Table Of ContentA 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
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Notices
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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).
