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CHONDRAL AND OSTEOCHONDRAL INJURIES
OSTEOCHONDRAL INJURIES OF THE KNEE
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CHONDRAL AND OSTEOCHONDRAL INJURIES Diagnosis and Management James M. Farmer, MD, David F. Martin, MD, Carol A. Boles, MD, and Walton W. Curl, MD
Chondral and osteochondral injuries are relatively common in the weightbearing joints of the lower extremity. The pathology can range from a simple contusion of the articular cartilage and subchondral bone to a fracture involving the cartilage alone or cartilage and underlying subchondral bone together. The mechanism of injury is from one of three types of trauma: compaction, shearing, or avulsion.26Because the injury is usually subtle and causes little to no dysfunction, the diagnosis of acute injuries is delayed. Occasionally, the injury is severe enough to cause a significant effusion, hemarthrosis, or ligament disruption. Even in such cases, the osteochondral injury often goes undiagnosed. In the past, plain radiography, arthrography, and joint aspiration were the only diagnostic modalities available to the clinician. Plain radiographs are not sensitive because the bone fragment tends to be small even when a large osteochondral defect is present. An arthrogram is quite good at detecting the defect; however, because it is an invasive study, a high index of suspicion is needed to justify its use. Joint aspiration is also invasive, but can demonstrate the presence of a hemarthrosis with fat droplets, indicative of an intraarticular fracture; however, aspiration cannot define the size or location of the injury. Recently, magnetic resonance (MR) imaging has been used to demonstrate marrow changes consistent with trabecular microfracture; MR imaging can be used to
From the Departments of Orthopaedic Surgery (JMF, DFM, WWC, CAB) and Radiology (CAB), Wake Forest University School of Medicine, Winston-Salem, North Carolina
CLINICS IN SPORTS MEDICINE VOLUME 20 * NUMBER 2 APRIL 2001
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evaluate the size and location of the injury. This should make earlier diagnosis and treatment of these lesions easier, leading to a better functional outcome for the patient. ARTICULAR CARTILAGE Anatomy and Histology
Articular cartilage is composed of a small population of chondrocytes, which produce an extensive extracellular matrix. The matrix is composed of primarily type I1 collagen and proteoglycan aggregate. The chondrocyte directs the synthesis, maintenance, degradation, and repair of the articular cartilage. It responds to several different stimuli, including mechanical load, composition of the surrounding matrix, growth factors, and cytokines6 The collagen and proteoglycan interact to form a tightly packed network. The collagen gives the articular cartilage stiffness and strength, and the proteoglycan, with its hydrophilic nature, gives the cartilage shock absorption and resistance to deformation. Each layer of cartilage has a unique composition and structure (Fig. 1).The superficial zone constitutes 10% to 20% of the articular cartilage, and is composed of densely packed collagen fibers aligned parallel to the joint surface. The middle zone makes up approximately 40% to 6O%, and is composed of loosely packed collagen, an abundance of proteoglycan,
Figure 1. The histology of articular cartilage. STZ = superficial zone. (From Mow VC, Zhu W, Ratcliffe A: Structure and Function of Articular Cartilage and Meniscus. In Mow VC, Hayes WC [eds]: Basic Orthopaedic Biomechanics. New York, Raven Press 1991; with permission.)
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and few chondrocytes. The deep zone makes up 30% to 40% and is characterized by abundant chondrocytes and tightly packed collagen fibers arranged perpendicular to the osteochondral junction, anchoring the cartilage to the bone. The tide mark represents calcified cartilage adjacent to the subchondral bone.21 Normal articular cartilage has a multilaminar appearance on high-resolution MR imaging, which correlates with these histologic layers.30
Articular Injury and Repair
Injury to the articular cartilage results from mechanical stress. The stress can be a suddenly applied load or a repetitive load. Either method can overload the cartilage, resulting in damage. Compaction fractures occur as a result of a direct force applied perpendicular to the joint surface. Examples include a direct blow to the patella, or sudden impaction of the lateral femoral condyle against the tibia during subluxation with an acute anterior cruciate ligament tear. Shearing fractures occur when the force is applied parallel to the joint surface. This can occur during patellar dislocation as the patella forcibly slides across the lateral femoral condyle. Avulsion fractures occur when ligaments or tendons exert a traction force on the bone. Examples include avulsion of the tibia eminence by the anterior cruciate ligament or the medial femoral condyle by the posterior cruciate ligament.', 4, 15, 22, 23, 27 These forces applied to the joint can result in microdamage to the cartilage without gross disruption; disruption of the cartilage alone; or fracture of the cartilage and the underlying subchondral bone. When the injury is limited to the cartilage alone, without surface disruption, diagnosis is difficult. A decrease in proteoglycan concentration, increased tissue hydration, and altered collagen structure can be seen histologically, but no clinically useful method for detection is currently available.6 When a chondral injury has occurred, the patient can present with pain, effusion, or mechanical symptoms. The lesion can be detected using MR imaging, arthrogram, or arthroscopy. The inflammatory response is not evoked secondary to the lack of blood supply to cartilage. Therefore, the chondrocytes attempt to fill the defect by increasing synthesis of the matrix. This response is usually inadequate, leading to an alteration of joint mechanics and degeneration of the adjacent cartilage.6 Osteochondral injuries result in significant hemarthrosis due to fracture of the highly vascular subchondral bone. Patients present with pain, effusion, and mechanical symptoms. Joint aspiration reveals hemarthrosis with a supernatant layer of fat if allowed to stand for 15 minutes.27A fibrin clot is formed with activation of the inflammatory response. The inflammatory mediators stimulate migration of mesenchyma1 cells, which differentiate into chondrocytes that produce type I and I1 collagen to fill the defect. The repair can remodel to form a functional articular surface if the defect is small, but most often the area degener-
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ates over time, leaving exposed subchondral bone." This can result in significant pain and progressive deformity. LESIONS OF THE KNEE Microtrabecular Fractures
The knee is a frequent site for chondral and osteochondral lesions. Occult subchondral trabecular microfractures, known as bone bruises, occur in greater than 80% of patients sustaining complete anterior cruciate ligament rupture.15Although these lesions sometimes can be detected acutely on plain radiographs, they often go relatively unnoticed until continued episodes of giving way cause deepening of the lesion with sclerosis, making them easily detectable on plain radiographs as the "lateral notch sign" (Fig. 2). Mechanism of this osteochondral injury is thought to be impaction of the tibia into the sulcus terminalis of the lateral femoral condyle during acute or chronic subluxation of the tibia, similar to a Hill-Sachs lesion in the shoulder.' The extent of the injury can range from an occult bone bruise detectable only by MR imaging, to osteochondral fracture. The clinical significance of bone bruises is yet to be determined. Johnson studied 10 patients with complete anterior cruciate ligament tears and found that all 10 patients had gross evidence of articular cartilage injury arthroscopically correlated with areas of altered marrow signal on MR imaging. Biopsy specimens of the injured cartilage revealed chondrocyte injury and death, loss of proteoglycan, increased tissue hydration, and osteocyte necrosis. Two patterns of injury were noted. Reticular lesions represent hemorrhage and edema limited to the medullary bone, and occurred in approximately two thirds of the cases. Geographic lesions occurred in 25% of the cases and represent injury contiguous with the articular surface. Reticular lesions showed complete resolution on repeat MR imaging at 6 to 12 months, whereas 62% of patients with geographic lesions showed evidence of osteosclerosis, cartilage thinning or loss, and accompanying osteochondral defects at 6 to 12 months follow up.15 Similar trabecular microfractures have been documented following isolated medial collateral ligament injuries. Miller et a1 found bone bruises on MR imaging in 45% of the patients with grades I1 or I11 isolated medial collateral ligament injuries. The lesions with this injury tend to be more diffuse and less localized than those with anterior cruciate ligament injuries. The mechanism is thought to be impaction of the lateral tibia plateau into the lateral femoral condyle with the valgus load. Complete resolution of microfractures based on MR imaging appearance occurred in all patients over a 2- to 4-month f o l l o w - ~ p . ~ ~ Similarly, a retrospective study of patients with posterior cruciate ligament injuries at the Steadman-Hawkins Clinic found an 83% incidence of bone bruises. The location of the lesions depended on the mechanism
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Figure 2. Lateral (A) and Anteroposterior (AP) (B) radiographs of the right knee demonstrate a deepened lateral femoral notch (arrow). It is uncommon to see this on an AP view. C, The corresponding MR image demonstrates the deepened lateral femoral notch and the associated bone contusion extending up into the metaphases. There is also increased signal within the posterior lateral tibia indicating the kissing contusions during subluxation. (Courtesy of James M. Farmer. From Patterson-Smith, 6 [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
and associated ligamentous injuries.19These lesions ultimately can prove to be significant, and can be the cause of osteoarthritis following a cruciate ligament injury despite ligament reconstruction and restoration of stability. Several series have demonstrated the progression of degenerative changes in the knee despite acute reconstruction of the anterior cruciate ligament.10,l2 These degenerative changes could be attributed to articular lesions that occur with the initial injury.
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Osteochondral Lesions with Patellar Dislocations
Osteochondral lesions of the lateral femoral condyle, medial patellar facet, or both have been documented in 40% to 50% of patients following lateral patella dislocation4(Figs. 3,4). The mechanism is a shearing force applied tangential to the joint surface by the quadriceps muscle through the patella during relocation of the patellofemoral joint. Patients usually present with pain; hemarthrosis with fat droplets; and medial retinacular, medial patellar, and lateral femoral condylar tenderness, with or without mechanical symptoms of locking or catching. The patient often does not remember a frank dislocation, but commonly reports a painful "snap" at the time of injury. Rosenberg reported a series of 15 cases of osteochondral fracture of the lateral femoral condyle. All 15 patients gave a history of a twisting injury with the knee flexed, but only five patients reported a definite dislocation. Plain radiographs demonstrated a defect in the lateral femoral condyle in all cases. Operative findings revealed a fracture of the lateral margin of the lateral femoral condyle on the weightbearing portion of the condyle. One third of the patients had an additional lesion at the inferomedial margin of the patella. All patients with lesions on both the lateral femoral condyle and patella reported multiple injuries.30The patella is thought to apply the force necessary to cause the fracture, but it is not clear whether this occurs during dislocation or reduction, or if dislocation is even a requisite for the injury to occur. The patella is seated deeply in the trochlear groove during flexion,
Figure 3. A, Axial fat suppressed T2-weighted MR image of the knee demonstrates a cartilage defect of the lateral trochlea with increased signal in the underlying bone consistent with contusion. There is corresponding increased signal in the medial patella inferiorly. A cartilaginous loose fragment is identified within the joint effusion medially (arrow) B, Lateral fat suppressed T2-weighted MR image demonstrating the cartilage defects on the anterior aspect of the patella and the lateral trochlea (arrow). (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
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Figure 4. Axial T2-weighted image reveals the increased signal within the medial patella and the lateral femoral condyle corresponding to the kissing contusions of patellar dislocation. There is some increased signal at the medial retinacular attachment to the patella consistent with a partial tear (arrow). (Courtesy of James M. Farmer. From PattersonSmith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
and patellofemoral compression forces are high. A twisting injury with a strong quadriceps contraction with the knee flexed can drive the patella into the lateral femoral condyle, much like a wedge, producing a stellate chondral fracture. The dislocating patella can act more like a chisel to produce an osteochondral fracture.30The natural history of these lesions can lead to a condition indistinguishable from osteochondritis dissecans (OCD). This observation has led several authors to suggest unrecognized trauma as a primary etiology of OCD lesions in the knee.27,30 LESIONS OF THE ANKLE Osteochondral Lesions of the Talus
Osteochondral lesions involving the talar dome are relatively common, with an incidence recorded from 0.09% of all talar fractures to 6.5% of ankle sprains. Because they once were thought to result from ischemia leading to necrosis of the subchondral bone and subsequent fragmentation of the articular cartilage, the term osteochondritis dissecans was applied to these lesions. In 1959, Berndt and Harty reviewed the literature and presented their own experience with these lesions. They suggested a traumatic etiology for ”transchondral fract~res.”~, 11, 17, 33, 34 They felt that lateral talar lesions are produced when an inversion stress is applied to a dorsiflexed ankle, causing the anterior lateral aspect of the talus to impact the fibula. They described a similar mechanism when an inver-
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sion or external rotation stress is applied to a plantar flexed ankle, causing impaction of the posteromedial talus against the tibia (Fig. 5). Histologic examination of specimens in their study revealed necrosis and fibrosis in the subchondral trabecular bone with normal articular ~artilage.~ Subsequent series have supported a traumatic etiology for most osteochondral lesions of the talus, ranging from 75% to 100% for lateral lesions and 18% to 80% for medial lesi0ns.3~Because a large percentage of osteochondral lesions of the talus, especially in the medial talar dome, present without any history of trauma, other causes such as ischemia and systemic illnesses should be considered. Staging of Talar Lesions
Several staging systems have been developed for osteochondral lesions of the talus. The original system developed by Berndt and Harty was based on radiographic and intraoperative findings, although the practical application of this staging system has been limited to the radiographic findings. Stage I lesions represent a small area of subchondral compression. Stage I1 lesions are partially detached osteochondral
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Figure 5. The most common locations for osteochondral lesions on the talus: anterolateral and posteromedial. Stippled area represents stress. (From Berndt AL, Hatty M: Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 41A: 988-1020, 1959; with permission.)
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fragments. Stage I11 lesions are detached fragments that remain in situ. Stage IV represents a displaced osteochondral fragment (Fig. 6).3Several other systems using computed tomography (CT) scans, MR imaging, and arthroscopy have been developed since Berndt and Harty. Taranow et a1 have introduced a staging system that evaluates the bone lesion preoperatively using MR imaging and evaluates the cartilage condition using arthroscopy. MR imaging is good at evaluating the subchondral
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Figure 6. The state Berndt and Harty classification of osteochondral injuries. Stage one represents subchondral compression. Stage two represents partially detached osteochondral fragment. Stage three represents detached fragments remaining in sifu. Stage four represents displaced osteochondral fragment. (From Berndt AL, Harty M: Transchondral fractures [osteochondritis dissecans] of the talus. J Bone Joint Surg 41A:988-1020, 1959; with permission.)
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bone for marrow edema and necrosis of the subchondral bone; however, it is not as useful in evaluating the articular surface. In the system proposed by Taranow et al, Stage I is a bone bruise. Stage I1 lesions are subchondral cysts that develop from bone bruises. Stage I11 lesions are partially detached osteochondral fragments in situ. Stage IV lesions are displaced fragments. Further classification is based on the appearance of the articular cartilage surface at arthroscopy. Grade A represents viable intact cartilage, and grade B represents breech or nonviable articular Diagnosis of Talar Lesions Patients with osteochondral lesions of the talus typically present with pain either acutely following an ankle sprain or chronically after nonoperative treatment. They frequently have intermittent episodes of swelling and mechanical symptoms such as crepitus, catching, and giving way. Plain radiographs can be normal or reveal an osteochondral lesion. Routine anteroposterior, lateral, and mortise views should be obtained (Fig. 7). Special views with the ankle placed in dorsiflexion or plantarflexion can reveal anterolateral or posteromedial lesions, respectively. Radiographs of the contralateral ankle can reveal bilateral lesions in 10% of patients. When plain radiographs are normal, but clinical examination is abnormal, a bone scan can detect increased uptake in the area of the lesion. CT and MR imaging can identify and quantify the lesion better than plain radiographs and bone scanning, and should be obtained when conservative treatment fails to relieve symptoms (Fig. 8).
Figure 7. Mortise view of the right ankle demonstrates osteochondral injury of the lateral talar dome. There is an osteochondral fractures involving the lateral talar dome. This fracture is complete, in situ corresponding to a Berndt and Harty stage 111 lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
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Figure 8. Coronal T1-weighted image of the talus demonstrates changes from an osteochondral injury involving the medial talar dome. There is no separate fragment and the overlying cartilage is intact. This corresponds to a Berndt and Harty stage one lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
Treatment of Talar Lesions
Treatment for osteochondral lesions of the talus depends on the condition of the subchondral bone and overlying articular cartilage. A trial of nonoperative management including limited weightbearing and immobilization is advocated for stage I, 11, and medial stage I11 lesions. Operative management is advocated for lateral stage I11 lesions, all stage IV lesions, and patients for whom nonoperative management has failed.17 Delaying surgery for up to 1 year has not been shown to affect the outcome adversely even if surgical management ultimately is required.= The surgical options depend on the stage of the osteochondral lesion. Treatment for stage IV lesions is excision of the displaced fragment with drilling, abrasion, or curettage of the subchondral base. The repair process involved with this treatment will be discussed later. Stage I11 lesions can be treated with excision of the fragment or internal fixation of the fragment. Long-term studies regarding the outcome of internal fixation of osteochondral lesions of the talus are lacking, but the best candidates are younger patients with large lesions due to trauma. The choices for fixation include Kirschner wire, cancellous screws, Herbert screws, or bioabsorbable screws.32Treatment for stage I and I1 lesions typically is directed toward stimulating healing of the necrotic subchondral bone. Drilling of intact lesions can be performed in an anterograde fashion by means of arthroscopy or open arthrotomy. Retrograde drilling can be performed arthroscopically with fluoroscopic guidance. Drilling is thought to stimulate vascular inflow into the lesion, but there is no scientific evidence that this occurs. Anterograde drilling techniques necessarily violate the articular surface, whereas retrograde techniques do not require drilling through the articular cartilage. In
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addition, retrograde techniques allow curettage of necrotic bone and bone grafting of lesions. Kumai et a1 reported good results in 13 of 18 patients and fair results in 5 of 18 patients with stage I1 medial lesions treated with anterograde arthroscopic drilling. They found the results were much better in patients younger than 30 years of age.I7 Taranow et a1 performed a prospective study of patients with stage I11 and IV lesions treated with retrograde drilling, curettage, and bone grafting. They found immediate improvement in the American Orthopaedic Foot and Ankle Society Ankle-Hindfoot Scale of 25 points (53.9 to 82.6 points) and radiographic evidence of healing in 88% of patients.34 The long-term effect on the development of arthrosis is unknown at this time. Postoperative care following any of the surgical techniques will include limited weightbearing and various lengths of immobilization. Immobilization following drilling techniques for intact lesions will be brief. If ankle instability is present and stabilization procedures are required, they should be staged. The stabilization procedure should follow complete rehabilitation from the drilling technique because the postoperative immobilization after the stabilization necessarily will be longer than that required for the drilling technique.33 DIAGNOSIS OF OSTEOCHONDRAL LESIONS Diagnostic Algorithm Many osteochondral lesions can be diagnosed by plain radiography; however, radiographs can be normal in the presence of an osteochondral lesion. When a patient presents with pain, effusion, and mechanical symptoms with normal radiographs, further diagnostic workup is needed. There are several options to formulate a diagnosis. Bone scans are relatively inexpensive and can demonstrate increased uptake, but cannot quantify the exact size of the lesion or determine the condition of the articular cartilage. Anderson et a1 evaluated 14 patients with ankle sprains and persistent pain and found that a positive bone scan correlated with osteochondral lesions found on MR imaging in all 14 patients, whereas only 10 of 14 patients demonstrated osteochondral lesions on CT scan.33If the bone scan demonstrates an osteochondral lesion, the clinician can either proceed to arthroscopy or obtain a CT scan. CT scans demonstrate excellent definition of bony fragments and allow determination of size, location, and displacement of the fragments. CT is less sensitive in detecting trabecular microfractures than MR imaging. Recent MR scanning techniques such as MR arthrography, magnetization transfer imaging, and fast spin echo sequences have improved the visualization of chondral defects.26,30 MR imaging can detect subtle bone injuries that will require limited weightbearing and allow evaluation of soft tissues, which can be responsible for the patient’s symptoms. Finally, arthroscopy has the advantage of direct visualization of the articular surface and ability to treat the lesions, but cannot evaluate the condition
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of the underlying subchondral bone. Please refer to our diagnostic and treatment algorithm in the Appendix at the end of this article. TREATMENT OF OSTEOCHONDRAL LESIONS
General Principles Treatment of osteochondral lesions is determined based on the condition of the articular cartilage. Displaced osteochondral fragments can be excised and treatment directed toward the osteochondral defect, or they can be replaced and stabilized with internal fixation. Osteochondral defects can be treated with several methods, which attempt to fill the defect with either fibrocartilage or transplanted hyaline cartilage. Each is discussed in the following sections. Internal Fixation Internal fixation of large osteochondral fragments can be performed. It usually is indicated for large fragments following acute trauma in younger patients. Stable internal fixation can restore the articular surface and allow early range of motion of the joint. Most methods can be performed arthroscopically. The most commonly used devices are 0.062inch diameter smooth Kirschner wires placed through the fragment into the subchondral bone. Several pins are sometimes necessary to gain rotational control. Smooth pins can loosen, resulting in loss of fixation. Cahill reports using 0.062 K-wires that are bent 90°, 1 mm from the tip, and seating the bent distal tip into the articular cartilage and subchondral bone to gain better fixation than with straight pins. The pins subsequently are removed in a retrograde direction.6 Cannulated small fragment screws, Herbert screws, or Acutrak screws can be used to fix the fragment (Fig. 9A-D). Screws provide more rigid fixation than K-wires. Small fragment screws must be countersunk beneath the surface of the articular cartilage. The Herbert or Acutrak screws are ideal for articular surfaces because they do not have heads and are placed easily below the articular surface. Maxie reported the use of Herbert screws to stabilize partially detached osteochondral fragments in three patients. The screws were inserted arthroscopically through a transpatellar portal. All patients were full weightbearing immediately postoperatively and symptoms improved without complications up to 1 year later.I8Newer bioabsorbable polylactic acid screws can be used to provide fixation with the advantage of not requiring a second procedure for removal. No studies have been published using polylactic acid screws for this purpose. Finally, Gillespie reported results using corticocancellous bone harvested from cortical bone of the anterior tibia to secure osteochondral fragments. The corticocancellous strips act as shims to hold the osteo-
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Figure 9. Anteroposterior (A) and lateral (B) radiographs reveal an osteochondral lesion involving the medial femoral condyle. There are several small fragments within the lesion. These are better seen on the lateral radiographs (arrows). Postoperative radiographs reveal fixation of the fragments with Accutrack screws. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
chondral fragment in place, and are a source of bone graft to stimulate healing. He reported good or excellent results in 17 of 18 patients with radiographic evidence of union by 8 months. In addition, there is no need for a second procedure to remove hardware.13 Once a fragment is fixed, the joint should be taken through a full range of motion several
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times to ensure secure fixation and smooth motion. This information can be used to plan the postoperative rehabilitation. Excision, Debridement, and Marrow Stimulation Techniques
Treatment of osteochondral defects on the articular surface poses a significant challenge to the clinician. The natural history of these lesions depends on the size and location of the lesion. Most researchers hypothesize that large Outerbridge grade I11 and IV lesions cause overload of the subchondral bone with progression to gonarthrosis. Recent studies show significant chondrocyte damage overlying bone bruises. This damage also can lead to osteoarthritis." Removal of loose fragments, dkbridement of fragmented cartilage, and joint lavage can provide temporary relief of symptoms. In addition, picking, drilling, abrasion, and microfracture of the subchondral surface can stimulate the formation of a fibrin clot, which will facilitate mesenchymal cells to fill the defect with fibr~cartilage~,~~ (Fig. 10A-C). Steadman and Rodrigo reported improvement in the appearance of the articular surface following microfracture of the subchondral bone for full-thickness lesions. They reported better results in patients who received continuous passive motion (CPM) for 6 to 8 hours per day following microfracture. The number of patients who had no improvement was higher in the patients who did not receive CPM, and 45% still had exposed subchondral bone compared to 15% of patients who received CPM following microfract~re.~~ Their study demonstrated the importance of motion following marrow stimulation techniques. Fibrocartilage is stronger in tension than compression, as opposed to hyaline cartilage, which is stronger in compression than tension. Fibrocartilage is not a durable substitute, and long-term results have not been satisfying; however, these techniques can be the best alternative for large osteochondral defects on the weightbearing surface. Chondral and Osteochondral Transplants
Several chondral and osteochondral transplant procedures have been developed. The transplanted tissue can be either autogenous or allograft tissue and can consist of chondral elements alone or osteochondral transplants. Each method has the common goal of filling the defect with stable hyaline cartilage, and each has its own advantages and disadvantages. These treatment options are discussed below. Perichondral and Periosteal Grafts
Mesenchymal cells on the surface of periosteum and perichondrium can be stimulated to produce hyaline cartilage. The factors leading to
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Figure 10. A, Axial and fat suppressed TBweighted image reveals a large bone contusion within the lateral femoral condyle. The overlying cartilage is not well demonstrated. B, Lateral fat suppressed proton density weighted image reveals irregularity and thinning of the cartilage of the anterior lateral femoral condyle (arrows). C, Arthroscopic view of Outerbridge Stage 3 lesion of the lateral trochlea groove. D, Arthroscopic view following debridement. €, Drilling of same lesion. F; Arthroscopic view of similar lesion immediately after drilling. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
this proliferation are not completely known, but it has been shown that perichondrial and periosteal cells, when placed with the cambium layer facing the joint, will form hyaline ~artilage.~.*~ The perichondrial grafts are taken from rib cartilage, placed over a fibrin glue that fills the defect,
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and secured with the cambium layer facing the joint. Homminga et a1 performed this technique on 25 patients. Their experience with these grafts yielded good initial results, with improvement in Hospital for Special Surgery (HSS) Knee Score from 73 to 90 at 1 year. Results at 5to 7-year follow-up were disappointing, with 60% of the patients having endochondral ossification and delamination of the cartilage with resulting pain and d y s f ~ n c t i o n Despite .~~ the early optimism involving these grafts, they have not provided good long-term results. Autogenous and Allogenic Osteochondral Transplant Transplantation of intact articular cartilage with its underlying subchondral bone attempts to fill a defect with intact hyaline cartilage and, stable bony fixation. The ideal lesion for this treatment is the focal chondral or osteochondral defect on the femoral condyle or talus in a young patient. Normal surrounding hyaline cartilage reduces boundary shear and improves outcome.16Allograft transplantation can be used to repair larger defects. Fresh allografts are used because chondrocyte viability is diminished after freezing. The immunogenicity of human bone and cartilage is low; therefore no attempt is made to cross-match antigens between donors and recipient^.^ The transplants usually are performed by an arthrotomy, and the exact orthotopic site of the lesion is harvested from the donor specimen. The graft is secured with interference screws. Results of this transplant yielded 86% good or fair results when one joint surface was treated, and 53% good or fair results when two joint surfaces were treated.'j The disadvantages of this technique are potential disease transmission and difficulties associated with donor procurement. Autogenous osteochondral transplant, commonly called mosaicplasty or OATS (Arthrex, Inc) procedure, involves the placement of viable chondrocytes and the underlying cancellous bone, which unites quickly into the defect. Grafts 5.0 to 9.0 mm in diameter are harvested from the intercondylar notch or non-weightbearing portion of the femoral condyle near the patellofemoral joint. Grafts are press fit into the defect (Fig. 11). Hangody reported results on 57 patients with greater than 3 year follow up. The average modified HSS score was 90.7. Followup arthroscopy in 19 patients revealed the transplanted cartilage remained hyaline in nature and the gaps between the grafts had been filled with fibro~arti1age.I~ Bugbee reported good to excellent results on the modified HSS score in all patients, a 90% return to full competition level activities in patients less than 30 years of age, and a 63% return to full competition level activities in patients over 30 years of age.7 Mosaicplasty ideally is indicated for smaller focal lesions on the femoral condyle in younger patients. The results for patellofemoral lesions were less successful, with an average modified HHS score of 71.14 Autogenous Chondrocyte Transplant Transplantation of autogenous chondrocytes first was shown to be successful in a rabbit model in 1984. The first successful treatment of
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Figure 11. A, Arthroscopic view of Outerbridge Grade 4 lesion on the lateral femoral condyle. 6,Lesion following debridement and picking. C,Arthroscopic view 7 months later. D, Arthroscopic view following autologous osteochondral transplant. The arrows outline the two osteochondral plugs. Note the fibrocartilage covering the lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
osteochondral lesions in humans with autogenous chondrocyte transplant was performed and reported by Brittberg et a1 in 1994.5 The technique involves harvesting articular cartilage from a minor weightbearing area on the femoral condyle arthroscopically. Chondrocytes are isolated and amplified in an aseptic culture medium. This culture procedure results in an increase of chondrocytes by 10 to 20 times. The cells are then re-implanted by arthrotomy into the defect and held in place by a periosteal flap (Fig. 12). Several explanations for the repair process have been offered, but none have been proven. The first theory is that transplanted cells repopulate the defect and synthesize a new hyaline cartilage matrix. Another explanation is that the periosteal flap stimulates proliferation of the transplanted cells to fill the defect. Finally, the transplanted cells and periosteum are theorized to stimulate the surrounding chondrocytes to enter the defect and repair it.5 The end result of autogenous chondrocyte transplant has been shown to be a stable hyaline cartilage filled defect. The indications for autogenous chondrocyte transplant are a focal osteochondral lesion in an otherwise normal joint. Brittberg et a1 initially treated 23 patients with autogenous
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Figure 12. Technique for autogenous chondrocyte transplantation. (From Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 33:889-895,1994; with permission.)
chondrocyte transplant (16 femoral condyle lesions and 7 patellar lesions), and found 14 of 16 excellent or good results at 24-month follow up for condylar lesions and 2 of 7 excellent or good results at 36-month follow up for patellar lesions. Patients were evaluated by arthroscopy at 3 months and again at 12 to 46 months postoperatively. The hyaline cartilage was found to become more stable over time. Biopsy specimens taken at the second arthroscopy confirmed the histologic features of hyaline ~artilage.~ Since this original report, over 250 patients have been treated with autogenous chondrocyte transplant with greater than 80% improvement at 2-year f o l l o w - ~ p Degeneration .~~ of the new hyaline cartilage over time has not been reported. Autogenous chondrocyte transplant is an effective but technically demanding treatment for focal osteochondral lesions in younger active patients. SUMMARY
Osteochondral lesions are relatively common and usually occur as a result of trauma. They often are unrecognized acutely and lead to osteochondral defects and eventually osteoarthritis. Detection of these lesions has been aided by bone scan, CT, and MR imaging. Acute osteochondral fragments can be replaced and internally fixed. Chronic
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osteochondral defects can be treated with several methods designed to stimulate healing by either fibrocartilage or healing by transplantation of bone and cartilage or cartilage alone. The goal of all treatment methods is to provide a stable, congruent joint surface, restore function, and prevent the evolution of osteoarthritis in the injured joint. References 1. Bach 8, Warren R Radiographic indicators of anterior cruciate injury. In Feagin J (ed): The Crucial Ligaments Diagnosis and Treatment of Ligamentous Injuries About Knee. New York, Churchill Livingstone, 1988, pp 319-323 2. Berlet G, Mascia A, Miniaci A Treatment of unstable osteochondritis dissecans lessions of the knee using autogenous osteochondral grafts (mosaicplasty). Arthroscopy 15:312316, 1999 3. Bemdt AL, Harty M Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 41A988-1020, 1959 4. Boden B, Pearsall A, Garrett W, et al: Patellofemoral instability: Evaluation and Management. J Am Acad Orthop Surg 5:47-57, 1997 5. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 335389495,1994 6. Buckwalter, J, Mow V, Ratcliffe A: Restoration of injured or degenerated articular cartilage. J Am Acad Orthop Surg 2:192-201, 1994 7. Bugbee W, Convery F Osteochondral allograft transplantation. Clin Sports Med 18:6775, 1999 8. Cahill 8: Osteochondritis dissecans of the knee: Treatment of juvenile and adult forms. J Am Acad Orthop Surg 3237-247, 1995 9. Cahill 8: Treatment of juvenile osteochondritis dissecans and osteochondritis dissecans of the knee. Clin Sports Med 4:367-386, 1985 10. Daniel DM, Stone ML, Dobson B et al: Fate of the ACL injured patient: A perspective study. Am J Sports Med 226324544, 1994
11. Ferkel R Arthroscopy of the ankle and foot. In Mann R, Caghlin M (eds): Surgery of the Foot and Ankle, ed 6, vol. 1. St. Louis, Mosby, 1993, pp 1291-1299 12. Friederich N, OBrien W Gonarthrosis after injury of the anterior cruciate ligament: A multi-center long term study. Z Unfallchir Versicherungsmed 86:8149, 1993 13. Gillespie H, Day B: Bone peg fixation in the treatment of osteochondritis dissecans of the knee joint. Clinic Orthop 143125-130, 1979 14. Hangody L, Kish G, Karpati Z, et al: Mosaicplasty for the treatment of articular cartilage defects: Application in clinical practice. Orthopedics 21:751-756, 1998 15. Johnson D, Urban W, Cabom D, et al: Articular cartilage changes seen with magnetic resonance imaging, detected bone bruises associated with acute anterior cruciate ligament rupture. Am J Sports Med 26409414,1998 16. Kish G, Modis L, Hongody L: Osteochondral mosaicplasty for the treatment focal chondral and osteo chondral lesions of the knee and talus in the athlete rational, indications, techniques, and results. Clin Sports Med 18:4547, 1999 17. Kumai T, Takakura Y, Higashiyana I, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus. J Bone Joint Surg 81:1229-1235, 1999 18. Mackie I, Pemberton D, Maheson M: Arthroscopic use of the Herbert screw in osteochondritis dissecans. J Bone Joint Surg 72B:1076, 1990 19. Mair SD, Schlegel TF, Gill TJ, et al: Steadman-Hawkins Clinic. Presented at the American Orthopaedic Society for Sports Medicine Annual Meeting. Vail, CO, 1999 20. Mandelbaum B, Brane J, Fu F et al: Articular cartilage lesions of the knee. Am J Sports Med 26:853-861, 1998 21. Mankin H, Mow B, Buckwalter J, et al: Form and function of articular cartilage. In Simon S (ed): Orthopedic Basic Science, Rosemont, IL, American Academy of Orthopedic Surgeons, 1994, p p 1-44
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22. Milgram J, Rogers L, Miller J: Osteochondral fractures: Mechanisms of injury and fate of fragments. AJR Am J Roentgen01 130:651-658, 1978 23. Miller M, Osbome J, Gordon W The natural history of bone bruises: A prospective study of magnetic resonance imaging detected trabecular microfractures in patients with isolated medial collateral ligament injures. Am J Sports Med 26:15-19, 1998 24. Minas T, Nehrer S: Current concepts in the treatment of articular cartilage defects. Orthopedics 20:525-538, 1997 25. Mori R, Ochi M, Sakai Y, et al: Clinical significance of magnetic resonance imaging (MRI) for focal chondral lesions. Magn Reson Imaging 171135-1140, 1999 26. Mow VC, Zhu W, Ratcliffe A Structure and function of articular cartilage and meniscus. In Mow VC, Hayes WC (eds): Basic Orthopaedic Biomechanics, New York, Raven Press, 1991, pp 143-198 27. ODonoghue D: Chondral and osteochondral fractures. J Trauma 6(4):469481, 1966 28. Recht MP, Resnick D: Magnetic resonance imaging of articular cartilage: An overview. Top Magn Reson Imaging 9:328-336, 1998 29. Rodrigo JS, Steadman RJ, Sillman JF, et al: Improvement of full thickness chondral defect healing in the human knee after debridement and microfracture using continuous passive motion. Am J Knee Surg 1994:7109-116. 30. Rosenberg N: Osteochondral fractures of the lateral femoral condyle. J Bone Joint Surg 46A:1013-1026, 1964. 31. Sisto, D. The surgical treatment of full thickness osteochondral defects of the knee. Presented at American Orthopaedic Society for Sports Medicine Annual Meeting, Traverse City, MI, 1999 32. Speer K, Warren R, Wickiewicz T, et al: Observations on the injury mechanism of anterior cruciate ligament tears in skiers. Am J Sports Med 23:77-81, 1995 33. Stone J: Osteochondral lesions of the talar dome: J Am Acad Orthop Surg 464-73,1996 34. Taranow W, Bisignani G , Towers J, et al: Retrograde drilling of osteochondral lesions of the medial talar dome. Foot Ankle Int 20474-480, 1999
Address reprint requests to David F. Martin, MD Wake Forest University School of Medicine Medical Center Boulevard Winston-Salem, NC 27157
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APPENDIX +/- history of injury Pain Effusion Mechanical symptoms
Excision Internal Fixation SCW.
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Excise/Debride Picking, Drilling, Abrasion, Microfracture Autogenous Osteocbondral Transplantation Allograft Transplantation Autogenous Chondrocyte Transplantation
Diagnostic and treatment algorithm for chondral and osteochondral lesions. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
0278-5919/01 $15.00
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CHONDRAL AND OSTEOCHONDRAL INJURIES Diagnosis and Management James M. Farmer, MD, David F. Martin, MD, Carol A. Boles, MD, and Walton W. Curl, MD
Chondral and osteochondral injuries are relatively common in the weightbearing joints of the lower extremity. The pathology can range from a simple contusion of the articular cartilage and subchondral bone to a fracture involving the cartilage alone or cartilage and underlying subchondral bone together. The mechanism of injury is from one of three types of trauma: compaction, shearing, or avulsion.26Because the injury is usually subtle and causes little to no dysfunction, the diagnosis of acute injuries is delayed. Occasionally, the injury is severe enough to cause a significant effusion, hemarthrosis, or ligament disruption. Even in such cases, the osteochondral injury often goes undiagnosed. In the past, plain radiography, arthrography, and joint aspiration were the only diagnostic modalities available to the clinician. Plain radiographs are not sensitive because the bone fragment tends to be small even when a large osteochondral defect is present. An arthrogram is quite good at detecting the defect; however, because it is an invasive study, a high index of suspicion is needed to justify its use. Joint aspiration is also invasive, but can demonstrate the presence of a hemarthrosis with fat droplets, indicative of an intraarticular fracture; however, aspiration cannot define the size or location of the injury. Recently, magnetic resonance (MR) imaging has been used to demonstrate marrow changes consistent with trabecular microfracture; MR imaging can be used to
From the Departments of Orthopaedic Surgery (JMF, DFM, WWC, CAB) and Radiology (CAB), Wake Forest University School of Medicine, Winston-Salem, North Carolina
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evaluate the size and location of the injury. This should make earlier diagnosis and treatment of these lesions easier, leading to a better functional outcome for the patient. ARTICULAR CARTILAGE Anatomy and Histology
Articular cartilage is composed of a small population of chondrocytes, which produce an extensive extracellular matrix. The matrix is composed of primarily type I1 collagen and proteoglycan aggregate. The chondrocyte directs the synthesis, maintenance, degradation, and repair of the articular cartilage. It responds to several different stimuli, including mechanical load, composition of the surrounding matrix, growth factors, and cytokines6 The collagen and proteoglycan interact to form a tightly packed network. The collagen gives the articular cartilage stiffness and strength, and the proteoglycan, with its hydrophilic nature, gives the cartilage shock absorption and resistance to deformation. Each layer of cartilage has a unique composition and structure (Fig. 1).The superficial zone constitutes 10% to 20% of the articular cartilage, and is composed of densely packed collagen fibers aligned parallel to the joint surface. The middle zone makes up approximately 40% to 6O%, and is composed of loosely packed collagen, an abundance of proteoglycan,
Figure 1. The histology of articular cartilage. STZ = superficial zone. (From Mow VC, Zhu W, Ratcliffe A: Structure and Function of Articular Cartilage and Meniscus. In Mow VC, Hayes WC [eds]: Basic Orthopaedic Biomechanics. New York, Raven Press 1991; with permission.)
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and few chondrocytes. The deep zone makes up 30% to 40% and is characterized by abundant chondrocytes and tightly packed collagen fibers arranged perpendicular to the osteochondral junction, anchoring the cartilage to the bone. The tide mark represents calcified cartilage adjacent to the subchondral bone.21 Normal articular cartilage has a multilaminar appearance on high-resolution MR imaging, which correlates with these histologic layers.30
Articular Injury and Repair
Injury to the articular cartilage results from mechanical stress. The stress can be a suddenly applied load or a repetitive load. Either method can overload the cartilage, resulting in damage. Compaction fractures occur as a result of a direct force applied perpendicular to the joint surface. Examples include a direct blow to the patella, or sudden impaction of the lateral femoral condyle against the tibia during subluxation with an acute anterior cruciate ligament tear. Shearing fractures occur when the force is applied parallel to the joint surface. This can occur during patellar dislocation as the patella forcibly slides across the lateral femoral condyle. Avulsion fractures occur when ligaments or tendons exert a traction force on the bone. Examples include avulsion of the tibia eminence by the anterior cruciate ligament or the medial femoral condyle by the posterior cruciate ligament.', 4, 15, 22, 23, 27 These forces applied to the joint can result in microdamage to the cartilage without gross disruption; disruption of the cartilage alone; or fracture of the cartilage and the underlying subchondral bone. When the injury is limited to the cartilage alone, without surface disruption, diagnosis is difficult. A decrease in proteoglycan concentration, increased tissue hydration, and altered collagen structure can be seen histologically, but no clinically useful method for detection is currently available.6 When a chondral injury has occurred, the patient can present with pain, effusion, or mechanical symptoms. The lesion can be detected using MR imaging, arthrogram, or arthroscopy. The inflammatory response is not evoked secondary to the lack of blood supply to cartilage. Therefore, the chondrocytes attempt to fill the defect by increasing synthesis of the matrix. This response is usually inadequate, leading to an alteration of joint mechanics and degeneration of the adjacent cartilage.6 Osteochondral injuries result in significant hemarthrosis due to fracture of the highly vascular subchondral bone. Patients present with pain, effusion, and mechanical symptoms. Joint aspiration reveals hemarthrosis with a supernatant layer of fat if allowed to stand for 15 minutes.27A fibrin clot is formed with activation of the inflammatory response. The inflammatory mediators stimulate migration of mesenchyma1 cells, which differentiate into chondrocytes that produce type I and I1 collagen to fill the defect. The repair can remodel to form a functional articular surface if the defect is small, but most often the area degener-
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ates over time, leaving exposed subchondral bone." This can result in significant pain and progressive deformity. LESIONS OF THE KNEE Microtrabecular Fractures
The knee is a frequent site for chondral and osteochondral lesions. Occult subchondral trabecular microfractures, known as bone bruises, occur in greater than 80% of patients sustaining complete anterior cruciate ligament rupture.15Although these lesions sometimes can be detected acutely on plain radiographs, they often go relatively unnoticed until continued episodes of giving way cause deepening of the lesion with sclerosis, making them easily detectable on plain radiographs as the "lateral notch sign" (Fig. 2). Mechanism of this osteochondral injury is thought to be impaction of the tibia into the sulcus terminalis of the lateral femoral condyle during acute or chronic subluxation of the tibia, similar to a Hill-Sachs lesion in the shoulder.' The extent of the injury can range from an occult bone bruise detectable only by MR imaging, to osteochondral fracture. The clinical significance of bone bruises is yet to be determined. Johnson studied 10 patients with complete anterior cruciate ligament tears and found that all 10 patients had gross evidence of articular cartilage injury arthroscopically correlated with areas of altered marrow signal on MR imaging. Biopsy specimens of the injured cartilage revealed chondrocyte injury and death, loss of proteoglycan, increased tissue hydration, and osteocyte necrosis. Two patterns of injury were noted. Reticular lesions represent hemorrhage and edema limited to the medullary bone, and occurred in approximately two thirds of the cases. Geographic lesions occurred in 25% of the cases and represent injury contiguous with the articular surface. Reticular lesions showed complete resolution on repeat MR imaging at 6 to 12 months, whereas 62% of patients with geographic lesions showed evidence of osteosclerosis, cartilage thinning or loss, and accompanying osteochondral defects at 6 to 12 months follow up.15 Similar trabecular microfractures have been documented following isolated medial collateral ligament injuries. Miller et a1 found bone bruises on MR imaging in 45% of the patients with grades I1 or I11 isolated medial collateral ligament injuries. The lesions with this injury tend to be more diffuse and less localized than those with anterior cruciate ligament injuries. The mechanism is thought to be impaction of the lateral tibia plateau into the lateral femoral condyle with the valgus load. Complete resolution of microfractures based on MR imaging appearance occurred in all patients over a 2- to 4-month f o l l o w - ~ p . ~ ~ Similarly, a retrospective study of patients with posterior cruciate ligament injuries at the Steadman-Hawkins Clinic found an 83% incidence of bone bruises. The location of the lesions depended on the mechanism
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Figure 2. Lateral (A) and Anteroposterior (AP) (B) radiographs of the right knee demonstrate a deepened lateral femoral notch (arrow). It is uncommon to see this on an AP view. C, The corresponding MR image demonstrates the deepened lateral femoral notch and the associated bone contusion extending up into the metaphases. There is also increased signal within the posterior lateral tibia indicating the kissing contusions during subluxation. (Courtesy of James M. Farmer. From Patterson-Smith, 6 [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
and associated ligamentous injuries.19These lesions ultimately can prove to be significant, and can be the cause of osteoarthritis following a cruciate ligament injury despite ligament reconstruction and restoration of stability. Several series have demonstrated the progression of degenerative changes in the knee despite acute reconstruction of the anterior cruciate ligament.10,l2 These degenerative changes could be attributed to articular lesions that occur with the initial injury.
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Osteochondral Lesions with Patellar Dislocations
Osteochondral lesions of the lateral femoral condyle, medial patellar facet, or both have been documented in 40% to 50% of patients following lateral patella dislocation4(Figs. 3,4). The mechanism is a shearing force applied tangential to the joint surface by the quadriceps muscle through the patella during relocation of the patellofemoral joint. Patients usually present with pain; hemarthrosis with fat droplets; and medial retinacular, medial patellar, and lateral femoral condylar tenderness, with or without mechanical symptoms of locking or catching. The patient often does not remember a frank dislocation, but commonly reports a painful "snap" at the time of injury. Rosenberg reported a series of 15 cases of osteochondral fracture of the lateral femoral condyle. All 15 patients gave a history of a twisting injury with the knee flexed, but only five patients reported a definite dislocation. Plain radiographs demonstrated a defect in the lateral femoral condyle in all cases. Operative findings revealed a fracture of the lateral margin of the lateral femoral condyle on the weightbearing portion of the condyle. One third of the patients had an additional lesion at the inferomedial margin of the patella. All patients with lesions on both the lateral femoral condyle and patella reported multiple injuries.30The patella is thought to apply the force necessary to cause the fracture, but it is not clear whether this occurs during dislocation or reduction, or if dislocation is even a requisite for the injury to occur. The patella is seated deeply in the trochlear groove during flexion,
Figure 3. A, Axial fat suppressed T2-weighted MR image of the knee demonstrates a cartilage defect of the lateral trochlea with increased signal in the underlying bone consistent with contusion. There is corresponding increased signal in the medial patella inferiorly. A cartilaginous loose fragment is identified within the joint effusion medially (arrow) B, Lateral fat suppressed T2-weighted MR image demonstrating the cartilage defects on the anterior aspect of the patella and the lateral trochlea (arrow). (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
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Figure 4. Axial T2-weighted image reveals the increased signal within the medial patella and the lateral femoral condyle corresponding to the kissing contusions of patellar dislocation. There is some increased signal at the medial retinacular attachment to the patella consistent with a partial tear (arrow). (Courtesy of James M. Farmer. From PattersonSmith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
and patellofemoral compression forces are high. A twisting injury with a strong quadriceps contraction with the knee flexed can drive the patella into the lateral femoral condyle, much like a wedge, producing a stellate chondral fracture. The dislocating patella can act more like a chisel to produce an osteochondral fracture.30The natural history of these lesions can lead to a condition indistinguishable from osteochondritis dissecans (OCD). This observation has led several authors to suggest unrecognized trauma as a primary etiology of OCD lesions in the knee.27,30 LESIONS OF THE ANKLE Osteochondral Lesions of the Talus
Osteochondral lesions involving the talar dome are relatively common, with an incidence recorded from 0.09% of all talar fractures to 6.5% of ankle sprains. Because they once were thought to result from ischemia leading to necrosis of the subchondral bone and subsequent fragmentation of the articular cartilage, the term osteochondritis dissecans was applied to these lesions. In 1959, Berndt and Harty reviewed the literature and presented their own experience with these lesions. They suggested a traumatic etiology for ”transchondral fract~res.”~, 11, 17, 33, 34 They felt that lateral talar lesions are produced when an inversion stress is applied to a dorsiflexed ankle, causing the anterior lateral aspect of the talus to impact the fibula. They described a similar mechanism when an inver-
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sion or external rotation stress is applied to a plantar flexed ankle, causing impaction of the posteromedial talus against the tibia (Fig. 5). Histologic examination of specimens in their study revealed necrosis and fibrosis in the subchondral trabecular bone with normal articular ~artilage.~ Subsequent series have supported a traumatic etiology for most osteochondral lesions of the talus, ranging from 75% to 100% for lateral lesions and 18% to 80% for medial lesi0ns.3~Because a large percentage of osteochondral lesions of the talus, especially in the medial talar dome, present without any history of trauma, other causes such as ischemia and systemic illnesses should be considered. Staging of Talar Lesions
Several staging systems have been developed for osteochondral lesions of the talus. The original system developed by Berndt and Harty was based on radiographic and intraoperative findings, although the practical application of this staging system has been limited to the radiographic findings. Stage I lesions represent a small area of subchondral compression. Stage I1 lesions are partially detached osteochondral
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Figure 5. The most common locations for osteochondral lesions on the talus: anterolateral and posteromedial. Stippled area represents stress. (From Berndt AL, Hatty M: Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 41A: 988-1020, 1959; with permission.)
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fragments. Stage I11 lesions are detached fragments that remain in situ. Stage IV represents a displaced osteochondral fragment (Fig. 6).3Several other systems using computed tomography (CT) scans, MR imaging, and arthroscopy have been developed since Berndt and Harty. Taranow et a1 have introduced a staging system that evaluates the bone lesion preoperatively using MR imaging and evaluates the cartilage condition using arthroscopy. MR imaging is good at evaluating the subchondral
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Figure 6. The state Berndt and Harty classification of osteochondral injuries. Stage one represents subchondral compression. Stage two represents partially detached osteochondral fragment. Stage three represents detached fragments remaining in sifu. Stage four represents displaced osteochondral fragment. (From Berndt AL, Harty M: Transchondral fractures [osteochondritis dissecans] of the talus. J Bone Joint Surg 41A:988-1020, 1959; with permission.)
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bone for marrow edema and necrosis of the subchondral bone; however, it is not as useful in evaluating the articular surface. In the system proposed by Taranow et al, Stage I is a bone bruise. Stage I1 lesions are subchondral cysts that develop from bone bruises. Stage I11 lesions are partially detached osteochondral fragments in situ. Stage IV lesions are displaced fragments. Further classification is based on the appearance of the articular cartilage surface at arthroscopy. Grade A represents viable intact cartilage, and grade B represents breech or nonviable articular Diagnosis of Talar Lesions Patients with osteochondral lesions of the talus typically present with pain either acutely following an ankle sprain or chronically after nonoperative treatment. They frequently have intermittent episodes of swelling and mechanical symptoms such as crepitus, catching, and giving way. Plain radiographs can be normal or reveal an osteochondral lesion. Routine anteroposterior, lateral, and mortise views should be obtained (Fig. 7). Special views with the ankle placed in dorsiflexion or plantarflexion can reveal anterolateral or posteromedial lesions, respectively. Radiographs of the contralateral ankle can reveal bilateral lesions in 10% of patients. When plain radiographs are normal, but clinical examination is abnormal, a bone scan can detect increased uptake in the area of the lesion. CT and MR imaging can identify and quantify the lesion better than plain radiographs and bone scanning, and should be obtained when conservative treatment fails to relieve symptoms (Fig. 8).
Figure 7. Mortise view of the right ankle demonstrates osteochondral injury of the lateral talar dome. There is an osteochondral fractures involving the lateral talar dome. This fracture is complete, in situ corresponding to a Berndt and Harty stage 111 lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
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Figure 8. Coronal T1-weighted image of the talus demonstrates changes from an osteochondral injury involving the medial talar dome. There is no separate fragment and the overlying cartilage is intact. This corresponds to a Berndt and Harty stage one lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
Treatment of Talar Lesions
Treatment for osteochondral lesions of the talus depends on the condition of the subchondral bone and overlying articular cartilage. A trial of nonoperative management including limited weightbearing and immobilization is advocated for stage I, 11, and medial stage I11 lesions. Operative management is advocated for lateral stage I11 lesions, all stage IV lesions, and patients for whom nonoperative management has failed.17 Delaying surgery for up to 1 year has not been shown to affect the outcome adversely even if surgical management ultimately is required.= The surgical options depend on the stage of the osteochondral lesion. Treatment for stage IV lesions is excision of the displaced fragment with drilling, abrasion, or curettage of the subchondral base. The repair process involved with this treatment will be discussed later. Stage I11 lesions can be treated with excision of the fragment or internal fixation of the fragment. Long-term studies regarding the outcome of internal fixation of osteochondral lesions of the talus are lacking, but the best candidates are younger patients with large lesions due to trauma. The choices for fixation include Kirschner wire, cancellous screws, Herbert screws, or bioabsorbable screws.32Treatment for stage I and I1 lesions typically is directed toward stimulating healing of the necrotic subchondral bone. Drilling of intact lesions can be performed in an anterograde fashion by means of arthroscopy or open arthrotomy. Retrograde drilling can be performed arthroscopically with fluoroscopic guidance. Drilling is thought to stimulate vascular inflow into the lesion, but there is no scientific evidence that this occurs. Anterograde drilling techniques necessarily violate the articular surface, whereas retrograde techniques do not require drilling through the articular cartilage. In
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addition, retrograde techniques allow curettage of necrotic bone and bone grafting of lesions. Kumai et a1 reported good results in 13 of 18 patients and fair results in 5 of 18 patients with stage I1 medial lesions treated with anterograde arthroscopic drilling. They found the results were much better in patients younger than 30 years of age.I7 Taranow et a1 performed a prospective study of patients with stage I11 and IV lesions treated with retrograde drilling, curettage, and bone grafting. They found immediate improvement in the American Orthopaedic Foot and Ankle Society Ankle-Hindfoot Scale of 25 points (53.9 to 82.6 points) and radiographic evidence of healing in 88% of patients.34 The long-term effect on the development of arthrosis is unknown at this time. Postoperative care following any of the surgical techniques will include limited weightbearing and various lengths of immobilization. Immobilization following drilling techniques for intact lesions will be brief. If ankle instability is present and stabilization procedures are required, they should be staged. The stabilization procedure should follow complete rehabilitation from the drilling technique because the postoperative immobilization after the stabilization necessarily will be longer than that required for the drilling technique.33 DIAGNOSIS OF OSTEOCHONDRAL LESIONS Diagnostic Algorithm Many osteochondral lesions can be diagnosed by plain radiography; however, radiographs can be normal in the presence of an osteochondral lesion. When a patient presents with pain, effusion, and mechanical symptoms with normal radiographs, further diagnostic workup is needed. There are several options to formulate a diagnosis. Bone scans are relatively inexpensive and can demonstrate increased uptake, but cannot quantify the exact size of the lesion or determine the condition of the articular cartilage. Anderson et a1 evaluated 14 patients with ankle sprains and persistent pain and found that a positive bone scan correlated with osteochondral lesions found on MR imaging in all 14 patients, whereas only 10 of 14 patients demonstrated osteochondral lesions on CT scan.33If the bone scan demonstrates an osteochondral lesion, the clinician can either proceed to arthroscopy or obtain a CT scan. CT scans demonstrate excellent definition of bony fragments and allow determination of size, location, and displacement of the fragments. CT is less sensitive in detecting trabecular microfractures than MR imaging. Recent MR scanning techniques such as MR arthrography, magnetization transfer imaging, and fast spin echo sequences have improved the visualization of chondral defects.26,30 MR imaging can detect subtle bone injuries that will require limited weightbearing and allow evaluation of soft tissues, which can be responsible for the patient’s symptoms. Finally, arthroscopy has the advantage of direct visualization of the articular surface and ability to treat the lesions, but cannot evaluate the condition
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of the underlying subchondral bone. Please refer to our diagnostic and treatment algorithm in the Appendix at the end of this article. TREATMENT OF OSTEOCHONDRAL LESIONS
General Principles Treatment of osteochondral lesions is determined based on the condition of the articular cartilage. Displaced osteochondral fragments can be excised and treatment directed toward the osteochondral defect, or they can be replaced and stabilized with internal fixation. Osteochondral defects can be treated with several methods, which attempt to fill the defect with either fibrocartilage or transplanted hyaline cartilage. Each is discussed in the following sections. Internal Fixation Internal fixation of large osteochondral fragments can be performed. It usually is indicated for large fragments following acute trauma in younger patients. Stable internal fixation can restore the articular surface and allow early range of motion of the joint. Most methods can be performed arthroscopically. The most commonly used devices are 0.062inch diameter smooth Kirschner wires placed through the fragment into the subchondral bone. Several pins are sometimes necessary to gain rotational control. Smooth pins can loosen, resulting in loss of fixation. Cahill reports using 0.062 K-wires that are bent 90°, 1 mm from the tip, and seating the bent distal tip into the articular cartilage and subchondral bone to gain better fixation than with straight pins. The pins subsequently are removed in a retrograde direction.6 Cannulated small fragment screws, Herbert screws, or Acutrak screws can be used to fix the fragment (Fig. 9A-D). Screws provide more rigid fixation than K-wires. Small fragment screws must be countersunk beneath the surface of the articular cartilage. The Herbert or Acutrak screws are ideal for articular surfaces because they do not have heads and are placed easily below the articular surface. Maxie reported the use of Herbert screws to stabilize partially detached osteochondral fragments in three patients. The screws were inserted arthroscopically through a transpatellar portal. All patients were full weightbearing immediately postoperatively and symptoms improved without complications up to 1 year later.I8Newer bioabsorbable polylactic acid screws can be used to provide fixation with the advantage of not requiring a second procedure for removal. No studies have been published using polylactic acid screws for this purpose. Finally, Gillespie reported results using corticocancellous bone harvested from cortical bone of the anterior tibia to secure osteochondral fragments. The corticocancellous strips act as shims to hold the osteo-
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Figure 9. Anteroposterior (A) and lateral (B) radiographs reveal an osteochondral lesion involving the medial femoral condyle. There are several small fragments within the lesion. These are better seen on the lateral radiographs (arrows). Postoperative radiographs reveal fixation of the fragments with Accutrack screws. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
chondral fragment in place, and are a source of bone graft to stimulate healing. He reported good or excellent results in 17 of 18 patients with radiographic evidence of union by 8 months. In addition, there is no need for a second procedure to remove hardware.13 Once a fragment is fixed, the joint should be taken through a full range of motion several
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times to ensure secure fixation and smooth motion. This information can be used to plan the postoperative rehabilitation. Excision, Debridement, and Marrow Stimulation Techniques
Treatment of osteochondral defects on the articular surface poses a significant challenge to the clinician. The natural history of these lesions depends on the size and location of the lesion. Most researchers hypothesize that large Outerbridge grade I11 and IV lesions cause overload of the subchondral bone with progression to gonarthrosis. Recent studies show significant chondrocyte damage overlying bone bruises. This damage also can lead to osteoarthritis." Removal of loose fragments, dkbridement of fragmented cartilage, and joint lavage can provide temporary relief of symptoms. In addition, picking, drilling, abrasion, and microfracture of the subchondral surface can stimulate the formation of a fibrin clot, which will facilitate mesenchymal cells to fill the defect with fibr~cartilage~,~~ (Fig. 10A-C). Steadman and Rodrigo reported improvement in the appearance of the articular surface following microfracture of the subchondral bone for full-thickness lesions. They reported better results in patients who received continuous passive motion (CPM) for 6 to 8 hours per day following microfracture. The number of patients who had no improvement was higher in the patients who did not receive CPM, and 45% still had exposed subchondral bone compared to 15% of patients who received CPM following microfract~re.~~ Their study demonstrated the importance of motion following marrow stimulation techniques. Fibrocartilage is stronger in tension than compression, as opposed to hyaline cartilage, which is stronger in compression than tension. Fibrocartilage is not a durable substitute, and long-term results have not been satisfying; however, these techniques can be the best alternative for large osteochondral defects on the weightbearing surface. Chondral and Osteochondral Transplants
Several chondral and osteochondral transplant procedures have been developed. The transplanted tissue can be either autogenous or allograft tissue and can consist of chondral elements alone or osteochondral transplants. Each method has the common goal of filling the defect with stable hyaline cartilage, and each has its own advantages and disadvantages. These treatment options are discussed below. Perichondral and Periosteal Grafts
Mesenchymal cells on the surface of periosteum and perichondrium can be stimulated to produce hyaline cartilage. The factors leading to
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Figure 10. A, Axial and fat suppressed TBweighted image reveals a large bone contusion within the lateral femoral condyle. The overlying cartilage is not well demonstrated. B, Lateral fat suppressed proton density weighted image reveals irregularity and thinning of the cartilage of the anterior lateral femoral condyle (arrows). C, Arthroscopic view of Outerbridge Stage 3 lesion of the lateral trochlea groove. D, Arthroscopic view following debridement. €, Drilling of same lesion. F; Arthroscopic view of similar lesion immediately after drilling. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
this proliferation are not completely known, but it has been shown that perichondrial and periosteal cells, when placed with the cambium layer facing the joint, will form hyaline ~artilage.~.*~ The perichondrial grafts are taken from rib cartilage, placed over a fibrin glue that fills the defect,
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and secured with the cambium layer facing the joint. Homminga et a1 performed this technique on 25 patients. Their experience with these grafts yielded good initial results, with improvement in Hospital for Special Surgery (HSS) Knee Score from 73 to 90 at 1 year. Results at 5to 7-year follow-up were disappointing, with 60% of the patients having endochondral ossification and delamination of the cartilage with resulting pain and d y s f ~ n c t i o n Despite .~~ the early optimism involving these grafts, they have not provided good long-term results. Autogenous and Allogenic Osteochondral Transplant Transplantation of intact articular cartilage with its underlying subchondral bone attempts to fill a defect with intact hyaline cartilage and, stable bony fixation. The ideal lesion for this treatment is the focal chondral or osteochondral defect on the femoral condyle or talus in a young patient. Normal surrounding hyaline cartilage reduces boundary shear and improves outcome.16Allograft transplantation can be used to repair larger defects. Fresh allografts are used because chondrocyte viability is diminished after freezing. The immunogenicity of human bone and cartilage is low; therefore no attempt is made to cross-match antigens between donors and recipient^.^ The transplants usually are performed by an arthrotomy, and the exact orthotopic site of the lesion is harvested from the donor specimen. The graft is secured with interference screws. Results of this transplant yielded 86% good or fair results when one joint surface was treated, and 53% good or fair results when two joint surfaces were treated.'j The disadvantages of this technique are potential disease transmission and difficulties associated with donor procurement. Autogenous osteochondral transplant, commonly called mosaicplasty or OATS (Arthrex, Inc) procedure, involves the placement of viable chondrocytes and the underlying cancellous bone, which unites quickly into the defect. Grafts 5.0 to 9.0 mm in diameter are harvested from the intercondylar notch or non-weightbearing portion of the femoral condyle near the patellofemoral joint. Grafts are press fit into the defect (Fig. 11). Hangody reported results on 57 patients with greater than 3 year follow up. The average modified HSS score was 90.7. Followup arthroscopy in 19 patients revealed the transplanted cartilage remained hyaline in nature and the gaps between the grafts had been filled with fibro~arti1age.I~ Bugbee reported good to excellent results on the modified HSS score in all patients, a 90% return to full competition level activities in patients less than 30 years of age, and a 63% return to full competition level activities in patients over 30 years of age.7 Mosaicplasty ideally is indicated for smaller focal lesions on the femoral condyle in younger patients. The results for patellofemoral lesions were less successful, with an average modified HHS score of 71.14 Autogenous Chondrocyte Transplant Transplantation of autogenous chondrocytes first was shown to be successful in a rabbit model in 1984. The first successful treatment of
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Figure 11. A, Arthroscopic view of Outerbridge Grade 4 lesion on the lateral femoral condyle. 6,Lesion following debridement and picking. C,Arthroscopic view 7 months later. D, Arthroscopic view following autologous osteochondral transplant. The arrows outline the two osteochondral plugs. Note the fibrocartilage covering the lesion. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)
osteochondral lesions in humans with autogenous chondrocyte transplant was performed and reported by Brittberg et a1 in 1994.5 The technique involves harvesting articular cartilage from a minor weightbearing area on the femoral condyle arthroscopically. Chondrocytes are isolated and amplified in an aseptic culture medium. This culture procedure results in an increase of chondrocytes by 10 to 20 times. The cells are then re-implanted by arthrotomy into the defect and held in place by a periosteal flap (Fig. 12). Several explanations for the repair process have been offered, but none have been proven. The first theory is that transplanted cells repopulate the defect and synthesize a new hyaline cartilage matrix. Another explanation is that the periosteal flap stimulates proliferation of the transplanted cells to fill the defect. Finally, the transplanted cells and periosteum are theorized to stimulate the surrounding chondrocytes to enter the defect and repair it.5 The end result of autogenous chondrocyte transplant has been shown to be a stable hyaline cartilage filled defect. The indications for autogenous chondrocyte transplant are a focal osteochondral lesion in an otherwise normal joint. Brittberg et a1 initially treated 23 patients with autogenous
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Figure 12. Technique for autogenous chondrocyte transplantation. (From Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 33:889-895,1994; with permission.)
chondrocyte transplant (16 femoral condyle lesions and 7 patellar lesions), and found 14 of 16 excellent or good results at 24-month follow up for condylar lesions and 2 of 7 excellent or good results at 36-month follow up for patellar lesions. Patients were evaluated by arthroscopy at 3 months and again at 12 to 46 months postoperatively. The hyaline cartilage was found to become more stable over time. Biopsy specimens taken at the second arthroscopy confirmed the histologic features of hyaline ~artilage.~ Since this original report, over 250 patients have been treated with autogenous chondrocyte transplant with greater than 80% improvement at 2-year f o l l o w - ~ p Degeneration .~~ of the new hyaline cartilage over time has not been reported. Autogenous chondrocyte transplant is an effective but technically demanding treatment for focal osteochondral lesions in younger active patients. SUMMARY
Osteochondral lesions are relatively common and usually occur as a result of trauma. They often are unrecognized acutely and lead to osteochondral defects and eventually osteoarthritis. Detection of these lesions has been aided by bone scan, CT, and MR imaging. Acute osteochondral fragments can be replaced and internally fixed. Chronic
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osteochondral defects can be treated with several methods designed to stimulate healing by either fibrocartilage or healing by transplantation of bone and cartilage or cartilage alone. The goal of all treatment methods is to provide a stable, congruent joint surface, restore function, and prevent the evolution of osteoarthritis in the injured joint. References 1. Bach 8, Warren R Radiographic indicators of anterior cruciate injury. In Feagin J (ed): The Crucial Ligaments Diagnosis and Treatment of Ligamentous Injuries About Knee. New York, Churchill Livingstone, 1988, pp 319-323 2. Berlet G, Mascia A, Miniaci A Treatment of unstable osteochondritis dissecans lessions of the knee using autogenous osteochondral grafts (mosaicplasty). Arthroscopy 15:312316, 1999 3. Bemdt AL, Harty M Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg 41A988-1020, 1959 4. Boden B, Pearsall A, Garrett W, et al: Patellofemoral instability: Evaluation and Management. J Am Acad Orthop Surg 5:47-57, 1997 5. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 335389495,1994 6. Buckwalter, J, Mow V, Ratcliffe A: Restoration of injured or degenerated articular cartilage. J Am Acad Orthop Surg 2:192-201, 1994 7. Bugbee W, Convery F Osteochondral allograft transplantation. Clin Sports Med 18:6775, 1999 8. Cahill 8: Osteochondritis dissecans of the knee: Treatment of juvenile and adult forms. J Am Acad Orthop Surg 3237-247, 1995 9. Cahill 8: Treatment of juvenile osteochondritis dissecans and osteochondritis dissecans of the knee. Clin Sports Med 4:367-386, 1985 10. Daniel DM, Stone ML, Dobson B et al: Fate of the ACL injured patient: A perspective study. Am J Sports Med 226324544, 1994
11. Ferkel R Arthroscopy of the ankle and foot. In Mann R, Caghlin M (eds): Surgery of the Foot and Ankle, ed 6, vol. 1. St. Louis, Mosby, 1993, pp 1291-1299 12. Friederich N, OBrien W Gonarthrosis after injury of the anterior cruciate ligament: A multi-center long term study. Z Unfallchir Versicherungsmed 86:8149, 1993 13. Gillespie H, Day B: Bone peg fixation in the treatment of osteochondritis dissecans of the knee joint. Clinic Orthop 143125-130, 1979 14. Hangody L, Kish G, Karpati Z, et al: Mosaicplasty for the treatment of articular cartilage defects: Application in clinical practice. Orthopedics 21:751-756, 1998 15. Johnson D, Urban W, Cabom D, et al: Articular cartilage changes seen with magnetic resonance imaging, detected bone bruises associated with acute anterior cruciate ligament rupture. Am J Sports Med 26409414,1998 16. Kish G, Modis L, Hongody L: Osteochondral mosaicplasty for the treatment focal chondral and osteo chondral lesions of the knee and talus in the athlete rational, indications, techniques, and results. Clin Sports Med 18:4547, 1999 17. Kumai T, Takakura Y, Higashiyana I, et al: Arthroscopic drilling for the treatment of osteochondral lesions of the talus. J Bone Joint Surg 81:1229-1235, 1999 18. Mackie I, Pemberton D, Maheson M: Arthroscopic use of the Herbert screw in osteochondritis dissecans. J Bone Joint Surg 72B:1076, 1990 19. Mair SD, Schlegel TF, Gill TJ, et al: Steadman-Hawkins Clinic. Presented at the American Orthopaedic Society for Sports Medicine Annual Meeting. Vail, CO, 1999 20. Mandelbaum B, Brane J, Fu F et al: Articular cartilage lesions of the knee. Am J Sports Med 26:853-861, 1998 21. Mankin H, Mow B, Buckwalter J, et al: Form and function of articular cartilage. In Simon S (ed): Orthopedic Basic Science, Rosemont, IL, American Academy of Orthopedic Surgeons, 1994, p p 1-44
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22. Milgram J, Rogers L, Miller J: Osteochondral fractures: Mechanisms of injury and fate of fragments. AJR Am J Roentgen01 130:651-658, 1978 23. Miller M, Osbome J, Gordon W The natural history of bone bruises: A prospective study of magnetic resonance imaging detected trabecular microfractures in patients with isolated medial collateral ligament injures. Am J Sports Med 26:15-19, 1998 24. Minas T, Nehrer S: Current concepts in the treatment of articular cartilage defects. Orthopedics 20:525-538, 1997 25. Mori R, Ochi M, Sakai Y, et al: Clinical significance of magnetic resonance imaging (MRI) for focal chondral lesions. Magn Reson Imaging 171135-1140, 1999 26. Mow VC, Zhu W, Ratcliffe A Structure and function of articular cartilage and meniscus. In Mow VC, Hayes WC (eds): Basic Orthopaedic Biomechanics, New York, Raven Press, 1991, pp 143-198 27. ODonoghue D: Chondral and osteochondral fractures. J Trauma 6(4):469481, 1966 28. Recht MP, Resnick D: Magnetic resonance imaging of articular cartilage: An overview. Top Magn Reson Imaging 9:328-336, 1998 29. Rodrigo JS, Steadman RJ, Sillman JF, et al: Improvement of full thickness chondral defect healing in the human knee after debridement and microfracture using continuous passive motion. Am J Knee Surg 1994:7109-116. 30. Rosenberg N: Osteochondral fractures of the lateral femoral condyle. J Bone Joint Surg 46A:1013-1026, 1964. 31. Sisto, D. The surgical treatment of full thickness osteochondral defects of the knee. Presented at American Orthopaedic Society for Sports Medicine Annual Meeting, Traverse City, MI, 1999 32. Speer K, Warren R, Wickiewicz T, et al: Observations on the injury mechanism of anterior cruciate ligament tears in skiers. Am J Sports Med 23:77-81, 1995 33. Stone J: Osteochondral lesions of the talar dome: J Am Acad Orthop Surg 464-73,1996 34. Taranow W, Bisignani G , Towers J, et al: Retrograde drilling of osteochondral lesions of the medial talar dome. Foot Ankle Int 20474-480, 1999
Address reprint requests to David F. Martin, MD Wake Forest University School of Medicine Medical Center Boulevard Winston-Salem, NC 27157
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APPENDIX +/- history of injury Pain Effusion Mechanical symptoms
Excision Internal Fixation SCW.
BoIw WO PLaS
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Bone Scan
Excise/Debride Picking, Drilling, Abrasion, Microfracture Autogenous Osteocbondral Transplantation Allograft Transplantation Autogenous Chondrocyte Transplantation
Diagnostic and treatment algorithm for chondral and osteochondral lesions. (Courtesy of James M. Farmer. From Patterson-Smith, B [ed]: Wake Forest University Orthopaedic Manual. Winston-Salem, Wake Forest Press, 1999; with permission.)