d

Fig. 5.10  Selected successive craniocaudal images of the left knee. PD FS sequences in the axial plane from the upper of the patella (a) to the tibial plateau (d), showing— medial retinaculum (MR), vastus medialis oblique [VMO]

(image a), MPFL-medial patella-femoral ligament, (image b), MPTL-medial patella-tibial ligament (image c), MPML-medial patella-meniscal ligament (image d)

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a

b

Fig. 5.11  Selected successive craniocaudal images of the left knee. PD FS sequences in the axial plane, highlighting the vastus medial oblique muscle (a) and the medial patellofemoral ligament (b). There is edematous hemorrhagic infiltration in the VOM muscle (black arrow in circle image a) and the femoral portion of the MPFL (black

arrow in circle image b), following acute patellar dislocation. Note the lateral patellar facet chondropathy (white arrow image a) and bone contusion at the anterior portion of the lateral femoral condyle (asterisk), and in the inferomedial portion of the patella (white arrow)

and adductor tubercle to the superior medial border of the patella [24]. The close attachment of the MPFL to the deep aspect of the vastus medialis obliquus (VMO) makes both the ligament and muscle susceptible to damage in acute patellar lateral dislocations (Fig. 5.11). The medial patellotibial ligament runs from the inferior medial edge of the patella and inserts approximately 1.5 cm below the joint line of the tibia [21]. The medial patellomeniscal ligament is inserted on the anterior portions of the patella’s inferior and medial meniscus.

eral patellofemoral ligament, which provides superior lateral support for the patella; (b) the deep, transverse retinaculum, which is the primary restraint to medial displacement; and (c) the patellotibial band, which provides inferolateral support for the patella [22] (Fig. 5.12). Some studies report that the LPFL might not be present in all knees. Some report its presence in only two-thirds of knees [23, 24]. The width of the LPFL is about 16  mm, and the length is about 42.1 mm [25]. A correlation between the length of the LPFL and the width of the lateral patellar facet has been reported, with shorter LPFL correlating with wider lateral patellar facets [25]. The iliotibial tract inserts on the lateral tibial condyle (Gerdy’s tubercle) and provides anterolateral stability to the tibia (Fig. 5.13). The iliopatellar band connects the anterior aspect of the iliotibial tract and femur to the patella, forming an integral part of the lateral retinaculum [26]. The lateral retinaculum and ITB significantly affect the patellar position because of their attachments to the patella.

The Lateral Retinaculum and Iliotibial Band The lateral retinaculum comprises two major components: the superficial oblique and the deep, transverse retinaculum [21]. The superficial oblique retinaculum consists of a fibrous expansion from the vastus lateralis and iliotibial band (ITB), which inserts into the lateral border of the patella. The deep, transverse retinaculum consists of three major components: (a) the lat-

5.2  MRI Anatomy Normal Appearance

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a

b

,7

9/

c

d

/3 )

/3 7

Fig. 5.12  Selected successive craniocaudal images of the left knee. PD FS sequences in the axial plane highlight the fibrous expansion from the vastus lateralis oblique (VLO) and iliotibial band (ITB), which inserts into the lateral border of the patella (arrows image a, b). The deep, trans-

verse retinaculum consists of three major components: LPFL-the lateral patellofemoral ligament (image c), LPTL-lateral patellotibial ligament (image d), and the patelo-meniscal ligament (is not seen here)

To summarize the contributions of various anatomic structures to patellofemoral stability, stability in extension and early flexion (up to 30 degrees) is primarily dependent on the integrity and function of the medial soft tissue stabilizers,

both static (MPFL) and dynamic (VMO). Stability in greater degrees of flexion depends on the bony architecture and congruity of the femoral trochlea and the patella.

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a

b

Fig. 5.13  Coronal PD FS sequence (images a, b). The iliotibial tract (dotted arrow a) inserts on Gerdy’s tubercle (continuous arrow) and provides anterolateral stability to the tibia and inferolateral support for the patella. Partial

rupture of the ITT at the level of the tibial insertion following the first episode of lateral patellar dislocation (circle and arrow b)

5.3 MRI Patellar Measurements

cance for patellar height include: the Insall– Salvati index (ISI) [25, 35], modified Insall–Salvati index (MISI) [36], Caton– Deschamps index (CDI) [37], Blackburne–Peel index (BPI), the morphology ratio (MR) [26] and patellar trochlear index (PTI) [37]. All measurements were made on the sagittal slice showing the greatest patella length. The Insall–Salvati Index (ISI) is calculated by dividing the patellar tendon length by the maximum diagonal of the patellar bone in a knee radiograph. Like the radiographic measurement, patellar height can be reliably assessed on sagittal MR imaging using the patellar tendon: patella height ratio [29]. The length of the patella on the midsagittal slice is the distance between the anterior-­inferior and posterior-superior corners. The length of the patellar tendon is determined by measuring the shortest line drawn parallel to the most profound edge of the patellar tendon (Fig.  5.14). For the Insall–Salvati index, when there is an elongated lower pole of the patella, known as “Cyrano patella,” the index value may

Numerous patellofemoral measurements have been described to quantify abnormalities of the patellofemoral joint. Evaluation of the position and morphological aspect of the patella is predominately based on imaging, such as X-rays [25–28] and computed tomography [29]. More recently, magnetic resonance imaging gained popularity in imaging PF disorders. Anatomic instability factors were measured on MR images, including patellar height, patellar tilt, TT-TG distance, trochlear morphology (sulcus angle, trochlear depth, trochlear facet asymmetry, trochlear condyle asymmetry, and lateral inclination angle), and Patella Trochlear Index (PTI) [30–35].

5.3.1 MRI Measurements of Patellar Height in the Sagittal Plane Among the quantitative parameters evaluated in the sagittal MR sections with diagnostic signifi-

5.3  MRI Patellar Measurements

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remain within the normal range if patella Alta is present [38]. Using a formula based on the Patellar Morphology Index (Vertical length of the patella/length of the patellar articular surface), Grelsamer et  al. and Miller [35, 38] identified three variations involving the length of the articu-

lar surface of the patella and the shape of the lower pole of the patella which introduces error in the Insall–Salvatti Index. Grelsamer study [38] describes three types of patella based on the ratio between the patella’s length and the articular surface’s length. Most patellae exhibit a ratio between 1.2 and 1.5 and are classified as type I (Those with a greater than 1.5 give the appearance of having a long nose; this is type II. Those with a ratio of 1.2 (short nose) are type III (Fig. 5.15). Type I (85%) has an articular surface of normal length with a typical rounded lower pole and yields accurate ISI measurements. Type II (11%) has an abbreviated articular surface length, and an elongated lower pole (Cyrano Nose) understates patella Alta while overstating patella Baja in ISI measurements. Type III (4%) has a normal articular surface with a flattened lower pole with patella Alta overstated, and patella Baja understated in ISI measurements. These authors suggested that the Modified Insall–Salvatti Index (MISI) be used in conjunction with the ISI in patients with unusual patellar shapes or old fractures or Sinding-Larsen-Johansson disease where Fig. 5.14  T1 SE image in sagittal plane reveals high-­ the lower pole of the patella is abnormal or diffiriding (patellar ratio 1,51). According to the Insall–Salvati cult to evaluate. Several authors have studied the Index (ISI), the patellar height ratio is calculated by dividpatella’s sagittal position using MRI or have ing the length of the patellar tendon from the apex of the patella (continuous line B) to its attachment on the tibial introduced novel MRI measurements for patients tuberosity (dotted arrow) by the maximum diagonal with PF disorders. Other methods include the length of the patellar bone modified Insall–Salvati ratio, the Caton– a

b

Fig. 5.15  T1 SE images in the sagittal plane (A–C) highlighting the vertical length of the patella (continuous line a-A–C) and length of the patellar articular surface (dotted line b-A–C). Based on the ratio between the length of the patella and the length of the patella’s articular surface, there are three types of shapes of the lower pole of the patella. Type I (image A) has a normal-length joint surface

c

with the typical rounded pole and produces accurate ISI measurements. Type II (image B) has an abbreviated articular surface length, and an elongated lower pole (Cyrano Nose) understates patella Alta while overstating patella Baja in ISI measurements. Type III (image C) has a normal articular surface with a flattened lower pole with patella Alta overstated and patella Baja understated in ISI

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Deschamps index, the Blackburne-Peel index, and de Carvalho et al. [26, 36, 39]. These methods use the low end of the articular surface of the patella as one landmark, thus avoiding possible false-positive or false-negative results in case of an abnormal shape of the distal non-articulating facet of the patella. The Modified Insall–Salvatti Index (MISI) is obtained by dividing the distance between the inferior aspect of the articular surface of the patella and the insertion of the patellar ligament by the length of the patellar articular surface to avoid inaccuracies associated with the variability in the shape of the lower pole of the patella [40]. The normal value of MISI: 1.25 (range 1.2–2.1); patella Alta: >2 (Fig. 5.16). The authors recommended that the MISI be used with the ISI and that its primary value is in identifying cases of patella Alta in which the ISI is in question. With either method, there can be a problem in patients with Osgood-Schlatter’s disease, where it is difficult to identify the patellar tendon insertion. In these instances, the Blackburn-

Fig. 5.16  The Modified Insall–Salvatti Index (MISI) is obtained by dividing the distance between the inferior aspect of the articular surface of the patella and the insertion of the patellar ligament by the length of the patellar articular surface to avoid inaccuracies associated with the variability in the shape of the lower pole of the patella [41]. The normal value of MISI: 1.25 (range 1.2–2.1); patella Alta: >2

5 Patella

Fig. 5.17  PD FS image in sagittal plane highlights the Caton-Deschamps index (CDI) calculation. The distance between the inferior articular surface of the patella and the anterior corner of the superior tibial joint (dotted line a) is divided by the length of the articular surface (line b). Values less than 0.6 indicate patella Baja and values greater than 1.2 indicate patella Alta

Peel ratio, the Caton-Deschamps index, and de Carvalho’s index have been recommended as alternatives for radiographic evaluation. The Caton-Deschamps Index (CDI) for evaluating patellar height is the ratio of length between the inferior articular surface of the patella and the anterior lip of the tibia and the length of the patellar articular surface. Normal value range 0.6–1.2. Values less than 0.6 indicate patella infera, and values greater than 1.2 indicate patella Alta (Fig. 5.17). CDI is the most accurate diagnostic method because it relies on readily identifiable and reproducible anatomical landmarks; does not depend on radiograph quality, knee size, radiologic enlargement, or position of the tibial tubercle or patellar modification; and is unaffected by the degree of knee flexion between 10° and 80° [42]. CDI is the most useful method for describing patellar height after distalization of the tibial tubercle because it assesses the height of the patella relative to the tibial plateau.

5.3  MRI Patellar Measurements

The Ratio of de Carvalho’s Index is similar to the Caton-Deschamps index. Still, it replaces the denominator with the shortest length between the inferior margin of the patellar articular cartilage and the closest point on the anterior margin of the tibial plateau (Fig.  5.18). These methods share the advantage of being independent of the shape of the lower pole of the patella and the vagaries of identification of the patellar tendon insertion. Still, they are all easily obscured by arthritic or posttraumatic changes of the patella and femorotibial articulation [40] (Fig. 5.19). The Blackburn-Peel (BP) Ratio measures the ratio of the shortest distance between the inferior margin of the patellar articular surface and a line parallel to the proximal tibial articular surface and the length of the patellar articular surface. The mean normal Blackburne-Peel ratio (TA/PC) is 0.8, with patella Alta defined as >1.0 and patella Baja: 1.0 [26, 40]. The main disadvantage of this method is that the line drawn along the plateau is naturally associated with the tibial slope. If the slope exceeds normal, the patella Alta will not be correctly appreciated

between the patella and the trochlea and for assessing patellar height using MRI: the “patellotrochlear index” (PTI). This is a ratio between the maximum length of patellar articular cartilage and the length of trochlear articular cartilage (Fig. 5.21). The described patellotrochlear index measured on sagittal MR images is a reliable and reproducible method to determine the exact articular correlation between the patellofemoral joint and the patellar height [37]. The major advantages of this index are [37]: (1) exact measurement of the patellotrochlear articular congruence; (2) osseous form variations of the patella (i.e., long, nonarticular inferior pole) [38] do not affect the ratio; (3) differences of length and shape of the trochlea are considered; (4) variations of the patellar tendon attachment areas

5 Patella

Fig. 5.21  Patellotrochlear index (PTI). PD FS image in the sagittal plane with the greatest patellar length highlights the PTI calculation. Line (b) measurement of articular cartilage. Line (a) parallel to line (b), most superior femoral articular cartilage to the reference line. PTI = A/B-­0,47(the mean patellotrochlear index is 31.7%) [37]. PTI of less than 12.5% suggests the presence of patella Alta

are insignificant (Sinding-Larson-Johansson or Osgood-­Schlatter’s disease; after surgical interventions); (5) thicker radiolucent cartilage in children is visible; (6) no ionizing radiation exposure, and (7) measurements in 0° knee flexion is easier than in 30° of flexion. Each of the mentioned assessment methods of patella Alta has advantages and limitations. For example, although the Insall–Salvati ratio is one of the most commonly used methods and does not depend on the degree of knee flexion, it is affected by the patellar shape, particularly its inferior point, and measurement does not change after the tibial tubercle distalization procedure [41]. On the other hand, the PTI is significantly altered with knee flexion [43].

5.3.1.1 Patella Alta Patella Alta, or high-riding patella, is too high above the trochlear fossa and occurs when the patellar tendon is too long [39] (Fig. 5.22). The

5.3  MRI Patellar Measurements

a

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b

Fig. 5.22  Woman, 37-year-old, with anterior knee pain. PD FS images in the sagittal (a) and axial plane (b) reveal high-riding patella (ISI ratio-1,43), (image a), chronic rupture of ACL (arrow image a) associated with recurrent patellar dislocation with rupture and femoral disinsertion

of the medial patellofemoral ligament (arrow in circle image b) and cartilage fibrillation of both patellar facets (black oval circle b). Note: type A Dejour dysplasia is the second anatomical major risk factor for patellar dislocation (dotted line b)

patella serves as an anchor point for the various soft tissue components of the extensor apparatus, which allows a balance of the opposing forces at the knee. The extension is facilitated by shifting the plane of the anterior extensors to the knee’s central axis of flexion and extension, and the extension force is increased. The hyaline cartilage of the patellofemoral articulation also minimizes friction during the transmission of the force of the quadriceps mechanism across the knee joint. The vertical position of the patella relative to the femoral trochlea is recognized as an important element of normal knee function. In relaxed extension, the inferior pole of the patella is located within the superior margin of the femoral trochlear groove but not fully engaged with the trochlea and with no compressive force acting across the patellofemoral joint. As flexion begins, initial contact occurs between the distal, lateral edge of the patellar articular surface, and with increasing flexion, the area of contact between the patella and femur increases in area and moves superiorly and medially so that at full flexion

(1200), the medial facet contacts the lateral margin of the medial femoral trochlea [39]. Normally the patella is fully engaged with the trochlea at 20–30°. In patella Alta, the patella is abnormally elevated relative to the femoral trochlea, and engagement occurs later in flexion, with the contact area between the patella and trochlea diminished. So, patella Alta predisposes to tracking abnormalities and instability. In the patella Alta, the patellofemoral contact area has been suggested to be, on average, 19% less than normal [39]. Elevation of the patella by 8 mm can result in a 25% increase in the magnitude of contact force across the patellofemoral articulation [44]. This increase in compressive force with diminished contact area across the articulation results in abnormal stress on the articular cartilage, predisposing to chondromalacia and patellofemoral osteoarthrosis. Patella Alta has been associated with several knee disorders, with patellofemoral instability and recurrent patellofemoral dislocation among the strongest associations [34, 39, 40, 45].

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About 25% of the patients with acute patellar dislocation (APD) have a high-riding patella on MR images and accompany a stable patella in only 3% of cases [39]. A high-riding patella has been associated with chondral patellotrochlear defects (Fig. 5.23), chondropathy (Fig. 5.24), and patellofemoral osteoarthritis [40, 46, 47] (Fig. 5.25). Patella Alta has also been linked with other entities, including neuromuscular diseases such as poliomyelitis, Osgood-Schlatter’s disease (Fig.  5.26), Sinding Larsen Johanssen disease (Fig.  5.27), and patellar tendon-lateral femoral condyle friction syndrome [30, 32, 48, 49] (Fig. 5.28).

5.3.1.2 Patella Baja Patella Baja or patella infera (a low-riding patella) is characterized by the distal position of the patella in the femoral trochlea, a decreased distance between the inferior pole of the patella and the articular surface of the tibia, and/or a permanent shortening of the patellar tendon [50] (Fig. 5.29).

a

Fig. 5.24  Woman, 39-year-old, with anterior knee pain. PD FS images in the sagittal (a) and axial plane (b) highlight patella Alta measurement by the Caton-Deschamps index (1,5). Relaxation and angulation of the patellar tendon in the distal segment (arrow image a) and patellar

Fig. 5.23  Man, 53-year-old, with anterior knee pain accentuated when going up and downstairs. PD FS image in sagittal plane reveals high-riding patella (ISI ratio1,43), associated with patellar and trochlear chondral ­ defects (circles) compatible with patellotrochlear chondropathy

b

chondropathy are both facets (short arrows image b). Note: Dejour type C trochlear dysplasia (oblique dotted line) is the second anatomical major risk factor for patellar instability

5.3  MRI Patellar Measurements

a

Fig. 5.25  Girl, 43-year-old, with anterior knee pain, accentuated when going up and downstairs. PD FS image in the sagittal plane (a) reveals patella Alta associated with patellar and trochlear chondral defects (arrow and

109

b

circle). PD FS image in the axial plane (b) demonstrates patellotrochlear chondral lesions and narrowing of the joint space, an aspect compatible with patellofemoral osteoarthritis (oval circle b)

Fig. 5.27  Girl, 12-year-old, a gymnast with anterior knee pain. T1-weighted image, in the sagittal plane, reveals Fig. 5.26 Boy, 11-year-old, with anterior knee pain high patella according to the Caton-Deschamps index located on the subpatellar level at the patellar tendon’s (1.8), associated Sinding Larsen Johanssen disease, expetibial insertion. T1-weighted image, in the midsagittal rienced through the avulsion of a small bone fragment plane, reveals patella Alta, according to the Caton-­ from the contour of the lower pole of the patella and Deschamps index (1.7), associated with Osgood-­ enclosed in the patellar tendon (oval circle) Schlatter’s disease experienced through the avulsion of a bone fragment enclosed in the patellar tendon (thin arrow) and deep subpatellar bursitis (dotted arrow)

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a

b

Fig. 5.28  Woman, 47-year-old, with lateral infrapatellar knee pain. PD FS images in the sagittal (a), coronal (b), and axial plane (c) reveal high-riding patella (ISI ratio1.33) associated with superolateral Hoffa’s fat pad’s ­

c

impingement. High signal intensity (edema) in the superolateral aspect of Hoffa’s fat pad between the inferolateral aspect of the patella, patellar tendon, and the lateral femoral condyle (asterisk a–c)

in extension, unlike a normal patella, which does not engage with the trochlea. A low-riding patella is most common in the postoperative or posttraumatic knee because of decreased tension forces of the quadriceps muscle. Several conditions are associated with patella Baja, including rupture of the patellar ligament, patellar fracture, or quadriceps tendon rupture (Fig. 5.30). A low-riding patella or patella Baja is often associated with a limited knee range of motion, patellofemoral arthritis (Fig. 5.31), and Osgood-­ Schlatter’s disease [40, 51, 52] (Fig. 5.32). Several studies have reported the adverse effects of the inferior position of patella infera. These include anterior knee pain, joint stiffness, alterations in joint mechanics, a decreased lever arm and extensor lag, and reduced range of motion [40]. Fig. 5.29  Man, 27-year-old, with anterior knee pain. T1 SE image in the midsagittal plane reveals patella Baja, Insall–Salvati (IS) index (0,7). Note a small bone fragment separated from the anterior-upper contour of the patella enclosed in the quadriceps tendon (thick white arrow) and thickened subpatellar synovial plica (small black arrows)

Patella Baja may also be defined by an Insall– Salvati ratio of 0.8. In patients with patella infera, the patella is always in contact with the trochlea

5.3.2 MRI Measurements of Patellar Position in the Axial Plane Among the quantitative parameters evaluated in the axial MR sections with diagnostic significance in patellar instability (PI) include patellar facet asymmetry, patellar axis (PA) as described by Dejour et al. [52], and the lateral patellofemoral length (LPL), patellar tilt, and subluxation.

5.3  MRI Patellar Measurements

Fig. 5.30  Man, 39-year-old, with anterior knee pain after a complete rupture of the quadriceps tendon at the level of the muscle–tendon junction.T1SE image in the midsagittal plane reveals the low secondary position of the patella (black arrow), and laxity, curling, and wrinkling, of the patellar tendon (thin white arrow)

a

Fig. 5.32  Boy, 15-year-old, with anterior knee pain. PD FS in the midsagittal plane (a) reveals a low-riding patella, according to Caton-Dechamps Index, associated with Sinding Larsen Johanssen disease (white arrow) and

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Fig. 5.31  Boy, 15-year-old, with anterior knee pain. T1SE in the midsagittal plane reveals a low-riding patella, according to the Caton-Deschamps index, associated with Osgood-Schlatter’s disease experienced through the avulsion of a bone fragment enclosed in the patellar tendon (thin arrow) and thickened subpatellar synovial plica (dotted arrows)

b

Dejour trochlear dysplasia type A (continues and dotted lines b), partial femoral disinsertion of MPFL (white arrow b), and small chondral defect on the lateral patellar facet (black arrow b)

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5.3.2.1 Patellar Facet Asymmetry Axial slices were used to determine the patellar facet asymmetry, described as the ratio of the medial and lateral patellar facet lengths (Fig.  5.33). The medial patellar so-called “odd facet” was not included in the medial facet measurements to prevent overestimating the facet. The Wiberg classification in three basic patellar configurations is the most commonly used [4] (Fig. 5.4). It is considered that the Wiberg type III patella, where the lateral facet is prominent and the medial facet is small, is among the predisposing factors of patellar instability and chondromalacia. [53, 54]. Barnett’s [55] study has shown that patellar shape changes from proximal to distal in the dysplastic patella compared to the non-­ dysplastic patella. The patella’s cartilaginous and

a

b

5.3.2.2 Patellar Tilt and Subluxation Different methods were described for evaluating patellar tilt [56–58]. In the transverse plane, the patella should lie horizontally such that the medial and lateral borders are equidistant from the femur (Fig.  5.35). A lateral tilt can lead to lateral patellofemoral compression syndrome ­ when the lateral border is higher than the medial border [59] (Fig. 5.36). Patellar tilt (as an expression of MPFL insufficiency) is diagnosed by determining the lateral patellofemoral angle. The

c

Fig. 5.33  PD FS axial images of the right knee show the change in the shape of the patella from (a) proximal to (b) middle to (c) distal in patellofemoral dysplasia. The medial facet becomes smaller and more vertical than the

a

osseous contours become more dysplastic along their length, as the ratio increase shows. However, there was little change in the ratios in the normal control group, suggesting a more uniform shape throughout (Fig. 5.34).

b

lateral (curved lines a–c). Note, in image c, the trochlear cartilage has fully visualized the appearance of trochlear dysplasia Dejour type B (dotted line)

c

Fig. 5.34  PD FS axial image of the right knee in a normal subject show uniformity of the patellar morphology from (a) proximal to (b) middle to (c) distal. The medial and lateral facets are relatively equal in size throughout the patella

5.3  MRI Patellar Measurements

a

Fig. 5.35  PD FS image in the transverse plane in two patients. Normally, the patella should lie horizontally such that the medial and lateral borders are equidistant from the

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b

femoral condyles (image a). The patella is tilted when the lateral border is higher than the medial border (arrow image b), leading to lateral patellofemoral compression

bility [58]. In Escalla’s study [33], a lateral patellar tilt >11° reached the highest sensitivity for predicting objective patellar instability (92.7%). Lateral patellar tilt may occur with or without patellar lateralization (Fig. 5.38).

5.3.2.3 Lateral Displacement of the Patella Patella that did not fit into the trochlea in flexion and with the medial margin lateralized concerning a line perpendicular to the bicondylar line in the plane of the medial eminence of the femoral trochlea is considered to be displaced (Fig. 5.39). Lateralization of the patella in extension may be physiological. Fig. 5.36  PD FS image in the axial plane reveals a lateral patellar tilt (thick arrow) associated with a compressive syndrome due to a lateral patellofemoral conflict (star and thin arrow)

patellofemoral angle is demonstrated as the angle between a line drawn along the lateral joint facet of the patella and a line drawn along the anterior aspect of the femoral condyles (Fig. 5.37). Lateral patellar tilt is a sensitive marker for patellar insta-

5.3.2.4 The Tibial Tubercle–trochlear Groove Distance Tibial Tubercle–trochlear Groove (TT-TG) is evaluated by measuring the distance between the most anterior point of the tibial tuberosity and the deepest point of the trochlear groove using two lines drawn perpendicular to the tangent to the posterior borders of the femoral condyles [34, 58] (Fig.  5.40). An increased tibial tubercle–

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a

Fig. 5.37  The patellofemoral angle. PD FS image in the axial plane shows the patellofemoral angle, which demonstrates the angle between a line drawn along the lateral joint surface of the patella (line a) and a line drawn along

b

the anterior aspect of the condyles (line b). A medial opening angle indicates patellar tilt. A lateral patellar tilt >11° reached the highest sensitivity for predicting objective patellar instability (92.7%) [33]

a

b

c

d

Fig. 5.38  Axial PD FS images. (a) Patellar tilt without patellar lateralization (values of 2 mm or less are considered normal). (b) Mild subluxation (values from 2 to

5  mm) (c), Moderate subluxation (values from 5 to 10 mm) (d). Severe subluxation (values >10 mm)

5.4  Acute Patellar Dislocation/Subluxation, MRI Findings

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Fig. 5.39  PD FS image in the axial plane shows dysplastic trochlea with a lateral patellar displacement of 10 mm. A line drawn parallel to the posterior aspect of femoral condyles is a reference (line a). A line drawn perpendicular to the reference line indicates the largest anteroposterior diameter of the medial trochlear facet (line b). The distance of the medial margin of the patella from this perpendicular line is normal 145° (dotted lines), bone marrow contusion in the inferomedial portion of the patella (star), and the anterolateral portion of the lateral femoral condyle (double stars), known as a “kissing contusions”

traumatic patellar dislocations is hemarthrosis of the knee, caused by rupture of the medial restraints of the patella [96].

5 Patella

Patella Alta, or increased patellar height, has long been recognized as a risk factor for LPD [88]. With patella Alta, the patella does not become engaged within the trochlear groove until the knee is in more than 30° of flexion, leading to the reduced patellar contact area and decreased stability in shallow degrees flexion [68]. Patella Alta can be measured in full extension on MRI using the Insall–Salvati ratio. In this method, the patellar height ratio is calculated by dividing the patellar tendon’s length (from the patella’s apex to its attachment to the tibial tuberosity) by the longest superoinferior diameter of the patella. A patella height ratio of more than 1.3 is consistent with patella Alta [68]. Methods like the Insall– Salvati rarely on the osseous relationships of the patellofemoral joint and the position of the patella about the trochlea. However, the most important factor in patellar height determination is the position of the articular surface of the patella concerning the trochlear cartilage, and the osseous anatomy does not correspond to the articular cartilage surface [97]. The patellotrochlear index measures the real articular cartilage relationship and accurately reflects the functional patella height. The patellotrochlear index is the ratio of the length of the trochlear articular cartilage overlapping the patellar cartilage divided by the patellar cartilage length. More than 80% of index values document patella Baja, and less than 12.5– 18% indicate patella Alta [41, 98].

5.4.3.6 The Tibial Tubercle–Trochlear Groove (TT-TG) Distance Tibial tubercle lateralization was measured using the method described by Schoettle et al. [34]. An increased tibial tubercle–trochlear groove (TT-­ TG) indicates a lateralized tibial tuberosity or a medialised trochlear groove [34]. TT-TG is a reflection of the clinically measured Q angle. A high Q angle or TT-TG would exert lateral pressure on the patella during knee extension. If this is not counteracted by vastus medialis muscle contraction, it can predispose to lateral patellar subluxation and instability [99]. The literature has a degree of variability about an abnormally high TT-TG. TT-TG distance of more than 20 mm is believed to be nearly always associated with patellar instability [47]. The TT-TG is evaluated

5.4  Acute Patellar Dislocation/Subluxation, MRI Findings

by measuring the distance between the most anterior point of the tibial tuberosity and the deepest point of the trochlear groove using two lines drawn perpendicular to the tangent to the posterior borders of the femoral condyles [57].

5.4.4 Injury Mechanism of APD Acute dislocation may occur from a direct or an indirect mechanism of injury. The indirect mechanism of injury is responsible for 66–82% of acute patellar dislocations and occurs most commonly with cutting, pivoting, and squatting movements with sports and other strenuous physical activities [100]. Typically, the foot is planted, the femur is rotated internally, and/or the tibia is rotated externally, and there is a valgus force at the knee joint; in this position, sudden contraction of the quadriceps produces a strong laterally directed force vector, resulting in dislocation of the patella [101]. Dislocation from a direct injury mechanism is much less common when the patella is struck with a laterally directed blow. Most cases of acute patella dislocation reduce spontaneously as the knee is brought into extension, and therefore evaluation in the emergency room or doctor’s office may not readily provide the diagnosis. The patient may report feeling or hearing a “pop” or a “snap” and seeing/feeling their kneecap “move out of place,” followed by spontaneous reduction with a “clunk” as the knee is extended [102].

5.4.5 Clinical Examination of APD The clinical examination of the acutely dislocated patella can be difficult, depending on the presence of a spontaneous reduction and concomitant injuries. When the patella remains dislocated, the knee demonstrates a gross deformity and restricted knee motion. A large hemarthrosis is often present, and physical examination may be significantly limited by guarding due to pain and bleeding in the knee. If this is the case, arthrocentesis with hemarthrosis aspiration and injection of a short-acting local anesthetic should

121

be considered [101] and allows for a more accurate examination of the knee and quicker restoration of knee motion and strength. The examination should focus on ruling out fractures, injuries to major ligamentous stabilizers of the knee joint, and patellar stability. Careful palpation of the medial PF ligament (MPFL) is conducted at its patellar and femoral origins to help determine the location of soft tissue failure. A combination of hemarthrosis and a sports-related mechanism of injury may initially suggest a diagnosis of an anterior cruciate ligament (ACL) tear, and careful examination of anterior, posterior, varus, valgus, and rotational stability of the knee should be performed [102]. Patients may exhibit medial knee tenderness and ecchymosis (bruising) at the femoral origin of the MPFL, near the medial epicondyle and adductor tubercle, and injury to the MCL (which also originates in this area) should be ruled out. There is often tenderness over the medial facet and lateral femoral condyle. Less commonly, there is a palpable soft tissue defect adjacent to the medial facet, especially if there is a complete tear at the VMO insertion. The knee’s range of motion is usually very limited due to pain and apprehension; crepitus during motion (in a knee without preexisting arthritis) concerns osteochondral fracture and the presence of intra-­ articular fragments. Apprehension with attempted lateral translation at 30 degrees of knee flexion suggests patella instability, known as the “patella apprehension” test [101]. Direct tenderness may be noted just proximal to the medial epicondyle, indicating failure of the MPFL at its femoral origin (Bassett’s sign) [103].

5.4.6 MRI Findings After Acute Patellar Dislocation Previous studies [31, 47, 61, 62, 64, 69, 70, 74, 104, 105] have described a constellation of magnetic resonance (MR) imaging findings characteristic of acute patellar dislocation, which are helpful for diagnosis. These findings include injuries to the medial retinaculum and the medial patellofemoral ligament (MPFL), joint effusion, contusions of the medial patella and lateral femo-

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a

b

c

Fig. 5.47  Woman, 20-year-old, with knee pain after a fall, with sudden internal rotation of the right knee with the foot fixed. PD FS in the axial plane. (a) and in the coronal plane (b, c). MR images five days after primary patellar dislocation demonstrate focal bone marrow edema involving the inferomedial pole of the patella and the lateral aspect of the lateral femoral condyle (stars a–c), consistent with the “kissing contusions” characteris-

tic of lateral patellar dislocation injury. It should be noted that the patient has Dejour B femoral dysplasia as a predisposing anatomic major factor and edematous infiltration of the LPFM with the interruption and retraction of some fibers (black arrowhead image a) and patellar disinsertion (continuous arrow a and b). Minimally effusion retropatellar and in paracondylar recesses (asterisk)

ral condyle, osteochondral fragments, articular and epiphyseal cartilage lesions. This subsection aims to illustrate the MRI findings of acute lateral patellar dislocation and concomitant injuries, such as injuries of the medial patellofemoral ligament/retinacular complex, contusions of the medial patella and lateral femoral condyle; osteochondral and avulsion fractures (Fig. 5.47).

on PD FS-weighted images. Wavy or retracted fibers surrounded by effusion are suggestive of complete disruption. Injury to the medial patellar stabilizers in acute lateral patellar dislocations has been identified in previous MRI studies in 82%–100% of cases, with a sensitivity and accuracy of 85% and 90%, respectively [23, 31, 74, 93, 107, 108]. Between 10 and 20% of the injuries to the medial ligaments involve the midsubstance site (Fig. 5.49), 50% and 90% involve the patellar insertion (Fig. 5.50), and 10–20% involve femoral insertion (Fig.  5.51). Disruption of the ligaments at the patellar insertion is complete in one-third and partial in two-thirds of the cases [74, 81]. In one-fourth of cases, the MPFL ruptures at the femoral attachment can also occur in an avulsion tear of the epicondyle [65, 74] (Fig. 5.52). It is common to see multiple sites injury to the medial ligamentous restraints in 48% of cases in one study [47, 63, 74, 108], including hemorrhagic edematous infiltration of the VMO muscle. VMO edema or hemorrhage was evaluated on axial, coronal, and sagittal PD FS-weighted

5.4.6.1 Injuries to Medial Patellar Stabilizers Partial or complete disruptions of the medial retinaculum MPFL were evaluated into four regions: the medial retinaculum at its patellar insertion, the medial retinaculum at its midsubstance, and the MPFL at its femoral origin or combination [106]. A partial tear is characterized by an irregular appearance or the discontinuity of some fibers in the ligamentous body and/or the presence of intra-ligamentous or peri ligamentous edema (Fig. 5.48). A full-thickness tear of a medial stabilizer is seen in MR imaging as complete disruption of the ligament and the presence of local soft tissue edema, which gives a high signal intensity

5.4  Acute Patellar Dislocation/Subluxation, MRI Findings

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a

b

c

d

Fig. 5.48  Woman, 21-year-old, with acute lateral patellar dislocation and spontaneous relocation. Selected successive craniocaudal images of the right knee. PD FS sequences in the axial plane from the upper pole of the patella (a–c) to the tibial plateau (d) show the following associated injuries: partial tear of the medial retinacular complex, evidenced by edematous infiltration of VMO

(star image a), extensive surrounding edema of the MPFL (oval circle image b, c) and MPTL (oval circle and arrow image d) with the discontinuity of some ligament fibers (arrows image b–d) and focal bone marrow edema involving medial femoral condyle (asterisk image a–c). Note trochlear dysplasia Dejour type A/B as a predisposing factor for patellar dislocation (dotted line image b)

images and identified as increased signal i­ ntensity tracking along the inferior border of the vastus medialis muscle (Fig. 5.53). After rupture of the medial compartment, the patella typically does not fully return to its normal position, even after reduction. Most patients will show a lateral tilt or a subluxation after patellar dislocation (Fig. 5.54). Subluxation is evaluated subjectively or by drawing a line joining the summits of the medial and

lateral femoral condyles and dropping a perpendicular to this at the level of the summit of the medial condyle. The distance of the medial margin of the patella from this perpendicular line is normally 70%) of patients with instability [29, 135]. A prior dislocation is a significant risk factor for recurrent dislocation, and risk progressively increases with subsequent dislocations. Gender and positive family history also correlate to recurrence risk [121]. While first-time dislocations occur equally across sexes, recurrent dislocators tend to occur in women and have a positive family history of patellar instability [90].

5.5.2 MR Imaging Findings After Recurrent Patellar Dislocation The clinical history and physical findings may need to be revised to establish the exact nature of the injury. As a result, MRI can play a key role in diagnosing and delineating the extent of osseous and soft tissue injury essential for directing appropriate surgical management. The typical MRI findings after transient lateral dislocation of the patella have been well described in the litera-

5 Patella

ture. They include a bone contusion pattern involving the inferomedial pole of the patella and the anterolateral aspect of the nonarticular portion of the lateral femoral condyle [111].

5.5.2.1 Patellar and Lateral Condylar Injury (Bone Contusion and Osteochondral Injury) Bone marrow edema resulting from contusion of the medial aspect of the patella and the femoral condyle is a typical finding after patellar dislocation. Bone marrow edema presents high signal intensity on T2 images and low-signal intensity on T1-weighted images. Nearly half of the cases with osteochondral defects have the classic finding of a concave impaction deformity of the inferomedial patella, which is considered a particular sign of prior patellar dislocation [111] (Fig. 5.66). Impression of the osteochondral surface of the patella is predominant in impaction-­ type injuries, and separated bone fragments are the major finding in avulsion-type injuries. The radiologist’s diagnosis is pivotal because immediate surgery is indicated if lesions are larger than 1–2 cm, and surgery should ideally be performed within one week from the traumatic event [111]. The MR imaging appearance varies with the force of dislocation and the interval between the event and imaging [47]. Bone bruises of the medial patella border and the lateral femoral condyle are present in 100% of all patients undergoing a first-time traumatic patella dislocation. In contrast, the bruising bone incidence is markedly lower in patients with recurrent or chronic patella dislocations. This phenomenon is because the MPFL was injured with the first dislocation, and thus less energy is required for subsequent dislocations [136] (Fig. 5.67). The configuration of the articular surface of the patella is convex, whereas that of the trochlear groove is concave [111]. This configuration allows for a potential shearing injury to involve the articular surface of either the patella or the femoral condyle during the first stage of dislocation. During reduction, the articular surface of the medial aspect of the lower pole of the patella first impacts the nonarticular portion of the lateral femoral condyle, resulting in the classic bone

5.5  Recurrent Lateral Patellar Dislocation

135

contusion. The patella then bounces back into its normal position within the trochlear groove. The concave configuration of the trochlear groove protects its articular surface from injury during the patella’s reduction, whereas the patella’s convex shape places its articular cartilage at risk for injury during the reduction stage well [111]. The patella is at risk for a shearing or impaction injury during dislocation and reduction. However, the femoral articular surface is at risk only during dislocation is likely the reason for the higher incidence of articular cartilage lesions involving the patella [136].

Fig. 5.66  Woman, 37-year-old, known with recurrent lateral patellar dislocation. PD FS image in the axial plane highlights bone bruises of the medial patella border with a concave appearance (dotted curved line). The medial patellofemoral ligament appears infiltrated edematous with the interruption of some fibers (short arrows), patellar disinsertion (long arrow), and femoral disinsertion (long dotted arrow)

Fig. 5.67  Woman, 43-year-old, known with multiple episodes of lateral patellar dislocation in the last year. PD FS image in the axial plane highlights the complete loss of cartilage at the level of the lateral facet of the patella (oval image) and an osteochondral fragment (dotted arrow) with the appearance of an intra-articular free body. The anterior half of MPFL appears relaxed with the interruption of continuity of the posterior half as a stigma of repeated lateral patellar dislocations. Note the absence of typical bone marrow edema involving the inferomedial pole of the patella and the lateral femoral condyle’s anterolateral aspect due to the reduced energy required to produce subsequent dislocations

Effusion Knee joint effusion is a typical finding after a patellar dislocation. It is present in most patients, especially when imaging is performed immediately after the event [47] (Fig.5.68). The amount of effusion decreases with time (Fig.  5.69). The presence of effusion is not specific and may also be associated with other conditions. The amount

Fig. 5.68  Man, 39-year-old, presenting with anterior knee pain after a recent lateral patellar dislocation. PD FS image in the axial plane reveals complete disruption of the medial retinaculum at its patellar insertion (thick arrow) and extensive intra and periligamentous edema and fluid accumulation in the medial paracondylar space (star). Trochlear dysplasia Dejour type B (dotted line), patellar tilt (thick white arrow), thickening of the medial synovial fold (thin white arrow). The patella remaining in lateral patellar inclination

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136

a

b

Fig. 5.69  Man, 37-year-old, has multiple episodes of lateral patellar dislocation, presenting with anterior knee pain after lateral patellar dislocation, with the patella remaining in lateral patellar inclination. Axial PD FS-weighted image (a) shows trochlear dysplasia Dejour type B as the first predisposing factor for patellar dislocation (dotted line), chondral defect on the lateral patellar facet, and irregularity of the cartilage contour of the lat-

eral facet of the trochlea (oval image) and a reduced amount of fluid in the lateral paracondylar synovial recess (star). Sagittal PD FS image (b) shows a high patella appearance (ISI = 1,43) as the second predisposing factor for patellar dislocation and irregularity of the patellar cartilage contour (arrow b). Note lateral patellar tilt (arrow image a) and a small tibial cyst under the ACL insert (dotted arrow image b)

of fluid depicted with T2/PD fat sat sequences can be determined in the sagittal plane to differentiate abnormal effusion from the normal amount of joint fluid present. Joint effusion is defined as a fluid layer of more than 4  mm thickness in the suprapatellar recess on mid-line sagittal images and more than 10 mm in the lateral recess on lateral sagittal images [137]. If hemorrhage is present, fluid–fluid levels will be seen due to sedimentation of blood components, which may have intermediate or low PD FS signal intensity, depending on the age of the effusion. Effusion is often absent in patients with habitual dislocations. Because such patients have considerable instability, redislocation rarely causes new injury to the lax medial stabilizers [137].

important to recognize that the incidence and severity of these articular cartilage lesions are related to underlying anatomic factors (Figs. 5.70 and 5.71). Chondral and osteochondral lesions are often associated with traumatic high-energy patellofemoral dislocations (Fig.  5.72). At the same time, atraumatic (low-energy) patellofemoral dislocations in patients with significant patellofemoral risk factors have a much lower incidence of osteochondral damage [136]. Intuitively, the energy required for a dislocation is inversely proportional to the amount of patellofemoral dysplasia. Very shallow morphology (highly dysplastic) with little bony restraint will allow a dislocation at lower energy levels than normal morphology (Fig. 5.73). Nomura et  al. (2004) evaluated cartilage lesions of patients with recurrent dislocation. In this study, 70 knees were evaluated after patella dislocation and after redislocation. He found that 96% had articular cartilage lesions of the patella,

Cartilage Lesions in Patellofemoral Dislocations Recurrent patellofemoral dislocations are frequently associated with chondral injury. It is

5.5  Recurrent Lateral Patellar Dislocation

137

with 76% showing fissuring, most commonly over the central dome, and 77% with fissuring or erosions over the lateral facet [138]. For the detection of central cartilage defects, standard clinical pulse sequences are highly reliable if the lesions are large, such as grade III or IV.  The diagnostic accuracy for circumscribed thinning of patellar cartilage involving less than 50% of the cartilage thickness (grade I or II) is lower. Defects of the trochlear cartilage are rare, and care must be taken not to overlook them because they require immediate surgery if they are large (Fig. 5.74). Long-term changes in the patellofemoral joint may occur after chronic instability. For such long-term changes, MR imaging demonstrates signs of osteoarthritis and ligamentous damage of the medial patella in most cases [139] (Figs. 5.75, 5.76, and 5.77).

Fig. 5.70  Man, 37-year-old, presenting with anterior knee pain after a recent lateral patellar dislocation and spontaneous relocation, 9  months from the last episode. Axial PD FS image shows a femoral sulcus angle larger than 145° suggestive of trochlear dysplasia (dotted lines) and fissuring cartilage over the central dome patella (oval image). Also, a relaxed MPFL interrupted some fibers in the middle and femoral portion (arrows) following recurrent dislocation episodes

a

Fig. 5.71  Woman, 35-year-old, presenting chronic anterior knee pain accentuated when going up and downstairs. She is known for recurrent lateral patellar dislocation. Sagittal PD FS-weighted images (a) show a small chondral fragment in the lower 1/3 of the patellar cartilage (arrow image a). Axial PD FS image (b) shows complete loss of the cartilage at the lateral facet of the patella with the presence of a small chondral fragment with the appear-

The Medial Patellar Stabilizers Injury It has been shown that damage to the medial patellar stabilizers, including medial patellar retinaculum and the medial patellofemoral ligament (MPFL) injuries, is prevalent in 70–100% of b

ance of a free body in the lateral patellofemoral articular hemispace (oval circle and arrowhead b). Note the presence of two predisposing factors for lateral patellar instability-­patella Alta (image a) and Dejour A trochlear dysplasia (image b). Poor visualization of the posterior portion of the MPFL (thick arrow) indicates multiple episodes of lateral patellar dislocation and secondary chondral lesions

5 Patella

138

Fig. 5.72 Man, 41-year-old, presenting with anterior knee pain after recent traumatic lateral patellar dislocation and spontaneous relocation, 4  months from the last episode. Axial PD FS image shows the opening of the trochlear groove >150° compatible with a Dejour trochlear dysplasia type A (dotted lines) as a predisposing factor for patellar dislocation and fissuring cartilage over the lateral patellar facet (oval image). Effusion in paracondylar synovial recesses (stars) and edematous infiltration of MPFL in the posterior third with its femoral disinsertion (white dotted arrow). Note, Morel Lavallee acute seroma in the posttraumatic space created between the subcutaneous plane and the lateral retinaculum (black arrow)

a

Fig. 5.73 Woman, 42-year-old, presenting with knee pain after a recent lateral patellar dislocation and spontaneous relocation, four months from the last episode. Axial PD FS image shows severe trochlear dysplasia Dejour type D (dotted curved lines), dysplastic patella (Wiberg 3), lateral patellar tilt (thick arrow) with fixed subluxation, thickening of patellotrochlear cartilage thickness, and narrowing of patellofemoral joint space (oval circle). Effusion in the lateral femoral paracondylar recess (star). Stretching and relaxing MPFL with the interruption of some fibers in the posterior half including the femoral disinsertion (dotted arrow)

b

Fig. 5.74  Man, 37-year-old, presenting with chronic anterior knee pain exacerbated after a recent lateral patellar dislocation with spontaneous relocation. According to Outerbridge classification, sagittal, and axial PD FS images show a chondral defect in the middle portion of the trochlea affecting both

facets (black arrows a, b) compatible with grade 3 lesion. PD FS axial image (b) highlights a chondral defect lateral facet of the patella (white arrow a) corresponding to grade 3 Outerbridge classification. Trochlear dysplasia Dejour type A (dotted line).Patellar insertional tendinosis (white arrow a)

5.5  Recurrent Lateral Patellar Dislocation

Fig. 5.75  PD FS image in the axial plane highlights the irregularity of the cartilage surfaces at the level of both facets’ patella and femoral trochlea, the reduction of cartilage thickness (oval image), cystic reaction at the level of the patellar subchondral bone (arrowhead), and the narrowing of the patellar femoral joint space. Vague visualization of MPFL (continuous white arrows) and femoral disinsertion (dotted arrow) indicate multiple episodes of patellar dislocation and the cause of chondral lesions with the appearance of incipient patellofemoral osteoarthritis. Note trochlear dysplasia Dejour type A (dotted lines)

a

Fig. 5.76  A 37-year-old woman presents chronic anterior knee pain exacerbated after recent lateral patellar dislocation remaining with minimal subluxation. Selected successive craniocaudal images of the left knee in PD FS axial sequences, with the first image showing the trochlear cartilage (dotted line image a). Thickening and irregularity of the contour of the MPFL, including discontinuity of

139

cases of lateral patellar dislocation [68, 77, 89, 101, 107, 108]. The MPFL/medial retinacular complex is best seen on transverse and sagittal T1-weighted sequences as a well-defined, low-­ signal intensity band. The degrees of MPFL injury were divided into partial and complete tears. Partial MPFL tear manifestations were defined as thickening and irregularity of the contour, including discontinuity of normal fibers and intraligamentous or extensive periligamentous edema (Fig. 5.78). A complete MPFL tear manifestation is defined as completely discontinuous (Fig. 5.79) or absent fibers in the expected region of the MPFL.  Partial or complete disruption of the MPFL was evaluated at 3 locations: the patellar insertion (Figs.  5.80 and 5.81), the midsubstance, and the femoral attachment (Fig.  5.82). Simultaneous injury at more than one location of the MPFL was classified as a combined injury (COM). VMO edema or hemorrhage was evaluated on coronal PD FS-weighted images ­ and identified as increased signal intensity tracking along the inferior border of the vastus medialis muscle. Elevation of the VMO muscle was

b

some fibers and intraligamentous and periligamentous edema (double and single arrows image a, b). Dejour type B dysplasia is a predisposing factor (dotted line image a) and typical bone marrow edema involving the patella’s inferomedial pole (stars image a, b). Note patellar tilt with minimal lateral subluxation (dotted and black double arrow)

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140

a

b

Fig. 5.77  Man, 57-year-old, with recurrent lateral patellar dislocation. MR images in the axial plane (a) highlight the destruction of the patellar cortico-chondral junction of the lateral facet of the patella (small white arrows in the oval), the avulsion at the femoral level of the MPFL (thick white arrow), and fluid accumulation in the medial paracondylar synovial recession (star). Images in the sagittal

plane (b) confirm patellar cortico-chondral degenerative changes (oval image) and, in addition, fluid accumulation in the suprapatellar bursa (star) and the subpatellar Hoffa’fat pad (asterisk). Note the presence of two major anatomical factors predisposing to lateral dislocation of the patella: trochlear dysplasia Dejour type B image A (dotted line) and patella Alta (ISI = 1.53) [image b]

evaluated on sagittal T1-weighted images by measuring the shortest distance between the cortex of the medial femoral condyle and the VMO muscle fibers and by measuring the vertical distance from the adductor tubercle to the inferior margin of the VMO muscle in the coronal plane of the adductor tendon. In summary, transient lateral patellar dislocation is a common, often clinically unsuspected, injury to the knee in which MR imaging can

provide a definitive diagnosis and identify patients who will benefit from surgical management. Trauma alone rarely causes patellar dislocation in patients without underlying predisposing factors, making identifying abnormal patellofemoral relationships essential for predicting patients at risk for recurrent instability [47]. Surgery may be indicated when associated injuries or abnormal patellofemoral relationships are identified.

5.5  Recurrent Lateral Patellar Dislocation

141

Fig. 5.78 A 43-year-old woman had multiple lateral patellar dislocation episodes last year. PD FS image in the axial plane highlights multiple discontinuities of the body of the medial patellofemoral ligament (arrows) and disinsertion at the femoral origin (double arrow), associated with fluid accumulation in paracondylar synovial recesses (star). Note the presence of Dejour B trochlear dysplasia (dotted line) and a small reactive osteophyte on the anteromedial contour of the trochlea (black dotted arrow). Wiberg type 3 dysplastic patella shows complete loss of cartilage from the lateral facet (black arrows head) and is tilted laterally (long dotted arrow) with minimal subluxation (0.5 cm)

a

b

Fig. 5.79  Absence of MPFL fiber visualization (question marks b) following multiple patellar dislocations in a 43-year-old patient with Dejour trochlear dysplasia type C (dotted curved line c) and fixed lateral patellar subluxation (0.9  mm). We note the patellar chondral lesions Outerbridge grade 4 in the patella (arrow in oval circle a,

c

arrow c) and grade 3 in the trochlea. Avulsion of a small bone fragment at the patellar insertion of the LPFM (long arrow c, short dotted arrow b) and myxoid-degenerative infiltration at the patellar insertion of the quadriceps tendon (dotted arrow a) and, respectively, the patellar insertion of the patellar tendon (continuous arrow a)

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142

a

b

Fig. 5.80 Woman, 35-year-old, had recurrent lateral patellar dislocation of the right knee. Axial images (a, b) in PD FS sequences highlight the patellar disinsertion of the MPFL (arrows a, b) and focal bone contusion at the

a

Fig. 5.81 Man, 37-year-old, with multiple recurrent patellar dislocations in the last years.PD FS-axial images (a), highlight discontinuity of MPFL, at patellar and femoral disinsertion (white arrows a), intra and periligamentous infiltration with the breaking of some fibers (black arrows). Dejour type B dysplasia lateral, patellar tilt, hemorrhagic fluid accumulation in paracondylar synovial

level of the inferomedial portion of the patella and the anterolateral area of the lateral femoral condyle (asterisk a, b). Notice that Dejour type B dysplasia is a predisposing factor for patellar instability (dotted line)

b

recesses (stars), and contusion of the inferomedial portion of the patella (short white arrow). PDFS image in the coronal plane shows edematous infiltration of medial collateral ligament, medial retinaculum, and VMO.  Anterolateral area of the lateral femoral condyle (asterisk b)

5.6  Patellar Contusion and Fracture

143

The noninvasiveness and multiplanar capability of MR imaging makes it well suited to diagnosing this condition since pain and the presence of a hematoma, soft tissue swelling, and hemarthrosis may hinder clinical evaluation [143]. Bone bruises and occult fractures can result in substantial pain and are radiographically silent. MR imaging may diagnose these injuries because these conditions also alter signal intensity in the bone marrow [144].

5.6.1 Mechanism of Injury of Patellar Fractures

Fig. 5.82  Woman, a 20-year-old gymnast, had a second episode of patellar dislocation. The T1 SE image in the axial plane acquired highlight the complete rupture of the medial patellar femoral ligament at the femoral insertion level (arrow). Notice patellar inclination with minimal lateral subluxation (dotted arrow)

5.6 Patellar Contusion and Fracture Patellar fractures account for approximately 1% of all skeletal fractures and may result from direct, indirect, or combined injuries [140]. They are most prevalent in individuals between 20 and 50 and occur twice as often in men as in women [141]. Patellar fractures are the most common cause of disruption of the extensor mechanism, six times as frequent as soft tissue injuries such as quadriceps or patellar tendon rupture [142]. Fractures may be caused by excessive force through the extensor mechanism or a direct blow. Complications include stiffness, extension weakness, and patellofemoral osteoarthritis.

Patellar fractures are the result of direct, indirect, or combined injury. Direct injuries can be secondary to low-energy trauma (fall on the knee from sitting or standing height) or high-energy trauma (dashboard impact in a motor vehicle accident) [140]. Most commonly, though, the mechanism of injury combines direct and indirect patterns, i.e., a culmination of a direct blow, quadriceps contraction, and secondary joint collapse. The fracture pattern is not determined solely by the mechanism of injury but also depends on factors such as patient age, bone quality, and degree of knee flexion [140, 145]. With indirect injuries, the fracture mechanism involves failure of the extensor mechanism due to eccentric overload, typically a forceful contraction mechanism of the quadriceps with the knee in a flexed position. The most frequent indirect mechanism is a fall on the feet with eccentrical contraction of the quadriceps muscle [141]. When the force of the fall overwhelms the resistance to knee flexion, the extensor mechanism fails, resulting in a patellar fracture [146]. Sports-­related fractures of the patella are relatively seldom. However, acute patella dislocations are associated with osteochondral patella fractures and bone contusion or fractures of the lateral femoral condyle in up to 70% of cases [138, 147] (Fig. 5.83).

144

Fig. 5.83  A woman, 21-year-old, an athlete, had anterior knee pain after a patellar fracture following acute lateral patellar dislocation. PD FS image in the axial plane highlights the contusion of the infer-medial portion of the patella (black asterisk) and a small osteochondral fragment detached from the medial facet of the patella (thin arrow). Association of bone edema at the anterolateral portion of the lateral femoral condyle (white asterisk) flattening of the trochlear groove with the appearance of trochlear dysplasia Dejour type A (dotted line), patellar disinsertion of the medial patellofemoral ligament (thick arrow) and vag visualization of the medial patellofemoral ligament, represents typical changes after acute patellar dislocation with spontaneous relocation of the patella. Note a vertical chondral free body in the lateral paracondylar recess (white arrow)

5.6.2 Clinical and Imagistic Evaluation A patella fracture is diagnosed based on the injury mechanism, physical examination, and radiological findings. All patients who have directly impacted the anterior knee are suspected to be unable to actively extend their knee after flexion injury or fall [146]. The clinical investigation usually shows in displaced fractures a visible and palpable defect between the bone fragments, local hematoma, and hemarthrosis that occurs quickly and symmetrically on the anterior knee, as almost all patellar fractures communicate with the knee joint [141]. The complete inability to extend the

5 Patella

knee reveals a tear of the medial and lateral retinaculum in addition to the fracture (Fig.  5.84). Extending the knee does not exclude a fracture sufficiently since either the retinaculum, iliotibial band, or adductors can provide active knee ­extension in patellar fractures without significant displacement [141]. (Fig. 5.85). Evaluation of the soft tissue status is crucial as the degree of soft tissue damage determines the further course of the patient. In up to 25% of cases, a skin abrasion is present, interfering with the timing of surgery and the surgical approach [148]. Osteochondral fractures of the patella are usually a result of shear forces caused by a patellar dislocation and occur less frequently by a direct impact trauma of the patella [138, 147]. A CT scan, including multiplanar reconstructions, provides exact imaging of the fracture pattern in comminuted fracture patterns or suspected accompanying ligamentous, meniscal, or osteochondral injuries. A recent study showed that adding computed tomography to the evaluation led to changes in management plans in almost half of the cases [149]. The noninvasiveness and multiplanar capability of MR imaging makes it well suited to diagnosing this condition since pain and the presence of a hematoma, soft tissue swelling, and hemarthrosis may hinder clinical evaluation [143]. Magnetic resonance imaging (MRI) is used when a suspected radiographically occult patellar fracture. Occult fractures are MRI characterized by a linear band of low-signal intensity with all imaging sequences, surrounded by bone marrow edema adjacent to the fracture (Fig. 5.86). MRI is also highly sensitive for detecting cartilage damage, subchondral fracture, and contusion and provides additional information on the integrity of the soft tissue components of the extensor mechanism [145] (Fig. 5.87).

5.6.3 Types of Patellar Fractures: MRI Illustration 5.6.3.1 Sleeve Fractures Sleeve fracture was first reported in 1978 by Houghton and Ackroyd and occurred predomi-

5.6  Patellar Contusion and Fracture

a

145

b

c

Fig. 5.84  Man, 41-year-old, was involved in a car accident. Clinical findings include acute pain, inability to extend the knee actively, and a suprapatellar gap. Ambulation is impossible due to the inability to extend the knee and excruciating pain. MRI examination was performed one week after direct knee contusion in PD FS-weighted images in the sagittal plane (a, b) and axial plane (c). Complete rupture of the quadriceps tendon at the osteo-tendinous junction, with hemorrhagic fluid infiltration (circle and arrow image a, b). Complete break of the medial retinaculum at the patellar insertion level

a

b

(arrow image c), associated with an intra-articular bone fragment from the medial portion of the patella (dotted arrow images b and c). Hemorrhagic fluid accumulation in the lateral femoral pericondylar recess (star image c). Femoral disinsertion of the lateral retinaculum (double arrow image c). Diagnosis: Complete quadriceps tendon and medial retinaculum rupture with patellar fracture and intra-articular bone fragment. The patient was operated on by refixing the quadriceps tendon and medial retinaculum to the patella by anchors

c

Fig. 5.85  Woman, a 47-year-old, long-jump former athlete, had a patellar fracture and preserved joint mobility without limiting the extension. Clinical findings include chronic anterior left knee pain exacerbated when going up and downstairs. PD FS images in the sagittal plane (a), coronal plane (b), and axial plane (c) highlight a sagittal fracture line in the middle of the patella with extension

posteroanterior, from the subchondral level to the anterior cortex (arrows a–c). Note the integrity of the patellar stability ligament system (dotted white arrow) and a chondral defect (black arrow) with extension to the cortex of the medial patellar facet. In the context of prolonged sports activity and repetitive overload of the patella, the fracture line can be classified as a stress fracture

nantly in children, comprising approximately half of all patellar fractures [150]. It is caused by rapid muscle contraction and mainly occurs in the pediatric population due to the cartilaginous composition of the patella. The sleeve is avulsed more frequently than tendon rupture as this is felt to be the weaker component, with the tendon collagen

fibers at insertion being indistinct from the cartilaginous sleeve. Although sleeve fractures typically occur due to a noncontact injury, they can also occur due to falls [151, 152]. These fractures often involve the distal pole of the patella in the form of an osteochondral avulsion. The classical mechanism of injury for inferior fractures is a forceful

5 Patella

146

a

b

Fig. 5.86  A 45-year-old woman with anterior knee pain after a fall while skating. T1 SE (a) and PD FS image (b) in the sagittal plane show an area of a bone contusion in hyposignal T1 (image a) and hypersignal PD FS (image

a

b) in the antero-distal portion of the patella and an intraspongios fracture line in hyposignal both in T1 and PD FS (arrow a, b), not evident on radiograph (not shown here)

b

Fig. 5.87  A 51-year-old woman had chronic anterior knee pain, exacerbated by prolonged walking, climbing, and descending stairs. She has been known for multiple patellar dislocations in recent years. PD FS images in the sagittal plane (a) and axial plane (b) highlighted fragmentation of cartilage coverage in both facets of the patella and interruption of the subchondral cortex with subchondral cystic reaction (dotted rectangle). The presence of an

anterior cortico-subcortical separation should also be noted with the appearance of a medial-lateral transversely oriented fracture line, with a coronal extension from the upper pole to the lower pole of the patella (dotted arrows a and continuous arrows b). There are also two anatomical factors predisposing to patellar instability—patella Alta (image a) and Dejour trochlear dysplasia type B (dotted line image b)

quadriceps contraction with flexion of the knee, resulting in separation of the sleeve from the patella (Fig. 5.88). However, in superior sleeve fractures,

Klerx-Melis et  al. postulated that specific knee flexion causes more force to transmit through the superior pole than to the inferior pole Usually,

5.6  Patellar Contusion and Fracture

a

Fig. 5.88  Woman, a 23-year-old, gymnast with anterior knee pain under the patella, appeared after more intense and prolonged training. PD FS images in the sagittal plane (a) and the coronal plane (b), performed one week after

sleeve fractures of the patella in children occur in the inferior pole of the patella, very rarely in the superior pole. The reason can be explained that the immature osteochondral junction in a child is more vulnerable to injury than the enthesis of the fully ossified adult patella [153]. The diagnosis of a sleeve fracture can be easily missed. A combination of history, examination, and radiological studies has proven the most effective way of managing these cases [154]. On clinical examination, the patient presents with local pain, tenderness, swelling, and an inability to extend the knee fully. Soft tissue swelling may be visible, indicating haemarthrosis and significant trauma. Interpreting plain films of the children’s knees is challenging when an avulsed bony fragment is not apparent. At the initial presentation, a patellar sleeve fracture diagnosis may be difficult clinically and radiologically because there may be no visible bony fragment. Patella Alta on a plain film may be the only most prominent sign [151, 155, 156]. Grogan et  al. [157] describe four patterns of avulsion (sleeve) fractures: namely superior, which is the least common (Fig. 5.89); inferior, usually caused by an acute injury (Fig. 5.90); and medial, which

147

b

the onset of pain, show the avulsion of a small cortical fragment and the inflammatory infiltration of the lower pole of the patella (arrows a, b)

Fig. 5.89  Man, a 27-year-old, weightlifter with anterior knee pain located at a suprapatellar level after prolonged training and lifting heavy weights. Images T1 SE in the sagittal plane highlight the avulsion of a small bone fragment from the cortex of the upper pole of the patella (continuous black arrow in a circle). It also highlights a small cortical fragment detached from the patella’s anteroinferior contour at the patellar tendon’s insertion (short black arrow). Hypertrophy of the tibial apophysis with the presence of a vertical band in the T1 hyposignal with a tendency to separate from the adjacent tibial spongious bone (white arrows)

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148

a

b

Fig. 5.90  Boy, a 12-year-old, gymnast with anterior knee pain after performing an exercise with the right knee twisted and falling to the ground. On examination, the patient presented with local pain, tenderness, swelling, and an inability to extend the knee fully. MRI examination

was performed 2 weeks after the knee contusion. PD FS images in the sagittal plane (a) and coronal plane (b) revealed the avulsion of a bone fragment from the lower pole of the patella (white arrows a, b) and a small area of the bone marrow edema after avulsion (black arrows a, b)

accompanies an acute lateral dislocation of the patella (Fig. 5.91) and lateral, is a chronic stress lesion resulting from the repetitive tensile pull from the vastus lateralis muscle [157] (Fig. 5.92). Avulsion fractures of the lower pole of the patella may be associated with tears of the patellar tendon (Fig. 5.93). The tendon may be retracted or thickened. Sinding-Larsen-Johansson syndrome, defined as osteochondrosis of the distal pole of the patella at the tendinous insertion, is of uncertain etiology but is related to chronic traction injury. This condition may mimic a stress fracture of the patella, an osteochondral sleeve fracture, or an ununited ossification center [155, 158]. The injury is characterized by a focal area of decreased signal on T1-weighted images and increased signal intensity on fat-saturated PD images (Fig. 5.94).

5.6.3.2 Patellar Fractures Following Acute and Chronic Patellar Dislocation Patellar dislocation of the patella occurs in two separate stages [111]. The patella translates laterally along the lateral femoral condyle’s lateral aspect during the first stage. During the second phase of the injury, as the patella relocates, the inferomedial aspect impacts the anterolateral aspect of the lateral femoral condyle, resulting in the classic bone marrow edema seen on MR imaging as “kissing contusions” (Fig. 5.95). The lateral femoral condyle contusion is more anteriorly and peripherally than in pivot shift injury [111]. Osteochondral injuries are avulsion fractures or impaction injuries of the patella or femur with noticeable irregularity of the osteochondral surface. Nearly half of the cases with osteochon-

5.6  Patellar Contusion and Fracture

Fig. 5.91  Woman, 32-year-old, had an acute patellar dislocation by indirect mechanism, in the first episode. This sportswoman states that the patellar dislocation occurred during the internal twisting movement of the thigh, and the leg is fixed to the ground. She felt intense pain and the movement of the patella, followed by a spontaneous reduction after the knee extension. The PD FS image in the axial plane highlights a branched fracture trajectory at the patella’s infero-medial portion (white arrows) with the isolation of an unmoved bone fragment in an anteroinferior position (asterisk). A small chondral fragment is detached from the medial patellar facet (black arrow) and a horizontal fracture by anterolateral cortico-subcortical separation (dotted white arrow). The force of the lateral dislocation of the patella is also highlighted by the fluid accumulation with a lamellar aspect, located between the lateral patellofemoral ligament and the subcutaneous tissue, suggestive of a Morel Lavallee acute seroma (black dotted arrow). Note Dejour A patellar dysplasia (dotted line) is a predisposing anatomic factor for patellar instability

dral defects have the classic finding of a concave impaction deformity of the inferomedial patella, which is considered a particular sign of prior patellar dislocation [74] (Fig.  5.43). Impression of the osteochondral surface of the patella is predominant in impaction-type injuries, and separated bone fragments are the significant finding in avulsion-type injuries (Fig. 5.96). Completely

149

separated fragments, or intra-articular bodies, usually represent chondral or osteochondral fragments from the patella or femoral condyle (Fig.  5.97). Lateral patellar dislocation occurs during movement while the knee is in slight flexion (20° to 30°); Vastus lateralis contraction produces a significant lateral force on the patella applied on the trochlear articular surface. During that stage of dislocation, the patella lies along the trochlear anterolateral margin, giving rise to the classical pattern of injury involving the inferomedial pole of the patella and the non-weight-­ bearing portion of the anterolateral femoral condyle. The above pattern is typically defined as an impaction injury [119]. Patellar or lateral femoral condyle osteochondral fracture (OCF) represents the main complication after dislocation, ranging from 5% to 39% [120]. Patellar fractures may also be associated with chronic patellar dislocation (Fig.  5.98) and patellar lateral femoral friction syndrome (Fig. 5.99).

5.6.3.3 Types of Posttraumatic Patellar Fractures Several primary patellar fractures have been identified, with separate diagnostic, imaging, and management considerations [159]. Plain radiographs show that the fracture line orientation classifies patella fractures. The primary types include vertical, transverse, marginal, stellate, osteochondral, and comminuted [141, 144, 145, 160]. Patellar Vertical Fractures Vertical fractures demonstrate a fracture line that courses superiorly to inferiorly and may involve the main body of the patella or just the periphery [140] (Fig. 5.100). Sometimes these fractures can also be displaced. Cramer et  al. postulated that fractures with less than 3 mm displacement should be con-

5 Patella

150

a

Fig. 5.92  Woman, 43-year-old, had multiple patellar dislocations in recent years. PD FS images in the sagittal plane (a) and axial plane (b) highlight the presence of two major anatomical factors predisposing to patellar instability: patella Alta (image a) and Dejour patellar dysplasia type A (image b). There is an irregularity and a reduction

a

Fig. 5.93  Woman, 57-year-old, with avulsion fractures of the lower pole of the patella, associated with tears of the patellar tendon. T1 SE image in the sagittal plane (a) and PD FS in the sagittal plane (b) highlight avulsion of the lower pole of the patella (black arrow a and dotted white arrow b) with partial rupture of the patellar tendon

b

in the cartilage thickness covering the lateral patellar facet (images a, b) and a fine subchondral fracture of the lateral patellar facet (black arrows image b). Note the patellar and femoral disinsertion of the medial patello-femoral ligament (dotted arrows), its angulation, and relaxation in the anterior segment (continuous arrow)

b

(dotted black arrows a, b). Pre-patellar and superficial infrapatellar bursitis (asterisk). The patellar tendon appears thickened, edematous infiltrated, and has an irregular posterior contour (black arrow a and white arrow b). Minimal fluid accumulation in the deep infrapatellar bursa. (white arrow)

5.6  Patellar Contusion and Fracture

a

151

b

Fig. 5.94  Girl, 13-year-old, handball player, status post-­ acute lateral patellar dislocation, first episode. PD FS images in the coronal plane (a), sagittal plane (b), and axial plane (c) are highlighted according to the mechanism of dislocation characteristic of “kissing contusions.” Thus, the area of a bone contusion in the inferomedial lateral of the patella and the presence of a small bone frag-

c

ment detached from the infero-posterior contour of the patella and migrated inferiorly in the pretrochlear space (image a, b, star, and black arrow, c black arrow); area of bone edema on the anterolateral contour of the lateral femoral condyle (asterisk image c). The suprapatellar synovial plica is also thickened (dotted arrow images a, b)

sidered non-displaced [158]. Melvin and colleagues defined displacement as separating fracture fragments by more than 3  mm and/or articular incongruity by more than 2 mm [140].

Fig. 5.95  A 43-year-old woman had a recurrent patellar lateral dislocation last episode. Axial PD FS imaging highlights typical changes in recurrent patellar dislocations. First is the bone marrow edema in the inferolateral portion of the patella (circle) and the anterolateral part of the lateral femoral condyle (asterisk). In this case, two types of osteochondral fragments can be identified: impact-type (black arrows) and separation (white arrows). It also stands out the presence of a small chondral fragment detached intra-articularly at the level of the lateral patellar facet (black dotted arrow), Dejour trochlear dysplasia type A (dotted lines), patellar disinsertion of the medial patellofemoral ligament (thick white arrow), and Wiberg dysplastic patella type III (star)

Patellar Transverse Fractures Transverse fractures that occur in the medial-­ lateral direction are called transverse. Approximately 80% of these fractures occur in the middle to lower a third of the patella [145]. While the mechanism may be multifactorial, these injuries are typically associated with indirect longitudinal forces (Fig. 5.101). Up to two-­ thirds of transverse patellar fractures are displaced [4], raising suspicion for retinacular and extensor mechanism injury, i.e., tear to the medial and lateral patellar retinacula [140]. Marginal fractures of the patella are fractures of the edge of the patella that do not extend across the patella and are not associated with disruption of the extensor mechanism (Fig.  5.102). This type most commonly involves the lateral facet and results from direct compression of the patella on a hyper-flexed knee [161].

5 Patella

152

a

b

Fig. 5.96  Woman, 61-year-old, with recurrent patellar lateral dislocation. PD FS in the axial plane (a) and sagittal plane (b) highlight characteristic changes in recurrent patellar dislocations, expressed by the lateral patellar tilt (long arrow a), edematous infiltration, and femoral disinsertion of the medial patellofemoral ligament (dotted white arrows). A highlight is the detachment of an osteochondral fragment from the medial patellar facet and the intra-articular migration with free body appearance (short

a

arrow a and thick arrow b). Small osteophyte at the level of the anterior contour of the lateral femoral condyle (small white arrow A) and the bone fragment with a band appearance in the anterior lateral paracondylar recess (black dotted arrow a). Narrowing the patellofemoral joint space with osteochondritis appearances (oval image b). Myxoid-edematous infiltration at the tibial insertion of the patellar tendon with the appearance of tendinosis (thin white arrow b)

b

Fig. 5.97  Woman, a 56-year-old, former sportswoman, had a recurrent patellar lateral dislocation. PD FS images in the sagittal (a) and axial plane (b) highlight the presence of an intra-articular osteochondral fragment (black dotted arrow) and a linear fracture path with the anteroposterior extension (black arrows a and short white

arrows b) with non-spacing fragments. The are two anatomical factors predisposing to patellar instability: patella Alta (image a) and Dejour trochlear dysplasia type A (dotted line b), Wiberg patellar dysplasia type III, (asterisk) with lateral tilt (thick arrow b)

5.6  Patellar Contusion and Fracture

a

Fig. 5.98  Woman, 47-year-old, with multiple recurrent patellar lateral dislocations in the last 10  years. PD FS images in the sagittal plane (a) and axial plane (b) show Wiberg type III patellar dysplasia with marked cartilage thickness reduction at the patella’s lateral facets and the femoral trochlea (dotted arrow b) narrowing the lateral patello-femoral joint direct contact with the lateral femoral condyle (thick white arrow), with the appearance of

a

Fig. 5.99  Man, a 63-year-old, with anterior knee pain exacerbated during the last weeks after falling on the left knee. MRI examination, performed three weeks after the traumatic episode, highlights in the PD FS sequences in the coronal plane (a) and in the axial plane (b), an area of bone edema in the central paramedian portion of the patella (asterisks image

153

b

femoral condyle friction syndrome. Fracture line in the middle portion of the patella with anteroposterior extension (dotted lines a and arrowhead b) and a small chondral fragment in the patello-femoral medial space (black dotted arrow b). The medial patelo-femoral ligament infiltrated in the posterior half, with the interruption of some fibers (thin white arrows) and femoral disinsertion (long dotted arrow)

b

a, black arrow b), that extends cranially and distally with a fracture line throughout the entire patella. Appeearance of Dejour trochlear dyplasia type A expressed by the widening of the trochlear grove by more than 150 degrees (dotted line b). Preserved integrity of the quadriceps, patellar tendons, and retinacula (dotted arrows image a)

5 Patella

154

a

b

Fig. 5.100  Man, a 37-year-old tiler, known for anterior knee an acute trauma by hitting the right knee. T1SE in the sagittal plane A, B (image B is zoomed). An irregular fracture trajectory in the vertical plane is evident from the

upper pole of the patella (black arrow) to the lower pole (white arrow) with the presence of an extended area of edema at the lower anterior 1/3 level (asterisk a, b)

Patellar Stellate Fractures Stellate fractures result from a direct blow to the patella with the knee in a partially flexed position [140]. Approximately 65% of these injuries are non-displaced [161] (Fig. 5.103). In an extensive comminuted fracture with displacement, the transverse component may extend into the medial and lateral retinacula (Fig. 5.104).

Comminuted Fractures These fractures are usually in the central or distal third of the patella (Fig.  5.105). As a result of direct trauma (mostly due to blows or falls on flexed knee), it can cause damage to the articular cartilage of the patella and femoral condyles.

5.6  Patellar Contusion and Fracture

155

a

b

c

d

Fig. 5.101  Man, a 31-year-old sportsman, long jumper, has the appearance of a transverse fracture at both knees, with lines of separation between the anterior cortex of the knee and the subcortical bone. PD FS images in the axial plane (a) and sagittal plane (b) highlight an anterior cortico-­subcortical separation with the appearance of a medial-lateral transversely oriented fracture line (white arrows right knee a) with a coronal extension from the upper pole to the lower pole of the patella (white arrows b). Patellar and trochlear cartilages, the quadriceps and patellar tendons, and the retinacula have preserved integ-

rity. In the left knee (c, d), images show the same aspect of anterior cortico-subcortical separation with the appearance of a medial-lateral transversely oriented fracture line (white arrows c) with a coronal extension from the upper pole to the lower pole of the patella (white arrows d). In addition to the patellar insertion of the patellar tendon, the mucoid-inflammatory infiltration is visible on the PD FS image as hypersignal with an aspect of tendinosis (black arrow d). Small fluid accumulation at the level of the deep subpatellar bursa, with the appearance of bursitis (white dotted arrow d)

156

Fig. 5.102  Man, a 33-year-old football player, presents a right marginal patellar fracture after direct contact trauma. PD FS image) in the coronal plane shows a vertical fracture along the medial edge of the patella (blackhead arrows)

Fig. 5.103  Appearance of stellate fracture through direct contact of the knee in semiflexion in a 31-year-old athlete. The PD FS image in the coronal plane highlights the presence of incomplete fracture trajectories with a stellate appearance at the level of the anterior portion of the patella and an associated inflammatory congestive process in the pre- and peripatellar soft parts (arrows)

5 Patella

Fig. 5.104  Man, a 43-year-old former triple jump athlete, has chronic anterior knee pain, accentuated in the last month after a blow to the side of his left knee. The pain was associated with reduced joint mobility and extension of the left leg. MR images of the left knee in the PD FS axial plane highlighted the presence of an anterior cortico-­ subcortical separation with the appearance of a medial-­ lateral transversely oriented fracture line (white arrows), associated with an area of a contusion in the lateral portion of the patella (star), and extension in the structures of the lateral retinaculum, that is interrupted at the patellar insertion (black double arrow) and thickened by edematous infiltration (short white arrows). An irregularity and focal reduction of the patella and femoral trochlea cartilage, narrowing the patellofemoral joint space (oval circle and black arrows)

5.7  Bipartite Patella

a

157

b

c

Fig. 5.105  Patella Alta. Comminuted fracture of the proximal half of the patella with slightly intra-articularly displaced fragments (images a, b) and laterally (image c).

Thickening and mucoid-inflammatory infiltration of the patellar tendon with the appearance of tendinitis-­ tendinosis (dotted arrow image b)

5.7 Bipartite Patella

who regularly participate in strenuous sports [170, 172–175]. Only 1–2% of persons with bipartite patella have symptoms sufficient to cause them to seek medical attention [169]. In 58% of patients with a symptomatic bipartite patella, the onset of pain is at 12–14 years of age [170]. The most common symptom is pain in the separated fragments during or after strenuous activity. Patients sometimes complain of pain during knee bending or when climbing stairs. Localized tenderness over the separated fragments is the most common physical finding [165, 166]. Movement at the interface between the bipartite fragment and the body of the patella is the cause of knee pain. This movement presumably causes pain in most symptomatic patients [163, 165]. In adults, bipartite patella becomes symptomatic following a minor injury, such as a blow to the knee, or a significant injury, such as acutely displaced separation of the bipartite fragment [170, 175, 176]. Rarely in middle-aged or elderly patients, a severe injury such as a fall causes separation of the bipartite fragment and rupture of the quadriceps tendon [177]. The Saupe classification describes the bipartite patella according to the location of the secondary ossification center [178]. Type I is at the inferior pole of the patella and is seen in 1% of cases. Type II is at the lateral margin of the patella and constitutes 20% of cases (Fig.5.106). Type

The patella starts to ossify between 3 and 5 years, from central to peripheral, reaching its mature form before adolescence [162]. Ossification can occur via a single or, more commonly, from multiple ossification centers that gradually coalesce [163]. Approximately half of them coalesce during childhood and adolescence [164]. In the remaining individuals, this superolateral accessory ossification center may fail to unite with the main portion of the patella, leading to patella partita—a developmental anomaly of ossification-­type patella partita [164–166]. The reported incidences of bipartite patella in studies that included more than 1000 patients were between 0.2% [167] and 1.7% [168]. Bipartite patella is more common in men than women. The reported man/woman ratios were 3.0 [165] and 4.3 [169]. The reported incidences of bilateral involvement were 25% [170] and 43% [169], and can be a cause of pain if there is a disruption of synchondrosis [171].

5.7.1 Clinical Features and Classification of Bipartite Symptomatic bipartite patella is observed in adolescents and young athletes, especially those

158

Fig. 5.106  The type II bipartite patella. PD FS image in the coronal plane highlights the lateral bone fragment (asterisks) and the space between the patellar body of the patella and the bipartite bone fragment (arrow)

5 Patella

Fig. 5.107  The type III asymptomatic bipartite patella. T1 SE image in the coronal plane highlights the superolateral bone fragment (asterisks) and the space between the patellar body of the patella and the bipartite bone fragment (arrow). The bipartite bone fragment (dotted arrow) and the lack of bone marrow edema are observed both in the body of the patella and in the bipartite bone fragment

III is in the superolateral patella and is the most common, found in 75% of cases (Fig. 5.107).

5.7.2 MR Findings Associated with an Asymptomatic Bipartite Patella Findings associated with asymptomatic bipartite patella include edema in the bipartite fragment (usually type III) and on the adjacent patella (Fig. 5.108) and abnormal fibrous tissue and cartilage discontinuity [162, 164, 166] (Fig.  5.109). Edema at the bipartite fragment and on the adjacent patella were evaluated and divided into two groups: “edema present” or “edema absent” [172]. The signals within the synchondrosis were analyzed and divided into three groups and recorded as cartilage signal, fibrous signal, and fluid signal [172] (Fig. 5.110). There are variations in the exact size and position of the fragment, lateral, or superolateral fragments can be observed. The lateral retinacu-

Fig. 5.108  Type III symptomatic bipartite patella. PD FS image in the coronal plane highlights the superolateral bone fragment (asterisks) and the space between the bipartite fragment and the main patellar bone (long arrow). Bone marrow edema in adjacent bones and synchondrosis inflammatory changes (white dotted arrows)

5.7  Bipartite Patella

159

lum is inserted, and the excess tension at the level of the lateral retinaculum and moved can generate local pain [173] (Fig.  5.111). MRI

highlights widening the space between the bipartite fragment and the main patellar bone fragments and inflammatory changes in synchondrosis. Also, MRI is an excellent radiological method for evaluating fragment morphology and assessing the relationship between the fragment and the patella [179]. A detailed evaluation of the fragment is important in guiding the surgical approach to the treatment and evaluating the relationship between the main patellar bone and the fragmented side [175]. Bipartite patella is sometimes misdiagnosed as a fracture because the images of both these conditions may appear very similar [180] (Fig. 5.112).

5.8 Dorsal Defect of the Patella

Fig. 5.109  Type III bipartite patella. PD FS image in the axial plane highlights the superolateral bone fragment (asterisks), an abnormal fibrous tissue (white arrow), and interfragmentary cartilage discontinuity (dotted arrow). Note the continuity of the patellar cartilage at the level of the bipartite bone fragment (black arrow)

a

b

Fig. 5.110  Man, a 61-year-old, had bipartite patella type III and chronic anterior knee pain exacerbated by a recent fall on the left knee. PD FS images of the left knee in the sagittal plane (a), coronal plane (b), and axial plane (c) confirmed the presence of the bipartite patella and revealed the presence of a bright fluid signal (same as the joint fluid) within the synchondrosis (white arrows a–c).

Dorsal defect of the patella (DDP) is common in conventional radiography and MRI during the first decades of life. It is also located in the superolateral quadrant and is commonly associated with bipartite/multipartite patella [181]. DDP is believed to be an ossification anomaly, possibly stress induced, considering histological evidence of avascular necrosis at the site of the dorsal

c

Note the presence of Dejour trochlear dysplasia type A (dotted line c), femoral avulsion of the medial patellofemoral ligament (long arrow c), and accumulation with inhomogeneous fluid signal (short black arrows c) in the upper and retro patellar synovial recesses. The appearance of superficial and infrapatellar bursitis (star a)

5 Patella

160

a

b

Fig. 5.111  A 43-year-old woman with chronic anterior knee pain, bipartite patella type III, and episodes of recurrent patellar dislocation. PD FS images of the left knee in the sagittal plane (a) and axial plane (b) confirmed the presence of the bipartite patella with the widening of the synchondrosis (black arrow a and dotted arrows b). The widening of the synchondrosis space is due to the tractions of the lateral patellofemoral ligament, which is

inserted on the bipartite fragment (thick arrow b). Note the presence of two predisposing anatomical factors, patella Alta (image a) and Dejour trochlear dysplasia type A (dotted lines b), and the stigmas of recurrent patellar dislocations: femoral disinsertion of the medial patellofemoral ligament (long thin arrow b), rupture of fibers in the posterior third (short arrow b) and chondral defect on the lateral facet of the patella (short black arrow b)

5.8  Dorsal Defect of the Patella

a

161

b

Fig. 5.112  PD FS image in the coronal plane (a) highlights an irregular fracture line separating a lateral bone fragment miming a bipartite patella. The recent traumatic

episode and marginal edema in both bone components (asterisks) confirm the diagnosis of patellar fracture. Image b shows a typical appearance of a bipartite patella

defect [182, 183]. When visualizing DDP, plain radiographs give a clear image of a round radiolucent lesion with a peripheral sclerotic margin in the superolateral aspect of the patella. DDP is demonstrated as a hyperintense focal contour abnormality [184] on an MRI fluid-sensitive series. In the presence of persistent symptoms, this imaging technique is helpful in the evalua-

tion of defects in the articular cartilage [184, 185] (Fig.  5.113). Though DDP is primarily asymptomatic, some studies have shown that in cases where articular cartilage in-folds into the bony perforation or where the defect in the underlying bone disrupts the articular surface, DDP can become symptomatic and may need to be treated surgically [184, 186].

5 Patella

162

a

Fig. 5.113  Dorsal defect of the patella in a 27-year-old man with knee pain following a blow to the left knee. PD FS image in the axial plane (a) shows a subchondral defect with irregular cartilage on the lateral patellar facet

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167 high jump, and basketball are all associated with sleeve fractures affecting the take-off leg. Eur J Radiol Extra. 2006;59:67–70. Link: https://tinyurl. com/y4vv9uxx 154. Yassa R, Oputa TJ, McNair M, Michaud R. Superior patellar sleeve fracture: a case report and review of the published evidence. Open J Trauma. 2019:2640–7949. 155. Valentino M, Quiligotti C, Ruggirello M.  Sinding Larsen-Johansson syndrome: a case report. J Ultrasound. 2012;15:127–9. 156. Wu M, Fallon R, Heyworth BE.  Overuse injuries in the pediatric population. Sports Med Arthrosc. 2016;24:150. 157. Grogan DP, Carey TP, Leffers D, Ogden JA. Avulsion fractures of the patella. J Pediat Orthop. 1990;10:721e30. 158. Cramer KE, Moed BR. Patellar fractures: contemporary approach to treatment. J Am Acad Orthop Surg. 1997;5(6):323–31. 159. Lamoureux C. et  al. Patella fracture imaging medscape. Updated: Sep 14, 2020. 160. Ali Yousef MA, Rosenfeld S. Acute traumatic rupture of the patellar tendon in pediatric population: case series and review of the literature. Injury. 2017;48(11):2515–21. 161. Dowd GS. Marginal fractures of the patella. Injury. 1982;14:287–91. 162. Kavanagh EC, Zoga A, Omar I, Ford S, Schweitzer M, Eustace S.  MRI fi in bipartite patella. Skelet Radiol. 2007;36(3):209–14. 163. Dwek JR, Chung CB. The patellar extensor apparatus of the knee. Pediatr Radiol. 2008;38(9):925–35. 164. Oohashi Y, Koshino T, Oohashi Y. Natural history of the superolateral bipartite fragment of the patella in children. J Orthop. 2010;7(4):e5. 165. Bourne MH, Bianco AJ.  Bipartite patella in the adolescent: results of surgical excision. J Pediatr Orthop. 1990;10:69–73. 166. Oohashi Y, Noriki S, Koshino T, Fukuda M. Histopathological abnormalities in painful bipartite patellae in adolescents. Knee. 2006;13:189–93. 167. Paas HR.  Zur Frage der Patella partita und ihrer Entste- hung unter besonderer Beru¨cksichtigung der Schra¨gteilung. Dtsch Z Chir. 1931;230:261–77. 168. Blumensaat C.  Patella partita-Traumatische Spaltpatella- Patellarfraktur. Arch Orthop Chir. 1932;32:263–28. 169. Weaver JK. Bipartite patellae as a cause of disability in the athlete. Am J Sports Med. 1977;5:137–43. 170. Oohashi Y, Koshino T, Oohashi Y. Clinical features and classification of bipartite or tripartite patella. Knee Surg Trau- matol Arthrosc. 2010;18:1465–9. 171. Kjellin I. Developmental variants, MRI Web clinic. 2009. 172. Akdag T, Guldogan ES, Coskun H, Turan A, Hekimoglu B.  A Magnetic resonance imaging for diagnosis of bipartite patella: usefulness and relationship with symptoms. Pol J Radiol. 2019;84:e491–7. https://doi.org/10.5114/pjr.2019.91163.

168 173. Flores DV, Gómez CM, Pathria MN.  Layered approach to the anterior knee: normal anatomy and disorders associated with anterior knee pain. Radio Graphics. 2018;38:2069–101. 174. Oohashi Y.  Developmental anomaly of ossification type patella partita. Knee Surg Sports Traumatol Arthrosc. 2015;23:1071–6. https://doi.org/10.1007/ s00167-­014-­2887-­7. 175. Canizares GH, Selesnick FH. Bipartite patella fracture. Arthroscopy. 2003;19:215–7. 176. Iossifidis A, Brueton RN.  Painful bipartite patella following injury. Injury. 1995;26:175–6. 177. Woods GW, O’Connor DP, Elkousy HA. Quadriceps tendon rupture through a superolateral bipartite patella. J Knee Surg. 2007;20:293–5. 178. Knochenmark SH, der Kniescheibe S.  Deutsch Z Chir. 1943;258:386. 179. Adachi N, Ochi M, Yamaguchi H, Uchio Y, Kuriwaka M.  Vastus lateralis release for painful bipartite patella. Arthroscopy. 2002;18:404–11. 180. Ma J, Shi F, Huang C, Shanzhi G. Forensic identification of bipartite patella misdiagnosed as patella

5 Patella fracture. J Forensic Sci. 2017;2017, 62(4) https:// doi.org/10.1111/1556-­4029.13357. 181. Mellado JM, Salvado E, Ramos A, Camins A, Sauri A. Dorsal defect on a multi-partite patella: imaging findings. Eur Radiol. 2001;11:1136–9. 182. Ho VB, Kransdorf MJ, Jelinek JS, Kim CK. Dorsal defect of the patella: MR features. J Comput Assist Tomogr. 1991;15:474–6. 183. van Holsbeeck M, Vandamme B, Marchal G, Martens M, Victor J, Baert AL. Dorsal defect of the patella: concept of its origin and relationship with bipartite and multipartite patella. Skelet Radiol. 1987;16:304–11. 184. Gerrie BJ, McCulloch PC, Labis JS, Lintner DM, Harris JD.  A case report and differential diagnosis of lytic patellar lesion. Orthopaedic J Sports Med. 2016;4(9):2325967116665580. https://doi. org/10.1177/2325967116665580. 185. Monu JU, De Smet AA. Case report 789: dorsal defect of the left patella. Skelet Radiol. 1993;22:528–31. 186. Gamble JG. Symptomatic dorsal defect of the patella in a runner. Am J Sports Med. 1986;14:425–7.

6

Patellar Tendon and Tibial Tubercle

6.1 Introduction The knee extensor mechanism comprises the quadriceps muscle and tendon, medial and lateral patellar retinaculum, patella, patellar tendon, and tibial tubercle [1]. The patellar tendon, by definition, is a ligament as it connects bone (patella) to bone (tibial tubercle). Tendons are soft connective tissue designed to efficiently transfer loads generated by muscles to the skeletal system, facilitating joint movement [2, 3].

6.2 Normal MRI Anatomy of Patellar Tendon Fibers of the rectus femoris tendon course over the patella and contribute to the patellar tendon. The origin on the inferior nonarticular pole of the patella is juxtaposed with the articular cartilage on the deep side and becomes confluent with the periosteum of the patella anteriorly. It inserts proximally onto the anterior lip of the patella and distally on the tibial tubercle connecting the quadriceps muscle to the lower leg [4]. A growth plate separates it from the tibial shaft in childhood and adolescence. Because the growth plate does not contribute to the overall length of the bone, it is called an apophyseal rather than an epiphyseal plate [5]. The superior part of the ligament overlies the infrapatellar fat pad, and the inferior part overlies

the deep infrapatellar bursa. In adults, the patellar tendon is around 25–40 mm wide in the coronal plane, 4–5  mm deep in the sagittal plane, and 4–6 cm long [4]. The patellar tendon attachment to bone (patella or tibia) forms fibrocartilaginous enthesis with four distinct tissue zones–dense fibrous connective tissue, uncalcified fibrocartilage, calcified cartilage, and bone [5]. The patellar tendon lacks a well-developed proper paratendon, while the posterior surface of the tendon, which is in direct contact with the fat pad, is highly vascularized and innervated. According to Duri et  al. [6], the pain intensity in some patients with patellar tendinopathy (PT) is due to the involvement of a fat pad. Patellar tendon pathology usually involves the enthesis sites. It most commonly involves the inferior pole of the patella but can also involve the tibial tubercle or proximal aspect of the patella in the quadriceps tendon [5]. The normal tendon comprises types I and II collagen fibers, surrounded by a paratenon consisting of loose connective tissue, not a synovial sheath [7]. The blood supply has been postulated to contribute to patellar tendinopathy [8]. The patellar tendon receives its vascularization through the anastomotic ring, which lies in the thin layers of loose connective tissue covering the dense fibrous expansion of the rectus femoris. The blood supply to the proximal portion of the patellar tendon enters precisely around the region most commonly affected by patellar tendinopathy—the proximal posterior aspect of the tendon [8]. A

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_6

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a

b

Fig. 6.1  A T1 SE sagittal image (a) in a patient with a normal patellar tendon reveals a homogeneously low signal intensity along its entire length and displayed distinct margins (arrows). A PD FS image axial view (b) demon-

strates the normal semilunar appearance of the patellar tendon, with a convex anterior border and well-defined posterior rim (arrows)

commonly held belief is that the patellar tendon has a “relatively avascular osseotendinous junction” [9]. Because the patellar blood supply is derived from the genicular arteries and the quadriceps and patellar tendons arc supplied secondarily, the tendon–osseous junctions have relatively decreased vascularity, which may be an important contributory factor to rupture [7]. On MR images, the normal patellar tendon presents a homogenous low signal intensity on all sequences (Fig. 6.1). A normal patellar tendon should not exceed 7 mm in AP diameter [4, 7]. In the axial view, the patellar tendon is crescent shaped.

weighted images with fat suppression (PD FS). On axial images, the direction of phase encoding should be left to right to prevent pulsation artifacts from the popliteal artery [10]. Coronal sequences are of limited value for the patellar tendon due to volume averaging artifacts and the non-orthogonal slice orientation [4].

6.3.1 Patellar Tendinopathy

A disease of the tendon, known as tendinopathy, is characterized by pain and reduced mobility and functionality. The etiology and progression of the disease are not well known, leading experts 6.3 MRI Pathological Findings to coin the term “tendinopathy” to describe the of Patellar Tendon condition’s clinical presentation [11, 12]. Tendinopathy is a broad term encompassing In daily practice, for the characterization of painful conditions in and around the tendon due lesions of the extensor mechanism, including the to overuse. It commonly affects the extensor patellar tendon, we use a standard MRI protocol, mechanism (including the patellar tendon) which includes the following: Sagittal spin-echo around the knee and is termed “jumper’s knee” T1-weighted images (T1 SE), Sagittal proton [12, 13]. Though Jumper’s Knee was once density-weighted images with fat suppression referred to as patellar tendonitis, it is now well (PD FS), or short tau inversion recovery (STIR) established in histopathologically and images. Other sequences in the standard protocol ­biochemically analyzed tissue samples excised are Coronal proton density-weighted images with from the patellar tendons of patients with acute fat suppression (PD FS) and Axial proton density-­ symptoms of Jumper’s Knee that inflammatory

6.3  MRI Pathological Findings of Patellar Tendon

cellular infiltrates are absent [14, 15]. This confirms that the disease mechanism in Jumper’s Knee is degenerative tendinopathy (tendinosis) rather than inflammatory tendinitis [16]. In the setting of patellar tendinopathy associated with Jumper’s knee, the area of abnormal signal intensity on MRI corresponds to a region of tenocyte hyperplasia, angiofibroblastic tendinosis, loss of coherent collagenous architecture, and micro tears [17].4It is characterized by an initial reactive or inflammatory response followed by the stage of degeneration. The prevalence of patellar tendinopathy is greatest in young adults engaged in high-demand sports that involve running, jumping, and cutting movements. It has been estimated to range from 40%–50% in elite volleyball players and 35%–40% in high-level basketball players [18]. It can also affect sedentary individuals, and an estimated prevalence of 14.2% is seen in the general population [19]. The exact etiology of the disease is still unknown. However, various risk factors have been identified that may contribute to patellar tendinopathy development [4].

6.3.1.1 Risk Factors Intrinsic and extrinsic risk factors cause PT. Extrinsic risk factors. Training volume and frequency are PT’s most common extrinsic risk factors [20]. Training on hard courts and synthetic tracts can increase the risk. However, using sprung wooden floors for indoor games has reduced the chance of injury. Reduced shock absorption of sporting shoes and shoe surface interaction are also factors that can trigger the condition. Intrinsic risk factors. Researchers have reported several intrinsic risk factors for PT, such as height, weight, waist-to-hip ratio, the lenght and strength of the hamstings, quadriceps and calf muscles, the range of motion of the lower extremities, and limb length others [21–24]. Various studies found a strong correlation between tight hamstring and quadriceps muscles with PT. Witvrouw E. et al. reported greater hamstring and quadriceps muscle flexibility in healthy athletes than in athletes with PT [25]. However, no difference was found between subjects with PT and healthy controls in the study conducted by Crossley KM et al. [26]. Crossley KM et al. found no association between hop test perfor-

171

mance and tendinopathy [26]. Biomechanical abnormalities, such as pes planus, limb length discrepancy, and patella Alta, also increased the risk of the development of PT in both athletic and nonathletic populations [23, 25, 27]. Conflicting results were found in numerous studies investigating the association of anthropometric characteristics with PT.  Zwerver J et  al. reported that athletes with PT would be taller, heavier, and younger than their counterparts without PT [19]. Increased waist circumference was associated with an increased risk of PT, especially among males [22].

6.3.1.2 Pathogenesis The great incidence of tendon injuries in the population and the failure rate of up to 25% of the available conservative treatments have made this field one of the most interesting alternative biological approaches [28]. The study of the microenvironment of tendinopathy is a key factor in improving tendon healing. There is still debate about the true role of inflammation and overload in activating the processes [29]. Both factors gradually produce degenerative changes in the tendon structure due to qualitative and quantitative alterations of tenocytes [30]. Histological tendinopathy has primarily been considered a degenerative pathological process of a non-­ inflammatory nature as the presence of acute inflammatory cells in chronic tendinopathy has never been confirmed [29]. However, thanks to newer research tools, convincing evidence that includes an increasing number of inflammatory cells in pathological tendons [31] has started to appear, showing that the inflammatory response is a key component of chronic tendinopathy [32]. Increasing cytokines, inflammatory prostaglandins, and metalloproteinases (MMPs), along with tendon cell apoptosis, seem to be provoked by continuing mechanical stimuli [33]. In this context, an alternative antiinflammatory and immunomodulatory approach that replaces the traditional anti-inflammatory modalities may provide another potential opportunity to treat chronic tendinopathies [29]. Macroscopically, the patellar tendon of patients with Jumper’s knee contains soft, yellow-brown, and disorganized tissue [14, 32, 33]. This macro-

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scopic appearance is called “mucoid” degeneration [34, 35].

6.3.1.3 MRI Features of the Patellar Tendinopathy MRI gives excellent soft tissue contrast, identifies the exact location and extent of tendon involvement, and helps exclude other clinical conditions such as bursitis and chondromalacia [36]. MRI is useful for surgeons to assess the severity of patellar tendon disease and determine how much tendon tissue to excise [14]. On MRI, infrapatellar tendinopathy produces focal areas of intermediate signal intensity on T1SE and high signal intensity on PD FS images. The localization of the injury can classify patellar tendinopathy. The most frequently affected zone is the inferior pole of the patella, in the deeper part of the tendon, often on the medial side [15, 37] (Fig. 6.2). This zone represents the area of maximum tension during exercise. Similarly, patellar tendinopathy may affect several areas of the tendon (middle, distal, including insertion into the tibial tuberosity) or may spread throughout the body of the patellar tendon (Figs.  6.3, 6.4, and 6.5). Patellar tendinopathy is often associated with the high or low position of the patella, and both increase the risk of PT development in athletic and nonathletic

a

b

Fig. 6.2  Focal patellar tendinopathy (Jumper’s knee) at the level of the proximal portions of the patellar tendon. A 54-year-old woman with anterior knee pain after walking, climbing, and descending stairs. T1 SE in the sagittal plane (a) highlights an area with an intermediate signal at the proximal portion of the patellar tendon without thickening (black arrow). PD FS in the sagittal plane (b) high-

Fig. 6.3  Patellar bifocal tendinopathy (Jumper’s knee) in a woman, 41-year-old. PD FS image in the sagittal plane (a) highlights an area with an increased signal in the proximal portions of the patellar tendon in the posterior half (thick black arrow), with minimum thickening. At the level of the distal third, an intratendinous, vertical band with an increased signal (short black arrow) suggests a degenerative mucoid infiltration—minimal fluid accumulation in the deep subpatellar bursa (dotted arrow). Note that the elongated lower pole of the patella (Cyrano Nose) understates patella Alta while overstating patella Baja in ISI measurement (asterisk)

c

lights the minimal thickening of the proximal portions of the tendon and the increase of signal intensity (black arrow). The corresponding PD FS axial image reveals that the area of focal tendinosis preferentially involves two medial thirds of tendon fibers (arrows c), a typical finding in early Jumper’s knee. Note the minimum fluid signal in the deep subpatellar bursa (dotted arrow)

6.3  MRI Pathological Findings of Patellar Tendon

Fig. 6.4  Patellar tendinopathy affecting the distal patellar tendon, including insertion of the tibial tuberosity in a man 53-year-old former runner with anterior knee pain after prolonged walking, climbing, and descending stairs. PD FS image in a sagittal plane shows patellar tendon body thickening, an area with an increased signal at the level of the proximal portion of the patellar tendon in the posterior half (white arrow), distal posterior contour irregularity (black arrow), and areas with an intermediate signal at the tibial insertion (dotted arrows)

a

b

Fig. 6.6  Patella Alta is associated with diffuse tendinopathy in a woman of 23 years old, an athlete with pain over the inferior pole of the patella limiting flexion and extension movements. T1 SE (a) and PD FS (b) images in the sagittal plane highlight patella Alta (ISI-1.58), associated with patellar tendon tendinopathy, expressed by mucoid infiltration in vertical bands with increased signal both T1

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Fig. 6.5  Patellar tendinopathy extended to the entire patellar tendon—a man, 47-year-old, with pain over the patella’s inferior pole, limiting flexion and extension movements. PD FS image in sagittal plane highlights intratendinous vertical linear infiltrations with increased signal, from patellar origin to tibial insertion (arrows). There is an inflammatory process in the anterosuperior portion of Hoffa tissue, with a pseudocystic appearance (oval circle). Note patella Alta (ISI-1.41) and minimal fluid accumulation in deep subpatellar bursitis (dotted arrow)

c

SE and PD FS along the entire length of the tendon (arrows a, b). There is an increase in the signal of Hoffa tissue at the border between the patellar tendon and the lateral femoral condyle with the appearance of impingement syndrome (thick arrow b, c). Image of superficial subpatellar bursitis (black arrow)

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a

b

Fig. 6.7  Patella Baja associated with diffuse tendinopathy. A 33-year-old man, and athlete, with chronic anterior knee pain. PD FS image in the sagittal plane highlights patella Baja (ISI-0,8), associated with patellar tendon tendinopathy, expressed by focal and short vertical lines of mucoid infiltration with increased signal along the entire

length of the tendon (arrows a). Minimum fluid signal in the deep subpatellar bursa (dotted arrow a). PD FS image in the axial plane shows an increase of the signal in two medial thirds of the tendon width under the patellar insertion (black arrows in circle b)

populations (Figs. 6.6 and 6.7). Irritation of the infrapatellar bursa at the distal part of the patellar tendon, in his insertion in the tibial tuberosity, often coexists with distal patellar tendinopathy (Fig. 6.8). Bone marrow edema in the inferior pole of the patella is a recognized associated finding (Fig. 6.9). There is a relationship between the alteration of the Hoffa fat pad and patellar tendinopathy [38] (Fig.  6.10). An alteration of the fat pad must be correctly diagnosed to apply the appropriate therapeutic protocol. In the sagittal and axial plane, marked tendinopathy, focal or diffuse, is easy to see on T1SE or PD FS images. A fluid-filled split is

compatible with a partial tear is seen within the proximal tendon on the PD FS in a sagittal image (Fig. 6.11). In chronic tendinopathies, areas of increased signal intensity were observed in both T1SE and PD FS images. Other common MRI findings include focal or diffuse thickening of the tendon with increased anteroposterior diameter in the affected region (Figs. 6.12 and 6.13). Calcification or ossification within the tendon may be seen as well-defined low-signal areas on all sequences (Fig. 6.14). Summary. Role of MRI in patellar tendinopathy: a) Identification of exact location and the extension of the tendon involvement; b) Exclusion

6.3  MRI Pathological Findings of Patellar Tendon

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of other conditions such as bursitis, chondromalacia; and c) Quantification of the size of the patellar tendon to be excised during surgery [4].

6.3.2 Sinding-Larsen-Johansson Syndrome and Patellar Sleeve Fractures

Fig. 6.8  Focal distal tendinopathy, associated with deep infrapatellar bursa and adjacent Hoffa inflammation in a man, 41-year-old, a former gymnast with chronic anterior knee pain at the subpatellar level, without trauma. PD FS image in the sagittal plane highlights an increased intratendinous signal in the distal portion of the patellar tendon, including the tibial insertion (black arrow in an oval circle), suggestive of a degenerative mucoid focal infiltration with the appearance of partial rupture. Secondary irritative reaction, expressed by deep subpatellar bursitis and inflammation of the Hoffa tissue overlying the bursa (white arrow and asterisk)

a

b

Fig. 6.9  Focal proximal patellar tendinopathy with bone marrow edema in the inferior pole of the patella. A former woman athlete, 47-year-old, , with chronic anterior knee pain accentuated by prolonged walking and going up and downstairs. PD FS image in the sagittal plane (a), axial

This condition, called Sinding-Larsen and Johansson syndrome, was described independently by Sinding-Larsen in 1921 and Johansson in 1922 [39]. The syndrome is seen in adolescents typically between 10 and 14 years of age but most often in males who play sports (football, running, volleyball, gymnastics) [40, 41]. The etiology appears to be traction tendinitis with de novo calcification in the proximal attachment of the patellar tendon, which had been partially avulsed [7]. Symptoms include limited knee motion and swelling and tenderness over the lower patella. Sinding-Larsen-Johansson syndrome is self-limiting and complete recovery can be expected when the closure of patella growth plate [7].

c

plane (b), and coronal plane (c) highlight a small area with an increased signal at the level of the proximal portions of the patellar tendon (arrows in circles a, b, c), with bone marrow edema in the inferior pole of the patella (asterisk in circle a, b, c)

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b

a

Fig. 6.10  Patellar tendinopathy associated with inflammation and pseudocystic transformation of Hoffa fat pad. A woman, 57-year-old, with anterior chronic pain localized to the inferior pole of the patella. T1 SE- image (a) and PD FS image in the sagittal plane (b) highlight diffuse thickening of the patellar tendon, more obvious at the level of the proximal third (double arrow b), irregularity of the anterior con-

a

Fig. 6.11  Focal acute proximal patellar tendinopathy. A 31-year-old man athlete triple jump with recent anterior knee pain appeared after more intense training, with no history of trauma. PD FS images in the sagittal plane (a), and axial plane (b), highlight an area with fluid increase signal at the level of the proximal portions of the patellar tendon (dotted arrow a) and prepatellar, under the proximal inser-

tour along its entire length, and intratendinous thin vertical lines with intermediate signal T1 (arrows image a) and increased signal in PD FS (dotted arrows b). Hoffa adipose tissue appears infiltrated edematous with inhomogeneous hyposignal over the entire surface (asterisk image a) and diffuse inflammation and pseudocyst image (asterisk image b). Image of deep subpatellar bursitis (thin dotted arrow b)

b

tion of the patellar tendon (long arrow a), with the appearance of partial disinsertion. An intratendinous vertical line with an increased signal is also highlighted. The corresponding PD FS axial image reveals that the area with fluid signal partially interrupts the continuity of the tendon at the level of the patellar insertion in the medial third (arrows in circle b). See also deep subpatellar bursitis (arrow image a)

6.3  MRI Pathological Findings of Patellar Tendon

a

177

b

Fig. 6.12  Diffuse thickening of the patellar tendon. A 39-year-old woman former handball player. PD FS image in the sagittal plane (a) shows fusiform thickening of the patellar tendon, more pronounced in the middle portion (double arrow), with no signal alteration within the tendon. Note the

a

Fig. 6.13  Focal thickening of the patellar tendon in the proximal half. A 59-year-old woman former runner with chronic anterior knee pain, accentuated when walking, climbing, and descending stairs, limiting flexion and extension movements. PD FS image in the sagittal plane (a) and coronal plane (b) shows degenerative mucoid

wide insertion of the tendon on the tibial apophysis (vertical line and small arrows a) and high-­riding patella (arrow a). PD FS image in the axial plane shows loss of semilunar morphology of the patellar tendon and the convex contour of the tendon in the lateral half (double arrow b)

b

infiltration of the proximal half of the patellar tendon, interruption of fiber continuity (asterisk a, b), and increased anteroposterior (1.8 cm) and transverse diameters (3.6  cm). Note also deep subpatellar bursitis with enclosure of fluid material (arrow image A) and diffused Hoffa fat pad inflammation (star a)

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178

a

Fig. 6.14  The appearance of chronic tendinopathy in two different patients: (1a) A 57-year-old man athlete with anterior knee pain and limited flexion and extension movements.T1SE-MR image in sagittal plane highlights the diffuse thickening of the patellar tendon, more obvious at the tibial insertion (double arrow), the irregularity of the anterior and posterior contours, fine and short intratendinous vertical lines with T1SE intermediate signal (arrow) and a small bone fragment embedded in the prox-

a

Fig. 6.15 Sinding-Larsen-Johansson syndrome. A 12-year-old girl gymnast with anterior knee pain after performing an exercise with the right knee twisted and falling to the ground. On clinical examination, the patient presented with local pain, tenderness, swelling, and an inability to extend the knee fully. PD FS images in the sagittal plane (zoomed image a) and coronal plane (b) revealed high signal and thickening of the proximal patellar tendon

b

imal portion of the patellar tendon (dotted arrow). (2b) A 59-year-old woman former volleyball player has chronic subpatellar knee pain and limited flexion and extension movements. PD FS-MR image in the sagittal plane highlights the appearance of the high-rinding patella (ISI-­ 1,48), with diffuse thickening of the patellar tendon, contour irregularity, and the absence of intratendinous mucodegenerative infiltrations. Minimum accumulation of fluid in the deep subpatellar bursa (arrow)

b

(1,2 cm) with adjacent marrow edema in the inferior pole of the patella (black arrow, double arrow, and white arrow a) and diffuse Hoffa’s fat tissue edema (asterisk a). The corresponding PD FS axial image reveals Hoffa’s fat edema in the proximal posterior portion of the proximal patellar ligament with a width of 1.3  cm (asterisk and double arrow b). Note the discontinuity of the patellar tendon with the appearance of partial rupture (short arrow b)

6.3  MRI Pathological Findings of Patellar Tendon

179

edema of Hoffa’s fat pad (Fig. 6.15), swelling of the cartilage, and fragmentation of the lower pole of the patella (Fig. 6.16). Patellar sleeve fractures are specific to the pediatric population [42]. In this injury, the cartilage of the inferior pole of the patella is pulled off the patella, often with a small avulsed bone fragment (Fig.  6.17). The mechanism that facilitates this injury is a vigorous contraction of the quadriceps muscles applied to a flexed knee [43]. Plain radiographs generally demonstrate a small bone fragment inferior to the lower pole of the patella, patella Alta, and a joint effusion [42]. However, it has been shown that the extent of the cartilaginous and soft tissue injury is often severely underestimated on plain radiographs [42]. For this reason, MR imaging is a critical tool for assessing the true extent of injury to the extensor mechanism. In many cases, the MR imaging findings of a patellar sleeve avulsion mirror those seen on plain radiographs: an avulsed bone fragFig. 6.16  Sinding-Larsen-Johansson syndrome with the ment, the increased signal intensity of the surseparation of the lower pole of the patella. A 13-year-old girl gymnast with anterior knee pain located subpatellar rounding soft tissues, and bone marrow edema of appeared after a fall on the knee. On clinical examination, the patella (Fig.  6.18). The joint effusion may the patient presented with local pain, tenderness, swelling, also be present if the fracture extends into the and an inability to extend the knee fully. PD FS image in joint. However, there have also been cases in the coronal plane reveals irregularity of the lower contour of the patella and the presence of an area of edema and which no bone fragment was avulsed, and MR cortical bone fragments (black arrows) and an osteocarti- imaging demonstrated a nondisplaced osteolaginous fragment (dotted arrow) chondral fracture. Fat-suppressed images (PD FS) show a hypointense fracture line surrounded by high-signal intensity bone marrow edema and 6.3.2.1 MRI Features of Sinding-Larsen-­ an adjacent linear hyperintense defect in the carJohansson Syndrome tilage at the inferior pole of the patella (Fig. 6.19). and Patellar Sleeve Fractures MRI can depict all the manifestations of Sinding-­ Sinding-Larsen-Johansson syndrome (Fig. 6.20a) Larsen-­Johansson syndrome: edema at the infe- shows the similarities and differences between rior pole of the patella and in the proximal portion other conditions with identical MRI semiology as of the patellar tendon, thickening of the patellar PT-jumper’s knee. SLJ is seen in adolescents tendon at the patellar attachment, and diffuse typically between 10 and 14 years of age and is

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180

a

Fig. 6.17 Avulsed osteochondral fragment from the anteroinferior lower pole of the patella. An 11-year-old girl gymnast with anterior knee pain located subpatellar after a fall on the left knee. The patient presented with local pain, tenderness, and swelling on clinical examination. T1 SE and PD FS images in the sagittal plane

b

revealed cortical bone fragments (black arrows a and white arrow b) detached and embedded in the proximal portion of the patellar tendon. There is a small area of edema with hyposignal T1 SE and hypersignal PD FS at the fragment’s detachment site (white arrow A and black arrow b). Note, the association with patella Alta (ISI-1,4)

6.3  MRI Pathological Findings of Patellar Tendon

a

Fig. 6.18  Avulsed osteochondral fragments in a patient with patella Alta. A 14-year-old boy, a basketball player with anterior knee pain located under the patella. The patient presented with local pain, tenderness, and swelling on clinical examination. PD FS images in the sagittal plane (a) and zoomed image (b) revealed an osteochondral bone fragment (black arrow b), avulsed from the

181

b

antero lower pole of the patella (white arrow b). There is also a small cortical fragment not detached on the anterior contour of the lower pole of the patella (black dotted arrow). It is an inflammatory reaction in Hoffa tissue adjacent to the described changes (asterisk b). Note the high position of the patella (ISI-1,44)

182 Fig. 6.19  A 12-year-old gymnast with anterior knee pain twisted and fell to the ground after performing an exercise with the right knee. On clinical examination, the patient presented with local pain, tenderness, swelling, and an inability to extend the knee fully. PD FS zoomed image in the sagittal plane revealed a hypointense fracture line at the lower pole of the patella (black arrows) surrounded by high-signal intensity bone marrow edema. A small osteochondral fragment (white arrow) is also highlighted above. See a high signal and slight thickening of the posterior portion of the proximal patellar tendon (long white arrow). Also, there is a slight thickening of the subpatellar synovial plica (thick dotted white arrow)

6  Patellar Tendon and Tibial Tubercle

6.3  MRI Pathological Findings of Patellar Tendon

a

a

183

b

c

S L J S

b

a

b

c

P T J K

Fig. 6.20  Two conditions with identical MRI appearance  – SLJD (a) and PT-jumper’s knee (b). (a). Focal thickening of the patellar tendon in the proximal half of the patellar tendon. A 12-year-old football player with subpatellar anterior knee pain, accentuated when walking, climbing, and descending stairs, limiting flexion and extension movements. PD FS images in the sagittal plane (A), coronal (B), and axial (C) highlight focal edema at the inferior pole of the patella (black dotted arrow A, B) and in the posterior proximal portion of the patellar tendon with thickening (black arrow A, B, C). (b). Focal

thickening of the patellar tendon in the proximal half of the patellar tendon. A 37-year-old man handball player with subpatellar anterior knee pain, worse after intense training. PD FS images in the sagittal plane (A) and axial plane (B) highlight focal edema at the proximal patellar tendon (black arrow A, B) and Hoffa’s fat pad edema in the anterosuperior portion (asterisk). Note that the differential diagnosis between these two conditions with identical MRI is made by the presence of growth cartilage in the first case (SLJD) and its absence (fusion) in the second case (PT jumper’s knee)

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6.4 Patellar Tendon Rupture

Fig. 6.21  Sinding-Larsen-Johansson syndrome associated with Osgood-Schlatter’s disease. A 16-year-old boy with anterior knee pain subpatellar and proximal tibial. PD FS image in the sagittal plane revealed a low patella position in relation to the femur and tibia and a shortening of the patellar tendon with the appearance of a patella infera. High-signal intensity in the posterior portion of the proximal patellar tendon (black arrow) is associated with avulsion and inclusion in the patellar tendon of a detached bone fragment from the tibial tuberosity (long white arrow). Note patellar tendon thickening at the tibial insertion (double arrow) and tibial tuberosity hypertrophy (asterisk) with an unwelded small bone fragment (short white arrow)

Rupture of the patellar tendon is a relatively infrequent yet disabling injury, most commonly seen in patients under 40  years of age. Overall, patellar tendon rupture is the third most common injury to the extensor mechanism of the knee, following patellar fracture and quadriceps tendon rupture [44, 45]. It occurs during athletic activities when the flexed knee resists a violent contraction of the quadriceps muscle group. Rupture usually represents the final stage of degenerative tendinopathy resulting from repetitive microtrauma to the patellar tendon [46]. This injury may also occur during less strenuous activity in patients whose tendons are weakened by systemic illness or the administration of local or systemic corticosteroid medications [47]. The ­ diagnosis is based on a painful, palpable defect in the substance of the tendon, an inability to extend the knee against gravity completely, and the existence of patella Alta confirmed by lateral radiographs [46]. Magnetic resonance imaging is the method of choice to detect and characterize patellar tendon rupture and highlight the associated lesions.

6.4.1 Classification and MRI Appearance

Some authors grouped patellar tendon ruptures into three categories according to the location of self-limiting in that it resolves within the disruption: the distal pole of the patella, ten12–18 months. PT occurs in people aged 25–50 don midsubstance, or tibial tubercle [7, 30, 34]. years who practice sports activities involving Patellar tendon rupture can occur secondary to running, squatting, stair ambulation, jumping, acute trauma (Fig. 6.22) or long-standing tendon climbing, and other activities that overload the irritation secondary to repetitive microtrauma flexion and extension movements and are non-­ (Fig.  6.23). Therefore, the patellar tendon most self-­limiting (Fig.  6.20b). Sinding-Larsen-­commonly ruptures near its proximal end of the Johansson syndrome is associated with inferior pole of the patella. Osgood-Schlatter’s disease (Fig. 6.21). Given that considerable force is needed to rupture a healthy tendon, ruptures likely occur in areas of preexisting disease. Patellar tendon rupture often occurs in the setting of long-standing

6.4  Patellar Tendon Rupture

185

a

b

Fig. 6.22  A 37-year-old man with anterior knee pain, swelling, and inability to extend the knee after a car accident. On local clinical examination, swelling of the distal thigh, anterior face, and medial and lateral soft parts of the left knee was observed. A palpable defect was felt at the subpatellar level. PD FS images in the sagittal (a) and axial plane (b) revealed a complete rupture of the patellar tendon at the patellar insertion (white arrow), marked swelling in the upper half, fragmentation (asterisk), and fluid-filled space between the tendon fragments (star a). Thickening of the patellar tendon in the lower half (double arrow), hemorrhagic fluid infiltration, and interruption of

a

b

Fig. 6.23  A 53-year-old woman, a former athlete known for chronic patellar tendinopathy, exacerbates subpatellar pain after a long walk. T1 SE image (a) and PD FS image in the sagittal plane (b) highlight the chronic tendinopathy of the proximal half of the patellar tendon, expressed by degenerative mucoid infiltration and increase of the anteroposterior diameter, more than 1.1 cm (double arrow ab). Edematous infiltration of the Hoffa’s fat pad and the

some fibers (short white arrows) with the appearance of posttraumatic tendinitis. Contusive hemorrhagic changes in the soft parts of the prepatellar and infrapatellar, medial, and lateral face of the knee, expressed by rupture and femoral disinsertion of both retinaculum (arrows b). Besides, it stands out, fluid collections (black dotted arrows A, B) in hypersignal PD FS, located in the posttraumatic space created between the subcutaneous fat and the underlying prepatellar and both retinacula fascia (black dotted arrows B), aspect suggestive of a Morel Lavalle lesion (acute posttraumatic seroma)

c

distension of the deep infrapatellar bursa (white arrow a and black arrow b). PD FS image (c) highlights the rupture of some fibers in the posterior upper half of the tendon and their posteroinferior retraction (black arrows c). See also an edematous infiltration of the Hoffa fatty tissue and accumulation of hemorrhagic fluid in the deep subpatellar bursa (asterisk). MRI Diagnostic: partial nontraumatic rupture of the patellar tendon

186

Fig. 6.24  Partial bifocal rupture of the patellar tendon in a patient with chronic tendinopathy. A 62-year-old woman known for chronic patellar tendinopathy exacerbates subpatellar pain after a long walk. PD FS image in the sagittal plane shows angulation and relaxation of the patellar tendon. Focal degenerative mucoid infiltration is noticed in the sites of maximum stress of the tendon-tibial insertion (black dotted arrow in white circle) and middle third (black dotted arrow in black circle), with the interruption of the continuity of the fibers. The rupture is the final result of chronic tendon degeneration due to repetitive microtrauma

6  Patellar Tendon and Tibial Tubercle

patellar tendon irritation, and the rupture results from chronic tendon degeneration due to repetitive microtrauma. Histopathologically ruptured tendons studied by Kannus et  al. demonstrated changes consistent with chronic inflammation and degeneration [48] (Fig. 6.24). Patellar tendon rupture can occur at three distinct locations with a proximal avulsion of the tendon, with or without bone from the inferior pole of the patella being the most common (Fig. 6.25). The strain at the tendon-inferior pole patella interface is three to four times higher than at the midsubstance of the tendon [49]. The other two possible locations for rupture include the midsubstance (Fig. 6.26) of the tendon and an avulsion of the patellar tendon from the tibial tubercle (Fig.  6.27). Patellar tendon rupture due to indirect trauma has been considered the end stage of a long-standing chronic tendon degeneration secondary to repetitive microtrauma [50]. Partial tears of the patellar tendon (PPTT) were found in

6.4  Patellar Tendon Rupture

a

187

b

Fig. 6.25  A 57-year-old woman with avulsion fractures of the lower pole of the patella, associated with tears of the patellar tendon. T1 SE image in the sagittal plane (a) and PDW SPAIR image in the sagittal plane (b) highlight avulsion of the lower pole of the patella (black arrow A and dotted black arrow b) with partial rupture of the patellar tendon (dotted white arrows a, b). The patellar tendon

a

Fig. 6.26  A 41-year-old man with a complete rupture of the patellar tendon in the middle third of the patellar tendon. On local clinical examination, swelling of the patellar tendon and a palpable defect was felt at the subpatellar level.T1 SE image in the sagittal plane (a) and PD FS

under the patella appears thickened (double arrows a and b) with an inhomogeneous structure and diffuse posterior contour (black arrows a and white arrows b). Hoffa fatty tissue edema in the posterosuperior portion. Prepatellar and superficial infrapatellar bursitis (star a). Thickening of the subpatellar synovial plica (black dotted arrow a)

b

image in the sagittal plane (b) show the complete rupture (white arrow a, and black arrow b) and posterior retraction of the inferior fragment on the tibial plateau (asterisk). See also the elevated position of the patella with the femur and tibia, secondary to the traction of the quadriceps

6  Patellar Tendon and Tibial Tubercle

188

a

b

Fig. 6.27  A 43-year-old man, a former basketball player, with an avulsion of the patellar tendon from the tibial tubercle, known for patellar tendinopathy of both knees. During a recreational game, he underwent an eccentric quadriceps muscle contraction with his foot on the ground, slightly bent. T1 SE image in the sagittal plane (a) and PD FS image in the sagittal plane (b) confirm an avulsion of the patellar tendon at the level of the insertion on the tibial

a

b

Fig. 6.28  A 43-year-old man with partial rupture of the patellar tendon, a known athlete with chronic focal tendinopathy at the patellar insertion. PD FS images in the sagittal plane (a), coronal plane (b), and axial (c) highlight an area with an increased signal at the level of the proximal

tubercle (circle and arrows images a, b), with the presence of a small bone fragment torn from the cortex of the tibial apophysis, well highlighted on the PD FS sequence (white arrow). The striated aspect of the patellar tendon is noticed due to the more obvious linear, vertical, degenerative mucoid infiltrations in the PD FS sequence (short black arrows a, b). Secondary diffuse infiltration of Hoffa’s fat pad (star)

c

portions of the patellar tendon (asterisk) over its entire depth (double arrow a, and over 1.2 cm wide b). Partial patellar tendon rupture is associated with edematous infiltration of the anterosuperior portion of Hoffa’s fat pad (star a, c)

6.4  Patellar Tendon Rupture

a

Fig. 6.29  A 21-year-old basketball player with a partial rupture of the patellar tendon at the patellar insertion. PD FS image in the sagittal plane (a) highlights an area with increased signal (asterisk a), thickening (double arrow a), and discontinuous fibers at the infrapatellar level of the

189

b

patellar tendon (arrow a). The edematous infiltration of adjacent Hoffa’s fat pad (star), is also highlighted. PD FS image in the coronal plane (b) through the patellar tendon shows a focal, vertical, hyperintense signal within the patellar tendon (asterisk b), consistent with a partial rupture

190

6  Patellar Tendon and Tibial Tubercle

6.5 Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

Fig. 6.30 A 21-year-old man practicing recreational sports, known with an OS disease, presents with anterior knee pain in the subpatellar level and at the tibial insertion of the patellar tendon; the pain is accentuated when hitting the ball. The PD FS sequence in the sagittal plane highlights patella Alta (ISIM-1.4) and the edematous infiltration of the patellar insertion of PT and its partial disinsertion (white arrow in the oval circle). Avulsion separation of the tibial tubercle from the tibial epiphysis (white dotted arrow)

the posterior and posteromedial portions of the tendon (Figs. 6.28, 6.29, and 6.30). The most sensitive predictor for a PPTT tear was the tendon’s thickness, in which thickness > 8.8 mm strongly correlated with a tear [51]. Summary. A knee MRI is an appropriate diagnostic study for a suspected patellar tendon rupture. It is the most sensitive imaging modality and can differentiate partial from complete tendon rupture. It helps determine the exact location of the rupture, the presence of any tendon degeneration, the position of the patella, and any concomitant intraarticular knee lesions.

The Osgood-Schlatter’s disease was first described in 1903 and is a traction apophysitis of the tibial insertion of the patellar tendon caused by the repetitive strain on the quadriceps femoris muscle [52]. It is one of the most common causes of knee pain in adolescents and usually presents in young males aged 10–14  years [53]. Rapid growth and increased physical activity predispose to the development of this condition during early adolescence. The immature patellar tendon–tibial tubercle junction is highly susceptible to submaximal, repetitive tensile stress resulting from high-intensity sports activity [6]. The incidence is higher in athletes compared to non-­ athletes, with 21% in athletes compared to 4.5% in non-athletes [54, 55]. It is most commonly unilaterally, but approximately 20–30% of patients will have a bilateral presentation [56]. It is a self-­ limiting condition, with a resolution of symptoms in about 90% of cases with or without some form of conservative treatment, and although the symptoms disappear after the closure of the growth plate in most cases, in some patients, they may persist [57].

6.5.1 Pathophysiology and MRI Findings The tibial tubercle, or tibial tuberosity, comprises a relatively soft apophyseal cartilage that is not as strong as bone. It develops as a secondary ­ossification center that provides attachment for the patellar tendon. Bone growth exceeds the ability of the muscle-tendon unit to stretch sufficiently to maintain previous flexibility leading to increased tension across the apophysis. The physis is the weakest point in the muscle–tendon– bone attachment (as opposed to the tendon in an adult) and, therefore, is at risk of injury from repetitive stress [58]. With the repeated contraction of the quadriceps muscle mass, especially with repeated forced knee extension as seen in sports requiring running and jumping (basketball, football, gymnastics), softening and partial

6.5  Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

avulsion of the apophyseal ossification center may occur with a resulting osteochondritis [59]. Knowledge of the normal development of the tibial tuberosity is essential for understanding the pathogenesis of Osgood-Schlatter’s disease. It is important to understand the four stages of tubercle development. Cartilaginous, apophyseal, epiphyseal, and bony stages have been described by Ehrenborg et al. [60]. During the cartilaginous stage of tuberosity development, soft tissue findings, including tendon thickening, prepatellar edema, and deep infrapatellar bursitis, dominate. MRI allows for identifying tuberosity marrow edema and subtle avulsive injury to the secondary ossification center, resulting in transverse clefts in the damaged ossifying cartilage that may not initially be apparent on radiographs [61]. The cartilaginous and apophyseal stages are separated by the appearance of the secondary ossification center. Next, the epiphyseal stage occurs when the ossification centers of the proximal tibial epiphysis and tubercle join. This results in the

191

Fig. 6.32  Normal ossification of the tibial tuberosity apophysis during 11–14 years.T1 SE image of the knee of a 13-year-old girl shows the ossification of the tibial tubercle apophysis (asterisk) in isosignal with the bone marrow of the tibial epiphysis except for a distal cartilaginous portion in the hyposignal (arrow)

continuity of the tubercule with the proximal tibial epiphysis. Last, the bony stage is distinguished by the fusion between the ossified tuberosity and the proximal tibial metaphysis. The bony stage occurs in girls by age of 15 years and boys by age of 17 years [60, 62]. The appearance and closure/fusion of the tibial tubercle occur in the following sequence pattern [58]:

Fig. 6.31  The T1 SE image of the knee of a 9-year-old girl shows a normal tibial tuberosity that appears in the hyposignal on the entire volume corresponding to the cartilaginous substrate (asterisk in the oval circle). Tibial growth plates (dotted arrows) and perifragmentary inflammatory reaction (dotted arrow)

–– The tibial tubercle is completely cartilaginous up to a certain age (age 18 years [63–65] (Fig. 6.33). The ossification of the anterior tibial tuberosity starts distally, the proximal part fuses with the

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192

a

Fig. 6.33 Tibial tuberosity apophysis fuses with the proximal tibial epiphysis (aged 14–18  years). PD FS image of the knee of a 15-year-old boy (a) shows the partial fusion of the tibial tuberosity apophysis with the proximal epiphysis of the tibial (arrows A) and the opening of the tibial growth cartilages (short arrows A). T1 SE image of the knee of a 17-year-old girl shows complete fusion of

a

Fig. 6.34  A 12-year-old gymnast has anterior knee pain at the subpatellar level corresponding to the tibial insertion of the patellar tendon. The pain started insidiously 2 weeks ago and gradually worsened.T1 SE (a) and PD FS (b) images in the sagittal plane demonstrate a lentiform bone fragment detached from the anterior contour of the

b

the tibial tubercle with the proximal tibial epiphysis (long arrow b) and inclusion of the growing tibial cartilage (short arrows b) Note, * Fasciculata muscle Articularis Anterior knee genus (asterisk and oblique line). It elevates the superior synovial membrane during knee extension, thus preventing compression of the synovial folds between the femur and the patella

b

tibial tubercle (white arrows a, b) with the interposition of a liquid blade (black arrow b) communicating with the deep infrapatellar bursa (dotted arrow a, b). Bone marrow edema in the tibial apophysis (white asterisk a and black asterisk b) and the tibial edge of the growth plate (short black arrows a, b)

6.5  Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

rest of the epiphysis, and the distal part fuses with the tibia. Osgood-Schlatter’s disease is a common cause of anterior knee pain in the skeletally immature athletic population. It occurs secondary to repetia

c

Fig. 6.35  A 13-year-old football player with anterior pain in his right knee located at the level of the tibial tuberosity. At first, the pain was low intensity and gradually intensified with activity without preceding trauma. On local clinical examination, an enlarged prominence at the tibial tubercle was present, with tenderness over the site of patellar tendon insertion. At rest, the pain could be reproduced by the resistant extension of the knee and the active and passive flexion.T1 SE image in the sagittal plane (a) showed the thickening of the distal and insertional portions of the patellar tendon (arrow a) and diffuse hyposignal at the level of the tibial apophysis (asterisk a). PD FS image in the sagittal plane (b) highlights the bone

193

tive strain and microtrauma from the force applied by the strong patellar tendon at its insertion into the relatively soft apophysis of the tibial tubercle [58]. This force results in irritation and severe cases, avulsion of the tibial tubercle b

d

marrow’s edema at the tibial apophysis level and a small bone fragment in the tibial insertion of the patellar tendon (dotted arrow b). An anti-inflammatory and resting treatment was recommended. The second examination was performed 6 weeks after the onset of pain.T1 SE image (C) and PD FS image in the sagittal plane (d) showed the separation of a lentiform bony fragment from the tibial tubercle (white arrows c, d) and an accumulation blade with the fluid signal between the separated fragment and the tibial apophysis (white dotted arrow d). See edema of the bone marrow in the tibial apophysis (asterisk c, d). Diagnostic: Tibial tuberosity apophysitis in the acute-sub-­ acute stage

194

Fig. 6.36  A 15-year-old boy with persistent anterior knee pain located at the level of the tibial tuberosity. PD FS image in the sagittal plane shows partial fragmentation of the tibial tuberosity with a small bone fragment detached from the tibial apophysis and embedded in the patellar tendon (long arrow). Accumulation with fluid signal in the deep infrapatellar bursa (dotted arrow) with a fine liquid blade migrated on the posterodistal contour of the patellar tendon (short dotted arrow), suggestive aspect for acute tibial apophysitis

apophysis. The force increases with higher activity levels, especially after rapid growth. Rarely trauma may lead to a complete avulsion fracture. MRI has a high sensitivity in evaluating tibial tuberosity pathology and associated soft tissue

6  Patellar Tendon and Tibial Tubercle

changes (Fig.  6.34). The imaging appearance varies with the severity of the insult and the stage of maturation of the tibial apophysis [61]. During the cartilaginous stage of tuberosity development, soft tissue findings, including tendon thickening, prepatellar edema, and deep infrapatellar bursitis, dominate (Fig.  6.35). MRI allows for identifying tuberosity marrow edema and subtle avulsive injury to the secondary ossification center, resulting in transverse clefts in the damaged ossifying cartilage that may not initially be apparent on radiographs [61]. Once the tibial ­ tubercle has started to ossify, bone fragmentation and disordered ossification become apparent on radiographs and MRIs. The isolated appearance of an irregular ossification center associated with surrounding inflammatory changes suggests the development of acute tibial apophysitis (Fig.  6.36). The following image presents anterior tibial apophysitis associated with bony edema of overload in the proximal tibial cartilage and distal femoral growth cartilage (Fig. 6.37). MRI also allows to highlight of the fragmentation of the tibial tuberosity, avulsion of some bone or cartilaginous fragments that can be separated (Fig. 6.38) or included in the patellar tendon (Fig. 6.39), Hoffa fatty tissue inflammation effusion of the deep infrapatellar bursa (Fig. 6.40). Most patients undergo spontaneous healing, and the bone fragments reunite with the tibia; symptoms may resolve even if the fragments do not fully incorporate [66]. In some patients, the unstable avulsed fragments displace proximally and form symptomatic non-united ossicles, often

6.5  Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

a

Fig. 6.37  Anterior tibial apophysitis is associated with bony edema of overload in the proximal growth tibial cartilage and distal femoral growth cartilage. A 13-year-old girl gymnast, after a fall from the bar, hits her right knee. T1 SE (a) and PD FS (b) images in the sagittal plane demonstrate bone marrow edema (hyposignal T1-a and hypersignal PD FS- b) adjacent to both sides of the proximal

a

Fig. 6.38  Fragmentation of the tibial tuberosity with avulsion and separation of two bone fragments in a 19-year-old boy with chronic patellar tendinopathy and symptomatic sequelae of Osgood-Schlatter’s disease. T1 SE image (a) and PD FS image (b) in the sagittal plane

195

b

tibial growth plate (white asterisk a, black asterisk b), associated with a slight enlargement of the growth plate (short black arrows b). A small portion of the tibial tuberosity’s ossification center, which can be expected at this age, is not yet ossified (dotted arrow). Note diffuse edema of the bone marrow in the distal metaphysis of the femur (star)

b

demonstrate fragmentation of the tibial tuberosity with separation of two bone fragments (oval circle a, b) and perifragmental inflammatory reaction (black arrow b). Note the appearance of chronic patellar tendinopathy (short white arrows b)

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196

a

b

Fig. 6.39  A 34-year-old man weightlifter, known for chronic patellar tendinopathy of the right knee during training, feels intense pain in the right knee at the subpatellar level (under the patella). T1 SE (a) and PD FS (b) images in the sagittal plane show complete avulsion of the

patellar tendon from the tibial apophysis and separation from the tibial epiphysis (white arrows a, b). Note degenerative mucoid infiltration in the posterior portion of the patellar tendon with the appearance of chronic tendinopathy (dotted arrows b)

6.5  Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

a

b

Fig. 6.40  A 23-year-old football player with anterior tibial apophysitis in the subacute stage. T1 SE (a) image in the sagittal plane shows an area of bone marrow edema in the tibial tuberosity, diffusely contoured with an inhomogeneous structure (asterisk a) and fluid signal in the deep subpatellar bursa (star a). PD FS image in the sagit-

a

197

b

Fig. 6.41  Chronic active form of Osgood–Schlatter’s disease, with symptoms, persists into adulthood. A 63-year-old man presented with anterior knee pain almost daily, being more intense in physical activities that required weight lifting. T1 SE (a) and PD FS images in

tal plane (b) confirms the presence of bone marrow edema in the tibial tuberosity (asterisk) and its fragmentation with multiple small bone fragments (short arrows b), partial disinsertion of the patellar tendon (dotted arrow), and serosanguineous fluid in the deep infrapatellar (star b) with extension in the Hoffa’s fat pad

c

d

the sagittal (b), coronal (c), and axial (d) planes showed tibial tubercle fragmentation (images a, b, c, and d) and degenerative mucoid infiltration of the patellar tendon (black arrows b) with the appearance of chronic tendinopathy

6  Patellar Tendon and Tibial Tubercle

198

a

b

Fig. 6.42 A 53-year-old man known with Osgood– Schlatter’s disease of the right knee presents with pain and limitation of flexion and extension when running and during activities that involve lifting weights. MR image T1SE in the sagittal plane (a) and PD FS image in the sagittal

a

Fig. 6.43  A 17-year-old boy with patella Alta associated with Osgood Schlatter disease. T1 SE (a) and PD FS images in the sagittal plane reveal high patella, according to the Caton-Deschamps index (greater than 1.2), associated with Osgood-Schlatter’s disease with avulsion a bone

c

plane (b) and axial plane (c) highlight marked hypertrophy of the tibial tuberosity (asterisk in oval circles a, b, and c) up to the level of the proximal articular surface of the tibia and shortening of the patellar tendon (double arrow b)

b

fragment from the anterior tuberosity enclosed in the patellar tendon (arrows a and b). Hypertrophy of the lower two-thirds of the tibial tuberosity (dotted arrow a and b)

6.5  Osgood-Schlatter Syndrome and Tibial Tubercle Avulsion Fractures

a

Fig. 6.44  A 16-year-old girl with patella infera associated with Osgood-Schlatter’s disease. T1 SE (a) and PD FS images (b) in the sagittal plane reveal the low position of the patella in relation to the femur and the tibia according to IS index (0,73), associated with Osgood-Schlatter’s disease experienced through the avulsion from the upper

199

b

third of the anterior tuberosity, a bone fragment enclosed in the patellar tendon (arrows a, b). High insertion of the patellar tendon over the entire height of the tibial tuberosity (dotted line a). The ossification center of the tibial tuberosity is in the ossification process (dotted arrow)

6  Patellar Tendon and Tibial Tubercle

200

ing, the main physical result in O ­ sgood-­Schlatter’s Disease acute phase (Osgood-Schlatter Recalcitrant Disease) (Fig. 6.45).

References

Fig. 6.45  Recalcitrant Osgood-Schlatter’s disease in a 19-year-old girl. Sagittal PD FS image of the knee shows hypertrophy and fragmentation of the tibial tuberosity with areas of inter-fragmentation edema (asterisks in the oval circle). Avulsion separation of a bone fragment from the anterosuperior contour of the tibial tuberosity, pulled proximally by the patellar tendon. (white dotted arrow). The fluid collection deep into the patellar tendon corresponds to deep infrapatellar bursitis (black arrows)

associated with patellar tendinosis. The disease can take a chronic active course in such cases, with symptoms persisting into adulthood Fig. 6.41. In chronic inactive Osgood-Schlatter’s disease with sequelae ‘appearance, MRI shows marked hypertrophy of tibial tuberosity with extension to the articular surface and shortening of the patellar tendon (Fig.  6.42). A high incidence of Osgood-Schlatter condition is in patients with patella Alta (Fig.  6.43) and patella Baja (Fig. 6.44), presumably because of increased tension on the tibial tuberosity [67]. Reactive, secondary heterotopic bone formation occurs at the insertion site of the patellar tendon. MR imaging demonstrates bone marrow edema in the tibial tubercle region and edema of the surrounding soft tissues, resulting in visible and painful swell-

1. LaPrade MD, Kallenbach SL, Aman ZS, Moatshe G, Storaci HW, Turnbull TL, Arendt EA, Chahla J, LaPrade RF.  Biomechanical evaluation of the medial stabilizers of the patella. Am J Sports Med. 2018;46(7):1575–82. [PubMed] 2. Thorpe CT, Screen HRC.  Tendon structure and composition. In: Ackermann PW, Hart DA, editors. Metabolic influences on risk for tendon disorders. 1st ed. Cham: Springer International Publishing; 2016. p. 3–10. 3. O'Brien M.  Anatomy of tendons. In: Maffulli N, Renström P, Leadbetter WB, editors. Tendon injuries: basic science and clinical medicine. London: Springer; 2005. p. 3–13. 4. Nayak M, Yadav R.  Patellar Tendinopathy. Jumper Knee. 2019; https://doi.org/10.5772/ intechopen.8464217. 5. Benjamin M, Kumai T, Milz S, Boszczyk BM, Boszczyk AA, Ralphs JR. The skeletal attachment of tendons—tendon “entheses.”. Comp Biochem Physiol A Mol Integr Physiol. 2002;133(4):931–45. 6. Duri ZA, Aichroth PM, Wilkins R, Jones J.  Patellar tendonitis and anterior knee pain. Am J Knee Surg. 1999;12(2):99–108. 7. Peace KAL, Lee JC, Healy J.  Imaging the infrapatellar tendon in the elite athlete. Clin Radiol. 2006;61(7):570–8. https://doi.org/10.1016/j.crad. 2006.02.005. 8. Scapinelli R.  Blood supply of the human patella. J Bone Joint Surg (Br). 1967;49:563–70. 9. McLoughlin RF, Raber EL, Vellet AD, et al. Patellar tendinitis: MR features, with suggested pathogenesis and proposed classification. Radiology. 1995;197:843–8. 10. Mosher TM. MRI of knee extensor mechanism injuries overview of the knee extensor mechanism, July 22, 2020. 11. Almekinders LC, Weinhold PS, Maffulli N. Compression etiology in tendinopathy. Clin Sports Med. 2003;22(4):703–10. 12. Maffulli N.  Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14(8):840–3. 13. Blazina ME, Kerlan RK, Jobe FW, Carter VS, Carlson GJ.  Jumper’s knee. The Orthopedic Clinics North Am. 1973;4(3):665–78. 14. David S. Levey Jumper’s Knee, MRI Web Clinic — December 2006. 15. Yu JS, Popp JE, Kaeding CC, Lucas J.  Correlation of MR imaging and pathologic findings in athletes

References undergoing surgery for chronic patellar tendonitis. AJR. 1995;165:115–8. 16. Benjamin M, Toumi H, Ralphs JR, Bydder G, Best TM, Milz S. Where tendons and ligaments meet bone: attachment sites (entheses) in relation to exercise and/ or mechanical load. J Anat. 2006;208:471–90. 17. Pudda G, Ippolito E, Postacchini F.  A classification of Achilles tendon disease. Am J Sports Med. 1976;4:145–50. 18. Lian OB, Engebretsen L, Bahr R.  Prevalence of Jumper's knee among elite athletes from different sports: a cross-sectional study. Am J Sports Med. 2005;33(4):561–7. 19. Zwerver J, Bredeweg SW, van den Akker-Scheek I.  Prevalence of Jumper's knee among nonelite athletes from different sports: a cross-sectional survey. Am J Sports Med. 2011;39(9):1984–8. 20. Visnes H, Bahr R.  Training volume and body composition as risk factors for developing Jumper’s knee among young elite volleyball players. Scandinavian J Med Sci Sports. 2012; https://doi.org/10.1111/j.1600-­0838.2011.01430.x. Source: PubMed 21. Stuhlman CR, Stowers K, Stowers L, Smith J.  Current concepts and the role of surgery in the treatment of Jumper’s knee. Orthopedics. 2016;39(6):1028–35. 22. Malliaras P, Cook JL, Kent PM. Anthropometric risk factors for patellar tendon injury among volleyball players. Br J Sports Med. 2007;41(4):259–63. 23. Cook JL, Kiss Z, Khan K, Purdam CR, Webster K.  Anthropometry, physical performance, and ultrasound patellar tendon abnormality in elite junior basketball players: a cross-sectional study. Br J Sports Med. 2004;38(2):206–9. 24. Culvenor AG, Cook JL, Warden SJ, Crossley KM. Infrapatellar fat pad size, but not patellar alignment, is associated with patellar tendinopathy. Scan J Med Sci Sports. 2011;21(6):e405–11. 25. Witvrouw E, Danneels L, Asselman P, D'Have T, Cambier D.  Muscle flexibility as a risk factor for developing muscle injuries in male professional soccer Players. A prospective Study. Am J Sports Med. 2003;31(1):41–6. 26. Crossley KM, Thancanamootoo K, Metcalf BR, Cook JL, Purdam CR, Warden SJ. Clinical features of patellar tendinopathy and their implications for rehabilitation. J Orthop Res. 2007;25(9):1164–75. 27. Cook JL, Khan K, Harcourt PR, et  al. A cross-­ sectional study of 100 cases of Jumper's knee managed conservatively and surgically. Br J Sports Med. 1997;31:332–6. 28. Lohrer H, David S, Nauck T.  Surgical treatment for Achilles tendinopathy  – a systematic review. BMC Musculoskelet Disord. 2016;17:207. https://doi. org/10.1186/s12891-­016-­1061-­4. 29. Abat F, et  al. Current trends in tendinopathy: consensus of the ESSKA basic science committee. Part II: treatment options. J Exp Orthopaed. 2018;5:38. https://doi.org/10.1186/s40634-­018-­0145.]. 30. Abate M, Silbernagel KG, Siljeholm C, Di Iorio A, De Amicis D, Salini V, Werner S, Paganelli

201 R.  Pathogenesis of tendinopathies: inflammation or degeneration? Arthritis Res Ther. 2009;11(3):235. 31. Dean BJ, Gettings P, Dakin SG, Carr AJ.  Are inflammatory cells increased in painful human tendinopathy? A systematic review. Br J Sports Med. 2016;50(4):216–20. Rees JD, Stride M, Scott A (2014) Tendons  – time to revisit inflammation. Br J Sports Med 48(21):1553–1557] 32. Jonathan D.  Rees, Matthew stride, Alex Scott, tendons – time to revisit inflammation. Br J Sports Med. 2014;48:1553–7. https://doi.org/10.1136/bjsports-­ 2012-­091957. 35.Raatikainen T, Karpakka J, Puranen J, et al. Operative treatment of partial rupture of the patellar ligament. A study of 138 cases. Int J Sports Med 1994;15:46–9 33. Andres BM, Murrell GA. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res. 2008;466(7):1539–54. 34. Khan KM. Patellar tendinopathy: some aspects of basic science and clinical management. Br J Sports Med. 1999; https://doi.org/10.1136/bjsm.32.4.346. Source: PubMed 35. Ferretti A, Ippolito E, Mariani P, et al. Jumper’s knee. Am J Sports Med. 1983;11:58–62. 36. Nuhmani S, Muaidi Q.  Patellar tendinopathy: a review of literature. J Clin Diagn Res. 2018; https:// doi.org/10.7860/JCDR/2018/35797.11605. ózsa L, Kannus P.  Human tendons. Champaign, IL: Human Kinetics, 1997:576 37. Malliars P, Cook J, Purdam C, Rio E. Patellar tendinopathy: Clinical diagnosis, load management, and advice for challenging case presentations. J Orthop Sports Phys Ther. 2015;45(11):887–98. Epub 21 Sep 2015. https://doi.org/10.2519/jospt.20. 38. Ward ER, Andersson G, Backman LJ, Gaida JE. Fat pads adjacent to tendinopathy: More than a coincidence? Br J Sports Med. 2016;50(24) https://doi. org/10.1136/bjsports-­2016-­096174. 39. Keret D, Wientroub S. Apofisitis. In: De Pablos J, editor. La rodilla infantil; 2003. p. 109–10. 40. Iwamoto J, et  al. "radiographic abnormalities of the inferior pole of the patella in juvenile athletes." the. Keio J Med. 2009;58(1):50–3. 41. Iwamoto J, Takeda T, Sato Y, Matsumoto H.  Radiographic abnormalities of the inferior pole of the patella in juvenile athletes. Keio J Med. 2009 Mar;58(1):50e3:50. 42. Valentino M, Quiligotti C, Ruggirello M.  Sinding-­ Larsen-­ Johansson syndrome: a case report. J Ultrasound. 2012;15:127e12. 43. Hagner W, Sosnowski S, Kazin˜ski W, Frankowski S. A case of Sinding-Larsen-Johansson and Osgood-­ Schlatter disease in both knees. Chir Narzadow Ruchu Ortop Pol. 1993;58(1):13e5. 44. Ramseier LE, Werner CM, Heinzelmann M.  Quadriceps and patellar tendon rupture. Injury. 2006;37(6):516–9. [Medline] 45. Cancienne JM, Gwathmey FW Jr, Diduch DR.  Quadriceps and patellar tendon disruption. Scott WN, Diduch DR, Hanssen AD, Iorio R, Long WJ, eds. Insall & Scott surgery of the knee. 6th ed. Philadelphia: Elsevier; 2018. 967–985.

202 46. Matava MWJ. Patellar Tendon Ruptures. J Am Acad Orthop Surg. 1996;4:287–96. 47. Christopher C. Annunziata, Patellar Tendon Rupture Workup, Updated: Mar 30, 2021. 48. Kannus P, Józsa L.  Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J Bone Joint Surg Am. 1991;73(10):1507–25. [Medline] 49. Hunter Hsu; Ryan M. Siwiec Patellar Tendon Rupture Last Update: January 21, 2020. 50. Kelly DW, Carter VS, Jobe FW, Kerlan RK. Patellar and quadriceps tendon ruptures—Jumper’s knee. Am J Sports Med. 1984;12(5):375–80. [Medline]. 51. Lynch S, Ahmad CS.  Stavros Thomopoulos, Charles Popkin rethinking patellar Tendinopathy and partial patellar tendon tears: a novel classification system. Am J Sports Med. 2020; https://doi. org/10.1177/0363546519894333. 52. Osgood RB.  Lesions of the tibial tubercle occurring during adolescence. Boston Med Surg J. 1903;148:114–7. https://doi.org/10.1056/ NEJM190301291480502. 53. Tsakotos G, Flevas DA, Sasalos GG, Benakis L, Tokis AV. Osgood-schlatter lesion removed arthroscopically in an adult patient. Cureus. 12(3):e7362. https://doi. org/10.7759/cureus.7362. 54. MacEwen GD.  In: Herring JA, editor. Tachdjian’s pediatric Orthopaedics. 3rd ed. Philadelphia: W.B. Saunders; 2002. 55. Micheli LJ, Purcell L, editors. The adolescent athlete. A practical approach. New  York: Springer Science; 2007. p. 289–323. 56. Gholve PA, Scher DM, Khakharia S, Widmann RF, Green DW.  Osgood Schlatter syndrome. Curr Opin Pediatr. 2007;19:44–50. 57. Krause BL, Williams JP, Catterall A.  Natural history of Osgood-Schlatter disease. J Pediatr Orthop. 1990;10:65–8. 58. James M.  Smith; Matthew Varacallo. Osgood Schlatter Disease, Last Update: July 30, 2021.

6  Patellar Tendon and Tibial Tubercle 59. Seyfettinoğlu F, Köse Ö, Oğur HU, Tuhanioğlu Ü, Çiçek H, Acar B. Is there a relationship between patellofemoral alignment and Osgood-Schlatter disease? A case-control study. J Knee Surg. 2020;33(1):67–72. [PubMed] 60. Ehrenborg G, Engfeldt B.  The insertion of the ligamentum patellae on the Tibial tuberosity. Some views in connection with the Osgood-Schlatter lesion. Acta Chir Scand. 1961;121:491–9. 61. Hirano A, Fukubayashi T, Ishii T, Ochiai N. Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol. 31:334–42. 62. McKoy BE, Stanitski CL.  Acute Tibial Tubercle Avulsion Fractures. Orthop Clin N Am. 2003;34(3):397–403. https://doi.org/10.1016/ S0030-­5898(02)00061-­5. 63. Watanabe H, Fujii M, Yoshimoto M, Abe H, Toda N, Higashiyama R, Takahira N.  Pathogenic factors associated with Osgood-Schlatter disease in adolescent man soccer players: a prospective cohort study. Orthop. J Sports Med. 2018;6(8) [PMC free article] [PubMed]:232596711879219. 64. Indiran V, Jagannathan D. Osgood-Schlatter disease. N Engl J Med. 2018;378(11):e15. [PubMed] Gholve PA, Scher DM, Khakharia S, Widmann RF, Green DW. Osgood Schlatter syndrome. Curr Opin Pediatr 2007;19(1):44–50 65. Itoh G, Ishii H, Kato H, Nagano Y, Hayashi H, Funasaki H. Risk assessment of the onset of Osgood-­ Schlatter disease using kinetic analysis of various motions in sports. PLoS One. 2018;13(1):e0190503. [PMC free article] [PubMed] 66. Rosenberg ZS, Kawelblum M, Cheung YY, Beltran J, Lehman WB, Grant AD. Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features. Radiology. 1992;185(3):853–8. 67. Flores DV, Gómez CM, Pathria MN.  Layered approach to the anterior knee: Normal anatomy and disorders associated with anterior knee. Radiographics. 2018;38:2069–101. https://doi. org/10.1148/rg.2018180048.

7

Intracapsular and Extra Synovial Peripatellar Fat Pads

7.1 Introduction There are three well-defined fat pads within the knee joint, each interposed between the joint capsule externally and the synovium-lined joint cavity internally [1]. The peripatellar fat pads include: Hoffa’s (infrapatellar) fat pad (HFP), the anterior suprapatellar (quadriceps) and the posterior suprapatellar (), fat pad (Fig. 7.1). The infrapatellar free space between the patellotibial tendon, the anterior portion of the femoral condyles, intercondylar fossa, and anterior horns of both menisci and ACL is occupied by the adipose tissue of Hoffa’s fat pad (HFP). It is a buffer to protect anterior knee joint structures from traumatic aggression. It has a rich innervation, and its damage is a common cause of anterior knee pain. Magnetic resonance imaging (MRI) has become a commonly used modality in evaluating the infrapatellar Hoffa’s fat pad (HFP) pathology.

Fig. 7.1  MRI Anatomy of the peripatellar fat pads. T1 SE image in the sagittal plane shows (1) Infrapatellar fat pad (Hoffa’s fat pad), which is inferior to the patella, posterior to the patellar tendon, and anterior to the intercondylar notch. (2)The anterior suprapatellar fat pad (Quadriceps), located superior to the patella, posterior to the quadriceps tendon and anterior to the suprapatellar recess. (3) The posterior suprapatellar prefemoral fat pad is anterior to the distal shaft of the femur and posterior to the suprapatellar recess

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_7

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204

7.2 Normal MRI Anatomy and Physiology of Peripatellar Fat Pad 7.2.1 Infrapatellar Fat Pad (Hoffa’s Fat Pad—HFP) MRI Anatomy and Physiology of Hoffa’s fat pad (HFP). On the sagittal plane, the HFP is bordered by the inferior pole of the patella superiorly, the joint capsule and patellar tendon anteriorly, the proximal tibia and deep infrapatellar bursa inferiorly, and the synovium-lined joint cavity posteriorly [1] (Fig. 7.2a). On the transverse plane, the HFP is located between the patellar retinacula and patellar tendon anteriorly and the trochlear surface of the femur posteriorly (Fig. 7.2b). It is also attached directly to the menisci anterior horns inferiorly and the tibia periosteum [2]. HFP comprises fat lobules separated by thin fibrous cords (Fig.  7.3). It also contains much

a

Fig. 7.2 (a) MRI Anatomy of Hoffa’s fat pad in the sagittal (a) and axial plane (b). T1SE image in sagittal plane (a). Hoffa’s fat pad is an intracapsular but extra-synovial structure with limited Anterior—Patellar tendon (1). Superior—Inferior pole of the patella (2). Inferior—The anterior proximal tibia contour (3) and deep subpatellar bursae (4). Posterior—Anterior contour of femoral condyles (5), the intercondylar notch, and the anterior cruciate ligament (6). T1 SE image in the axial plane (b).

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

larger septae—such as the infrapatellar synovial plica, which is well imaged at MRI as a low signal intensity structure of variable size and thickness on T1SE images [3]. The infrapatellar synovial plica can be followed from its femoral origin from the anterior part of the intercondylar notch up to its distal attachment to the inferior pole of the patella [4] (Fig. 7.4). Also known as the ligamentum mucosum; it is a normal anatomical structure representing remnants of synovial membranes from embryological development [2]. It is the most common plica in the knee, and sometimes it can become symptomatic [4]. The transverse meniscomeniscal ligament connects the lateral meniscus’s anterior edge to the medial meniscus’s anterior end, which runs inside the posterior aspect of the fat pad (Fig.  7.5). The deep infrapatellar bursa is interposed inferiorly between the patellar tendon and proximal tibia posteriorly. It has the shape of the letter “V,” ­limited by the anterior distal patellar tendon, the

b

Hoffa’s fat pad is located between the patellar retinacula and patellar tendon anteriorly and the trochlear surface of the femur posteriorly; 1-Patellar tendon, 2-Lateral patello-­ tibial ligament, 3-Medial patello-tibial ligament, 4-The anterior horn of the lateral meniscus, 5-The anterior horn of the medial meniscus, 6-Intercondiliar fossa. Lateral margins of HFP, known as alar plicae, protrude in the joint and project posteriorly along with the anterior horn of the meniscus [1, 29]

7.2  Normal MRI Anatomy and Physiology of Peripatellar Fat Pad

a

b

Fig. 7.3  MRI normal appearance of Hoffa infrapatellar tissue. Images in the sagittal plane, TI SE (a), PD FS (b), and T1 SE in the axial plane (c) show low signal foci seen within the fat pad that represent soft tissue thickening and blood vessels (small black arrows a, c, and white arrows b). The structural background is adipose tissue with

a

205

c

hypersignal T1 SE (image a, c) and hyposignal on the fat-­ suppressed sequences (image b). The infrapatellar fat pad contains a framework of connective tissue septa interspersed among fat lobules [2, 16]. It is richly vascularized and innervated and plays its role in biomechanical support and neurovascular supply of adjacent structures [1, 11]

b

Fig. 7.4  The infrapatellar synovial plica (the ligamentum mucosum). T1 SE image (a) and PD FS image (b) show infrapatellar synovial plica, which can be followed from its origin from the anterior part of the intercondylar notch

up to its distal attachment into the inferior pole of the patella (black arrow a, and white arrow b). It is the most common plica in the knee and can become pathological due to inflammation or posttraumatic rupture

tibial margin in the back, and the adipose layer of Hoffa’s fat pad superiorly (Fig.  7.6). A deep infrapatellar bursa is present in 20–70% of individuals. It does not communicate with the knee joint [5]. The interface between the posterior aspect of the fat pad and the adjacent joint space consists of several synovial recesses separated by fat projections or alae. Knowing the synovial recesses

within the infrapatellar fat pad is essential when evaluating the knee for joint effusion and diagnosing intraarticular bodies. Intraarticular fluid in quantities as small as 1 ml can be normally found in the knee joint between the infrapatellar fat pad and the femoral condyles [6]. As the amount of fluid increases, two normal synovium-lined clefts along the posterior aspect of the fat pad become distended [6]. One is located superiorly in a verti-

206

a

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

b

Fig. 7.5  Transverse menisco-meniscal ligament. PD FS images in the axial plane (a) and coronal plane (b) show the menisco-meniscal ligament, which connects the ante-

rior horn of the lateral meniscus to the anterior horn of the medial meniscus. It runs inside the posterior aspect of the Hoffa fat pad (arrows a, b)

Fig. 7.6  The deep infrapatellar bursa. PD FS image in sagittal plane highlights deep infrapatellar bursa (thick white arrow), which is interposed inferiorly between the patellar tendon anteriorly (white dotted arrow) and the proximal tibia posteriorly (black dotted arrow). LaPrade [90] described a fat apron extending down from the infrapatellar fat pad (star), dividing the deep infrapatellar bursa into an anterior (one asterisk) and posterior space (two asterisks)

cal orientation (suprahoffitic recess); the other is anterior to the menisci in a horizontal direction (infrahoffitic recess) (Fig.  7.7). The HFP comprises adipocytes and adipose connective tissues containing collagen embedded in an amorphous ground substance containing glycosaminoglycans [7]. Hoffa’s fat pad also contains pluripotent cells that differentiate into osteoblasts and chondrocytes, unlike subcutaneous fat. It can be divided into inner and outer tissues [8]. The inner tissue is the pad’s core with hard pillow-like adipose tissue with cushioning properties, whereas the outer tissue is a soft adipose tissue surrounding the inner tissue. It was described that the inner tissue might undergo a compressive load, and the outer tissue may undergo a tensional load [7]. The HFP has space-filling properties in the joint cavity, which implies an essential role in joint function, such as secreting synovial fluid [9], promoting lubrication [10], and shock absorption [7]. The vascular supply of Hoffa’s fat pad derives from the superior and inferior geniculate arteries, with a central area left paucivascular [11]. Two vertical arteries are posterior to the patellar ten-

7.2  Normal MRI Anatomy and Physiology of Peripatellar Fat Pad

Fig. 7.7  Synovial recesses within the infrapatellar fat pad. PD FS image in the sagittal plane shows both recesses from the Hoffa’s fat; one is located superiorly (suprahoffitic) in a vertical orientation (white arrow), and the other is located inferior (infrahoffitic), anterior to the menisci in a horizontal orientation (dotted arrow). Visualization and characteristics of these recesses depend on the amount of joint effusion

don’s lateral margins, supplied by the superior and inferior genicular arteries [11]. These vertical arteries interconnected by two or three horizontal arteries are located superior to, inferior to, and, when three are present, at the level of the tibial plateau [11]. The Hoffa’s fat pad, richly innervated, receives branches from the femoral, common peroneal, and saphenous nerves. It also contains a high density of type IV afferent nerve endings, which explains the significant levels of pain perceived when the adipose structure is affected by pathologic processes [12]. Hoffa’s fat pad is the most sensitive tissue within the knee joint, eliciting severe pain on endoscopic palpation, and nociceptive fibers have been found in adipose patients with anterior knee pain [13, 14]. Structurally it is composed of adipose tissue similar to subcutaneous fat [14]. Besides, adipocyte tissue in the HFP contains macrophages, lymphocytes, granulocytes, and nociceptive nerve fibers that could partly be responsible for anterior

207

pain [15]. It is thought to improve the distribution of the lubricant effect of intra-articular joint fluid by increasing the synovial surface [16] and reducing the loading impact by absorbing forces generated in the knee joint [17]. Even under extreme starvation conditions where subcutaneous fat is eliminated, preservation suggests a central role in knee joint homeostasis [18]. The HFP was shown to be a source of cytokines, adipokines, and lipid mediators in knees with OA [19, 20]. It is also a site of inflammatory and mesenchymal stem cells [21]. The role of HFP is not limited to the liberation of chemical mediators but might also be mechanical, considering its anatomy. A recent study focused on sex differences of the healthy HFP and showed that men displayed significantly greater HFP volume/body weight than women, a finding unexplained to date [22]. Hoffa’s fat pad (HFP) is a deformable structure that easily adapts to the knee joint’s changing contours during movement, helping to distribute synovial fluid and acting as a protective cushionbetween articular surfaces [23]. The main function of HFP is to reduce friction between the patella, patellar tendon, and deep skeletal structures. It prevents pinching of the synovial membrane and facilitates vascularized adjacent structures. The importance of peripatellar fat pads in normal knee kinematics is demonstrated because Hoffa’s fat pad resection alters patellar biomechanics [24]. Due to its close contact with cartilage and bone surface, the HFP may contribute to joint homeostasis by reducing the impact of loading and absorbing forces generated in the knee joint [17]. Hoffa’s fat pad (HFP) is richly innervated and a source of anterior knee pain. Patients with abnormalities of the HFP on MRI are often but not always symptomatic [2].

7.2.2 Suprapatellar Fat Pad Two fat pads are located suprapatellar anterior, the quadriceps suprapatellar fat pad, and the posterior prefemoral fat pad. The quadriceps suprapatellar fat pad is superior to the patella, posterior to the quadriceps tendon, and anterior to the suprapatellar recess. A

208

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

normal suprapatellar fat pad lies on the patellar base and is rather triangular (Fig. 7.2(2)). It fills the gap between the posterior aspect of the quadriceps tendon and the superior aspect of the retro patellar cartilage, increasing the congruency of the extensor mechanism. Posteriorly, the suprapatellar joint recess, an upward extension of the knee joint cavity, separates the supra-patellar fat pad from the prefemoral fat pad, which sits immediately anterior to the femur [25–28]. The prefemoral fat pad is anterior to the distal shaft of the femur and posterior to the suprapatellar recess (Fig.  7.2(1). During normal flex-­ extension of the knee, the suprapatellar fat pad prevents friction between the quadriceps tendon and femoral condyle, and the prefemoral fat pad prevents direct contact between the patella and distal shaft of the femur.

Cyclops lesions

7.3 MRI Pathological Findings of Infrapatellar Fat Pad

7.3.1 Intrinsic Pathology of Infrapatellar Fat Pad

A variety of pathological processes can affect the infrapatellar fat pad. They are usually classified into intrinsic, primarily from the Hoffa tissue, and extrinsic, resulting from the secondary involvement pad.

7.3.1.1 Hoffa’s Disease Albert Hoffa described Hoffa’s disease for the first time in 1904 [30]. Hoffa’s initial pathogenesis attributed to inflammation, hypertrophy, and fibrosis of the infrapatellar fat pad impinged the tibia and femur during extension. Recent arthroscopic studies also supported this hypothesis [2, 31, 32]. Hoffa’s disease is a syndrome of IPFP impingement that is thought to result from acute or repetitive knee trauma, causing inflammation and bleeding. It has two clinical phases, acute and chronic [14, 32]. Trauma to the knee is the most common cause of Hoffa’s disease and is responsible for 85% of cases [29]. Acute posttraumatic cases are characterized by nonspecific symptoms such as pain, swelling, bruising, and functional impairment with knee flexion deformity. Traumatic injuries of the anterior compartment of the knee involving Hoffa adipose tissue may act by direct acute contact (Figs. 7.8 and 7.9) or indirect noncontact injury (Figs.  7.10 and 7.11) or may act by repetitive chronic microtrauma (Figs.  7.12 and 7.13). Acute traumas also include traumatic patellar dislocations [33] (Fig.  7.14) and postsurgical

Pathological Spectrum of Hoffa’s Disease [1, 14, 16, 29] Intrinsic Hoffa Disease Oedema at the Superolateral aspect of Hoffa’s fat pad Intracapsular chondroma Localized nodular synovitis Post-arthroscopy / post-surgery fibrosis Shear injury Extrinsic Intra-articular Joint effusion Intra-articular bodies Meniscal cyst Ganglion cyst

Synovial. Pigmented villonodular synovitis Synovial hemangioma Primary synovial chondromatosis Chondrosarcoma Rheumatoid, seronegative arthritis Synovitis secondary to osteoarthritis Extracapsular Patellar fracture Patellar tendon rupture Sinding-Larsen-Johansson disease Deep infrapatellar bursitis Osgood-Schlatter’s disease

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Fig. 7.8  Direct trauma to the anterior compartment of the knee associated with secondary inflammation of Hoffa tissue (hoffitis) in a 34-year-old man with anterior knee pain after a trauma to the left knee by falling off the motorcycle. PD FS image in sagittal (a) and axial plane (b) highlight hemorrhagic edematous infiltration of the patellar

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tendon and the anteroinferior portion of the patella (arrow and asterisk a), associated with inflammation and secondary hypertrophy of the subpatellar adipose tissue with inhomogeneous increased signal intensity (star a, b) that suggest acute hoffitis

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Fig. 7.9  Edematous-hemorrhagic infiltration of Hoffa’s tissue after a complete rupture of the patellar tendon. A 37-year-old man was the victim of a road accident resulting in a complete rupture of the patellar tendon. PD FS images in coronal (a), axial (b), and sagittal (c) show complete rupture of the patellar tendon in with distal

retraction of the lower fragment (arrows a, c). Edematous-­ hemorrhagic infiltration of Hoffa’s tissue, intra-hoffatic areas with increased signal intensity (asterisk a–c), and hypertrophy of the subpatellar adipose tissue (dotted double arrows a, b)

complications (Fig. 7.15) or damage to Hoffa’s fat layer by patellar maltracking [23, 34] (Fig.  7.16) or post ACL reconstruction (Fig. 7.17). Either acute or chronic, traumas can lead to local bleeding and inflammation—the most frequent causes of HFP-­ related pain

(Fig. 7.18) and eventually to a variety of arthrofibrosis lesions, such as posttraumatic or postarthroscopic fibrosis and postsurgical fibrosis [16–19]. Traumatic injury to the infrapatellar plica can also occur and result in signal changes within the fat pad following the ligamentum

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Fig. 7.10  An acute ACL ruptured in a 31-year-old man, a football player who suffered a knee injury by noncontact trauma, like a type Pivot Shift mechanism. PD FS image in the middle sagittal plane (a) and lateral parasagittal (b) show complete rupture of the ACL (thick arrow a), with secondary inflammation and subpatellar adipose tissue (dotted double arrow and star a) with low-intensity intra-­ hoffatic areas in the T1SE sequence (star b). Note the

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characteristic complications of the ACL rupture—the anterior translation of the tibia (1.1 cm) toward the femur (vertical long dotted arrow and double arrow b), and the typical Segond lesion (short arrow b) and perilesional tibial edema (asterisk b). There is also edematous infiltration of the posterior cruciate ligament (asterisk a) and the distal portion of the patellar tendon (short dotted double arrow a)

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Fig. 7.11  Inflammatory reaction of the Hoffa tissue’s posterior portion after noncontact ACL rupture and the medial meniscus in a 31-year-old football player. PD FS image in the sagittal plane (a, b) and axial plane (c) show areas with increased signal intensity in the posterior portion of Hoffa fatty tissue (asterisk a–c) with a reactive

inflammatory substrate, following acute ACL rupture (arrow b) and bucket handle rupture of medial meniscus, manifested by posterior double cruciate sign (arrow a) and “inverted “medial meniscus, with intercondylar meniscal fragment (arrow c)

mucosum (Fig.  7.19) or may be affected in patients who engage in overloaded activities repetitive flexion and extension movements (Fig. 7.20). History of prior sports-related trauma is often present in infrapatellar plica injuries

[35]. In addition to intra-hoffitic edema, MR imaging displays associated traumatic injuries or inflammation and hypertrophy of the Hoffa tissue secondary to acute ACL rupture (Fig. 7.21).

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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Fig. 7.12  Inflammation of HFP by repetitive chronic microtrauma in a 41-year-old professional cycling patient, after intense training for 2 weeks. PD FS image in the sagittal plane (a) and axial plane (b) show inflammation of the Hoffa tissue expressed by the homogeneous

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increase of the signal (star a, b) and the hypertrophy of two lateral thirds with mass effect (black arrow b). Small accumulation with fluid signal in the deep subpatellar bursa (arrow a)

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Fig. 7.13  Inflammation of HFP by repetitive chronic microtrauma in a 27-year-old fencer with the appearance of a secondary hoffitis. PD FS image in the sagittal plane (a) and axial plane (b, c) shows inflammation of the Hoffa

tissue expressed by the inhomogeneous increase of the signal (star a–c). Small fluid accumulation exists in the suprapatellar recess (small black arrow a) and the intercondylar notch (asterisk a)

In the chronic phases, fibrin and hemosiderin have low signal intensity on Tl- and PD FS images. Fibrous tissue may be transformed into fibrocartilaginous tissue, sometimes ossified [3]

(Fig. 7.22). Because ossification also may present with low signal intensity, the correlation of MR imaging appearances with radiographic findings is essential to differentiate fibrosis from

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Fig. 7.14  Cystic transformation of Hoffa fat tissue in a patient with multiple patellar dislocations in the presence of two major anatomic risk factors for patello-femoral instability: patella Alta and trochlear dysplasia type B (not exposed) and with secondary patellar tendinosis. T1 SE image in the sagittal plane (a) and PD FS image in the sagittal plane (b), coronal (c), and axial plane (d), high-

light the multi-cystic transformation of Hoffa tissue (asterisks a–d) and degenerative mucoid infiltration of the patellar tendon in the distal half and at the tibial insertion ((black arrow and dotted arrows b). Note the appearance of secondary patelo-femoral osteoarthritis expressed by reduced patelo-trochlear cartilage thickness and narrowing of the patelo-femoral space

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Fig. 7.15  Postsurgical complication (Chronic Hoffitis) in a 31-year-old athlete after ACL reconstruction. Six months postoperatively, clinically, the patient presented anterior knee pain and a limited range of articular motion. PD FS image in the sagittal plane (a, b) highlights anteriorization of the tibial tunnel (white arrow a, b) with ante-

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Fig. 7.16  Hoffa’s fat pad damage by a microcystic transformation in a 47-year-old patient with patellar maltracking. T1SE in the lateral parasagittal plane (a) and PD FS in the axial plane (b) highlight the signal change-T1

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rior cortical disruption of the tibial tunnel (dotted arrow b, c) irritation of the Hoffa’s fat pad, with increased diffuse signal PD FS, with thinning and fibrotic retraction of the patellar tendon (black dotted arrow a, b), compatible ​with a secondary chronic hoffitis/diffuse arthrofibrosis

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hyposignal (white asterisk) and PD FS hypersignal (black asterisk), with microcystic degeneration of Hoffa adipose tissue. Patella Alta and patellar tendinopathy (white arrow a, b)

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Fig. 7.17  Acute hoffitis in a 25-year-old man, after ACL hyposignal T1 (asterisk a, b) and hypersignal PD FS (star reconstruction. Sagittal and axial images T1 SE (a, b) and c–e) compatible with a postsurgical diffuse inflammatory PD FS (c–e) show tissue signal changes in the Hoffa-­ process of the acute hoffitis type

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Fig. 7.18  Acute trauma to the right knee, associated with local bleeding and inflammation of Hoffa fat pad in a 44-year-old man. PD FS image in the sagittal plane at two levels, mediosagittal (a) and medial parasagittal (b), highlight the increased signal of Hoffa tissue (star a, b). An edematous-hemorrhagic fluid blade that delimits the ante-

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rior portion along the entire length of the patellar tendon (black arrows a, b) and the pretibial portion of Hoffa fat (white arrows) with the appearance of acute edematous-­ hemorrhagic hoffitis. Note the tibial septate bone cyst below the PCL insertion (double arrows a, b) and infrapatellar superficial bursitis (asterisk)

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Fig. 7.19  Posttraumatic rupture of the subpatellar synovial plica, associated with secondary focal hoffitis in a 25-year-old rugby player with rupture of both cruciate ligaments and posterior capsule. PD FS image in the sagittal plane shows thickening of the subpatellar synovial plica (thick white arrow), angulation of the trajectory (thin white arrow), and liquid delimitation (short black arrow). Also, a small fragment of the subpatellar synovial envelope (dotted white arrow) and inflammation of the Hoffa tissue, with the appearance of secondary focal hoffitis (star), stand out. Notice the rupture of both cruciate ligaments, the thickening of the posterior capsule (white arrow) and partial tibial desininsertion (thick white arrow). The complete suprapatellar plica (black arrow) divides the suprapatellar pouch into a suprapatellar compartment (double asterisk) and an articular compartment (asterisk)

Fig. 7.20  Ruptured infrapatellar synovial plica, associated with reactive hoffitis in a 29-year-old football player. The sagittal PD FS image highlights the infrapatellar synovial plica fragment (white arrow), and the increased signal of inflamed Hoffa adipose tissue (star), with the appearance of reactive hoffitis. Effusion in the suprapatellar synovial recess (asterisk). Note the interruption of the posterior articular capsule in the distal third (dotted arrow)

ossification [1]. Symptoms in the chronic phase are infrapatellar discomfort or pain exacerbated when going up and down stairs and lifting heavy weights. Movements are usually well-preserved [29]. Hoffa’s test is a useful aid in diagnosis. In this test, the examiner takes up the flexed knee and presses the thumbs of both hands deeply along the sides of the patellar tendon just below the patella. A positive sign elicits a sharp pain at the terminal extension while extending the flexed knee [36] https://www.msn.com/nl-­nl/ feed?theme=light.

7.3.1.2 Superolateral Hoffa’s Fat Pad Edema Superolateral Hoffa’s fat pad edema (SHFP) is a common finding in routine knee MR imaging studies, with a reported prevalence of 13% in a sample of middle-aged individuals with or at risk of osteoarthritis and 50% in a small cohort of 16 asymptomatic female volleyball players [37, 38]. Numbers on the prevalence in the general population are not available [39]. On MR imaging, sagittal and axial fluid-sensitive images reveal increased signal intensity in the superolateral portion of Hoffa’s fat pad, between the lateral femoral condyle and patellar tendon, described as edema (Fig. 7.23). SHFP is a correlate of patellar lateral femoral friction syndrome (PLFFS), which was characterized for the first time in the literature in 1999 by Bruker et  al. [32], who

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Fig. 7.21 A 57-year-old man with inflammation and hypertrophy of the Hoffa tissue secondary to acute ACL rupture. T1 SE and PD FS images in the sagittal plane (a, b) highlight the hypertrophy of Hoffa tissue (star a, b), widening the patello-tibial angle (double arrow a, b) and a slight curvature by the mass effect of the patellar tendon (white arrow a, b). Uneven increased signal with

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micronodular appearance well expressed on the PD FS image (asterisks). Note, rupture of the ACL with the distal fragment lying on the tibial plateau (long white arrow) and superficial prepatellar and infrapatellar bursitis (black dotted arrows), patellar and tibial insertional tendinopathy (black arrows b)

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Fig. 7.22  A 51-year-old woman with Hoffa’s disease in the chronic stage has low signal intensity on both sagittal Tl SE and PD FS images (white arrows a–c). Fibrous tis-

sue may be transformed into fibrocartilaginous tissue, sometimes even ossify Sagittal T1 SE (dotted arrow d)

called it infrapatellar fat pad impingement in a study of eight patients, and then by Chung et al., in a study of 42 patients [34] where the term

patellar tendon-lateral femoral condyle friction syndrome was introduced [36]. Patellar lateral femoral friction syndrome (PLFFS) is thought to

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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Fig. 7.23  A 17-year-old girl with focal increased signal intensity in the superolateral portion of Hoffa’s fat pad. PD FS images in sagittal (a), coronal (b), and axial (c) planes reveal focal increased signal intensity in the super-

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olateral portion of Hoffa fat pad (asterisk a–c), between the lateral femoral condyle (white arrow) and patellar tendon (dotted arrow c)

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Fig. 7.24  Focal increased signal intensity in the superolateral portion of Hoffa’s fat pad in a 25-year-old woman with patella Alta and subtle patellar maltracking. PDFS image in the sagittal plane (a) reveals focal increased signal intensity in the superolateral portion of Hoffa fat pad (asterisk), patella Alta (ISI-1,53), reduction of patellar cartilage thickness, and narrowing of the patelo-femoral joint space with osteoarthritis appearance (short white arrows a). Small contusive area in the anterior portion of the lateral femoral condyle (dotted white arrow a). PDFS images in the axial plane (b) reveal lateral patellar inclina-

tion (arrow b), with minimal lateral patellar subluxation (double arrow) and small synovial effusion in the lateral paracondylar recess (star), and Dejour type B trochlear dysplasia (dotted line b). Image c in the axial plane reveals focal increased signal intensity in the superolateral portion of Hoffa’s fat pad, between the lateral femoral condyle (white arrow c) and patellar tendon (dotted arrow c), and vague visualization of the body of the lateral patelo-­ femoral ligament, following recurrent lateral patellar subluxations (thin white arrows c)

be a sensitive indicator of subtle patellar maltracking, as several studies have reported strong associations between its presence and morphologic abnormalities and signs detected and described by magnetic resonance imaging (MRI) in a population of patients with anterior knee pain [36, 40–43]. The knees with SHFP have anatomi-

cal predispositions for instability, primarily with patella Alta (Fig.  7.24), patellar tilt more than 13,5° (Fig.  7.25), and a tibial tuberosity–trochlear groove distance (TT-TG) more than 10 mm (Fig.  7.26) and a trochlear prominence of more than 4  mm [36]. In 35% of patients, patellar chondropathy is visible (Fig.  7.27). Moreover,

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Fig. 7.25  A 15-year-old boy with anterior knee pain by going up and down stairs and on long walks. After a football game, he felt intense pain under the patella of his right knee. PD FS images on both knees (RK, LK) in the sagittal plane (a), coronal plane (b), and axial plane (c, d) reveal focal increased signal intensity in the superolateral portion of the Hoffa’s fat pad (asterisk images a, b, d— both knee), patella Alta right knee (RK-ISI-1,53) and left

knee (LK-ISI-1,51), lateral patellar tilt at both knees (images c-right and left knee). Note the stigma of an acute lateral dislocation, a small contusion in the inferior medial portion of the patella on the right (short white arrow c), an area of bone edema on the anterolateral margin of the lateral femoral condyle (arrow d), and patellar rupture of medial patella tibial ligament (arrow image d–LK)

48% of patients have patellar or trochlear subchondral abnormalities [36] (Fig. 7.28). The classic symptoms are anterior knee pain when climbing and descending stairs (patella syndrome). A decreased range of motion, crepitus, moderate joint effusion, and peri ligamentous swelling may be observed next to the patellar ligament [44].

tive trauma related to hyperextension, rotational sprains, and genu recurvatum [49] (Fig.  7.29). First, trauma induces inflammation and hemorrhage. Secondly, hypertrophy of the inflamed fat pad predisposes crushing and impingement [50]. MR imaging in standard sequences demonstrates a heterogeneous mass within the infrapatellar fat pad, with the high signal intensity representing chondroid matrix or edema on fat suppression sequences and areas of low signal intensity representing calcification or ossification. Intracapsular chondroma is a rare chondroma characteristically located inferior to the patella (Fig. 7.30). The literature describes many IFP tumors or tumor-like lesions such as primary or secondary synovial chondromatosis, synovial sarcoma, para-articular chondroma, giant cell tumor focal pigmented villonodular synovitis, chondrosarcoma, lipoma, ganglion cysts, and hemangioma [16]. Intracapsular osteochondroma is a rare form of chondroma and is characteristically located inferior to the patella [26]. Some have considered this

7.3.1.3 Intracapsular Chondroma Chondroma is a benign tumor mainly arising from bones (enchondroma—osteochondroma or exostosis), infrequently in the soft tissues (hand, feet), and rarely in para-articular location, most often the knee [45, 46]. The pathogenesis of soft tissue osteochondroma is unclear, but several theories exist [1]. It may occur due to metaplasia from mesenchymal cells due to acute or repetitive trauma related to hyperextension of the knee and subsequent inflammation and hemorrhage [47, 48]. Some authors consider it the end stage of Hoffa’s disease resulting from acute or repeti-

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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entity an end-stage form of Hoffa disease, given its similar location within the infrapatellar fat pad and similar pathologic feature of ossifying cartilaginous metaplasia [49].

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7.3.1.4 Localized Nodular Synovitis Villonodular synovitis is a benign proliferative disorder classified radiologically into diffuse or localized forms [51]. The localized form, known as localized nodular synovitis, is believed to represent a reactive process or possibly a true neoplasm [52]. Unlike in diffuse form, the hemosiderin deposition in  localized nodular synovitis is highly variable and may be absent. Although the localized form most commonly affects the tendon sheaths of the hands, the giant cell tumor can also occur in the anterior part of the knee, including the infrapatellar fat pad area [53–55]. The clinical manifestations of localized nodular synovitis of the knee are nonspecific. A retrospective review of 26 cases of localized nodular synovitis of the knee by Dines et al. demonstrated that vague pain was the most common presenting complaint (92% of patients). In contrast, mechanical symptoms such as locking or restricted knee motion were rare [56]. Mechanical symptoms occur more commonly in cases involving localized nodular synovitis of a large size sandwiched into a small space between joint structures such as the infrapatellar fat pad [57]. However, although the infrapatellar fat pad is a common

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Fig. 7.26  A 15-year-old boy with four anatomical factors at risk of patellar instability: high patella, (not shown). Dejour trochlear dysplasia type C, patellar inclination greater than 13°, and tibial tuberosity—trochlear groove distance (TT-TG). PD FS axially through the deepest point of the trochlea (vertical continuous line a) and a line parallel to the trochlear line through the anterior part of the tibia tuberosity (vertical dashed line b), image b, highlights the TT-TG distance of more than 10  mm (double line). Note that focal increased signal intensity in the superolateral portion of Hoffa’s fat pad (arrow image a)

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Fig. 7.27  A 53-year-old woman with anterior chronic left knee pain and multiple lateral patellar dislocations with spontaneous relocation. PD FS images in the sagittal plane (a), coronal (b), and axial (d) show focal increased signal intensity in the superolateral portion of the Hoffa’s fat pad (asterisk) and three anatomical risk factors for patellar instability: patella Alta (image a), patellar inclina-

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tion with fixed subluxation (image c) and trochlear dysplasia, Dejour type A (image d). The presence of changes consequent to the lateral patellar dislocations-­ chondropathy of the lateral facet of the patella (arrows in oval circle image a, c) and the patellar disinsertion of the medial patelo-femoral ligament (arrow image d)

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Fig. 7.28  A 45-year-old woman with anterior chronic left knee pain and multiple lateral patellar dislocations with spontaneous patellar relocation. PD FS images in the sagittal plane (a) show patella Alta (ISI-1.5), focal increased signal intensity in the superolateral portion of the Hoffa’s fat pad (asterisk), reduction of patellar cartilage thickness in the distal half (arrow in an oval circle). PD FS image in the axial plane (b, c) reveals lateral patel-

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lar inclination (thick arrow b) and direct contact between the lateral facet of the patella and the lateral femoral condyle, closure of the lateral patellofemoral angle, and damage to the patelo-trochlear cartilage (arrows in circle b). Image c shows focal increased signal intensity in the superolateral portion of Hoffa fat pad (asterisk) and trochlear dysplasia Dejour A (dotted line)

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Fig. 7.29  A 50-year-old woman, a housekeeper with anterior knee pain, presented with pain at the subpatellar level about 7  months ago after a minor trauma that was exacerbated when going up and down. MRI examination 1 month after the onset of pain revealed inflammation and hypertrophy of Hoffa’s fad pat with the appearance of acute Hoffitis. The present examination was performed 6 months after the onset of pain in the sequences T1 SE

and PD FS in the sagittal plane, highlighting the infrapatellar tissue’s edema (asterisk a–c). The presence in the central portion of Hoffa fat of a node inhomogeneous hyposignal T1 SE and intermediate signal PD FS (star a–c) is compatible with the development of an intrahoffitic condrom. Hoffa’s fat pat containt pluripotent cells that can differentiate into chondrocytes and osteoblasts [91]

site for localized nodular synovitis, a large localized nodular synovitis in the fat pad does not always result in mechanical symptoms because the fat pad can tolerate significant volume

changes such as those which occur during knee motion [16, 53]. MRI demonstrates one or more nodules with well-defined margins in the infrapatellar adipose

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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Fig. 7.30  A 55-year-old man with sub-patellar pain and limitation of left knee joint movements. T1SE images in the sagittal plane (a), and axial plane (b), show in the posterosuperior portion of the Hoffa tissue a round-oval formation (1.3/0.9  cm) inhomogeneous T1 hyposignal (arrows a, b) and inhomogeneous intermediate signal in

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PD FS representing calcification (arrow c) and increased signal in the periphery, representing the edematous delimitation (asterisk). The lesions were arthroscopically excised and histologically confirmed as intracapsular chondroma

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Fig. 7.31  A man, 39  years old, with chronic anterior knee pain and limitation of flexion and extension movements. T1SE image in the axial plane shows two nodules with well-defined edges, one in inhomogeneous hyposignal (arrow a) and another with mixed, intermediate (asterisk a) and hyposignal signal accentuated at the level of the posterior contour (dotted arrow a), located in the posterior portion of the infrapatellar adipose tissue. PD FS images

in the axial plane (b) and the sagittal plane (c) highlighted the nodules with a heterogeneity of the intermediate signal (asterisk b, c) and accentuated, discontinuous hyposignal at the edges (arrows b, c). There is inflammation of adipose tissue adjacent to the villonodular synovial nodules. Areas of low signal intensity within the lesions suggest the presence of hemosiderin

tissue (Fig. 7.31). The signal intensity characteristics of the mass are variable and include high signal intensity on fat suppression sequences MR images from edema and low signal intensity with all pulse sequences from hemosiderin or fibrosis. Hemosiderin is differentiated from fibrosis when magnetic susceptibility effects are noted on gradient-­echo (GRE) MR images. Hemosiderin appears as an area of strong hypointensity (or

“blooming”) on GRE MR images compared to conventional SE images and is most conspicuous when long echo times are used in localized nodular synovitis of the knee. The ability of MRI to delineate the extent of disease and to differentiate pigmented villonodular synovitis (PVNS) from its related localized forms is essential, as the entities differ considerably in terms of treatment approach and their typical response to surgical excision [53].

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7.3.1.5 Post-Arthroscopy and Post-­ Surgery Fibrosis HFP scars may result from previous surgery or arthroscopy as an excessive fibrotic response during the repair process [16, 46, 48]; postsurgical fibrosis is usually ill-defined or confluent [16], while post-arthroscopic fibrosis generally manifests as bands coursing through the fat pad (Fig.  7.32). The arthroscopic portals commonly penetrate the infrapatellar fat pad, including the anterolateral, anteromedial, and central portals [57]. Postsurgical fibrotic changes within the HFP are usually asymptomatic [2]. However, a careful investigation of other possible origins of the patient’s pain must be made before considering fibrosis of HFP as the cause [5].

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injury to the knee and has been described as an indirect sign of anterior cruciate ligament (ACL) injury [58]. The linear fluid collection is typically visualized on T2-weighted images as an area of increased signal intensity within the fat pad at the level of the menisci (Fig. 7.33). Additional signs of an ACL injury usually are evident [19].

7.3.2 Extrinsic Pathology of Infrapatellar Fat Pad Due to its close relationship with several anatomical structures, the HFP is secondarily involved in adjacent disorders. These include Intra-articular and Anterior Extracapsular injuries.

7.3.2.1 Intra-Articular Pathology Parameniscal Cysts A meniscal cyst is an infrequent diagnosis, with an estimated 1–8% [59–61]. The extrusion of synovial fluid causes meniscal cysts through a horizontal or complex meniscal tear [62]. Meniscal cysts may present as intrameniscal cysts (Fig.  7.34) or para meniscal cysts (Fig. 7.35) based on their location relative to the meniscus. The association between a parameniscal cyst and an underlying meniscal tear is considered to be strong support for the theory that a meniscal cyst results from fluid extrusion through a meniscal tear [63] (Figs. 7.36 and 7.37). A parameniscal cyst is a well-defined fluid collection adjacent to a meniscus. Meniscal cysts located anteriorly can bulge into the infrapatellar fat pad (Fig.  7.38). They may show lobulations and ­internal septations and rarely produce bony erosions (Fig.  7.39). Parameniscal cysts of the medial meniscus are less common than the lateral (Fig.  7.40). Parameniscal cysts of the lateral meniscus are more commonly palpable than the Fig. 7.32  Post-arthroscopic fibrosis of HFP in a 29-year-­ medial meniscus cysts [60]. Even though there old patient with suspected partial ACL rupture. PD FS are no “special tests” to evaluate meniscal cysts image in the sagittal plane highlights a low signal fibrosis specifically, physical examination maneuvers to band, with the vertical arrangement in the posteromedial portion of Hoffa tissue corresponding to the central evaluate meniscal tears may be used due to the arthroscopic portal (thick white arrow). The fibrotic tissue association of parameniscal cysts with meniscal is imbedded in the inflammation of the Hoffa fat with the tears [64]. MR Imaging is typically considered appearance of secondary hoffitis (asterisks). Fluid accu- the “gold standard” for a suspected meniscal cyst mulation with distension of the suprapatellar synovial recess (star). Note the minimum angular contour of the due to its ability to delineate the cyst and assess the menisci. The MRI imaging of a cystic strucACL (thin white arrow) 7.3.1.6 Shear Injury A linear collection of fluid within the substance of the infrapatellar fat pad may occur with a shear

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Fig. 7.33  A linear collection of fluid within the substance of the infrapatellar fat pad may occur with a shear injury to the knee and has been described as an indirect sign of anterior cruciate ligament (ACL) injury [58]. The linear

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fluid collection typically is visualized on T2-weighted images as an area of increased signal intensity within the fat pad at the level of the menisci

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Fig. 7.34  The T1SE (a) and PD FS (b) images in the coronal plane show an intrameniscal cyst in the lateral meniscus in hyposignal T1 (dotted arrow a) and in hypersignal PD FS (continuous arrow b)

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Fig. 7.35  PD FS image in the sagittal plane shows a linear intrameniscal tear in the posterior horn of the medial meniscus (dotted arrow), which continues with a small parameniscal cyst (continuous arrow)

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Fig. 7.37  Palpable mass on the lateral side of the knee in a 47-year-old woman, painful on prolonged walking, which reduces its volume in flexion and increases in extension. PD FS images in coronal (a), sagittal (b), and axial plane (c) show a tear in the body of the lateral menis-

Fig. 7.36  PD FS image in coronal plane highlights an intrameniscal body of lateral meniscus arrow that continue with parameniscal cyst (asterisk and oval circle), that occupies the space under lateral collateral ligament

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cus (arrow a), fluid effusion, and a septate parameniscal cyst extending below the LCL (star a–c). Note the presence of synovial fluid under the body of the lateral meniscus (asterisk a)

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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Fig. 7.38  A 47-year-old man presents with anterior knee pain and limitation of flexion and extension. PD FS images in sagittal (a), and axial plane (b), show a parameniscal cyst in the infrapatellar adipose layer image(star a, b) that continues with a horizontal tear in the lateral

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Fig. 7.39  A 43-year-old woman has lateral knee pain, limited flexion and extension movements, and a palpable mass on her lateral side. Coronal (a) and axial (b) PD FS images show a multiseptate and multiloculated parameni-

meniscus, with increased signal intensity on a (arrow). The parameniscal cyst is ruptured beyond its wall, has an inhomogeneous structure, and communicates with the deep subpatellar bursa (double arrow and dotted arrow)

b

scal cyst (arrows a, b) of the horn of the lateral meniscus, extending into the lateral collateral ligament space and in the postero-lateral portion of Hoffa’s fat pad

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

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a

b

Fig. 7.40  A 53-year-old woman has chronic pain in the right knee and a palpable mass on the medial face of the knee, which reduces its volume in flexion and increases extension and limited flexion and extension movements. Coronal (a), sagittal (b), and axial (c) PD FS images show

ture that continues with a horizontal or complex meniscal rupture, with low signal intensity on T1SE images and high signal intensity on PDFS images, suggests diagnosing a parameniscal cyst. Surgical excision, aspiration, and steroid injections are current treatment options. However, recurrence rates are high when managed conservatively [65].

c

the appearance of multiseptate (arrows a–c), large multiloculated medial parameniscal cyst (stars a–c). The marked distension of the medial collateral subligamentary space is noticeable (double arrow a)

Lesions rarely occur within the HFP, most commonly ganglion cysts [68, 69]. Ganglion cysts (GC) may be extra-articular, intraarticular, periosteal, or intraosseous but are not associated with meniscal tears [61]. The literature on the subject is still confusing, with both terms used interchangeably [70]. The first type—GC, is the commonest and arises from the joint capsule, ligaments, bursae, tendon sheaths, or subchonGanglion Cyst dral bone [71], perhaps from synovial herniation MRI features distinguish two common musculo- or tissue degeneration [72]. They usually are skeletal lesions, Ganglion cysts (GC) and associated with the cruciate ligaments and may Synovial cysts (SC). A GC is a cystic, tumor-like be multilocular or lobulated. At MR imaging, lesion of unknown origin delimited by dense con- ganglion cysts manifest as cystic lesions with nective tissue filled with gelatinous fluid rich in fluid signal intensity on T1-weighted images and hyaluronic acid and other mucopolysaccharides high signal intensity on fat suppression sequences. [66]. On the other hand, an SC is a juxta-articular A ganglion cyst would not be continuous with a fluid-filled collection lined by synovial cells, meniscal tear if one were coincidentally present which histologically distinguishes them from and thus can be differentiated from a meniscal other juxta-articular fluid collections, most cyst in cases where both meniscal injury and ganimportantly from GC. It represents a joint fluid’s glion cysts occur (Fig. 7.41). Hoffa’s ganglia are focal extension that may or may not communi- most commonly in contact with the anterior horn cate with the joint [66]. Also, this fluid collection of the lateral meniscus [73]. Because of this premay extend in any anatomic direction, in opposi- dilection, Saddik et al. hypothesized that the gantion to a synovial effusion with its well-­ glia of the IPFP may result from degeneration of circumscribed anatomic boundary, the joint the transverse ligament, which connects the antecapsule, which guides its extension in a more pre- rior horns of the lateral and medial meniscus [16] dictable direction [67]. Cysts and Cyst-like (Fig. 7.42). Other authors pointed to compressive

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

a

227

b

Fig. 7.41  Hoffa parameniscal cyst versus Hoffa ganglion cyst. Two PD FS images in the sagittal plane. The first image (a) belongs to a patient with a parameniscal cyst of the anterior horn of the lateral meniscus. (the same patient illustrated in 7.39 A). The continuity of the cyst with a meniscal tear from the anterior horn (black arrow a) and rupture of the cyst (dotted black arrow) with the drainage

a

b

of fluid in the deep subpatellar bursa with the appearance of bursitis are noted. The second image (b) belongs to other patient with a large ganglion cyst with a multilocular (asterisk b) and septate (small black arrows) appearance, developed in the Hoffa fatty tissue in the postero-lateral portion, in contact with the body of the lateral meniscus, (dotted line)

c

Fig. 7.42  A 27-year-old man presents with anterior knee pain and limitation of flexion and extension. T1SE in the sagittal plane and PD FS images in the sagittal and axial plane highlight in the posteromedial portion the presence

of an oval image with clearly outlined inhomogeneous hyposignal T1 and hypersignal PD FS, developed by degeneration of the anterior intermeniscal transverse ligament (arrows a–c)

injury of the meniscal periphery with resultant degenerative changes extending into surrounding soft tissues rather than within the meniscus [74, 75]. Surgical excision, aspiration, and steroid injections are treatment options; however, recurrence rates are high when managed conservatively [76].

The Cyclops Lesion A cyclops lesion is a soft tissue mass extending through the intercondylar region anterior to the ligament graft and the apex of the IPFP [16] (Fig. 7.43). The cyclops lesion is a complication after arthroscopic treatment of ACL injury [46, 77] (Figs.  7.44 and 7.45). Localized anterior

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a

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Fig. 7.43  Nodular arthophybrosis (cyclops lesion) postsurgical history of anterior cruciate ligament reconstruction (ACLR). A 32-year-old man with ACLR 2  months prior presented anterior knee pain during activity and incomplete extension of the knee. T1 SE image in the sagittal plane and PD FS images in sagittal (b), coronal (c), and axial plane (d) highlight lobular nodular image in the

a

b

d

posterior apex of Hoffa’s fat pad (arrows), with a low signal on T1 and heterogeneous signal on PD FS images. Some fluid is also surrounded (arrows a–c). The infrapatellar fat pad has internal fibrous low signal tissue (asterisk a, b). Note the integrity of the intercondylar graft (dotted arrow b)

c

Fig. 7.44  A 27-year-old man with ACL reconstruction with anterior knee pain and limited right knee extension 5 weeks after surgery. Sagittal T1 SE and PD FS images highlight the ACL graft (thick arrow) with preserved continuity in the intercondylar notch and normal MRI signal. It also highlights the presence of a fusiform soft tissue mass (small arrows a–c) in the inhomogeneous hyposig-

nal T1 SE (white asterisk a, c) and intermediary to low-­ intensity PD FS signal extending through the intercondylar region just anterior to the graft ligament and the apex of the IPFP with the appearance of localized anterior arthrofibrosis. Pseudocystic changes in Hoffa fatty tissue at the subpatellar level in hyposignal T1 SE and hypersignal PD FS (star a–c)

arthrofibrosis has around a 1–9.8% frequency rate after anterior cruciate ligament (ACL) reconstruction [78] and is known to be the second most complication after ACL reconstruction [79]. The first is graft impingement due to anterior placement of the tibial tunnel after ACL reconstruction causing knee extension loss [80]. Other reasons for loss of knee extension can be due to Hoffa’s fat pad fibrosis, knee capsular contracture, suprapatellar or intercondylar adhesions, and patellar

entrapment [80]. Loss of full extension after anterior cruciate ligament (ACL) reconstruction, with the development of an audible and palpable “clunk” with terminal extension, was first described by Jackson and Schaefer as “cyclops syndrome” [81]. This syndrome, which results from a fibrous nodule, has recently been described in patients who have sustained ACL injury but have not undergone reconstructive surgery [81]. Cyclops nodules are also described in the post-

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

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c

Fig. 7.45  A 31-year-old woman had undergone ACL reconstruction for knee instability 6  months ago. The patient presented with stiffness, pain, and difficulty in extension. On physical examination, the patient had difficulty extending her right leg.T1SE in the sagittal plane shows anterior to the tibial tunnel a small nodule in isosig-

nal with the intensity of adjacent muscles (arrow a). PD FS images in sagittal (b) and axial plane (c) confirm the presence in the deep portion of the intercondylar fossa of a small oval node with mixed-signal—peripheral intermediate and increased signal inside (white arrows b, c), delimited by synovial fluid (asterisk b, c)

traumatic knee with a clinically and radiologically intact ACL [81]. It can be attributed to microtrauma leading to subclinically torn ACL bundles in such situations [79]. The pathogenesis of the Cyclops lesion is multifactorial. It is considered a natural fibroproliferative reaction secondary to remnants after drilling, ACL stump tissue, torn graft fibers, and impingement of the exposed fibers of the ACL on the intercondylar notch [80]. It can also be a result of the inadequate placement of the graft. Histopathology of Cyclops lesion shows that it contains central granulation tissue surrounded by adjacent dense fibrous tissue. Over time, the cyclops evolve from an early stage showing fibrosis to a late stage showing fibrocartilaginous dense, soft tissue. MR imaging is the modality for identifying cyclops nodules after ACL reconstruction. In 31 patients, Bradley et  al. found MR imaging to be 85% sensitive, 85% specific, and 85% accurate in ­ detecting cyclops nodules [46]. Magnetic resonance imaging is the primary postoperative investigative tool to evaluate failed ACL reconstruction and complications such as cyclops lesions, graft instability, disruption, extension loss, and hardware fracture. Magnetic resonance imaging is also a modality for postoperative reinjury and preoperative planning for repeat surgery [81].

7.3.2.2 Hoffa’s Fat Pad Anterior Extracapsular Disorders The articular cavity of the knee is limited anteriorly and extracapsular by the extensor system composed of the quadriceps tendon, patella, patellar ligament, and tibial tubercle. If the extent of anterior extracapsular disorders is significant, the adjacent infrapatellar fat pad may be involved [1]. Examples of such involvement include patellar contusion (Fig.  7.46), patellar fracture (Fig.  7.47), and patellar sleeve fracture (Fig. 7.48). A patellar slip fracture is defined as an avulsion of a small fragment of bone from the distal pole of the patella, along with its articular cartilage, periosteum, and retinaculum, which is removed from the main body of the patella. An acute injury causes the fracture due to the strong contraction of the quadriceps with the knee bent [82]. Other extracapsular disorders lesions that affect Hoffa fatty tissue are patellar tendon rupture (Fig. 7.49), fragmentation of the tibial tubercle (Fig.  7.50), Sinding-Larsen-Johansson disease (Fig.  7.51), Osgood-Schlatter’s disease (Fig. 7.52), and direct injuries to the anterior face of the knee (Fig. 7.53).

230

a

Fig. 7.46  Contusion of the lower half of the patella with inflammation of the Hoffa fatty tissue. T1 SE image (a) and PD FS (b), in the sagittal plane highlight an area of bone contusion in the lower half of the patella (asterisk a,

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

b

b), associated with inflammation of the Hoffa fatty tissue expressed by the presence of linear beams in hyposignal T1 and hypersignal PD FS (star a, b)

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

Fig. 7.47  Comminutive fracture in the upper half of the patella involving Hoffa fatty tissue in a 47-year-old man with patella Alta. T1 SE image in the sagittal plane highlights a comminutive fracture in the patella’s upper half, expressed by a complete oblique linear trajectory (white arrow) and two small fragments grouped without displacement (circle image). The appearance of chronic hoffitis expressed by the reduced volume of the infrapatellar fatty tissue (double arrow) and vertical fibrous lines (black dotted arrows) in hyposignal T1 SE. Patellar chronic tendinopathy (black arrows)

231

Fig. 7.48 A 14-year-old girl with Sinding-Larsen-­ Johansson disease, patellar sleeve fracture, and secondary hoffitis. Sagittal T1SE imaging shows repetitive posttraumatic damage of the proximal end of the patellar tendon inserted into the inferior pole of the patella. Avulsion of a small bone fragment (white arrow) from the cortex of the lower pole of the patella (black arrows) and its inclusion in the proximal portion of the patellar tendon (dotted arrow) that appears thickened (double arrow). It represents a chronic traction injury of the immature osteotendinous insertion—the appearance of secondary chronic hoffitis (star)

232

a

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

b

Fig. 7.49 A 37-year-old man with edematous-­ Edematous-hemorrhagic infiltration of intra-Hoffatic hemorrhagic infiltration of the Hoffa tissue after acute areas with diffuse increased signal intensity (star a, b), rupture of the patellar tendon. Sequential PD FS image in with the appearance of secondary acute hoffitis. Note fluid the mediosagittal plane (a) and medial-parasagittal (b) accumulation and distension of the suprapatellar synovial shows complete rupture of the patellar tendon at the tibial recess (double arrows a, b) with the prefemoral fat cominsertion (black arrow in circle a) and incomplete rupture pressive effect (thin dotted white arrows a, b). Fluid-­ in the medial parasagittal plane (black arrow in circle b), hemorrhagic accumulation, distension of the posterior and reactive small fluid accumulation in the deep infrapa- capsule (thick white arrow a, b), and Jumper’s knee tenditellar bursa (asterisk a, b). Small bone fragments detached nopathy (black dotted arrow) from the tibial spine (thick white dotted arrow).

7.3  MRI Pathological Findings of Infrapatellar Fat Pad

a

Fig. 7.50  Fragmentation of the tibial tubercle with the involvement of Hoffa fatty tissue in a 27-year-old man. T1SE and PD FS images in the sagittal plane highlight the fragmentation of the tibial tubercle (black arrow a and white arrow b), with the avulsion of small bone fragments

a

Fig. 7.51 A 13-year-old girl with Sinding-Larsen-­ Johansson disease and superior secondary hoffitis. Sagittal PD FS imaging (a) shows repetitive posttraumatic damage of the proximal end of the right patellar tendon as it inserts into the inferior pole of the patella (black arrow) and a

233

b

in the deep infrapatellar bursa (black dotted arrow a and white dotted arrow b), and fluid-hemorrhagic accumulation in the bursa and Hoffa tissue (asterisk a, b). The appearance of acute hoffitis in the posterosuperior portion (star)

b

small area of contusion at the inferior pole of the patella (white arrow). The zoomed PD FS (b) image highlights the secondary edematous infiltration in the upper portion of the Hoffa fatty tissue (asterisk)

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Fig. 7.52  A 19-year-old boy with Osgood-Schlatter’s disease associated with chronic hoffitis. Sagittal T1 SE highlights the appearance of patella Alta (ISI-1.5) and the presence of a small bone fragment detached from the anterior contour of the tibial epiphysis embedded in the patellar tendon (white arrow). The appearance of chronic hoffitis expressed by the presence of vertical fibrous bands of different thicknesses in hyposignal T1SE (black arrows)

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

Fig. 7.53  Direct trauma to the anterior compartment of the knee, associated with secondary inflammation of Hoffa tissue (hoffitis). A 34-year-old man with anterior knee pain after a trauma to the left knee by falling off a motorcycle. PD FS image in the sagittal plane highlights hemorrhagic edematous infiltration of the patellar tendon, anterior soft tissues, the anteroinferior portion of the patella (double arrow and asterisk), and the anterosuperior portion of the tibial epiphysis (asterisk in the circle). Associated with inflammation and secondary hypertrophy of the infrapatellar adipose tissue with inhomogeneous increased signal intensity (star), that suggest acute posttraumatic hoffitis. Note interruption of ACL graft (dotted arrow)

7.4 MRI Pathological Findings of Suprapatellar Fat Pad Introduction There are suprapatellar fat pads: anterior quadriceps fat pad and posterior prefemoral fat pad. During normal flexion-extension of the knee, the anterior quadriceps suprapatellar fat pad prevents friction between the quadriceps tendon and femoral condyle, and the posterior prefemoral fat pad prevents direct contact between the patella and distal shaft of the femur.

7.4  MRI Pathological Findings of Suprapatellar Fat Pad

7.4.1 MRI Pathological Findings of Anterior (Quadriceps) Suprapatellar Fat Pad Quadriceps Fat Pad Lesion The quadriceps or suprapatellar fat pad is a normal fat pad positioned between the distal ­ quadriceps tendon anteriorly and the suprapatellar recess posteriorly. It usually measures 6 mm (range, 4–8  mm) in women and 7  mm (range, 5–9 mm) in men [25]. The quadriceps fat pad (QFP), also called the suprapatellar fat pad, is located between the quadriceps tendon and the suprapatellar recess of the knee joint. It is the smallest fat pad and has a triangular shape with an average thickness of eight ±2 mm in men and seven ±2 mm in women [25, 26]. The gap is between the posterior part of the quadriceps tendon and the superior posterior aspect.It is separated posteriorly from the prefemoral fat pad by the joint recess. The suprapatellar recess, an extension of the knee joint, does not possess a capsule. Therefore, the posterior surface of the quadriceps fat pad and a segment of the distal quadriceps tendon are lined with synovium [25]. These synovial-lined surfaces come in contact with the trochlea during knee flexion, increasing the extensor mechanism’s congruency. a

b

Fig. 7.54 A 27-year-old male basketball player with anterior knee pain. PD FS images in the sagittal plane (a) coronal (b), and axial (c) show suprapatellar fat-pad

235

An additional anterior knee structure, the articular muscle, is found deep relative to the quadriceps muscle, is present in all individuals, and is routinely visualized on MR images [83]. It originates from the femur as one to seven muscle bundles and inserts on the suprapatellar recess. It applies tension to the suprapatellar recess during knee extension, protecting the relatively redundant suprapatellar recess from entrapment between the femur and the patella [83]. The criterion for the quadriceps fat pad mass effect on the suprapatellar recess is a posterior convex border [26] (Fig. 7.54). The quadriceps tendon is continuous with the fat pad and contains the most adipose tissue between its fibers at its enthesis, also called endotenon fat [28]. The term ‘quadriceps fat-pad impingement’ syndrome (QFPIS) has been used to describe an inflammatory process within the anterior suprapatellar fat, manifested on MRI as a high PD FS signal, low T1 signal, and mass effect on the quadriceps tendon. Quadriceps fat pad syndrome (QFPIS) is a rare cause of anterior knee pain and is characterized clinically by tenderness over the superior pole of the patella and pain on deep knee flexion [26, 39] (Fig. 7.55). In symptomatic cases, true impingement is described with compression of the fat pad between the posterior surface of the quadriceps tendon, the superior

c

swelling indicated by convex posterior border (arrow a) and high signal intensity of suprapatellar fat pad (asterisk a–c). No other internal derangement not identified

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a

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

b

Fig. 7.55  A 44-year-old man with Quadriceps fat pad impingement syndrome (QFPIS) and tenderness over the superior pole of the patella and pain on deep knee flexion. T1 SE (a) and PD FS (b) images in the sagittal plane highlight hypertrophy of the suprapatellar fat pad (black double arrow a, b) with a typical convex appearance (white

dotted arrow a, b). Accumulation with fluid signal in the distal part of the suprapatellar synovial recess (white star a, black star b). Note, articularis genus muscle prevents the synovial membrane’s impingement between the patella and the femur (white arrow a, b) [92]

edge of the patella, the medial patellar synovial recess, and even the trochlea on maximum knee flexion (Fig. 7.56). Similar to Hoffa’s syndrome, histological changes have been reported [27] with an inflammatory reorganization, vasculitis with vascular thrombosis, and metaplasia [84]. In the absence of clinical findings, a diagnosis of QFPIS cannot be made based solely on MRI findings because quadriceps fat pad edema (QFPE) may be present in the absence of anterior knee pain [26, 27]. Oedema of the suprapatellar fat pad is found in 12–14% of patients undergoing knee MR imaging, but its relationship to anterior knee pain is controversial [28, 29]. In other words, QFPS is a clinical entity; however, QFPE is an imaging finding and may be related to anterior knee pain (Fig.  7.57) or may not [39] (Fig.  7.58). Similar histologic changes suggest suprapatellar fat pad

edema may be similar to Hoffa disease [28]. However, it has also been suggested that suprapatellar fat pad edema may result from repetitive friction against the trochlea during high-angle knee flexion. The term “impingement” has been increasingly used for suprapatellar fat pad edema [7, 23, 34], although no evidence supports this condition’s mechanical origin. Prior retrospective studies showed no association between suprapatellar fat pad edema and measurement of patellar maltracking [29]. On MRI imaging, suprapatellar fat edema shows an increase in size with heterogeneous signal strength compared to subcutaneous fat with a convex posterior edge and mass effect on suprapatellar joint recess, with high signal on fat-saturated images and sensitivity to fluid and low signal on T1-weighted images (lower than subcutaneous fat).

7.4  MRI Pathological Findings of Suprapatellar Fat Pad

a

b

d

c

e

Fig. 7.56  A 27-year-old man with tenderness over the superior pole of the patella and by deep palpation of the quadriceps tendon. T1 SE (a) and PD FS images in the sagittal plane (b, e), coronal plane (c), and axial plane (d) highlight the suprapatellar fat pad in hyposignal on the T1 SE (white asterisk a) and hypersignal in PD FS (b–e),

a

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b

Fig. 7.57  A 20-year-old woman athlete with tenderness over the superior pole of the patella. T1 SE (a) and PD FS images in coronal (b) and axial planes highlight quadriceps fat pad edema that occurs in hyposignal T1 (asterisk

compatible with an edematous substrate. Zoom image in sagittal PD FS (e) highlights myxoid-edematous infiltration of both vastus medial, lateral, and intermediate tendons with interruption of some fibers consistent with partial rupture of the quadriceps tendon, associated with the insertional tendinitis/tendinosis (arrows e)

c

a) and hypersignal PD FS (asterisk b, c). Note the absence of sensitivity and pain on palpation of the patellar insertion of the quadriceps tendon and the upper pole of the patella

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b

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d

Fig. 7.58  A 40-year-old woman with 2 months of anterior right knee pain and movement restriction history. Sagittal T1 SE image (a) shows mild hypertrophy of the quadriceps suprapatellar fat pad (QSFD) and moderate hyposignal representing edematous infiltration (white asterisk a) compared to the intensity of the fat under the

skin (black asterisk a). PD FS images in sagittal (b), coronal(c), and axial (d) planes confirm QSFD hypertrophy and edematous substrate that induces mass effect on suprapatellar joint recess (short arrow b) and prefemoral fat pad in the distal portion (double asterisk c, d)

7.4.2 MRI Pathological Findings of Suprapatellar Posterior Prefemoral Fat Pad

suprapatellar bursa [85]. With the knee at maximum extension, this fat pad may be compressed between the posterior surface of the patella and the anterior femoral cortex, resulting in chronic impingement rarely described in the literature [85, 86]. However, a rare clinical finding and less known than the anterior suprapatellar and infrapa-

The posterior suprapatellar, or prefemoral, fat pad is located anterior to the femur and is separated anteriorly from the quadriceps fat pad by the

7.4  MRI Pathological Findings of Suprapatellar Fat Pad

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d

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f

Fig. 7.59  Prefemoral fat pad impingement syndrome (PFPIS) induced by tumoral lesion causing the fatty tissues of the anterodistal femur to impinge. A woman 47-year-old with anterior pain of the right knee, which appeared insidious a month ago during prolonged walking, and later at rest and when climbing stairs. T1 SE (a) and PD FS images in sagittal(b), axial (c), coronal (d), highlights distally, at the level of the prefemoral fat pad and retropatellar in the proximal half, the presence of a

fusiform mass with inhomogeneous hyposignal in all sequences (arrows a–d), with mass effect on the prefemoral fat as prefemoral fat pad impingement syndrome. The image t2med3  in the axial plane (arrow image e) highlights the aspect of magnetic susceptibility due to the hemosiderin content. The patient underwent arthroscopic surgery, and the histopathological examination established the diagnosis of villonodular synovitis (image f)

tellar fat pad, prefemoral fat pad impingement syndrome (PFPIS), is considered one of the underlying causes of anterior knee pain (AKP) [85, 87, 88]. PFPIS is generally induced by tumorous lesions (Fig.  7.59). That occurs at the same site, such as lipomas (Fig. 7.60) and lipoma arborescent, causing the fatty tissues of the anterodistal femur to impinge—however, very few reports of PFIS induced by normal adipose tissue. Suguru Koyama and his colleagues reported a case of PFIS caused by normal adipose tissue located superolateral to the patellofemoral joint (PF) and inside the suprapatellar sac, which was excised on

arthroscopic examination [89]. A similar case is presented in (Fig. 7.61). Prefemoral FPIS is associated with an edematous and hyperplasia fat pad [88] with superficial non-­ encapsulated fibrous changes. It often presents a mass-like protrusion of fatty tissue into the suprapatellar pouch and a small joint effusion. These findings are most easily evident on MRI. Patients may report anterior knee pain proximal to the superior pole of the patella. In addition, intermittent mechanical symptoms can occur if the fibrotic fat pad snaps over the femoral, exacerbated by knee extension and prolonged standing (Fig. 7.62).

7  Intracapsular and Extra Synovial Peripatellar Fat Pads

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a

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Fig. 7.60 Prefemoral fat pad impingement (PFPIS) induced by nodular lesion, causing the anterodistal femur’s fatty tissues to impinge. A 21-year-old man with anterior pain of the right knee during prolonged walking and restriction in the range of motion when climbing stairs.T1 SE (a) and PD FS images in sagittal (b) highlight

a

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Fig. 7.61  Prefemoral fat pad impingement syndrome (PFPIS) induced by normal adipose prefemoral tissue. A 43-year-old woman with a difficulty in walking. One week before the presentation, she experienced discomfort in the right anterior knee joint with no prior injury, and the symptom progressed into pain the following period. There was no joint swelling, but the patient showed severe restriction in the range of motion due to pain. There was

a nodular, oval mass, of 1.2 / 0.8 cm, with inhomogeneous isosignal T1 and PD FS, within the prefemoral fat pad. Minimal synovial reaction in deep infrapatellar synovial recess (dotted arrow b). The patient underwent arthroscopic surgery, and the histopathological examination established the diagnosis of fibrolipoma

c

tenderness at the medial femorotibial (PF) joint and the proximal side of the PF joint. T1 SE (a) and PD FS images in sagittal (b) and axial plane (c) revealed the prefemoral fat pad (asterisk a–c) with normal signal in T1 and PD FS images. The hyperplasia of the fat pad was located superomedially and into the medial femoropatellar joint (double arrow); there were mild synovial reactions (asterisk c) and no fibrous septa

References

a

241

b

Fig. 7.62  Prefemoral fat pad impingement syndrome (PFPIS) induced by posttraumatic rupture of distal prefemoral fat following lateral patellar dislocation. T1 SE in the sagittal plane (a) and PD FS images in sagittal (b) and axial plane (c) highlight an image with an irregular oval appearance, detached from the middle portion of the prefemoral fat in homogeneous hypersignal (T1) and

References 1. Jacobson JA, Lenchik L, Ruhoy MK, Schweitzer ME, Resnick D. MR imaging of the infrapatellar fat pad of Hoffa. Radio Graphics. 1997;17:675–91. 2. Draghi F, Ferrozzi G, Urciuoli L, Bortolotto C, Bianchi S.  Hoffa’s fat pad abnormalities, knee pain and magnetic resonance imaging in daily practice. Insights Imaging. 2016;7:373–83. https://doi. org/10.1007/s13244-­016-­0483-­8. 3. Magi M, Barca A, Bucca C, Langerance V. Hoffa disease. Ital Onhop Traumatol. 1991;17:211–6. 4. de Lange-Brokaar BJ, Ioan-Facsinay A, van Osch GJ, Zuurmond AM, Schoones J, Toes RE, et  al. Synovial inflammation, immune cells and their cytokines in osteoarthritis: a review. Osteoarthr Cartil. 2012;20:1484e99. 5. Roemer FW, Jarraya M, Felson DT, Hayashi MD, Crema D, Loeuille AG.  Magnetic resonance imaging of Hoffa’s fat pad and relevance for osteoarthritis research: a narrative review. Osteoarthr Cartil. 2016;24:383e397. 6. Schweitzer ME, Falk A, Benhoty D, Mitchell M, Resnick D.  Knee effusion: normal distribution of fluid. AJR. 1992;159:361–3. 7. Jiang L-F, Fang J-H, Li-Dong W. Role of infrapatellar fat pad in osteoarthritis: pathological process of knee osteoarthritis: future applications in treatment. World J Clin Cases. 2019;7(16):2134–42. https://doi. org/10.12998/wjcc.v7.i16.2134. 8. Nakano T, Wang YW, Ozimek L, Sim JS.  Chemical composition of the infrapatellar fat pad of swine. J Anat. 2004;204:301–6. https://doi.org/10.1111/ j.0021-­8782.2004.00283.x. [PMID: 15061756]

c

hyposignal (PDFS), [star image a, b], migrated distally in the suprapatellar synovial recess with moderate fluid accumulation. Notes-lateral patellar subluxation (thick white arrw), also can see trochlear Dejour dysplasia type C (dotted curved line) and fluid accumulation in the retro pattelar space (dotted black arrrow)

9. Davies DV, White JE.  The structure and weight of synovial fat pads. J Anat. 1961;95:30–7. [PMID: 13720093] 10. MacConaill MA. The movements of bones and joints; the synovial fluid and its assistants. J Bone Joint Surg Br. 1950;32-B:244–52. https://doi.org/10.1302/0301-­ 620X.32B2.244. [PMID: 15422026] 11. Kohn D, Deiter S, Ruden M. Arterial blood supply of the infrapatellar fat pad. Anatomy and clinical consequences. Arch Orthop Trauma Surg. 1995;114(2):72– 5. https://doi.org/10.1007/BF00422828. 12. Biedert RM, Sanchis-Alfonso V. Sources of anterior knee pain. Clin Sports Med. 2002;21:335e47. vii. 13. Witonski D, Wagrowska-Danielewicz M. Distribution of substance-P nerve fibers in the knee joint in patients with anterior knee pain syndrome. A ­ preliminary report. Knee Surg Sports Traumatol Arthrosc. 1999;7:177e83.29. 14. 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;26:773e7. 15. Clockaerts S, Bastiaansen-Jenniskens YM, Runhaar J, Van Osch GJ, Van Offel JF, Verhaar JA, et  al. The infrapatellar fat pad should be considered as an active osteoarthritic joint tissue: a narrative review. Osteoarthr Cartil. 2010;18:876e82. 16. Saddik D, McNally EG, Richardson M.  MRI of Hoffa’s fat pad. Skelet Radiol. 2004;33:433e44. 17. Pan F, Han W, Wang X, Liu Z, Jin X, Antony B, et al. A longitudinal study of the association between infrapatellar fat pad maximal area and changes in knee symptoms and structure in older adults. Ann Rheum Dis. 2014; https://doi.org/10.1136/ annrheumdis-­2013-­205108.

242 18. Ioan-Facsinay A, Kloppenburg M.  An emerging player in knee osteoarthritis: the infrapatellar fat pad. Arthritis Res Ther. 2013;15:225. 19. Conde J, Scotece M, Lopez V, Abella V, Hermida M, Pino J, et al. Differential expression of adipokines in infrapatellar fat pad (IPFP) and synovium of osteoarthritis patients and healthy individuals. Ann Rheum Dis. 2014;73:631e3. 20. Eymard F, Pigenet A, Citadelle D, FlouzatLachaniette CH, Poignard A, Benelli C, et  al. Induction of an inflammatory and prodegradative phenotype in autologous fibroblast-like synoviocytes by the infrapatellar fat pad from patients with knee osteoarthritis. Arthritis. Rheumatol. 2014;66:2165e74. 36e38. 21. Klein-Wieringa IR, Kloppenburg M, BastiaansenJenniskens YM, Yusuf E, Kwekkeboom JC, El-Bannoudi H, et  al. The infrapatellar fat pad of patients with osteoarthritis has an inflammatory phenotype. Ann Rheum Dis. 2011;70:851e7. 22. Diepold J, Ruhdorfer A, Dannhauer T, Wirth W, Steidle E, Eckstein F.  Sex-differences of the healthy infra-patellar (Hoffa) fat pad in relation to intermuscular and subcutaneous fat content e data from the osteoarthritis initiative. Ann Anat. 2015;200C:30e6. https://doi.org/10.1016/j. aanat.2014.12.004. 23. Brukner P, Khan K. Anterior knee pain. In: Clinical sports medicine. 3rd ed. Sydney: McGraw-Hill; 2006. p. 464–94. 24. Bohnsack M, Wilharm A, Hurschler C, Rühmann O, Stukenborg-Colsman C, Wirth CJ.  Biomechanical and kinematic influence of a total infrapatellar fat pad resection on the knee. Am J Sports Med. 2004;32:1873–80. 25. Staeubli HU, Bollmann C, Kreutz R, Becker W, Rauschning W.  Quantification of intact quadriceps tendon, quadriceps tendon insertion, and suprapatellar fat pad: MR arthrography, anatomy, and cryosections in the sagittal plane. AJR. 1999;173:691–8. 26. Roth C, Jacobson J, Jamadar D, Caoili E, Morag Y, Housner J.  Quadriceps fat pad signal intensity and enlargement on MRI: prevalence and associated findings. AJR. 2004;182:1383–7. 27. Shabshin N, Schweitzer ME, Morrison WB.  Quadriceps fat pad edema: significance on ­magnetic resonance images of the knee. Skeletal Radiol. 2006;35:269–74. 28. Apostolos NT, Karantanas H.  Suprapatellar fat-pad mass effect: MRI findings and correlation with anterior knee pain. AJR. 2013;200:W291–6. https://doi. org/10.2214/AJR.12.8821. 29. Singh VK, Shah G, Singh PK, Saran D. Extraskeletal ossifying chondroma in Hoffa’s fat pad: an unusual cause of anterior knee pain. Singap Med J. 2009;50(5):e189–92. 30. Hoffa A.  The influence of the adipose tissue with regard to the pathology of the knee joint. JAMA. 1904;43:795–6. 31. Kumar D, Alvand A, Beacon JP.  Impingement of infrapatellar fat pad (Hoffa’s disease): results of

7  Intracapsular and Extra Synovial Peripatellar Fat Pads high-portal arthroscopic resection. Arthroscopy. 2007;23:1180–6. e1181 32. Brukner PD, McConnell J, Bergman AG, Bealieu CF, Matheson GO.  Infrapatellar fat pad impingement: correlation between clinical and MR findings. Med Sci Sports Exerc. 1999;31(5 Supplement):S294. 33. Schwaiger BJ, Wamba JM, Gersing AS, Nevitt MC, McCulloch CE, Link TM. Signal intensity alteration in the suprapatellar fat pad is associated with degeneration of the patellofemoral joint over 48 months – data from the osteoarthritis initiative. Osteoarthr Cartil. 2016;24:S267–8. 34. Chung CB, Skaf A, Roger B, Campos J, Stump X, Resnick D.  Patellar tendon-lateral femoral condyle friction syndrome: MR imaging in 42 patients. Skelet Radiol. 2001;30:694–7. 35. Cothran RL, McGuire PM, Helms CA, Major NM, Attarian DE. MR imaging of infrapatellar plica injury. AJR Am J Roentgenol. 2003;180:1443e7. 36. Barbier-Brion B, Lerais J-M, Aubry S, Lepage D, Vidal C, Delabrousse E, Runge M, Kastler B.  Magnetic resonance imaging in patellar lateral femoral friction syndrome (PLFFS): prospective case-­ control study, diagnostic and interventional. Imaging. 2012;93:e 171–e18. 37. Widjajahakim R, Guermazi A, Jarraya M, et  al. The relation of patellofemoral joint alignment and trochlear morphology to superolateral Hoffa’s fat pad edema: the most study. Osteoarthr Cartil. 2016;24:S423. 38. Mehta K, Wissman R, England E, Dheurle A, Newton K, Kenter K.  Superolateral Hoffa’s fat pad edema in collegiate volleyball players. J Comput Assist Tomogr. 2015;39:945–50. 39. Jarraya M, Diaz LE, Roemer FW, Arndt WF, Goud AR, Guermazi A. MRI findings consistent with peripatellar fat pad impingement: how much related to patellofemoral Maltracking? Magn Reson Med Sci. 2018;17:195–202. https://doi.org/10.2463/mrms. rev.2017-­0063. 40. Campagna R, Pessis E, Biau DJ, et al. Is superolateral Hoffa fat pad edema a consequence of impingement between lateral femoral condyle and patellar ligament? Radiology. 2012;263:469–74. 41. De Smet AA, Davis KW, Dahab KS, Blankenbaker DG, del Rio AM, Bernhardt DT. Is there an association between superolateral Hoffa fat pad edema on MRI and clinical evidence of fat pad impingement? AJR Am J Roentgenol. 2012;199:1099–104. 42. Jibri Z, Martin D, Mansour R, Kamath S. The association of infrapatellar fat pad oedema with patellar maltracking: a case-control study. Skelet Radiol. 2012;41:925–31. 43. Matcuk GR, Cen SY, Keyfes V, Patel DB, Gottsegen CJ, White E, A.  Superolateral Hoffa fat-pad edema and patellofemoral maltracking: predictive modeling. AJR Am J Roentgenol. 2014;203:W207–12. 44. Larbi A, et  al. Hoffa’s disease: A report on 5 cases, ­ diagnostic and interventional. Imaging. 2014;95:1079–84. https://doi.org/10.1016/j. diii.2014.06.009.

References 45. Maheshwari AV, Jain AK, Dhammi IK. Extraskeletal paraarticular osteochondroma of the knee  – a case report and tumor overview. Knee. 2006;13:41–414. 46. Bradley DM, Bergman AG, Dillingham MF.  MR imaging of cyclops lesions. AJR Am J Roentgenol. 2000;174(3):719–26. 47. Turhan E, Doral MN, Atay AO, Demirel M. A giant extrasynovial osteochondroma in the infrapatellar fat pad: end stage Hoffa’s disease. Arch Orthop Trauma Surg. 2008;128(5):515–9. Epub 2007 Jul 24 48. Helpert C, Davies AM, Evans N, Grimer RJ. Differential diagnosis of tumours and tumour-like lesions of the infrapatellar (Hoffa’s) fat pad: pictorial review with an emphasis on MR imaging. Eur Radiol. 2004;14:2337–46. 49. Krebs VE, Parker RD.  Anhroscopic resection of an extrasynovial ossifying chondroma of the infrapatellar fat pad: end-stage Hoffa’s disease? Anhroscopy. 1994;10:301–4. 50. Ingabire MI, Deprez FC, Bodart A, T.  Puttemans1, soft tissue chondroma of Hoffa’s fat pad. JBR–BTR. 2012;95:15–7. 51. Jelinek JS, Kransdorf MJ, Utz JA, et  al. Imaging of pigmented villonodular synovitis with emphasis on MR imaging. AJR. 1989;152:337–42. 52. Cavanaugh RC, Schwamm HA.  Radiologic pathologic correlation of the month from AFIP. Radiology. 1971;100:409–14. 53. Huang G, Lee C, Chan WP, Chen CY, Yu JS, Resnick D. Localized nodular synovitis of the knee: MR imaging appearance and clinical correlates in 21 patients. Am J Roentgenol. 2003;181:539–43. 54. Hantes ME, Basdekis GK, Zibis AH, Karantanas AH, Malizos KN.  Localized pigmented villonodular synovitis in the anteromedial compartment of the knee associated with cartilage lesions of the medial femoral condyle: report of a case and review of the literature. Knee Surg Sports Traumatol Arthrosc. 2005;13:209–12. 55. Mandelbaum BR, Grant TT, Hanzman S, et  al. The use of MRI to assist in diagnosis of pigmented villonodular synovitis of the knee joint. Clio Onhop. 1986;231:135–9. 56. Reicher MA. The spectrum of knee joint disorders. In: Mink JH, Reicher MA, Crues III JV, Deutsch AL, editors. MRI of the knee. 2nd ed. New York, NY: Raven; 1993. p. 333–99. 57. Shahriaree H.  Anhroscopic technique and normal anatomy. In: Shahriaree H, editor. O’Connors textbook of arthroscopic surgery. 2nd ed. Philadelphia, PA: Lippincott; 1992. p. 255–83. (Fig 8). 58. Robenson PL, Schweitzer ME, Banolozzi AR, Ugoni A.  Anterior cruciate ligament tears: evaluation of multiple signs with MR imaging. Radiology. 1994;193:829–34. 59. Anderson JJ, Connor GF, Helms CA.  New observations on meniscal cysts. Skelet Radiol. 2010;39(12):1187–91.[7] 60. Campbell SE, Sanders TG, Morrison WB. MR imaging of meniscal cysts: incidence, location, and clinical

243 significance. The American Journal of oentgenology. 2001;177(2):409–13. 61. de Smet AA, Graf BK, Del Rio AM. Association of parameniscal cysts with underlying meniscal tears as identified on MRI and arthroscopy. The American Journal of Roentgenology. 2011;196(2):W180–6. 62. Burk DL, Dalinka MK, Kanai E, et al. Meniscal and ganglion cysts of the knee: MR evaluation. AJR. 1988;150:331–6. 63. McCarthy CL, NcNally EG.  The MRI appearance of cystic lesions around the knee. Skelet Radiol. 2004;33:187–209. 64. Chen H. Diagnosis and treatment of a lateral meniscal cyst with musculoskeletal ultrasound. Case Rep Orthop. 2015;2015:432187, 3 pages. https://doi. org/10.1155/2015/432187. 65. Hulet C, Souquet D, Alexandre P, Locker B, Beguin J, Vielpeau C.  Arthroscopic treatment of 105 lateral meniscal cysts with 5-year average follow-up. Arthroscopy. 2004;20(8):831–6. 66. Francesca D, Beaman MD, Jeffrey J, Peterson MD. MR imaging of cysts, ganglia, and bursae about the knee. Radiol Clin N Am. 2007;45(6):969–82. 67. Giard M-C, Pineda C. Ganglion cyst versus synovial cyst? Ultrasound characteristics through a review of the literature. Rheumatol Int. 2014; https://doi. org/10.1007/s00296-­014-­3120-­1. 68. Kim JY, Jung SA, Sung MS, Park YH, Kang YK. Extra- articular soft tissue ganglion cyst around the knee: focus on the associated findings. Eur Radiol. 2004;14(1):106–11. 69. Bui-Mansfield LT, Youngberg RA.  Intraarticular ganglia of the knee: prevalence, presentation, etiology, and management. AJR Am J Roentgenol. 1997;168(1):123–7. 70. Narváez JA, Narváez J, Aguilera C, De Lama E, Portabella F.  MR imaging of synovial tumors and tumor-like lesions. Eur Radiol. 2001;11(12):2549–60. 71. Janzen DL, Petefy CG, Forbes JR, Tirman PFJ, Genant HK. Cystic lesions around the knee joint: MR imaging findings. AJR. 1994;I63:155–61. 72. Marra MD, Crema MD, Chung M, et  al. MRI features of cystic lesions around the knee. Knee. 2008;15(6):423–38. 73. Kim MG, Kim BH, Choi JA, Lee NJ, Chung KB, Choi YS, et  al. Intra-articular ganglion cysts of the knee: clinical and MR imaging features. Eur Radiol. 2001;11:834e40. 74. Pedowitz RA, Feagin JA, Rajagopalan S. A surgical algorithm for treatment of cystic degeneration of the meniscus. Arthroscopy. 1996;12:209e12. 75. Lantz B, Singer KM.  Meniscal cysts. Clin Sports Med. 1990;9:707e25. 76. Prasad N, Kalekar T, Kharat A. A large lateral parameniscal cyst of the knee associated with bucket handle tear. 2020; https://doi.org/10.35100/eurorad/ case.17027. Published on 03.11.2020 77. Dhanda S, Sanghvi D, Pardiwala D.  Case series: cyclops lesion  - extension loss after

244 ACL reconstruction. Indian J Radiol Imaging. 2010;20:208–10. 78. Pujol N, Colombet P, Potel JF, Cucurulo T, Graveleau N, Hulet C, et  al. Anterior cruciate ligament reconstruction in partial tear: selective anteromedial bundle reconstruction conserving the posterolateral remnant versus single-bundle anatomic ACL reconstruction: preliminary 1-year results of a prospective randomized study. Orthop Traumatol Surg Res. 2012;98:S171–7. 79. Kharat A, Garg S, Singh A, Kulkarni V.  Magnetic resonance imaging of cyclops lesion as a cause of persistent morbidity after anterior cruciate ligament reconstruction. www.mjdrdypu.org, DOI:https://doi. org/10.4103/0975-­2870.169932. 80. Recht MP, Piraino DW, Cohen MA, Parker RD, Bergfeld JA.  Localized anterior arthrofibrosis (cyclops lesion) after reconstruction of the anterior cruciate ligament: MR imaging findings. AJR Am J Roentgenol. 1995;165:383–5. 81. Runyan BR, Bancroft LW, Peterson JJ, Kransdorf MJ, Berquist TH, Ortiguera CJ. Cyclops lesions that occur in the absence of prior anterior ligament reconstruction. Radiographics. 2007;27:e26. 82. Xie L, Xu H, Zhang L, Xu R, Guo Y. Sleeve fracture of the adult patella: case report and review of the literature. Medicine. 2017;96(32):e7096. https://doi. org/10.1097/MD.0000000000007096. 83. Puig S, Dupuy DE, Sarmiento A, Boland GW, Grigoris P, Greene R.  Articular muscle of the knee: a muscle seldom recognized on MR imaging. AJR. 1996;166:1057–60. 84. Huberti HH, Hayes WC, Stone JL, Shybut GT. Force ratios in the quadriceps tendon and ligamentum patellae. J Orthop Res. 1984;2:49–54.

7  Intracapsular and Extra Synovial Peripatellar Fat Pads 85. Borja MJ, Jose J, Vecchione D, Clifford PD, Lesniak B. Prefemoral fat pad impingement syndrome: identification and diagnosis. Am J Orthop. 2013;42:E9–11. 86. Grando H, Chang EY, Chen KC, Chung CB.  MR imaging of extrasynovial inflammation and impingement about the knee. Magn Reson Imaging Clin N Am. 2014;22:725–41. 87. F. Lapègue, N. Sans et al, Imaging of traumatic injury and impingement of anterior knee fat, https://doi. org/10.1016/j.diii.2016.02.012. 2211-5684/© 2016 Editions fran¸ caises de radiologie. Published by Elsevier Masson SAS 88. Kim YM, Shin HD, Yang JY, Kim KC, Kwon ST, Kim JM.  Prefemoral fat pad: impingement and a mass-­ like protrusion on the lateral femoral condyle causing mechanical symptoms. A case report. Knee Surg Sports Traumatol Arthrosc. 2007; 89. Koyama S, Tensho K, Shimodaira H, Iwaasa T, Horiuchi H, Kato H, Saito N.  Hyperplastic fat pad. 2018;2018:3583049. https://doi. org/10.1155/2018/3583049. 90. LaPrade RF.  The anatomy of the deep infrapatellar bursa of the knee. Am J Sports Med. 1998;26(1):129–13. 91. Wickham MQ, Erickson GR, Gimble JM, Vail TP, Guilak F. Multi- potent stromal cells derived from the infrapatellar fat pad of the knee. Clin Orthop Relat Res. 2003;412:196–212. 92. Grob K, Gilbey H, Manestar M, Ackland T, Kuster MS.  The anatomy of the articularis genus muscle and its relation to the extensor apparatus of the knee. JB JS Open Access. 2017;2(4):e0034. https:// doi.org/10.2106/JBJS.OA.17.00034. Published online 2017 Nov 28, PMCID: PMC6133144,PMID: 30229230

8

Intra-articular Structures, the Synovial Lining, Patellofemoral Osteoarthritis

8.1 Introduction The knee’s synovial membrane is the knee capsule’s inner aspect which produces synovial fluid to aid in the lubrication of the knee joint and provides nourishment through diffusion. It is also reflected in the articular margins of the femur, tibia, and patella. It does not cover the menisci or the cruciate ligaments posteriorly and is separated from the fibrous capsule by the popliteus tendon. The knee joint is a complex anatomical structure that hosts various pathological processes. Many of these conditions can either primarily or secondarily affect the various synovial compartments of the joint, the latter being exquisitely demonstrated in magnetic resonance imaging (MRI), particularly in the presence of a joint effusion [1]. Approximately 0.5  ml of synovial fluid is present in a normal knee joint [1, 2]. The synovial lining of the knee joint consists of several interconnected compartments.

8.2 MRI Compartments 8.2.1 Central Compartment Anteriorly, the synovial membrane is attached to the patellar articular margins before extending circumferentially beneath the aponeuroses of the vastus medialis and lateralis to attach to the anterior femoral shaft (Fig. 8.1).

Fig. 8.1  Anatomy of the synovial central compartment. PD FS image in the axial plane highlights the anterior aspect of the synovial membrane. It is attached to the articular edges of the patella (short white arrows), extends circumferentially (black arrows) under the vastus medialis aponeurosis (single asterisk), lateral retinaculum (double asterisk), and attaches anteriorly to the femoral shaft (triple asterisk). The retropatellar joint space and paracondylar recesses are filled with synovial fluid (black asterisks)

Below the patella, the infrapatellar fat pad of Hoffa displaces the membrane posteriorly, away from the ligamentum patellae. Within Hoffa’s fat pad, a superior vertically orientated supra-­

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 I. I. Codorean, I. B. Codorean, Clinical-MRI Correlations of Anterior Knee Pain, https://doi.org/10.1007/978-3-031-39959-6_8

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Fig. 8.2  A superior, vertically orientated supra-hoffatic and an inferior, horizontal infra-hoffatic recess within Hoffa’s fat pad. PD FS image in the sagittal plane in a 16-year-old boy highlights within Hoffa’s fat pad the presence of the vertically oriented upper intrahoffatic synovial recess (continuous white arrow) and the lower synovial recess with horizontal orientation (dotted arrow). There is also evidence of fluid accumulation in the suprapatellar bursa (double asterisk) and intraarticular retropatellar (single asterisk)

hoffatic and an inferior, horizontal infra-hoffatic recess may be demonstrated [3] (Fig. 8.2). These are commonly linear (Fig.  8.3 ) or sometimes globular in shape (Fig. 8.4) and can be present with or without coexisting joint effusion. On either side of the patella, reduplications of the membrane extend inferiorly and project into the joint cavity as alar folds or plicae [4] (Fig.  8.5). Sometimes, these combine with the central infrapatellar fold to form the ligamentum mucosum, which attaches to the intercondylar fossa of the femur, anterior to the anterior cruciate ligament (ACL) insertion (Fig. 8.6). A horizontal cleft is present in the posterior aspect of the infrapatellar fat pad and appears in approxi-

Fig. 8.3  Linear intrahoffatic with a minimal amount of synovial fluid. The PD FS image in the sagittal plane highlights the presence of two intrahoffatic synovial recesses with a thin linear appearance, the upper vertical (solid arrow) and the lower horizontal (dotted arrow)

mately 90% of individuals on MR imaging [5]. This cleft is lined with synovial tissue and can be variably shaped, a linear shape being the most common. It is located anterior to the distal insertion of the anterior cruciate ligament on the tibia, with the ligament mucosum forming the roof of the cleft (Fig.  8.7). The central portion then extends medially and laterally, covering the anterior aspects of the cruciate ligaments (Fig.  8.8) before being reflected from the sides of the PCL onto the adjoining fibrous capsule (Fig.  8.9). This portion divides the knee cavity into medial and lateral components with an interposed ­extra-­synovial space containing the cruciate ligaments [6, 7]. Along with the medial and lateral aspects of the capsule, the synovial lining extends inferiorly from the articular margins of the femur as far as the meniscal attachments. The peripheral surfaces of the menisci themselves are not covered by the synovial membrane (Fig. 8.10).

8.2  MRI Compartments

Fig. 8.4  Supra- and infrahoffatic synovial recesses with a globular appearance due to synovial fluid effusion. PD FS image in the sagittal plane in a 27-year-old man with anterior pain in his right knee after a fall at a football game, highlights fluid accumulation in both supra and infrahoffatic recesses with a globular appearance (asterisks). Note the fluid accumulation in the suprapatellar synovial recess and the visualization of the Zindron III suprapatellar fold (black arrow). Angulation of the anterior contour of the ACL (white arrow) is compatible with a partial rupture of the anteromedial bundle: superficial pre- and infrapatellar bursitis (black dotted arrow)

8.2.2 Suprapatellar Pouch Superiorly extending from the upper surface of the patella, a large pouch is between the anterior quadriceps tendon and the femur’s anterior surface (Fig.  8.11). The articularis genu muscle arises from the anterior surface of the lower part of the body of the femur and inserts into the synovial membrane at the junction of the suprapatellar pouch and proper joint cavity (Fig.  8.12). It functions to pull the suprapatellar pouch during knee extension, thereby stabilizing the suprapatellar pouch and allowing the patella to glide freely without friction over the femur [8, 9].

247

Fig. 8.5  Reduplications of the synovial membrane project into the joint cavity as synovial plicae. PD FS image in the sagittal plane in a 43-year-old man highlights the reduplication of the synovial membrane, which medially extends as a thin hypointense band, from the medial patellofemoral ligament (black arrow) to the medial femoral condyle (white arrow) with an aspect of the medial synovial plica Sakakibara Type C. Laterally, the synovial reduplication extends from the patellofemoral ligament (black dotted arrow) to the edge of the patella (white dotted arrow)

8.2.3 Posterior Femoral Recesses As the membrane extends posteriorly from both sides of the femur, recesses are formed between the posterior portion of both femoral condyles and the deep surface of the gastrocnemius’s lateral and medial heads. In the midline, the posterior capsular recess may be identified behind the PCL as an extension from the medial femorotibial compartment [10, 11] (Figs. 8.13 and 8.14).

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a

Fig. 8.6  Ligamentum mucosum. PD FS image in the sagittal plane in a 63-year-old woman highlights the presence of the mucous ligament, which originates in the intercondylar fossa, anterior to the intermeniscal transverse ligament (white arrow a, b), with a curvilinear trajectory in Hoffa fatty tissue (short arrow a, b) and is inserted on the

Fig. 8.7  Mucosum ligament forming the roof of the oval infrahoffatic recess. PD FS image in the sagittal plane shows the infrapatellar synovial recess (asterisk), which is distended with a globular appearance and covered by the mucosum ligament (arrow)

b

lower pole of the patella (white dotted arrow). The degenerative mucoid infiltration of the anterior cruciate ligament is noted, expressed by loss of fascicular and fibrillar appearance (asterisk a, b), known as the “ACL celery stalk sign”

8.2  MRI Compartments

a

Fig. 8.8  The deep part of the central recess of the synovial membrane covers the anterior aspects of the cruciate ligaments. PD FS image in the sagittal plane (a) and axial plane (b) in a 23-year-old woman shows fluid accumulation in the deep portion of the synovial membrane (aster-

Fig. 8.9  Pericruciate recesses. PD FS image in axial plane in a 32-year-old woman shows fluid on either side of the ACL (white dotted arrows) and PCL (asterisk and white arrow). Notes, the stigmas of a recent lateral patellar dislocation expressed by edematous infiltration of the medial patellofemoral ligament (short black arrows), rupture of the fibers (long black arrow), femoral disinsertion (double arrow), and area of edema in the lateral portion of the lateral femoral condyle (black dotted arrow) are highlighted

249

b

isk a, b), adjacent to the anterior cruciate ligament (white arrow a, b) and posterior cruciate ligament (dotted arrow a, b). Notes, retropatellar fluid accumulation (double asterisk a) and deep infrapatellar bursa (arrowhead a)

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a

Fig. 8.10  Perimeniscal synovial recesses. PD FS image in coronal (a, b). Both knees in the coronal plane in a 47-year-old woman show lateral femoral-tibial perimeniscal recesses of the right knee (continuous white arrows a) and its lateral homolog of the left knee (dotted white

b

arrows B), which do not cover peripheral surfaces of the menisci. Note the incomplete subchondral fracture line at the medial tibial condyle (thick arrow a) and rupture of the root of the lateral meniscus of the left knee (colored arrow B)

8.2  MRI Compartments

Fig. 8.11  Synovial Suprapatellar pouch in a man with old rupture of both cruciate ligaments. A sagittal PD FS image of a 42-year-old man shows a large pouch filled with synovial fluid (asterisk) formed between the quadriceps tendon (white arrow) and the femur (black arrow). The supra patellar bursa communicates with the retropatellar articular space (dotted black arrow), and the suprapatellar (short white arrow) and infrapatellar recesses (white dotted arrow) are expanded by the synovial fluid. Notes fragmentation of the anterior cruciate ligament (thick white arrow), absence of the posterior cruciate ligament (star), and rupture of the posterior capsule (interrupted arrow)

251

Fig. 8.12  The articularis genu muscle in a 13-year-old boy. This muscle arises from the anterior surface of the femur (white arrow) and inserts into the synovial membrane at the junction of the suprapatellar pouch and proper joint cavity (black arrow). It should be mentioned that the distal insertion of the articularis genu muscle in this child is made by two separate bundles (continuous and dotted black arrows). Its function is to pull and stabilize the suprapatellar pouch during knee extension, allowing the patella to glide freely without friction over the femur [8]

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a

Fig. 8.13  Posterior synovial recesses. PD FS images in the sagittal (a) and axial (b) planes in a 21-year-old man highlight a fluid signal band (continuous white arrow a) in the posterior recesses, deep to the lateral head of gastrocnemius (dotted short white arrow a). Axial image (b) shows fluid in both posterior recesses (asterisks and con-

b

tinuous white arrow b), deep to the medial and lateral head of gastrocnemius (dotted white arrow b). Here is a fluid accumulation in the suprapatellar synovial recess (double asterisk) and intraarticular retrotrochlear space (black arrow)

8.3  Synovial Plicae of the Knee

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8.3.1 Embryology and Anatomy

Fig. 8.14  Fluid accumulation in the posterior capsular recess after a rupture in the bucket handle of the medial meniscus. PD FS in the sagittal plane shows fluid accumulation in the posterior capsular recess (single asterisk), thickening of the posterior capsule (continuous white arrow), and an irregular band image in hyposignal with double PCL appearance, compatible with a rupture in the bucket handle of the medial meniscus (dotted arrow). Fluid accumulation in the suprapatellar synovial recess (double asterisk) and intraarticular retrotropatellar (black arrow)

8.3 Synovial Plicae of the Knee Synovial plicae of the knee are folds in the joint’s lining, thought to represent remnants from embryologic development [2]. They are common incidental findings on cadaveric, arthroscopic, and MRI examinations [4, 12]. On macroscopic examination, normal folds are thin, flexible folds with a synovial lining around the fibroelastic connective tissue protruding into the joint. The corresponding MRI appearance is a thin, linear, hypointense object in the joint that is connected to the synovial mucosa, often outlined by joint fluid [3, 13]. The infrapatellar plica was first reported by Vesalius in the sixteenth century [2]. Pipkin was the first investigator to focus on plicae as an etiology for knee symptoms in 1950 [14].

The knee develops from mesodermal elements and is initially separated into three compartments, medial, lateral, and suprapatellar [7]. The membrane separating the compartments is resorbed between the ninth to twelfth week of gestation, forming a single joint compartment by the sixteenth week. One theory of plica formation hypothesizes that the plicae are remnants of this embryologic membrane that are not properly resorbed [7]. Another theory of plica formation is based on the observation that the knee is initially filled with mesenchymal tissue at 7 weeks gestation [9]. Cavitations within the mesenchyme coalesce to form the joint cavity within 10 weeks. In this theory, plicae are thought to represent areas of incomplete cavitation, with differentiation of residual mesenchymal tissue into synovial folds [9]. The synovium is a thin specialized membrane lining the diarthrodial joint surfaces, bursae, and tendon sheaths. The synovium provides nutrition and lubrication to the joint cartilage by fluid secretion [15].

8.3.2 Classification and Imaging Appearance of Synovial Plicae of the Knee Joint In general, synovial plicae are classified based on their shapes and sizes. Four synovial plicae of the knee have been described based on location [13]: suprapatellar, infrapatellar, medial patellar, and lateral patellar plica (Fig. 8.15). The incidence of synovial plicae depends on the studied patient populations: cadavers, open knee surgeries, knee arthroscopies, or knee MR examinations. The prevalence of plica syndrome varies, ranging from 11 to 87% for suprapatellar plicae and 18 to 60% for mediopatellar plicae [16]. The most commonly reported range is 20–25% of the population [16]. Infrapatellar plicae may be present in around 65% of patients [17]. Lateral plicae and their rates are not well known, with most of the studies from Japan [18, 19]; its range is around 1–2%. In an arthroscopic study of 400 knees, the

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Fig. 8.15 Normal suprapatellar synovial plica in a 50-year-old man with joint effusion. The sagittal PD FS image shows the suprapatellar synovial plica that appears as a thin band of low-intensity signal with an oblique trajectory to the prefemoral fat layer (black arrow) and a posterior perforation (dotted arrow). The plica is delimited by the synovial fluid (asterisk) from the suprapatellar bursa that appears distended and communicates with the retropatellar articular space (double asterisk). Note that the sign of the posterior double cruciate ligament is highlighted (white arrow), suggestive of a bucket handle meniscus tear

rates are 87% for suprapatellar plica, 86% for infrapatellar plica, 72% for mediopatellar plica, and 1.3% for lateral patellar plica [11]. Synovial plicae may become symptomatic because of plica syndrome or injury. MR Imaging plays a crucial role in detecting synovial diseases, highlighting the presence of the plica, its exact location, and measurement before irreversible joint damage. Synovial plicae are seen best on MRI, appearing as bands of low-signal intensity thin and pliable within the high signal intensity joint fluid: suprapatellar (Fig.  8.16), medial patellar (Fig.  8.17), infrapatellar (Fig.  8.18), and lateral patellar (Fig. 8.19). Pathologic plicae are hypertrophied with loss of elasticity (Figs.  8.20 and 8.21), calcified, hyalinized, and fibrotic. The thickened fibrotic plica becomes tight and rigid,

forming a bowstring over the medial femoral condyle and irritates the synovium of the condyle with repeated knee joint movement; in secondary mechanical synovitis; as a consequence, this will lead to softening and degeneration of the articular cartilage and the development of chondromalacia [19] (Fig. 8.22). Because of the high soft tissue contrast resolution of MRI, besides synovitis diagnosis, joint effusion, articular cartilage, subchondral bone, ligaments, muscles, and juxta-­ articular soft tissues can be evaluated. Damage in intra-articular structures, particularly cartilages, generally occurs due to pathologic processes involving the synovium, leading to irreversible joint destruction [20]. Symptomatic plicae are usually present in active patients undertaking repetitive knee movement (Figs. 8.23, 8.24, and 8.25). Symptomatic plicae may cause dull pain in the anteromedial aspect of the knee; the pain may be intermittent or aggravated by physical activity and can be associated with locking, giving way, and clicking within the joint [21]. Pain is located in the area medial to the patellar area above the joint line and the superomedial patellar area [16, 21]. Synovial plicae are found in many knees. They are asymptomatic but may become diseased when subject to an inflammatory process, commonly due to overuse or trauma [9, 12, 15–17]. A symptomatic plica will result in a constellation of symptoms highlighted by intermittent knee pain termed plica syndrome [12, 19]. Plica syndrome is a clinical diagnosis in which the symptoms and physical findings are associated with a pathologic plica. Broom and Fulkerson reviewed 730 arthroscopies performed in a sports injuries clinic and found that 28 patients (3.8%) had a pathologic plica implicated as a cause of symptoms [18]. Plica syndrome is most commonly due to the medio-patellar plica. The patient typically presents with medial patellar pain, usually above the joint line, exacerbated during flexion-­ extension of the knee, and asymptomatic. Pain may be due to chondromalacia of the patella and medial femoral condyle from repetitive contact with the mediopatellar plica [13]. Physical findings may include crepitation, effusion, and palpable pain.

8.3  Synovial Plicae of the Knee

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a

b

Fig. 8.16  Medial patellar plica. PD FS images in axial (a) and sagittal plane (b) show a thin uniform hypointense band in the medial patellofemoral synovial recess (arrows a, b), outlined by a joint effusion

a

Fig. 8.17  Infrapatellar plica. Girl 14-year-old gymnast reports anterior left knee pain after intense training. T1SE image (a) and PD FS image (b) in the sagittal plane show a thin hypointense band (white arrow a, b) that originates from the anterior part of the intercondylar notch (white

b

dotted arrow a, b) and courses through Hoffa’s fat pad to insert on the inferior pole of the patella (blackhead arrow a, b). Note that edematous infiltration of the patellar tendon at the patellar insertion (dotted black arrow a, b) is a possible cause of anterior knee pain

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a

b

Fig. 8.18  Lateral patellar plica. PD FS images in axial (a) and coronal plane (b) highlight a lateral fold as a thin hypointense band (arrows a, b), delimited by the articular fluid from the lateral synovial recess (dotted arrows a, b)

Fig. 8.19  A thick medial and lateral patellar synovial plicae in a patient with complete anterior cruciate ligament rupture. PD FS image in axial plane highlights thickened medial synovial plica with a diffuse outline at the insertion on medial femoral condyle (continuous black and dotted white arrows) in a 20-year-old man with ACL rupture five weeks ago (not shown). Only the bone contusion characteristic of the “Pivot Shift” rupture mechanism is noticed at the level of the lateral femoral condyle in the middle third (single asterisk). The contusion of the inferomedial portion of the patella (double asterisk) and the thickening and edematous infiltration of the lateral synovial plica (black dotted arrow) are also highlighted

Fig. 8.20  A thick synovial infrapatellar plica in a patient with chronic rupture of the anterior cruciate ligament. PD FS image in the sagittal plane highlights infrapatellar plica that appears thickened with a diffuse outline along the entire path (short white arrow) from the intermeniscal transverse ligament (long white arrow) to the lower pole of the patella (dotted arrow) in a 37-year-old man. Chronic ACL rupture in the middle third (thick white arrow). Note an irregular area of a bone contusion in the posterior portion of the tibial epiphysis (star)

8.3  Synovial Plicae of the Knee

Fig. 8.21  Thickened mediopatellar plica, following the lateral dislocation of the patella in a 14-year-old girl, with two anatomical factors at risk of patellar instability: patella Alta (not shown) and Dejour type B trochlear dysplasia (dotted line). The axial PD FS image highlights the thickened mediopatellar plica, with an irregular band appearance in the hyposignal, located in the medial patelo-femoral synovial recess (double arrow and black arrows), which separates it into a posterior portion (single asterisk) and an anterior portion (double asterisk), which communicates with the articular space of the lateral patellofemoral recess (triple asterisk). Note the lateral inclination of the patella (thick white arrow) and a small synovial cyst in the lateral part of the lateral patellar facet (black dotted arrow)

8.3.2.1 Suprapatellar Plica The suprapatellar plica is the second most common plica after the infrapatellar plica, with a reported prevalence of up to 89% at autopsy [2]. Alternative names include superior plica, supramedial plica, medial suprapatellar plica, or ­suprapatellar septum. It is responsible for the division of the suprapatellar pouch from the knee. The suprapatellar plica courses from the anterior femoral metaphysis to the posterior quadriceps tendon and from the medial to the lateral wall of the joint [17]. The medial portion may merge with a medial patellar plica if present. In some cases, it may cause suprapatellar bursitis and chondromalacia [21]. This plica has

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Fig. 8.22  Thickened mediopatellar plica with synovial irritation and development of chondromalacia in a 33-year-old man. PD FS image in the axial plane highlights the thickening of the mediopatellar plica, degeneration of the articular cartilage in the medial half of the medial facet of the patella, expressed by chondral defect extending to the subcortical bone, compatible with a grade III / IV chondromalacia (arrows in a circle). Some accumulation of retropatellar fluid in the medial patellofemoral joint (asterisk). Lateral patellar plica with MRI normal appearance (dotted arrow)

varying shapes: an entire tissue plane (Fig. 8.26) or a porta. Zidorn examined suprapatellar plicae by direct observation in 210 knees from 149 adult cadavers and classified them into four groups [22]. Type I: also called septum completum, in this type, there is a septum separating the knee joint from the suprapatellar bursa (Fig. 8.27). Type II: also known as septum perforatum, in this type, there are one or more openings of different sizes in the septum that separates the knee joint from the suprapatellar bursa. (Fig. 8.28) Type III: also known as septum residuale, is a fold usually located on the medial side separating the knee joint from the suprapatellar bursa (Figs. 8.29 and 8.30). Type IV: also known as septum extinctum, in this type, the septum that separates the knee joint from the suprapatellar bursa is completely involuted (Fig.  8.31). Suprapatellar plicae are usually asymptomatic.

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variation of the suprapatellar plica can have clinical significance. Pigmented villonodular ­ synovitis, synovial osteochondromatosis, hemophilia, and septic arthritis may be isolated to the suprapatellar bursa because of a complete septum. If the orthopedic surgeon is unaware of its existence, he may rupture the complete septum and unnecessarily contaminate the knee joint with the pathology in the suprapatellar bursa [13]. Intra-­ articular loose bodies may become lodged in the suprapatellar bursa due to a checkvalve mechanism after passing through the porta from the joint. Infection or PVNS may be confined to the suprapatellar bursa by a suprapatellar plica (Fig.  8.34); this plica may contribute to chondromalacia’s pathogenesis or suprapatellar bursitis [25–28].

Fig. 8.23  Symptomatic suprapatellar synovial plica* in a cyclist with anterior pain in the right knee. A 32-year-old professional cyclist with right knee pain, accentuated by physical activity during training. The sagittal PD FS image highlights the complete suprapatellar synovial plica (long colored arrow), which appears with a thickened path (double arrow) from the quadriceps tendon to the femur inflammatory infiltrated with an increased signal. It is bounded by the synovial fluid of the suprapatellar bursa, which separates it into two compartments, the upper and the lower. Note the image of a bilocular septate Baker cyst with a homogeneous structure. It is the only cause of anterior knee pain and falls into synovial fold syndrome*

Inflammation of the suprapatellar plica can occur and progress similarly to the medial plica syndrome, although less frequently. Suprapatellar plicae may also impinge on the medial femoral condyle during flexion, limiting patellar mobility and causing chondral damage [19, 23, 24]. Compartmentalization of the suprapatellar bursa may occur due to a complete Type I or Type II plica with a small porta that separates the suprapatellar bursa from the knee joint; there is no communication between these two compartments (Fig. 8.32). This results in a palpable suprapatellar mass and pain due to trapped fluid. When the suprapatellar plica is absent, the articularis genu insertion can be seen at the synovial cavity’s upper limit (Fig.  8.33). The complete septum

8.3.2.2 Medial Patellar Plica The medial patellar plica is the most frequently symptomatic knee plica, although it is less common than suprapatellar or infrapatellar plicae [28]. The mediopatellar plica most classically produces plica syndrome and has been referred to in the literature as plica synovialis mediopatellaris, the meniscus of the patella, medial shelf, Aoki’s ledge, Iino’s band, and plica alaris elongate [17, 19, 23]. The medial fold is a large, free-­ edged structure that comes from under the medial retinaculum (Fig.  8.35) or the medial patellar femoral ligament (Fig.  8.36), or even from the medial wall of the synovial sac [19] (Fig. 8.37). It courses inferiorly and parallels the medial edge of the patella in the coronal plane and ends when it becomes continuous with the synovium, termed plicae Alaris, covering the infrapatellar Hoffa’s fat pad [12, 19, 23] (Fig. 8.38). In some cases, the mediopatellar plica may begin superiorly at the suprapatellar region’s vastus medialis oblique muscle level (Fig. 8.39). It may be either contiguous or separate from a suprapatellar plica (Fig. 8.40). The medial plica is often considered an intra-articular ligament, providing a mechanical link between the femoral condyle and the infrapatellar fat pad [29]. The medial plica is composed of relatively elastic tissues which asymptomatically conform to the changes in shape and lengths of the plica

8.3  Synovial Plicae of the Knee

a

Fig. 8.24  Thickening of the infrapatellar synovial plica in a 27-year-old sportsman with anterior cruciate ligament rupture (ACL). T1 SE image (a) and PD FS image (b) in the sagittal plane highlight an arcuate band of edema in

Fig. 8.25  Incidental highlighting of the suprapatellar plica divides the suprapatellar pouch into a suprapatellar compartment and an articular compartment in a patient with left knee trauma. PD FS image in the sagittal plane shows a complete suprapatellar plica (black arrow), which divides the suprapatellar bursa into an upper compartment (single asterisk) and an articular lower compartment (double asterisk). A tibial plateau fracture separates a bone fragment (star) and epiphyseal extension (arrows)

259

b

the infrapatellar fat pad along the course of the infrapatellar plica and the anterior portion of the Hoffa fatty tissue (black arrows and asterisk a, b). Partial ACL rupture (white arrows a, b)

Fig. 8.26  Suprapatellar plica as a complete tissue plane. T1 SE image in the sagittal plane in a 14-year-old girl highlights the suprapatellar synovial plica with the appearance of complete tissue without fluid content (full arrow). Note patella Alta and the presence of the articularis genus muscle (dotted arrow)

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a

Fig. 8.27  Suprapatellar plica Type I: also known as septum completum in a patient with anterior knee pain after twisting his left knee during a football game. PD FS image in sagittal (a) and axial plane (b) highlights the suprapatellar plica with a complete septum pattern and upward oblique orientation from the quadriceps tendon to the pre-

Fig. 8.28  Suprapatellar plica Type II: Septum perforatum. A 13-year-old girl with pain and joint effusion. The PD FS image in the sagittal plane highlights the fluid in the suprapatellar pouch, which outlines a suprapatellar plica with a slight uniform thickening (arrow) and a posterior perforation (dotted arrow). Septum perforatum has a narrow opening and separates the knee joint (single asterisk) from the suprapatellar bursa (double asterisk)

b

femoral fat pad (arrows a, b). It is thickened and separates the suprapatellar bursa into an upper (single asterisk a, b) and a lower articular compartment (double asterisk a, b). Thickening of the synovial wall in the lower compartment (dotted arrows a, b) with the appearance of synovitis

folds as the knee flexes and extends. In some patients, particularly those who may have had injuries or multiple surgeries over the medial aspect of the knee, the medial synovial plica may become very thick and fibrotic and catch over the medial aspect of the medial femoral condyle [30]. In all patients, the medial synovial plica will glide over the anteromedial aspect of the medial femoral condyle with flexion and extension of the knee. In most patients, this gliding motion of the plica will occur without any symptoms because of the knee’s high viscosity of the native synovial fluid. However, in patients with effusions, which decrease the viscosity of their synovial fluid, patients may either have crepitation or catching of their medial synovial plica with flexion and extension of the knee [31] (Fig. 8.41). This crepitation or catching can occur with patients while climbing stairs, squatting and bending, and other activities. The medial plica’s transverse width and lateral extent are variable [2].

8.3  Synovial Plicae of the Knee

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a

b

Fig. 8.29 Suprapatellar plica Type III: with septum residuale, located on a medial side, incidentally discovered in a woman with ACL acute rupture (not shown). A 34-year-old woman with anterior pain and swelling of the left knee. PD FS images in the sagittal (a), and axial plane

a

b

Fig. 8.30  Suprapatellar plica Type III: septum residuale, incidentally discovered on a skier after a fall. A 34-year-­ old man with anterior pain and swelling of the right knee. PD FS images in the sagittal (a), axial (b), and coronal

(b), highlight the medial sinovial fold (arrow a, b) and fluid in the medial suprapatellar bursa (single asterisk), which separate the fluid from the patellofemoral knee joint (double asterisk)

c

plane (c) highlight the lateral sinovial fold (arrow a–c) and a fluid collection in the suprapatellar bursa (single asterisk) and pericondylar femoral synovial recesses (double asterisk)

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a

Fig. 8.31  Suprapatellar plica Type IV: also known as septum extinctum, in this type, the septum that separates the knee joint from the suprapatellar bursa is completely involuted. A 46-year-old man, a former athlete, with chronic anterior pain in his right knee. T1SE image (a) and PD FS (b) in the sagittal plane highlights the fluid

a

Fig. 8.32 Compartmentalization of the suprapatellar bursa due to a complete Type I plica. A 37-year-old man presented after trauma with hemarthrosis and a palpable suprapatellar mass. PD FS image in sagittal (a) and coro-

b

collection in the suprapatellar bursa (asterisk a, b) and its distension (double arrow a, b). Note that the infrapatellar plica with a curvilinear trajectory from the intermeniscal transverse ligament (dotted arrow a, b) to the lower pole of the patella (horizontal white arrow) and fluid accumulation in the Hoffa fatty tissue (double asterisk)

b

nal plane (b) demonstrates thickened and irregular suprapatellar plica (arrow a, b), which divides the suprapatellar bursa into two separate compartments—suprapatellar (single asterisk) and retropatellar (double asterisk)

8.3  Synovial Plicae of the Knee

Fig. 8.33  When the suprapatellar plica is absent, the articularis genu insertion can be seen at the upper limit of the synovial cavity. PD FS image in the sagittal plane demonstrates thickened and irregular suprapatellar plica (asterisk); the articularis genu insertion can be seen at the upper limit of the synovial folds (arrows)

The width of the mediopatellar plica is graded according to the length of the medial facet of the patella: in grade 1, the medial plica does not extend to the medial edge of the patella; in grade 2, the plica extends to within the inner one-third of the medial facet of the patella; in grade 3, plica extends between the inner third and outer third of the medial facet of the patella; and in grade 4, plica extends beyond the outer third of the medial facet of the patella [32]. The anatomy of the medial plica itself is variable and thus can be classified into four types, A–D, according to a widely accepted and clinically significant scheme authored by Sakakibara [24, 25]. Type A and type B are largely asymptomatic because of their small size [12]. Type C and type D often become symptomatic due to their larger size and propensity to become trapped between the medial condyle of the femur and the patella [12, 19, 25, 27].

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Fig. 8.34  Free bodies blocked in the suprapatellar bursa due to a check valve mechanism in a 59-year-old woman with Zidron type II suprapatellar plica (septum perforatum) and synovial chondromatosis of the right knee. The PD FS sagittal image shows fluid accumulation in the suprapatellar pouch, Zidron type II suprapatellar plica (continuous black arrow), and free bodies in the upper suprapatellar compartment (white arrows). The absence of free bodies in the lower retropatellar synovial compartment (single asterisk) is explained by the perforated septum’s valve mechanism (black arrow and dotted line). Notes degenerative mucoid infiltration of the posterior cruciate ligament (triple asterisk), cyst ganglion under PCL insertion (double asterisk), and a free body in infrahoffatic synovial recess (white arrow)

Type A can be found as a cord-like, thin elevation of the synovial wall (Fig. 8.42). Type B presents as synovium with a shelf-like appearance, which is not wide enough to cover the anterior surface of the medial femoral condyle (Fig. 8.43). Type C has a similar shelf-like appearance but is larger and partially covers the anterior surface of the medial femoral condyle (Fig. 8.44). Furthermore, a type D medial plica exists similarly to a type C medial plica, except that it is additionally fenestrated and has pedunculated tags that may impinge upon the patella-­ femoral joint [12, 25, 27] (Fig. 8.45).

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Fig. 8.35  Medial plica originating below the medial retinaculum in a 15-year-old girl with lateral patellar dislocation, first episode. The axial PD FS image highlights the medial synovial fold (thick white arrow) that originates below the medial retinaculum (dotted arrow). The plica appears as a wide structure with free edges (short black arrows), is inserted on the upper part of the medial femoral condyle (thin white arrow), and separates the medial paracondylar recess into an anterior compartment (single asterisk) and a posterior one (double asterisk). Associated joint fluid is noted (single asterisk), as well as a small chondral defect on the lateral patellar facet (short white arrow)

Four synovial structures in the medial gutter may be mistaken as the medial plica: the anteromedial fringe of the synovium, the superomedial plica, the plica alaris elongate, and the transverse arcuate folds. The anteromedial fringe of the synovium is a structure that covers the anterior horn of the medial meniscus that can cause painful symptoms, similar to the mediopatellar plica when it has impinged. The superomedial plica may be mistaken as the medial plica, but it is part of the superior plica; noticing its location superior to the patella can differentiate this as a distinct entity. The plica alaris elongate can be found as a fold of synovium adjacent to the patella that can be distinguished from the medial plica with a skyline view of arthrography. The transverse arcuate folds lie at the base of the

Fig. 8.36  The thin medial plica originates below the medial patellofemoral ligament. Axial PD FS image in a 23-year-old woman highlights the medial synovial plica (black arrow) that originates below the medial patellofemoral ligament (white arrow) and has an ascending path to the medial femoral condyle. Note that a thin lateral synovial plica (short black arrow) originates below the lateral patellofemoral ligament (white dotted arrow)

medial gutter and may be confused with the medial plica [27, 33]. MRI findings of pathologic medial plicae include thickening and increased intrasubstance signal on T2-weighted images, fat saturation sequences, wide plica extending beyond the medial margin of the trochlear articular surface, corresponding to a Sakakibara Type C lesion fenestration, corresponding to a Sakakibara Type D lesion, focal fluid adjacent to the plica out of proportion to the overall amount of joint fluid, and interposition between the patella and femoral trochlea on multiple contiguous images [13] (Fig. 8.46). Jee et  al. reported overall sensitivity of 95% and specificity of 72% for MRI detection of symptomatic plicae in 55 patients. In their series, the incidence of symptomatic plicae increased when the medial plica extended beyond the medial margin of the patella into the patellofemoral joint [26]. Monabang et al. reviewed 9 cases

8.3  Synovial Plicae of the Knee

Fig. 8.37 The mediopatellar plica originates in the medial side of the synovial sac in a 45-year-old man with fluid accumulation in the suprapatellar bursa and retropatellar. The sagittal PD FS image shows the medial patellar plica (black dotted arrow) coming from the medial wall of the synovial sac at the medial edge of the patella (white and black continuous arrow). Notes, the second vertical medial plica, distal portion (white dotted arrow)

of arthroscopically significant medial patellar plicae and found that clinically significant plicae were interposed between the patella and trochlea on more axial slices than controls and had adjacent focal fluid collections [34]. Hayashi et  al. reported that larger (Sakakibara Type C) medial patellar plicae on MRI were associated with a higher likelihood of medial patellar cartilage damage on 342 knees [28]. The symptomatic plicae are the most common medial plicae that extend from the medial joint line to the adipose layer. Diagnosis of symptomatic plica is primarily based on clinical findings [21]. A thorough differential diagnosis is required to ascertain if the plica is the primary cause of knee pain. On physical examination, the medial patellar plica (MPP) test has a sensitivity of 90% and a specificity of 89% [12]. The MPP test is performed with the patient supine and the knee in

265

Fig. 8.38  Medial plica with inferior route and parallel to the medial edge of the patella in the coronal plane. PD FS image in the sagittal plane in the 17-year-old girl highlights the medial plica in the coronal plane as a vertical band (arrows) that descends on the medial facet of the patella and parallel to the medial edge of the patella

extension. Using the thumb, the examiner presses the inferomedial portion of the patellofemoral joint to insert the mediopatellar plica between the patella and the medial femoral condyle. While maintaining this pressure, the knee is flexed at 90 degrees. The MPP test is considered positive when the patient experiences pain in the knee in extension and relief of pain with the knee in 90 degrees of flexion [13]. It has been reported that the medial plica exists in 64–85% of healthy knees [35] and may be symptomatic in 2.8% of cases of knee pain [36]. When symptomatic local symptoms include: anteromedial knee pain in 75% of cases, clicking in 50% of cases, tenderness on palpation, reduced knee range of movement in 8% of cases, and difficulty with loading tasks [35]. These symptoms are not particularly specific to plica syndromes and can present with many other causes of knee pain [19].

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Fig. 8.39  The medial plica originates at the vastus medialis oblique muscle level. PD FS image in the axial plane at the upper level of the suprapatellar bursa in a 37-year-­ old man with suprapatellar bursitis highlights a medial synovial plica (white arrow) originating at the level of the vastus medial oblique muscle (star). The plica has free edges (short black arrows). Joint fluid is noted in the suprapatellar bursa (asterisk)

Asymptomatic synovial plicae may be found normally within the knee. Chronic inflammation secondary to direct trauma, repetitive sports activities, or other pathologic knee conditions affects the pliability of the synovial folds and can become symptomatic. With the motion of the knee, the thickened fibrotic plicae can irritate the synovium of the condylar margins, leading to inflammatory synovitis and articular cartilage wear [14, 15] (Fig. 8.47). The mediopatellar plica is most likely to cause problems when it becomes thickened, fibrotic, or bowstrung [26]. Mediopatellar plica may cause snapping and impingement within the medial PFJ during knee motion and are believed to contribute to degenerative chondral lesions in the medial PFJ compartment [15, 18, 25, 26]. Lyu and colleagues found that 97% of the symptomatic knees with arthroscopy-detected mediopatellar plica had degenerative cartilage damage on the edge

Fig. 8.40  Thin medial plica originating from the suprapatellar synovial pouch’s wall was incidentally detected. The sagittal PD FS image in a 27-year-old man with acute rupture of the anterior cruciate ligament (not shown) highlights a medial synovial plica (black arrow) originating from the suprapatellar synovial pouch (white arrow) that continues with the suprapatellar plica (black dotted arrows)

and the anterior part of the medial femoral condyle [37]. Christoforakis and colleagues demonstrated a significantly increased incidence of cartilage damage in the medial patella (47.7% vs. 27.5%, P