A Primer in Cartilage Repair and Joint Preservation of the Knee PDF
Preview A Primer in Cartilage Repair and Joint Preservation of the Knee
A Primer in Cartilage Repair and Joint Preservation of the Knee A Primer in Cartilage Repair and Joint Preservation of the Knee Editedby Tom Minas, MD, MS AssociateProfessor HarvardMedicalSchool Director,Cartilage RepairCenter, Brighamand Women’sHospital,ChestnutHill,Massachusetts 1600JohnF.KennedyBlvd. Ste1800 Philadelphia,PA19103-2899 APRIMERINCARTILAGEREPAIRANDJOINT PRESERVATIONOFTHEKNEE ISBN:978-1-4160-6654-5 Copyright#2011bySaunders,animprintofElsevierInc. Nopartofthispublicationmaybereproducedortransmittedinanyformorbyanymeans,electronicor mechanical,includingphotocopying,recording,oranyinformationstorageandretrievalsystem,without permissioninwritingfromthepublisher.Detailsonhowtoseekpermission,furtherinformationabout thePublisher’spermissionspoliciesandourarrangementswithorganizationssuchastheCopyright ClearanceCenterandtheCopyrightLicensingAgency,canbefoundatourwebsite:www.elsevier.com/ permissions. ThisbookandtheindividualcontributionscontainedinitareprotectedundercopyrightbythePublisher (otherthanasmaybenotedherein). Notices Knowledgeandbestpracticeinthisfieldareconstantlychanging.Asnewresearchandexperience broadenourunderstanding,changesinresearchmethods,professionalpractices,ormedicaltreatment maybecomenecessary. Practitionersandresearchersmustalwaysrelyontheirownexperienceandknowledgeinevaluating andusinganyinformation,methods,compounds,orexperimentsdescribedherein.Inusingsuch informationormethodstheyshouldbemindfuloftheirownsafetyandthesafetyofothers,including partiesforwhomtheyhaveaprofessionalresponsibility. Withrespecttoanydrugorpharmaceuticalproductsidentified,readersareadvisedtocheckthe mostcurrentinformationprovided(i)onproceduresfeaturedor(ii)bythemanufacturerofeach producttobeadministered,toverifytherecommendeddoseorformula,themethodanddurationof administration,andcontraindications.Itistheresponsibilityofpractitioners,relyingontheirown experienceandknowledgeoftheirpatients,tomakediagnoses,todeterminedosagesandthebest treatmentforeachindividualpatient,andtotakeallappropriatesafetyprecautions. Tothefullestextentofthelaw,neitherthePublishernortheauthors,contributors,oreditors, assumeanyliabilityforanyinjuryand/ordamagetopersonsorpropertyasamatterofproducts liability,negligenceorotherwise,orfromanyuseoroperationofanymethods,products,instructions, orideascontainedinthematerialherein. ISBN:978-1-4160-6654-5 AcquisitionsEditor:DanPepper DevelopmentalEditor:MarlaSussman PublishingServicesManager:PatriciaTannian ProjectManager:LindaVanPelt DesignDirection:LouForgione PrintedintheUnitedStatesofAmerica Lastdigitistheprintnumber: 9 8 7 6 5 4 3 2 1 Contributors Julie Glowacki, PhD Andreas H. Gomoll, MD OrthopedicsDepartment Cartilage RepairCenter OrthopedicResearch Laboratory BrighamandWomen’sHospital MedicalResearch Building HarvardMedicalSchool BrighamandWomen’sHospital ChestnutHill,Massachusetts Boston,Massachusetts Chapter5.Debridement,Microfracture, andOsteochondral Chapter2.Cartilage RepairandRegeneration Autograft TransferfortheTreatment ofCartilage Defects Chapter12.Meniscal AllograftTransplantation v Dedication Special Thanks IwouldliketodedicatethisbooktoLarsPeterson,MD, PhD, Gothenberg, Sweden. The reality of joint preser- vation in young patients with articular injuries has only Taking on the taskof writinga surgicaltext, considering become possible because of his vision and courage to the topic was dear to my heart and was what I did every persevere with the premise that cultured articular chon- day, at first seemed straightforward. However, it turned drocytesmayaffectrepair.Hetranslatedahypothesisto out to be quite the opposite and it wouldn’t have been a preclinical rabbit model in 1982 and then to clinical possible without my family by my side. I would like to application in 1987. thankmywifeDanaforherpatienceandencouragement He is a pioneer in the field of orthopedics. I thank and my two beautiful children, Krista and Lucas, who him and his co-workers Anders Lindahl, MD, PhD, havealwaysbeenthelightinmylife.Withouttheirlove, and Mats Brittberg, MD, PhD, for allowing me to be a enthusiasm,andsupport,thisbookwouldnothavecome part of their team. He has been a mentor and great to fruition. For this, I am forever grateful. friend over the years as we have tried to promote the I would also like to thank my parents, Mary and field of cartilage repair around the world. Angelo Minas, for their unconditional love and support Workingandknowinghimhasbeenatruehonorand throughout my life. I have always strived to emulate privilege. themintheirdedicationandcommitmenttobothfamily and career. Introduction The purpose of this book is to provide residents, fel- lows, and surgeons with a practical approach to the field of cartilage repair. Specialized surgical techniques have been developed combining previous principles of internal fixation, osteotomy, and ligamentous and meniscal surgeries, as well as newly developed cartilage repair techniques. Because joint preservation in young patients is a developing field, it is often confusing to residents, fellows, and experienced surgeons. I will attempt to outline and illustrate my approach using Lars Peterson, MD, PhD, and author – Tom Minas, my own experience, rationales, and surgical techniques. MD,MS,ontheirwaytoGreatSlaveLake,NorthWest Territories, Canada, 2005. vi Acknowledgments vii Acknowledgments My career has been influenced by many people, so of my patients and through outcomes research has I hope that I will not offend any by omission. James advanced the field of cartilage repair. Carl Winalski, Waddell, MD, and Robin Sullivan, MD (deceased), MD, Department of Radiology, first started the CRC who inspired me to be an orthopedist. Marvin Tile, with me as a collaborator in evaluating cartilage repair MD, a great mentor and friend who guided me in criti- by non-invasive methods. His expertise and teamwork cal thinking and the principles of internal fixation. has been invaluable. I would like to thank former mem- RobertSalter,MD(deceased),myorthopedicsprofessor bers, assistant Brenda Surowiec and research assistant at University of Toronto, who continued to inspire and Rosa Chiu, and my present team, assistants Jeannette encouragemeintomyclinicalpathofjointpreservation Vannan and Esther Prall. Physician assistant Courtney and cartilage repair. Clement Sledge, MD, who intro- Van Arsdale has been a great addition to our team. duced me to basic science cartilage repair in Boston. TimBryant,RN,BSN,hasbeeninvolvedinmypractice Thomas Thornhill, MD, my chairman, mentor, and since 1993, first as a surgical nurse and then as a friend, who helped me set up the Cartilage Repair Cen- research nurse. I thank him for his dedication, loyalty, ter (CRC) at the Brigham and Women’s Hospital and hard work, and friendship. He is responsible for the continues to encourage and advise me on new pathways excellent data collection and organization of our data- in cartilage repair. Richard Scott, MD, who has taught base and for helping to pass this on to our fellows and me so much about knee surgery and gave me the idea co-workers. Finally, Andreas Gomoll, MD, has been an to write this book. My basic science collaborators Julie enthusiastic and tireless researcher and partner at the Glowacki, PhD, and Shuichi Mizuno, PhD, who have CRC. His addition has brought new energy and ideas held me to a high standard of the scientific method for good clinical research and training for our residents and have encouraged me to translate our findings to and fellows. the bedside and vice-versa. Finally, in the light of full disclosure for those who Overtheyearsasthefieldofcartilagerepairhasdevel- readthisbook,IamaconsultanttoGenzymeBiosurgery, oped, my residents and clinical fellows have encouraged which cultures the autologous chondrocytes that are the me to compile a syllabus to guide them as they trained. topic of Chapter 7, and I am on the Scientific Advisory I hope this book will assist them in their management Board and have IP for ConforMIS—with royalties and of patients with this difficult problem. I thank them stock options—which manufactures custom resurfacing collectivelyfortheirenthusiasmandencouragement. implants and is the topic of Chapter 16. I would like to thank the members of my team at the CRC. Teamwork has resulted in excellent clinical care Foreword This is a timely and unique book by a world pioneer of intrinsic repair and regeneration processes, and a com- autologous cartilage transplantation—the first widely plete account of the systematic approach to diagnosis, successful cell-engineering procedure in surgery. patientmanagement,andthedetailsofthesurgicaltech- Tom Minas has compiled an impressive text embrac- niques and rehabilitation programmes for all types of ing the whole subject, tracing the etiology of articular problems. cartilage injury, breakdown, and repair and the chal- This is supplemented by a collection of fascinating lenges involved in development of modern treatment. and extremely challenging clinical problems and the This is combined with his personal contributions to “Minas touch” required to deal with them. the phenomenal success of this approach in the treat- Aconstantthemeistheneedforascientificallybased ment of acute osteochondral injuries in the knee as well surgical approach matching the patient’s goals with the as groundbreaking advances in treatment of early osteo- surgical possibilities, by employing a treatment algo- arthritis. His 15-year experience involving over 600 rithmbasedonhis5‘E’s—engagement,empathy,educa- patients with a variety of cartilage injuries has led to tion, enlistment, and end solution—which ensure that his personal philosophy of the optimal applications in a bothpatientandsurgeonareclearabouttherealisticout- very complex and sometimes controversial clinical field. comesofthetreatment.Thisiscombinedwithastrategy It is especially timely because of the considerable ofclinicaltrialswhereverpossible.Itisnotablethatinhis confusion concerning the appropriate indications for especiallydifficultgroupofosteoarthriticpatients,hehas cell-based and other therapies and the mushrooming of achievedan85%pluspatientsatisfactionrate different commercial products entering the market, Thisoutstandingbookisascientifictreatiseandstep- mostly untried. This is relevant because of the potential wise surgical guide as well as a visionary surgeon’s view to prevent and treat osteoarthritis, which is predicted to ofthismostexcitingofmusculoskeletaldevelopmentsof affect 20% of the population by 2020. the 21st century. It is beautifully presented and illu- Beginning in 1995, he stamped his own intellectual strated and a pleasure to read. rigour and surgical innovative techniques on the man- Itismyprivilegetohavehadaforetasteofaspecialist agement program, taking it from an exciting but rela- masterpiece. tively simple process to a varied and carefully planned treatment tailored to individual patients with early or George Bentley, MB, ChM, DSc, FRCS, latecartilagedamage,whichnowmayinvolvecorrection FRCCS (Ed), FMedSc of malalignment, ligament and meniscal injuries, Emeritus Professor of Orthopaedics advanced bony injury, or even osteoarthritis. University College, London The16chapterscovercurrentscientificknowledgeof Honorary Consultant Orthopaedic Surgeon cartilage properties, the etiology of damage and the Royal National Hospital, London viii 1 Chapter Chondral Injury and Osteoarthritis: The Impact of Articular Cartilage Lesions Tom Minas, MD, MS INTRODUCTION MENISCALINJURY PREVALENCEOFOA EFFECTOFRUNNINGANDOTHERSPORTS ALIGNMENT:TIBIOFEMORALAND PRESENTVERSUSFUTURETOTALKNEE ONOA PATELLOFEMORAL ARTHROPLASTYNUMBERS ANTERIORCRUCIATELIGAMENTINJURY CHONDRALDEFECTSIZE ECONOMICBURDEN POSTERIORCRUCIATELIGAMENTINJURY EFFECTOFBODYMASSINDEXONOA INTRODUCTION defects are the medial femoral condyle (up to 32%) and thepatella.2,3Mostaredetectedincidentallyduringmenis- Damage to the articular cartilage comprises a spectrum cectomy or anterior cruciate ligament reconstruction.1,4 of disease entities ranging from single, focal chondral Notably, despite the relatively high incidence, many of defects to more advanced degenerative disease and these defects are incidental in nature and asymptomatic. end-stage osteoarthritis (OA). Focal chondral defects Articular cartilage lesions have no spontaneous repair have long been implicated in the subsequent deve- potentialandhaveapropensitytoworsenwithtime.Even lopment of OA. Focal chondral defects result from though the natural history is not completely understood, various causative factors that may genetically predispose thoseinvolvedincartilagerepairagreeontheimportance to early breakdown and wear. of looking for background factors that predispose to the Genetics may predispose to early cartilage wear and formation of these defects—malalignment and compart- OA. In addition, metabolic, inflammatory, and deve- ment overload of the tibiofemoral or patellofemoral lopmentaldiseasesmayleadtoarticularcartilagedamage. compartment, joint laxity, contracture, meniscal insuf- These may include Gaucher disease, hemophilia, hema- ficiency, and, of course, genetic predisposition to OA— chromatosis,ochronosis,Ehlers-Danlossyndrome,Paget for which clinical, biologic, or genetic markers currently disease, acromegaly, avascular necrosis, neuropathic arelacking. arthropathy,andjointdysplasia. Patients are approximately evenly split in reporting a EFFECT OF RUNNING AND OTHER traumaticversusaninsidiousonsetofsymptoms.Athletic SPORTS ON OA activitiesarethemostcommonincitingeventassociated withthediagnosisofchondrallesions.1Traumaticevents anddevelopmentalcausativeagentssuchasosteochondri- Long-distance running and its relationship to the deve- tisdissecanspredominateinyoungeragegroups.Several lopment of OA is an issue of great interest. Several large studies have found high-grade chondral lesions studies have suggested that recreational long-distance (OuterbridgegradesIIIandIV)in5%to11%ofyounger running is not associated with progression of knee patients(<40years)andupto60%ofolderpatients(upto OA.5–8 However, the presence of risk factors such as 65 years).1–3 The most common locations for these obesity, muscle weakness, or previous joint injury can 2 Chondral Injury and Osteoarthritis: The Impact of Articular Cartilage Lesions CHAPTER 1 3 make the knee more susceptible to the demands asso- significant contributor to subsequent OA development. ciated with participation in sports or athletics.9 In con- Surgical repair of the ACL aims to restore normal trast to recreational involvement, participation in biomechanics to the knee. However, ACL repair has several athletic and sporting activities at the elite level not been shown to reduce the incidence of knee OA has been associated with an increased risk of lower- compared with nonoperative management.25 This extremity OA.10–12 These activities include sports finding may support the theory that it is the initial involvingtorsionandimpact,suchassoccer,weightlift- traumaandbonebruisingwithoverlyingcartilageinjury ing,andsprinting.13,14Ignoringaknowncartilageinjury and subsequent ligament failure that eventually lead to and continuing to participate in torsional impact sports, OA, which is my belief. such as soccer, has been shown to cause progression of Neuman et al26 reported that the primary risk factor articular cartilage injuries with development of large for development of knee OA after ACL injury was areas of delamination.15 Other studies have demon- whether a meniscectomy had been performed. This strated that known articular injury greater than 1cm2 finding seems to support the view that maintenance of has progressed to OA, with greater than 14-year fol- knee loading and chondroprotection from the meniscus low-up in more than half of patients allowed to partici- are important considerations in this issue. More inves- pate in sports.16 Even when known cartilage injuries tigation is needed to determine the causative factors are treated with articular cartilage repair by use of responsibleforearlyOAdevelopmentinthispopulation. microfracture or autologous chondrocyte implantation, OA may develop in as many as one third of patients17 POSTERIOR CRUCIATE LIGAMENT as early as 5 years after treatment. This may be due to INJURY missedaxialalignmentversustheseverityoftheinstigat- ing initial injury in producing articular cartilage injury because this has not been found with autologous The posterior cruciate ligament (PCL) is rarely injured chondrocyte implantation alone when alignment was compared to the ACL. Occasionally patients with PCL- carefully assessed and treated.18,19 injured knees are asymptomatic. When patients are symptomatic, they generally exhibit pain and disability rather than functional instability as seen in patients with ANTERIOR CRUCIATE LIGAMENT ACL-deficient knees. The medial femoral condyle is INJURY injured more frequently than the lateral femoral con- dyle.27,28 Varus alignment of the limb predisposes to Another consideration that often directly relates to par- medially based pain in this situation. To prevent further ticipation in athletics is injury to the anterior cruciate progressionofamedialarticularinjury,PCLreconstruc- ligament (ACL) and subsequent development of knee tion is recommended. However, valgus tibial osteotomy OA. This severe trauma is generally associated with combined with increased flexion in the sagittal plane bone bruising at the time of subluxation of the tibiofe- decreases posterior translation of the tibia and in itself moral joint with tear of the ACL.20,21 Biopsies of the mayunloadandaddenoughstability.Carefulassessment overlying articular cartilage to the bone bruise have of instability, alignment, and cartilage injury is required demonstrated that the superficial and middle zones of to determine an appropriate treatment pathway. articular cartilage have greater than 50% cartilage apoptosisinadditiontolossofproteoglycans,indicating MENISCAL INJURY severe injury to the overlying cartilage surface with a propensity for late articular cartilage loss and delamina- tion and the possibility of progression to OA.22 Bone The role of the meniscus in load distribution and shock bruisesinthestudyhavebeenshowntooccuringreater absorption has long been understood. The absence of a than 80% of ACL-injured knees.22 meniscus has been shown to predictably result in OA The untreated chronic ACL deficient knee has an of the affected compartment, with characteristic increased risk of articular cartilage injury, especially as radiographic changes such as flattening of the femoral the time from initial injury increases.23,24 condyles with peripheral osteophyte formation and Long-term follow-up of ACL-injured patients has sclerosis of the tibial surface.29–31 consistently demonstrated an association between ACL Ithasbeennotedthatthemedialcompartmentofthe injuryandthedevelopmentofkneeOA.Ithasbeenpos- knee develops these changes within 10 to 15 years after tulated that disruption of the normal mechanics of the total meniscectomy; however, the lateral compartment knee and continued instability with resultant shear may degenerate within 2 to 5 years after total menis- forces to the articular surfaces also predispose to injury cectomy. These findings led me to consider that the to the meniscus, which is the secondary stabilizer of compartments are quite different in their susceptibility the knee. Loss of the meniscus as a shock absorber is a to loss of the meniscus. The medial compartment 4 PART 1 DECISIONMAKING comprises60%oftheweight-bearingsurfacescompared articular cartilage degeneration by placing abnormal to 40% in the lateral compartment. The medial com- stressesonthearticularcartilage.33,34Correctiveosteot- partment is congruent in that the femoral articular sur- omy to normalize the forces of the tibiofemoral joint face is convex and the tibial articular surface is will arrest progression of disease and, in the event of concave. The broad medial collateral ligament in addi- cartilage repair, will improve the environment for opti- tion to the meniscus stabilizes the medial compartment mal reconstitution of the articular surface. such that there is a rolling motion of the femur on the Patellar lateral maltracking, patella baja, and arthro- tibia without translation and shear, hence the term fibrosisoftheinfrapatellarfatpadallresultinabnormal medial pivot with the medial side of the knee being rela- forces across thearticulation ofthe patellofemoraljoint. tively stable and the lateral side exposed to more shear. Isolated lateral patellar facet arthritic change may Themedialmeniscusdoesnotcapture theentiremedial develop withisolated lateral maltracking, and panpatel- femoral condyle because the anterior horn attachment lar articular loss is more common with patella baja and varies and often rolls off the anterior aspect of the tibia, patellar contracture. The underlying causes, which may providing less surface to the femoral articular condyle. require soft tissue releases, tibial tubercle osteotomy, Therefore, it is less crucial to the medial compartment vastus medialis obliquus quadriceps advancement, and other than the posterior horn of the medial meniscus, dysplasia of the trochlea, all must be addressed in order whichisloadedcontinuouslyduring flexion oftheknee. to halt the progression of disease or to allow cartilage The articular surfaces in addition to being congruous repair to pursue without overload and failure. have firmer and harder surfaces than the lateral com- partment. The increased stability, congruence, and CHONDRAL DEFECT SIZE hardnessaremoreprotectiveandinthepresenceofnor- mal alignment wear are slow to progress. However, varus alignment on the medial compartment usually The initiation of an articular cartilage defect frequently results in a more rapidly degenerating medial compart- is traumatic in more than half of the cases detected; mentinOA.Forthisreason,Iconsiderthemedialcom- the remainder arise insidiously.1 partment of the knee to be very alignment dependent. The progression of an articular cartilage lesion to a Thelateralcompartmentisverydifferent.Thelateral bipolar articular injury and then to OA ismultifactorial, tibial plateau surface is convex, and the articular surface as previously discussed. When considering cartilage is softer than in the medial compartment. The lateral repairforsuchadefect,thesizeofthedefectfactorsinto collateral ligament is thin and posteriorly based. It pro- the choice of repair. The natural history of disease for a vides little stability to the lateral compartment itself. known sizecartilagedefectisnot understood. However, However, the meniscus is almost circular and makes up even a small defect (e.g., 1cm2) may progress if activity for the lack of congruence of the tibial articulation to isunrestricted.16Withallotherfactorsbeingequalafter the femoral articulation. Loss of the lateral meniscus background factors have been corrected, the size of the therefore allows incongruence of the lateral compart- chondral defect is critical to the treatment being ren- ment and increased translation and shear with point dered for repair. If the defect is well shouldered when loadingofthefemoralcondyleonthesofterlateraltibial weight-bearing forces are placed across it (Figure 1–1), plateau articulation. This predisposes to rapid articular the shoulders take up the load, protecting the subchon- wear, as seen clinically. For this reason, I consider the dralboneofthedefectfromstimulationandhencepain. lateral compartment to be very meniscal dependent as No treatment of this defect may be needed if the defect opposed to the medial compartment, which is more isasymptomaticandcanbeobservedovertimetodeter- alignment dependent. mine progression of disease. In addition, a treatment that provides a fibrocartilage repair that protects and stabilizes the existing shoulders, thus dispersing the ALIGNMENT: TIBIOFEMORAL AND forces throughout the defect, may be adequate over PATELLOFEMORAL time. However, if the defect is large, the shoulders may not be participating in load bearing, and the subchon- The role of alignment in the progression of an articular dral bone of the defect then becomes abrasive to the cartilage injury and OA cannot be underestimated. opposite articular surface, producing bipolar degenera- Sharma et al32 noted that, in the presence of malalign- tive changes. A repair tissue for this situation would ment of the tibiofemoral joint, the risk of progression need to bear all of the forces, be sturdy, and have visco- ofarthritisinthekneewasfourtimesinthemedialcom- elastic mechanical properties that make it durable partment when varus of just 2 degrees and five times in and nonabrasive, such as hyaline articular cartilage. the lateral compartment when only 2 degrees of valgus These properties will determine treatment options for was present over an 18-month time course. Other stud- the patient and are discussed further in Chapter 4 (see ies have shown that malalignment plays a role in Figure 1–1).
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