Hip Cartilage Restoration: Overview 87 Lisa M. Tibor and Jeffrey A. Weiss Contents Introduction ........................................ 1082 Cartilage Basic Science: General ................ 1082 Structure and Composition ......................... 1082 Material Properties .................................. 1085 Mechanics of the Hip .............................. 1085 Contact Patterns .................................... 1086 Mechanical Causes of Articular Cartilage Defects .............................................. 1087 Clinical Characteristics of Hip Cartilage Defects .............................................. 1087 Treatment Options ................................ 1089 Nonoperative Management ......................... 1089 Primary Repair Versus Arthroscopic Debridement ........................................ 1089 Microfracture ....................................... 1092 Autologous Chondrocyte Implantation (ACI) and Matrix-Associated Chondrocyte Implantation (MACI) ............................... 1092 Autologous Matrix-Induced Chondrogenesis (AMIC) ........................... 1093 Osteochondral Autograft ........................... 1093 Osteochondral Allograft ............................ 1093 Allogenic Cartilage Graft ........................... 1094 Summary ........................................... 1094 References .......................................... 1094 Abstract Articular cartilage must resist mechanical load- ing modes that include compression, tension, and shear. The material characteristics of artic- ular cartilage are optimized for these roles and are intricately related to structure and compo- sition. When full-thickness chondral and osteochondral defects occur in the hip, they are painful, causing mechanical symptoms and inflammation as a result of cartilage break- down. These defects often progress over time. The treatment goals for cartilage restoration surgery are the resolution of symptoms, return to activity, and prevention of progressive dam- age. To achieve this, a preoperative plan is essential, and the nature of the lesion including size, location, underlying etiology, or associ- ated structural pathoanatomy must be known. Indications for treating a focal chondral defect in the hip include acute trauma with an unstable fragment, continued pain and symptoms despite conservative management, a visible chondral defect on preoperative imaging with a positive response to a diagnostic intra-articular injec- tion, and intra-articular loose bodies. The objec- tive of this chapter is to describe the current state of the art for restoration of focal articular cartilage defects in the hip. To support this objective, we review the basic structure and function of articular cartilage as well as the biomechanics of the hip and of focal defects. Subsequently, the clinical presentation, diagno- sis, and suspected underlying causes of damage L.M. Tibor (*) Kaiser Permanente Medical Center, South San Francisco, CA, USA e-mail: [email protected]J.A. Weiss Departments of Bioengineering and Orthopaedics, and Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, UT, USA e-mail: [email protected]# Springer Science+Business Media New York 2015 S.J. Nho et al. (eds.), Hip Arthroscopy and Hip Joint Preservation Surgery , DOI 10.1007/978-1-4614-6965-0_96 1081
Transcript
Hip Cartilage Restoration: Overview 87Lisa M. Tibor and Jeffrey A. Weiss
AbstractArticular cartilage must resist mechanical load-ing modes that include compression, tension,and shear. The material characteristics of artic-ular cartilage are optimized for these roles andare intricately related to structure and compo-sition. When full-thickness chondral andosteochondral defects occur in the hip, theyare painful, causing mechanical symptomsand inflammation as a result of cartilage break-down. These defects often progress over time.The treatment goals for cartilage restorationsurgery are the resolution of symptoms, returnto activity, and prevention of progressive dam-age. To achieve this, a preoperative plan isessential, and the nature of the lesion includingsize, location, underlying etiology, or associ-ated structural pathoanatomy must be known.Indications for treating a focal chondral defectin the hip include acute trauma with an unstablefragment, continued pain and symptoms despiteconservative management, a visible chondraldefect on preoperative imaging with a positiveresponse to a diagnostic intra-articular injec-tion, and intra-articular loose bodies. The objec-tive of this chapter is to describe the currentstate of the art for restoration of focal articularcartilage defects in the hip. To support thisobjective, we review the basic structure andfunction of articular cartilage as well as thebiomechanics of the hip and of focal defects.Subsequently, the clinical presentation, diagno-sis, and suspected underlying causes of damage
L.M. Tibor (*)Kaiser Permanente Medical Center, South San Francisco,CA, USAe-mail: [email protected]
J.A. WeissDepartments of Bioengineering and Orthopaedics, andScientific Computing and Imaging Institute, University ofUtah, Salt Lake City, UT, USAe-mail: [email protected]
# Springer Science+Business Media New York 2015S.J. Nho et al. (eds.), Hip Arthroscopy and Hip Joint Preservation Surgery,DOI 10.1007/978-1-4614-6965-0_96
to articular surfaces in the hip are reviewed.Finally, we discuss the available treatmentoptions, their relative indications, and theirpublished outcomes to date.
Introduction
Full-thickness chondral and osteochondral defectsin the hip are painful, causing mechanical symp-toms and inflammation as a result of cartilagebreakdown. In addition, these defects progressover time from increased mechanical stress onthe surrounding cartilage and from the increasedintra-articular inflammation. Thus, the treatmentgoals for cartilage restoration surgery in the hipare to improve pain and symptoms and to slow theprogression to osteoarthritis. Accordingly, thischapter focuses on treatments for focal full-thickness chondral or osteochondral defects.
Cartilage damage negatively influences the out-comes of open and arthroscopic management offemoroacetabular impingement (FAI) as well asthe outcome of acetabular reorientation for dyspla-sia [1, 2]. Conversely, untreated FAI or dysplasiacauses continued mechanical stress on an area ofrepaired cartilage, which negatively influences theoutcomes of cartilage surgery. Thus, identificationof bony pathoanatomy is an important part of thepreoperative planning for cartilage restoration sur-gery. In addition to FAI and dysplasia, there areseveral traumatic and nontraumatic causes of focalcartilage damage. Osteochondral lesions occur inpatients who had Perthes’ disease in childhood [3]and in those with femoral head avascular necrosisor osteochondritis dissecans lesions. Patients withfemoroacetabular impingement (FAI) frequentlyhave acetabular rim lesions and, less commonly,parafoveal defects [4]. Instability occurring as aresult of dysplasia causes chondral damage at thesuperior aspect of the acetabulum and femoralhead (Fig. 1) [5], whereas an episode of traumaticinstability in conjunctionwith FAI usually causes aposterior rim lesion and/or a parafoveal femoralhead defect (Fig. 2) [6]. Finally, a fall on the greatertrochanter can cause a lateral impact event, trans-mitting force to the central femoral head and/oracetabulum and causing cartilage damage [7].
When compared to what is known about carti-lage restoration in the knee, there is relatively littleinformation specifically about cartilage restora-tion in the hip. Currently, most cartilage repairstrategies for the hip are based on basic scienceand techniques that were developed for the knee.In the past decade, however, there has been adramatic improvement in magnetic resonanceimaging (MRI), arthroscopy, and open surgeryfor younger patients with hip pain. Theseimprovements should also lead to hip-specificcartilage science and restoration techniques. Theobjective of this chapter is to describe the currentstate of the art for treating focal articular cartilagedefects in the hip. To support this objective, wereview the basic structure and function of articularcartilage as well as the biomechanics of the hipand focal articular defects. Subsequently, the clin-ical presentation, diagnosis, and suspected under-lying causes of damage to articular surfaces in thehip are reviewed. Finally, we discuss the availabletreatment options, their relative indications, andtheir published outcomes to date.
Cartilage Basic Science: General
Articular cartilage must resist mechanical loadingmodes that include compression, tension, and shear.Thematerial characteristics of articular cartilage areoptimized for these roles and are intricately relatedto structure and material composition. This sectionprovides a brief review of these topics.
Structure and Composition
Articular cartilage is composed primarily of water,collagen, and large proteoglycans (Fig. 3, leftpanel). By wet weight, cartilage is 68–85 % water,10–20%collagen, 5–10%proteoglycan, and<5%other matrix molecules [8]. The interstitial fluidcontains dissolved electrolytes, predominantlyNa+, Ca2+, Cl�, and K+. Chondrocytes account forless than 10% of the total tissue volume [9] and areresponsible for the metabolic activity of cartilage.The primary collagen in articular cartilage is fibril-forming type II collagenwith variable orientation of
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Fig. 1 Images from a patient with dysplasia (a) whounderwent arthroscopy and periacetabular osteotomy (b).At the time of arthroscopy, she had full-thickness chondraldamage at the acetabular rim (c) and underwent
microfracture of the lesion (d) (Reprinted from [5], Copy-right# 2011 by American Orthopaedic Society for SportsMedicine, by permission of SAGE Publications)
Fig. 2 Episodes of traumatic hip posterior hip dislocationoccur with the hip in flexion and internal rotation, with aposteriorly directed force on the femur. If there is a camlesion present, the femoral head and neck can lever on theanterior acetabular rim. As the femoral head dislocates
posteriorly, chondrolabral damage can occur at the poste-rior labral rim, analogous to a bony Bankart lesion in theshoulder (Reprinted with permission from Springer Sci-ence+Business Media, from [6]. Copyright # 2012, TheAssociation of Bone and Joint Surgeons®)
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collagenfibers depending on the depth of the tissue.In the superficial zone (top 10–20 %), fibers areoriented parallel to the articular surface; in the mid-dle zone (middle 40–60 %), fibers are orientedrandomly; and in the deep zone (bottom ~30 %),the fibers are oriented perpendicularly to thesubchondral bone. Aggrecan accounts for 80–90% of all proteoglycan in cartilage. Chondroitin sul-fate, keratin sulfate, and hyaluronan are the primaryglycosaminoglycan (GAG) side chains in cartilage.Chondroitin sulfate and keratin sulfate have nega-tively charged sulfate and carboxyl groups that
make the chains anionic overall. Hyaluronan isnot sulfated and interacts with aggrecan and linkproteins to form large aggregates that areimmobilized in the extracellular matrix and whichconsequently stabilize the extracellular matrix.Since these charged proteoglycans are immobilizedwithin the extracellular matrix, the resulting chargeis referred to as the “fixed charge density.” Theproteoglycan distribution, and therefore the distri-bution of fixed charge density, varies through thecartilage depth. Aggrecan level is the lowest in thesuperficial zone and increases with depth [8].
Fig. 3 Cartilage structural features and their relationshipto continuum level mechanical behavior. Left panel – thestructure and orientation of collagen and proteoglycanaggregates determine the continuum level mechanical
behavior. Right panel – key features of continuummechan-ical behavior include tension–compression nonlinearity,anisotropy, viscoelastic material behavior, and swelling
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Material Properties
The structure of articular cartilage produces com-plex material behavior (Fig. 3, right panel).Because cartilage structure and composition varywith depth, material properties also vary withdepth [10–13]. The material behavior of cartilagevaries between species within the same joint,between joints within species, and spatially withineach joint within each species [14–16]. Cartilageexhibits nonlinear material behavior in bothtension and compression. Under uniaxial tensilestress, cartilage material behavior is primarilydetermined by the collagen fibrils. Thestress–strain curve in tension exhibits a toe regionfollowed by an approximately linear region due tothe uncrimping of collagen fibers followed byloading of straightened fibers [8]. Under uniaxialcompressive stress, the material response ofcartilage is governed by the proteoglycan matrixand fluid flow. The modulus of cartilage in tensionis approximately one to two orders of magnitudelower than in compression, a discrepancy knownas tension–compression nonlinearity [16]. Thischaracteristic is important for most modes ofcartilage deformation that are relevant to whole-joint mechanics.
Fluid–solid interactions, the intrinsicviscoelasticity of the solid phase, and fixed chargedensity causes flow-dependent viscoelasticity ofthe cartilage and swelling [17–19]. The cartilageswelling is caused by the fixed charge density ofthe tissue and charge–charge repulsion betweenclosely packed GAGs attracting interstitialfluid counterions [8]. Collagen primarily bearstensile stress, and thus the fibrillar collagenresists expansion of the solid matrix duringswelling [20].
Solutes, including nutrients and metabolicby-products, move through cartilage via diffu-sion. Solute diffusivity in cartilage is smallerthan in aqueous solution [8], and diffusivitydecreases as the tissue is compressed [21, 22].The size of the solute also influences solutediffusivity. For large solutes, cyclic loading canenhance diffusion but it has no effect on smallsolutes [23].
Mechanics of the Hip
The kinematics (motion) of the hip are primarilydetermined by the congruency of the articularsurfaces, their shape and curvature, the limits ofmotion imposed by bony contact between thefemur and acetabulum or labrum, and the jointreaction forces related to musculature and bodyweight. The stress at the articular cartilage layersand the cartilage contact area during articulationare determined by joint congruency, curvature,chondral thickness and material properties, andjoint load. Local joint congruency, defined as thecongruency of the two articulating surfaces in theregion of a particular point of contact, is in turn afunction of joint kinematics.
The magnitude and orientation of the abductormuscle force as well as the distance from the jointcenter counteracts the force from body weight, sothat the overall joint reaction forces across the hipare determined by the sum of these two oppositelydirected forces. Typical joint reaction forces duringsingle-leg stance are approximately three times thebody weight but vary as a function of activity. Thestudy by Bergman et al. is the most widely quotedreport on in vivo hip joint reaction forces [24].These investigators measured hip joint reactionforces during activities of daily living in patientswho had received a total hip replacement with atelemeterized load cell. Joint reaction forces rangedfrom2.4 times bodyweight during levelwalking to2.6 times body weight when walking downstairs.Independent of other factors, joint reaction forcesare decreased bymedializing the center of rotation.For example, this can occur nonsurgically by theuse of a cane in the contralateral hand, or surgicallyvia lateralization of greater trochanter, whichmoves the relative point of application of theabductor muscles farther from the joint center.
Although the normal hip is generally consideredto be a highly congruent joint, the local congruencyvaries with changes in joint orientation, such asflexion–extension or abduction–adduction. Fur-ther, congruency is often altered in joints withpathomorphologies such as acetabular dysplasiaand FAI. For a given joint reaction force, higher
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congruency generally implies a larger contact areaand thus lower contact stresses. If the global con-gruency is defined as, for instance, the congruencyof a pair of spheres to the articular surfaces, dys-plastic hips have a lower global level of congru-ency than normal hips. However, this does notnecessarily translate into higher local contactstresses since local congruency is not significantlydifferent between normal and dysplastic hips [25].
Contact Patterns
Areas of contact on the articular surfaces vary some-what with activity and motion during the activity inboth normal and pathomorphologic hips. In thenormal hips, the direction of loading and the loca-tion of chondral contact change frompredominantlysuperior–posterior during ascending stairs, to moresuperior duringwalking, to superior–anterior duringdescending stairs [26]. Predicted peak stress in nor-mal hips ranges from 7.52 � 2.11 MPa for heel-strike during walking (2.3 times the bodyweight) to8.66 � 3.01MPa for heel-strike during descendingstairs (2.6 times the body weight). Across all activ-ities of daily living, the contact area of the femur onthe acetabular cartilage occupies about a third ofthe total surface area. Even in the normal hips,
the distribution of contact stress is highlynonuniform due to local incongruities between thefemoral and acetabular cartilage. In addition, con-tact stress variesmore between different subjects fora single activity than between different activities fora single subject.
In the hips with acetabular dysplasia, theacetabulum is shallow. Dysplasia is typicallydiagnosed radiographically by an anterior and/orlateral center edge angle (CEA) less than 20–25�
and an acetabular index greater than 10�. Thesemeasures are indicative of a shallow acetabulumand an upwardly sloping sourcil, respectively.Patient-specific finite element (FE) predictions ofcontact area show that only the superior region ofthe acetabulum exhibits significantly differentlabral contact areas when comparing normal anddysplastic subjects [25] (Fig. 4). This suggeststhat during activities of daily living, the superiorlabrum in the dysplastic hip is loaded morethan other portions of the acetabular labrum.Predictions of labral load support corroboratethis finding – the labrum in dysplastic hipssupports loads that are 2.8–4.0 times larger thanthat of normal hips. These results are consistentwith clinical observations of labral hypertrophy,as well as the superior or anterosuperior locationof labral tears in the dysplastic hip [27–29].
Fig. 4 Cartilage contact pressure in coronal (top) andsagittal (bottom) slices of a representative normal hip(left), retroverted hip (middle), and dysplastic hip (right).Normal hips exhibited centered, distributed loading (leftcolumn). Contact in retroverted hips was moved medially
and superiorly with respect to normal hips (middle col-umn). In dysplastic hips, loading was shifted laterally, andin comparison to normal hips, a significantly higher per-centage of load was supported by the acetabular labrum[25, 30]
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In the hips with acetabular retroversion, theacetabulum opens more posterolaterally than nor-mal. This is recognized on anteroposterior radio-graphs by the presence of a crossover sign, whichindicates a prominent anterior acetabular wall, adeficient posterior acetabular wall, or both. Carti-lage contact in retroverted hips is focused in thesuperomedial acetabulum, whereas in normalhips, contact patterns are distributed over moreof the entire acetabulum (Fig. 4) [30]. Addition-ally, retroverted subjects tend to have patches ofmore medial contact.
Mechanical Causes of ArticularCartilage Defects
Focal cartilage defects often result from cartilagedelamination, typically due to shear loading thatcauses failure at the osteochondral interface. Invitro, both articular surface contact stress andmaximum shear stress have been shown to predictcartilage fissuring under impact loads [31, 32].The maximum shear stress during activity for thenormal hip tends to occur at the interface of theacetabular cartilage and subchondral bone, nearthe junction of the cartilage with the labrum [33].
For a specific joint, chondral defects greaterthan a certain size tend to increase in size, generatean inflammatory response in the joint, and ulti-mately lead to OA, while other smaller defectswill remain stable and not progress to disease[34]. Furthermore, a number of geometric factorscontribute to the variability in clinical successtreating osteochondral defects, as these factorsoften produce unfavorable conditions for theformation of new cartilage or the survival ofimplanted plugs, scaffolds, or cells [35].The major geometric factors are defect size, jointcurvature, joint congruence, cartilage thickness,and status of the rim of the defect. Increasedjoint curvature generally causes the rim of thedefect to experience higher stresses and strainsduring joint loading and articulation. This is fur-ther exacerbated if the joint surfaces are incongru-ent. Thinner regions of articular cartilage haveless ability to increase the local congruency dur-ing deformation since deformation is limited by
the reduced thickness. And, finally, if the rim ofthe defect is well defined and intact, the defect willbe more likely to remain stable and not progress inthe joint, whether it is repaired or not.
As illustrated in the upper panels of Fig. 5 for adefect in the femoral condyle of the knee, increas-ing defect size exposes the rim of the defect tohigher stresses and strain. Furthermore, in largerdefects, healing neocartilage or implanted plugsor cells are more exposed to deformation duringhealing, resulting in a progressively worse out-come independent of other factors. Because thecongruency of diarthrodial joints can vary as afunction of joint kinematics, a defect may besubjected to different degrees of loading as afunction of joint articulation. This is illustratedin the lower panels of Fig. 5 for the femoralcondyle of the knee as a function of knee flexion.
Clinical Characteristics of Hip CartilageDefects
There is no single history or physical examinationfinding that is pathognomonic for cartilage dam-age or chondral defects in the hip. There are,however, some predictable patterns of injury.Byrd reported a series of athletes who hadchondral damage after lateral impact events, sus-taining a blow to the greater trochanter during afall [7]. Because younger patients typically havelittle soft tissue to absorb the force of an impact,the force is transmitted to the central joint surface.The cartilage subsequently fails at the medialaspect of the femoral head. There may also be acorresponding lesion in the weight-bearing por-tion of the acetabulum just above the fossa, whichmay result from chondrocyte compression [7].Parafoveal chondral defects have been describedin athletes with FAI that participate in sports thatrequire rapid lower extremity flexion, torsion,and force. The lesion seems to occur fromimpingement-induced instability and translation,with incongruent hip motion causing high shearstresses and cartilage deformation [4]. Similarly,athletes who have a distinct hip subluxation ordislocation can have chondral injuries andligamentum teres tears around the fovea, as well
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as posterior labrum and cartilage injury [6].Finally, about 25 % of patients with a history ofPerthes’ disease in childhood have full-thicknesschondral defects [3]. Regardless of the proposedetiology, patients report some combination ofsharp groin or buttock pain, stiffness, clicking,popping, or catching [7, 36]. These symptomsare also characteristic of labral tears, and patientswith chondral defects frequently have a coexistinglabral tear [36].
No single exam maneuver is specific forchondral pathology. The location of the lesionmay influence the presence and nature of painwith weight-bearing or with specific exammaneu-vers. Pain with hip “logrolling” usually indicatessynovitis and/or a hip joint effusion. A full hipexamination including stance, gait, range ofmotion, strength, location of specific sites of ten-derness, and provocative maneuvers includingapprehension and impingement testing shouldbe performed. It is important to evaluate for
FAI or dysplasia, labral tears, compensatorytendinopathies, and compensatory gait patterns.Both FAI and dysplasia can cause or exacerbatechondral damage and should be addressed ifsurgery is planned.
All patients should have radiographs of the hipto evaluate for FAI, dysplasia, joint incongruity,and early arthritic changes. A CT scan with ver-sion analysis is helpful for further evaluation ofFAI or dysplasia, but does not image the cartilagedirectly. Cartilage defects are best seen with a highquality MRI or MR arthrogram of the hip. TheMRI should be performed with a 1.5T or 3Tmagnet and small-field-of-view coil. A combina-tion of coronal, sagittal, axial, and radial imagesbest characterizes the location, size, and natureof the defect. Cartilage imaging is, however,notoriously difficult. MRA is more effective fordetecting labral tears than cartilage damage, withsensitivity for chondral defects ranging from 47%to 81 %, specificity ranging from 66 % to 89 %,
Fig. 5 Effects of defectsize and joint curvature onfocal cartilage defects,shown for the femoralcondyle of the knee joint.Top panels – as defect sizeincreases, the rim of thedefect and healing tissuewithin the defect issubjected to increasinglyhigh strains during normaljoint loading.Bottom panels– joint congruency andcurvature often vary as afunction of joint orientation.These changes haveimplications for theeffective strains that a defectwill experience. As kneeflexion increases,congruency of the articularsurfaces and, thus contactarea, decreases whilecontact stresses and strainsincrease
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and accuracy of 67 % [36, 37]. Bony edemaadjacent to the defect can indicate recent trauma[7], or local overload [36].
Treatment Options
The treatment goals for cartilage restoration sur-gery are the resolution of symptoms, return toactivity, and prevention of progressive damage.To achieve this, a preoperative plan is essential,and the nature of the lesion including size, loca-tion, underlying etiology, or associated structuralpathoanatomy must be known. Indications fortreating a focal chondral defect in the hip includeacute trauma with an unstable fragment, contin-ued pain and symptoms despite conservative man-agement, a visible chondral defect on preoperativeimaging with a positive response to a diagnosticintra-articular injection, and intra-articular loosebodies. The timing of surgery depends on the typeof lesion, age of the patient, and any previousinterventions. Of note, patients who have loosebodies or unstable fragments should undergo sur-gery in a more urgent fashion because of thepotential for severe cartilage damage from aloose fragment within the joint.
Treatment options for cartilage defects includeconservative measures like activity modification,weight management, and viscosupplementationas well as surgical techniques like microfracture,second-generation ACI techniques, and oste-ochondral allografts (Figs. 6, 7, and 8) [38, 39].Specific technique chapters follow for each typeof cartilage restoration surgery; the discussion ofeach type of intervention in this chapter will focuson the basic science rationale for each techniqueand any published outcomes for the hip.
Nonoperative Management
For many patients with chondral defects, a trial ofnonoperative measurement is appropriate. Thisoften consists of activity modification or weightmanagement to decrease the mechanical loadacross the damaged area of cartilage. Physicaltherapy focusing on hip and core strengthening
may also help improve the muscular dynamicsaround the hip, particularly if there is a componentof instability [40, 41]. Patients frequently askabout nutritional supplements. The most wellknown of these is a combination of glucosamineand chondroitin. Individual trials have shownmixed results, and in meta-analysis, there was noclinically relevant effect on joint pain or jointspace narrowing [42].
Intra-articular cortisone injections may be usedto reduce symptoms from inflammation. How-ever, each injection has some risk of infection,soft tissue weakening, and possibly a microscopiceffect on the cartilage [43]. Multiple cortisoneinjections should not be the definitive manage-ment strategy for young patients who are potentialcandidates for cartilage restoration procedures.Platelet-rich plasma (PRP) has also been toutedas a possible treatment for cartilage defects orosteoarthritis. Advocates for intra-articular PRPinjections promote it as a topical application ofbiological factors that promote healing of thedefect. However, preparations of PRP vary andalthough the effective agent has been proposed, itis not definitively known [44]. There are two stud-ies of PRP injection for hip arthritis; other studiesof intra-articular PRP are for the knee or for thetalus. Most patients have some initial improvementwith gradual worsening over time [45]. Hyaluronicacid or viscosupplementation improves symptomsby a combination of antiinflammatory effects, res-toration of the viscosity of synovial fluid, and nor-malization of synovial cell hyaluronate synthesis[46]. It appears to be safe, without potential adverseeffects [46]. The results of hyaluronic acid injec-tions are mixed. In the hip, 45–60% of people havepain relief 6 months after injection [46].
Primary Repair Versus ArthroscopicDebridement
Primary repair can be considered for anosteochondral fragment especially in the settingof an acute trauma where the fragment shouldundergo fracture-type healing. If there is a purelychondral flap, the healing is less predictable. Casereports of direct repair have been published. These
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are limited, but the results are reported to be goodin the short-term follow-up [47]. Debridementof the flap removes a mechanical irritantand prevents the formation of loose bodies.This may allow symptoms to resolve and permitreturn to activity or sports [7]. Arthroscopyis definitive for diagnosis of an unstable flap if
the preoperative imaging was inconclusiveand arthroscopic debridement is often thedefinitive therapy. Occasionally, however, thelesion is larger than anticipated and a secondopen cartilage restoration procedure is indicated.Arthroscopic chondral debridement is often usedas the comparison procedure for other cartilage
Fig. 6 Currently, treatment decisions for cartilage resto-ration are based on the size and type of lesion (here,depicted for the knee). Small focal defects (<2 cm2) areoften treated with microfracture. Larger defects (2–3 cm2)can be treated with osteochondral autograft or cell-based
therapies like ACI, MACI, AMIC, or allogenicchondrocytes. Even larger defects (~4 cm2) are treatedwith allografts (Reprinted from [39] with permissionfrom Elsevier)
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Fig. 7 The treatmentstrategy for a chondraldefect can also beconsidered in the context ofthe matrix and scaffoldbeing applied. Currentlyused grafts may consist ofcells and matrix, as in thecase of an osteochondralallografts and autografts,and juvenile cartilageparticles, or just matrix as isthe case with devitalizedgrafts. In the future, cell-derived decellularized ECMproduced in vitro may alsobe a treatment option(Reprinted from [38] withpermission from Elsevier)
Fig. 8 Developmental progression of tissue-engineeringtherapies for articular cartilage repair. In general, cartilagerepair therapies are based on a strategy of reproducingnormal cartilage growth and development. Early strategieslike ACI rely on chondrocyte proliferation. Second-generation therapies like MACI or AMIC involve cellsimplanted in a matrix and covered with a membrane with
the goal of producing in situ cartilage. More recentlydeveloped therapies include implantation of juvenile carti-lage, with the goal of expansion and development intomature adult cartilage tissue. Future directions includedevelopment of larger constructs and potentially a biolog-ical joint replacement (Reprinted from [39] with permis-sion from Elsevier)
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restoration techniques. In the hip, debridementhas worse outcomes when compared with autolo-gous chondrocyte implantation (ACI) [48] ormicrofracture [49].
Microfracture
Microfracture consists of using a surgical awl ordrill to penetrate the subchondral bone at the baseof a cartilage lesion. The holes in the subchondralplate promote bleeding into the defect, withmigration of stem cells and formation of a“superclot,” ultimately resulting in the productionof reparative fibrocartilage within the defect [50].For microfracture to successfully producefibrocartilage, the defect needs to have verticalwalls of stable, normal cartilage, creating a“well-shouldered” lesion. This decreases shearand compression forces and protects the clot dur-ing healing, which is important because the sta-bility of the clot contributes to the success of theprocedure [51]. The advantages of microfractureare that it is technically straightforward, can beperformed arthroscopically, and is low-cost.The disadvantage of microfracture comparedto other cartilage repair techniques is that itproduces less Type II cartilage and has differentbiomechanical properties than hyaline cartilage,which may make the repair less durable than othertechniques. In addition, the overall concentrationof mesenchymal cells in the bone marrow islow and their chondrogenic potential declineswith age [52].
Microfracture is indicated for full-thicknesslesions in patients undergoing concomitant treat-ment of FAI or dysplasia. Most commonly, theseare acetabular rim lesions but, when technicallyfeasible, microfracture can also be used for smallfemoral head lesions (Fig. 6). It is contraindicatedfor lesions over 2 cm2, for patients not willing toendure postoperative non-weight-bearing or reha-bilitation, and for bipolar lesions. The results ofmicrofracture for lesions in the hip have generallybeen reported in combination with treatment forFAI [49]. One study reported better results withmicrofracture than with debridement, with the
greatest improvement seen by 8 weeks withmaintenance of the result for up to 12 months[49]. On second-look arthroscopy, patients hadfibrocartilage fill of most or all of the defect [49].Patients with more extensive lesions, however,still progress to arthroplasty and it seems that thetechnique is limited by the size and extent of thelesion.
Autologous Chondrocyte Implantation(ACI) and Matrix-AssociatedChondrocyte Implantation (MACI)
Both ACI and MACI involve harvesting autolo-gous chondrocytes, growing them in culture, andsubsequently implanting them [53] (Figs. 6 and 8).MACI and matrix-assisted chondrocyte trans-plantation (MACT) are second-generation tech-niques that utilize absorbable scaffolds tosupport the implanted chondrocytes duringhealing. Theoretically, ACI and MACI shouldrestore hyaline cartilage at the defect. Unfortu-nately, both ACI and MACI are two-stage pro-cedures, with a technically demanding secondstage performed via a surgical hip dislocationapproach. In the original technique, a periostealpatch is used to cover the implanted chondrocytes.Complications related to the periosteum are notinfrequent, although most surgeons who performACI regularly are now using a synthetic collagenmembrane.
ACI and MACI are indicated for symptomatic,unipolar, well-contained defects that are between2 and 10 cm2 and with less than 6–8 mm of boneloss. There has only been one outcomes studypublished for ACI or MACI in the hip. In thisseries, MACI was better than debridement at mid-term follow-up. It should be noted, however, thatall lesions were acetabular [48]. In addition,results tend to be worse when ACI is performedfor failed microfracture [54]. When compared tomicrofracture, the results of ACI tend to be stableor show a trend toward continued improvement.When compared with autograft transplant, theresults are similar, but the clinical response tendsto be slower [55].
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Autologous Matrix-InducedChondrogenesis (AMIC)
Essentially, AMIC is a second-generationmicrofracture technique. After the microfractureis performed, the fibrin gel is placed in the defectand a porcine collagen I/III matrix is sewn overthe lesion. This protects the clot and allows themesenchymal stem cells to differentiate [51].When compared to MACI, AMIC is less expen-sive and is a single-stage surgery. Furthermore,there is no autograft donor site morbidity. Becausethe technique involves sewing a membraneover the stabilized superclot, it does require asurgical hip dislocation approach. A modifiedall-arthroscopic version of the technique has alsobeen published [48].
AMIC is indicated for symptomatic full-thickness chondral and osteochondral lesionsin weight-bearing regions. The maximumrecommended size is as yet unknown, but a caseseries of patients who underwent AMIC for fem-oral head and acetabular lesions measuring morethan 2 cm2 has been published [56]. This seriesconsisted of six patients with a minimum of 1-yearfollow-up, all of whom had improved short-termfunction. In the knee, the published results arestable at 1–2 years, with improvements in bothoutcomes and activity scores [57]. Some patientshave developed intralesional osteophytes afterAMIC and some patients in each series stillprogressed to arthroplasty [57].
Osteochondral Autograft
Osteochondral autograft techniques involvetransplanting healthy, mature cartilage from anon-weight-bearing part of the hip or knee to thesite of a chondral defect (Fig. 7). The transplantedplug undergoes osseous integration with thesubchondral bone, and the transplanted cartilageintegrates with the adjacent host cartilage viafibrocartilage [58]. The advantage ofosteochondral autografting is that it places newmature hyaline cartilage into the defect in a single-stage procedure. Nonetheless, it is limited by
donor site morbidity, graft availability, and thepotential for dead space between the graftplugs [58].
Osteochondral autografts are indicated forsmall- to medium-sized focal lesions on the fem-oral head and acetabulum (2.5–4.0 cm2) (Fig. 6)[58]. Autografts are contraindicated for patientswith avascular necrosis and advanced osteoarthri-tis and for patients older than 50 [59, 60]. In thehip, there have been several case reports and caseseries of osteochondral autografts performed forvarying indications. These generally have goodresults in short-term follow-up [61]. Within alarger series of patients with Perthes’ disease,four patients underwent autografting, withanecdotally good results [62]. The exception tothis trend was a series of patients who underwentautografting for lesions caused by avascularnecrosis, who had uniformly poor results [60].
Osteochondral Allograft
Like osteochondral autografts, osteochondralallograft involves a cartilage transplant of intactviable cartilage and underlying subchondral boneinto a defect (Fig. 7) [63]. Cartilage is relativelyimmunoprivileged and has an avascular matrix,which means that the host immune reaction islimited [63]. As part of the healing process, allo-graft bone becomes necrotic and is reabsorbed viacreeping substitution. This provides a scaffold andsupports the articular surface during gradualincorporation [64].
Osteochondral allografts are indicated fortreatment of larger lesions or for lesions withsubstantial bone loss (Fig. 6). It has the advantageof precisely restoring the chondral surface archi-tecture in a single-stage procedure with viablehyaline cartilage. It can also be used for largedefects with no donor site morbidity [63]. Graftavailability can, however, be limited and the graftscan be expensive. There is some risk of rejection,incomplete incorporation, or disease transmissionas well. Finally, it can be technically demanding tomatch or size the allograft intraoperatively. Thereare only limited clinical reports available for
87 Hip Cartilage Restoration: Overview 1093
osteochondral allografting in the hip. Patientsreceiving fresh allografts performed via a surgicaldislocation approach for acetabular or femoralhead lesions had an average 25-point improve-ment in their Harris Hip Score at a minimum of2-year follow-up [65].
Allogenic Cartilage Graft
Allogenic cartilage grafting is the most recentlydeveloped cartilage repair technique. With thistechnique, the allogenic cartilage is a cell carrierand not a structural graft (Figs. 7 and 8). Thereare two types of allogenic cartilage grafting:morcellized cartilage allograft and allogenicchondrocyte implants. In the former, morcellizedjuvenile chondrocytes are placed into a defect.The chondrocytes then migrate out of thecartilage cubes and produce extracellularmatrix to fill the defect [66]. With allogenicchondrocyte implants, the cartilage is harvestedand subsequently enzymatically digested torelease and isolate the chondrocytes. The cellsare then mixed with alginate to form beads forimplantation [67].
The indications for allogenic cartilage graftingare similar to those for ACI: symptomatic unipolarwell-contained defects measuring 2–10 cm2 withless than 6–8 mm of bone loss. Both types ofchondrocyte grafting can be performed as asingle-stage procedure and the chondrocytesthemselves appear to be immunoprivileged via alack of surface allo-reactivity proteins [67]. Inaddition, if genetic rather than mechanical factorscontributed to the formation of the defect, allo-genic cartilage replaces the patient’s potentiallycompromised cells [67]. The disadvantages ofchondrocyte grafting are that the complicationsare similar to those for ACI, there is some risk ofdisease transmission because it is a donor tissue,and clinical results are limited. There are no clin-ical reports of allogenic cartilage grafting for thehip. In the knee, there is one case series thatreported significant and stable clinical improve-ment at a 5-year follow-up, but with a 19 % (4/21)failure rate [68].
Summary
There are many different techniques available forcartilage repair or restoration in the hip. Whencompared with the knee, the published resultsare limited. There are several reasons for this;however, the awareness of young adult hip diseaseis increasing and the hip preservation field as awhole is continuing to develop. This is likely toincrease the use of cartilage repair techniques forthe hip and concomitantly increase the number ofpublished clinical results.
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