The articular cartilage of diarthrodial joints serves severalimportant - PDF document

The articular cartilage of diarthrodial joints serves severalimportant functions: joint lubrication, stress distribution tosubchondral bone to minimize peak stress, and provision ofa smooth low-friction surface. Repetitive and acute impact,as well as torsional joint loading can damage articular carti-lage surfaces of the knee joint. Injury to articular cartilagecan lead to pain, swelling, joint dysfunction, and possiblyprogressive joint degeneration. Nonsurgical treatment op-tions include oral medications, simple bracing, and physicaltherapy. Surgical interventions range from simple arthro-scopic debridement to complex tissue engineering, includ-ing autologous chondrocyte implantation. To determine theproper treatment option, each patient's age, intensity ofsymptoms, activity level, and lesion characteristics shouldbe considered. The purpose of this chapter is to providea comprehensive overview of the etiology, diagnosis, andmanagement of articular cartilage lesions.EPIDEMIOLOGYChondral lesions affect approximately 900,000 Americanseach year, leading to more than 200,000 surgical proce-dures to treat high-grade lesions (grade III or IV), as de-scribed in the classification section of this chapter. Curl et418ARTICULARCARTILAGEINJURIESTAMARA K. PYLAWKARICHARD W. KANGBRIAN J. COLEal. completed a retrospective review of 31,5 16 arthroscopiesand identified chondral lesions in 63% of cases, of which41% were grade III and 19% were grade IV. Hjelle et al.prospectively evaluated 1,000 knee arthroscopies and iden-tified chondral or osteochondral lesions in 61% of the pa-tients, with 55% classified as grade III and 5% as grade IV.Chondral or osteochondral lesions vary in size and canoccur in isolation or exist as multiple lesions in a single joint.Articular cartilage damage of the knee joint most commonlyoccurs in the weight-bearing zone of the medial femoralcondyle (58% of all cartilage lesions in the knee). Othercommonly affected zones include the weight-bearing zonesof the lateral femoral condyle and patellofemoral joint.ORGANIZATION AND COMPOSITIONArticular cartilage consists of a large extracellular matrix(ECM) with highly specialized cells (chondrocytes) sparselydistributed throughout the tissue, composing approximately10% of the total wet weight of the tissue (Fig. 30-1). Chon-drocytes are responsible for the homeostasis of articularcartilage, including synthesis, secretion, and maintenanceof the ECM. This homeostasis is partially regulated bychondrocyte metabolic activity that responds to variousagents, including (but not limited to) cytokines, growth fac- Figure 30-4Photomicrograph of biopsy from fibrocartilage fillafter marrow stimulation technique demonstrating a distinct lack oforganizational structure and poor PG staining (hematoxylin andeosin,X 10).visible mechanical disruption limited to articular cartilage.These injuries are characterized as (but not limited to) chon-dral fissures, flaps, fractures, and chondrocyte damage. Lackof vascular integration, and therefore lack of migration, ofmesenchymal stem cells to the damaged area limits the repairof this type of injury. Mild repair occurs as chondrocytes startproliferating and synthesizing additional ECM; however,this response is short lived, and defects remain only partiallyhealed. Thus, normal articular cartilage that is adjacent tothe damaged site may undergo additional loading forces pre-disposing it to degeneration over time.Osteochondral injuries are defined by a visible mechani-cal disruption of articular cartilage and subchondral bone.Such injuries occur when there is an acute assault on theTABLE 30-2 OUTERBRIDGE CLASSIFICATIONOF CHONDRAL INJURIESGradeDescriptionI\tSoftening and swelling of cartilageII\tFissures and fragmentation in an area1/2inch or lessin diameterIII\tFissuring and fragmentation in an area with morethan'/2-inch diameter involvementIV\tErosion of cartilage down to subchondral boneBFigure 30-5A: Arthroscopic photograph demonstrating anOuterbridge grade III lesion of the medial femoral condyle. B:Arthroscopic photograph demonstrating an Outerbridge grade IVlesion of the medial femoral condyle.cartilage, leading to a fracture that penetrates deep into thesubchondral bone. Subsequent hemorrhage and fibrin clotformation elicit an inflammatory reaction. The clot extendsinto the cartilage defect and releases vasoactive mediatorsand growth factors, such as transforming growth factor43and platelet-derived growth factor, both implemented in therepair of such osteochondral defects. The resulting chon-dral repair tissue is a mixture of normal hyaline cartilageand fibrocartilage and is less stiff and more permeable thannormal articular cartilage. Such repair tissue rarely persistsand may show evidence of deterioration with depletion ofPGs, increased hydration, fragmentation and fibrillation,and loss of chondrocyte-like cells. Alternatively, osteochon-dritis dissecans is a condition that may be developmentalChapter 30/Articular Cartilage Injuries421 tory drugs, activity modification, and oral chondropro-tective agents such as glucosamine or chondroitin sul-fate.Glucosamine stimulates chondrocyte and synovio-cyte activities, whereas chondroitin inhibits degra-dative enzymes and prevents fibrin thrombus for-mation in periarticular tissue. These substancesimprove pain, joint line tenderness, range of mo-tion, and walking speed. No clinical data, however,show that these oral agents affect the mechanicalproperties or biochemical consistency of articularcartilage.€If nonsurgical management fails, a referral to an ortho-paedic surgeon should be considered._Indications that would suggest this type of referralare included in Box 30-1.Surgical TreatmentE!Treatment options to restore the articular cartilage sur-face involve consideration of many factors: defect size,Chapter 30/Articular Cartilage Injuries423ent, concomitant pathology, patient age, physical de-and level, and patient expectations.Articular cartilage lesions of similar size may havemany surgical options with no general consensusamong orthopaedic surgeons. TABLE 30-9 RESULTS OF OSTEOCHONDRAL ALLOGRAFTSH, hip (femoral head); F, femur; Tr, trochlea; P, patella; T, tibia.However, frozen osteochondral tissue lacks cel-lular viability.The prolonged cold preservation method in-creases the "shelf-life" of the graft to at least 28days and alleviates the scheduling difficultieswhile maintaining cell viability(78%at28dayspreservation); however, chondrocyte suppres-sion remains an issue.Incorporation and healing of allografts dependon creeping substitution of host bone to allograftbone.Postoperative rehabilitation consists of immedi-ate continuous passive motion and protectedweight-bearing for 6 to 8 weeks.This procedure is most often used as a secondarytreatment option in patients who have failed pre-vious attempts at cartilage repair.Tables30-8and30-9summarize the outcomesstudies for osteochondral autograft and allografttransplants.SUGGESTED READINGBrittberg M. Evaluation of cartilage injuries and cartilage repair. Osteo-logie 2000;9:17-25.Brittberg M, Lindahl A, Nilsson A, et al. Treatment of deep cartilagedefects in the knee with autologous chondrocyte transplantation.N Engl J Med 1994;331:889-895.Buckwalter JA. Articular cartilage injuries. Clin Orthop 2002;402:21-37.Chapter 30/Articular Cartilage Injuries5 years-95%10 years-80%15 years-65%20 years-46%Buckwalter JA, Hunzinker EB, Rosenberg LC, et al. Articular cartilage:composition, structure, response to injury, and methods of facilita-tion repair. In: Ewwing JW (ed), Articular Cartilage and Knee JointFunction: Basic Science and Arthroscopy. New York: Raven Press,1990:19-56.Bugbee WD. Fresh osteochondral allografting. Op Tech Sports Med2000;8:158-162.Caplan A, Elyaderani M, Mochizuki Y, et al. Overview of cartilagerepair and regeneration: principles of cartilage repair and regenera-tion. Clin Orthop 1997;342:254-269.Chu CR, Convery FR, Akeson WH, et al. Articular cartilage transplan-tation.Clinical results in the knee. Clin Orthop 1999;360:159-168.Curl W, Krome J, Gordon E, et al. Cartilage injuries: a review of 31,516knee arthroscopies. Arthroscopy 1997;13:456-460.Edwards RB, Lu Y, Markel MD. The basic science of thermally assistedchondroplasty. Clin Sports Med 2002;21:619-647.Hjelle K, Solheim E, Strand T, et al. Articular cartilage defects in 1,000knee arthroscopies. Arthroscopy 2002;18:730-734.Kish G, Modis L, Hangody L. Osteochondral mosaicplasty for the treat-ment of focal chondral and osteochondral lesions of the knee andtalus in the athlete. Rationale, indications, techniques and results.Clin Sports Med 1999;18:45-66.Mandelbaum BR, Romanelli DA, Knapp TP. Articular cartilage repair:assessment and classification. Op Tech Sports Med 8:90-97.Miller BS, Steadman JR, Briggs KK, et al. Patient satisfaction andoutcome after microfracture of the degenerative knee. J Knee Surg2004;17:13-17.Peterson L, Brittberg M, Kiviranta I, et al. Autologous chondrocytetransplantation: hiomechanics and long-term durability. Am JSports Med 2002;30:2-12.Poole A. What type of cartilage repair are we attempting to attain? JBone Joint Surg Am 2003;85:40-44.Sprague NF. Arthroscopic debridement for degenerative knee joint dis-ease. Clin Orthop 1981;160:118-123.Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical tech-nique and rehabilitation to treat chondral defects. Clin Orthop2001;391:5362-S369.429StudyNumber of PatientsMean Age (yr)LocationMean Follow-upResultsMeyers (1984)2116-50H63 mo80% successMeyers et al. (1989)3938F,T,P3.6 yr78% success22% failureGarret (1994)1720F3.5 yr94% successGross (1997)12335F,T,P7.5 yr85% successChu et al. (1999)5535F,T,P75 mo76% good/excellent16% failureBugbee (2000)12234F5 yr91 % success rate at 5 yr75% success rate at 10 yr5% failureAubin et al. (2001)6027F10 yr84% good/excellent20% failureShasha et al. (2003)65NAT12 yrKaplan-Meier Survival Rate: