Surgical Techniques in Sports Medicine
1st Edition

56
Surgical Treatment of Osteochondritis Dissecans of the Knee
Christina R. Allen MD
Marc R. Safran MD
History of the Treatment of Osteochondritis Dissecans
Osteochondritis dissecans (OCD) of the knee is a condition that causes separation or fragmentation of a segment of subchondral bone and overlying cartilage from the remaining underlying subchondral bone. With progression of the condition, this pathology may result in signs or symptoms correlating with the disease stage as it impacts on the integrity of the overlying articular cartilage.
Early signs or symptoms associated with intact cartilage over an OCD lesion may be related to cartilage softening or an alteration in the mechanical properties of the cartilage. At this early stage, the patient may complain of vague anterior knee pain and a variable amount of swelling that is typically intermittent and often related to activity level. In later stages, due to lack of underlying support of the cartilage, the patient may present with signs or symptoms of articular cartilage separation (cartilage flaps or “loose bodies” causing locking or catching symptoms), inflammatory synovitis, or a persistent or intermittent effusion. Because lesions may become symptomatic, surgical intervention may often be required. In 1840, Paré was the first to describe the removal of joint loose bodies, which were presumably osteochondral fragments.1 Operative treatment for unstable lesions has been traditionally attributed to Smillie,2 who developed a nail for open reduction and internal fixation of displaced and unstable lesions.
The incidence of OCD has been estimated at between 0.02% to 0.03% (based on a survey of knee radiographs) and 1.2% (based on knee arthroscopies).3,4 The highest rates appear among patients between 10 and 15 years of age, with rare instances in children under 4 or patients over 50 years of age. Higher rates among males are historically reported, with an approximate 2:1 ratio compared with females, though recent data suggest that this difference is lessening.5 Bilateral lesions, typically in different phases of development, are reported in 15% to 30% of cases and mandate assessment of both knees in all those presenting with this diagnosis.6 OCD lesions of the knee most commonly involve the lateral aspect of the medial femoral condyle (Fig. 56-1A,B). The lateral femoral condyle is less frequently involved, and patellar OCD lesions are even more rare.6,7
The etiology of osteochondritis dissecans remains unclear. König8 originally described the condition in 1888 and gave it a name indicative of his initial belief that OCD was due to an inflammatory reaction of both the bone and the cartilage. Current consensus regarding etiology is debatable, although an inflammatory etiology is unlikely, as recognized by König a decade later. Repetitive microtrauma, ischemia, epiphyseal abnormalities, osteochondral fracture, genetic predisposition, and endocrine abnormalities have all been postulated as potential contributors to development of OCD.
Clinically, Cahill5 and Mubarak and Carrol9 emphasized a distinction between two types of OCD as recognized by the osseous age of the patient at the time of symptom onset. Those with open physes are considered to have juvenile onset OCD, while those who are skeletally mature at the time of symptom onset have the adult form. Paradoxically, adult onset OCD may simply be a delayed onset of previously asymptomatic juvenile OCD that failed to heal and manifests later with loosening and joint degeneration. Skeletal age at onset of symptoms appears to be the most important determinant of prognosis and remains an essential factor directing the timing and nature of treatment decisions. Paletta et al.10 found that all patients with open physeal plates and increased activity on bone scan were more likely to heal their OCD lesion, while those without increased activity did not heal. In contrast, among patients
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with closed growth plates only 33% healed despite having a similar increase in activity within the lesion.
Fig. 56-1. The classic location for osteochondritis dissecans. AP radiographs demonstrates a lateral aspect of the medial femoral condyle OCD lesion before (A) and after (B) displacement.
Both radiographic and surgical classification systems for OCD lesions have been described, with few having clear prognostic significance. Using plain radiographs of the talus, Berndt and Harty11 classified OCD in four stages that describe the condition and position of the osteochondral fragment, ranging from compression of the subchondral bone to complete detachment of the fragment (loose body). Cahill and Berg12 describe a method of dividing the AP and lateral radiographs into 15 distinct zones. This alphanumeric system provides standardization for research and descriptive purposes, but has found limited clinical application to date with regard to treatment or prognosis.5
DiPaola et al.13 classified lesions according to appearance on magnetic resonance imaging (MRI) and correlated specific findings with the potential for fragment detachment. They described lesions containing fluid (high T2 signal) behind the subchondral fragment as potentially unstable, as this suggested a breach of the cartilage surface.The presence of a low T2 signal behind the fragment suggests that there is no fluid behind the fragment, indicating a stable fibrous attachment and potentially intact cartilage surface. Other reports suggest a similarly high level of confidence for predicting lesion stability using intra-articular gadolinium contrast.14
DiPaola’s classification system has proven to be reasonably accurate and predictive of the stability of lesions on arthroscopic examination. O’Connor et al.15 found an 85% correlation between preoperative MRI findings using DiPaola’s criteria and arthroscopic findings graded with Guhl’s arthroscopic classification system for OCDs.In Guhl’s16 system, OCD stages are defined by cartilage integrity and fragment stability. Type I lesions have softening of cartilage but no breach of the cartilage surface; type II lesions have breached cartilage but are stable. Type III osteochondral defects have a definable fragment that remains partially attached (flap lesion), type IV lesions constitute an osteochondral defect at the donor site with a resultant loose body in the knee joint.
Indications and Contraindications
No randomized, controlled clinical trials exist for either operative or nonoperative interventions for OCD of the knee. In general, physis maturity, dissection of the lesion from the adjacent subchondral bone or stability, size, and location of lesions and cartilage surface integrity have been used as predictive criterion for necessity of operative intervention.
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Fig. 56-2. Treatment algorithm for knee OCD.
Recently, a large multicenter review of the European Pediatric Orthopedic Society’s experience with treatment of OCD lesions was performed.6 Lessons from this study are derived from the knees of 318 juvenile patients and 191 adults. The authors of the study made several important distinctions and conclusions. They determined that if there are no signs of dissection (loosening), the prognosis is significantly better and that pain and swelling are not good indicators of fragment dissection. Additionally, plain radiographs and computed tomography (CT) scan are not useful in predicting dissection. Sclerosis on plain radiographs predicts a poor response to drilling. Further analysis demonstrated that lesions greater than 2 cm in diameter had a worse prognosis, and when there is evidence of dissection, surgical treatment results are better than nonsurgical. Lesions in the classical location of the lateral aspect of the medial femoral condyle had a better prognosis. Finally, although patients with adult onset symptoms had a higher proportion of abnormal findings on radiographs after the treatment period (42%), more than one in five of those with open epiphyseal plates (22%) had abnormal knee radiographs at an average of 3 years after starting treatment.
An algorithm for treatment decisions is outlined in Fig. 56-2, with the primary goal being to promote healing of lesions in situ and preventing displacement.
Nonoperative treatment through activity modification may include a wide spectrum of approaches that have historically included crutches for limited weight bearing, braces, or even casts for non-compliant patients. In patients without significant sports participation, prescribing a non–weight-bearing status and range of knee motion exercises may be beneficial to cartilage and help avoid the potential disaster of “cast disease” and arthrofibrosis. Our approach is to limit sports activities without immobilization, casting, or crutches, except for the noncompliant patient.
Choosing surgical intervention for managing OCD of the knee and selecting a strategy for repair, reconstruction, or removal of osteochondral lesions depends upon the stability of the osteochondral lesion and the integrity of the overlying cartilage. Essentially, the indications for operative treatment in skeletally immature patients are a symptomatic osteochondral fragment that is attached but not healing, a partially or completely detached fragment with a disrupted articular surface, and loose bodies. In skeletally mature individuals, lesions are less likely to heal with conservative treatment once fluid is dissecting under the fragment; therefore, symptomatic lesions and loose bodies are generally treated surgically.
Preoperative Imaging Studies
Three standard roentgenograms of the knee, bilateral posterior-anterior (PA) 30-degree bent knee (Rosenberg or notch
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view), axial (Merchant) view, and lateral weight-bearing exams are routine in the initial evaluation for OCD.17 Lesions of the weight-bearing surface of the femur are best seen with a flexed knee PA view and may help identify the lesions in the posterior condyles (Fig. 56-1A,B). Lateral radiographs allow recognition of the relative anterior-posterior location and identification of normal benign accessory ossification centers in the skeletally immature patient as described by Caffey et al.18 An axial view of the patella should be added, as it may uncover the unusual patella lesion. Plain radiographs also allow a baseline assessment of the lesion size, presence or absence of sclerosis, presence or absence or lesions in the contralateral knee, potential dissection, and assignment to one of several classification systems that are based on radiographic criteria.
MRI studies are also useful in quantifying the size of the lesion. Again, the studies of DiPaola et al.13 have shown that lesions containing fluid (high T2 signal) behind the subchondral fragment tend to be unstable and may require surgical treatment (Fig. 56-3), whereas lesions that demonstrate a low T2 signal behind the fragment indicate a stable fibrous attachment.
The use of bone scans may be beneficial in monitoring the healing progress of a stable lesion and may also be useful in predicting the healing potential of a lesion. As previously noted, Paletta et al.10 found that all patients with open physeal plates and increased activity on bone scan went on to heal their OCD lesions, while those without increased activity did not heal without surgical intervention. In contrast, among patients with closed growth plates only 33% healed despite having a similar increase in activity within the lesion.
Fig. 56-3. T2-weighted MRI of the knee demonstrating high signal behind osteochondral fragment, indicating an unstable fragment.
Surgical Techniques
Surgical treatment of osteochondral defects is usually performed under general anesthesia, possibly supplemented with a femoral nerve block for postoperative pain relief. Arthroscopic treatment is preferable because of decreased morbidity, although it may be necessary to perform a mini-arthrotomy or full arthrotomy in order to gain adequate access to the osteochondral defect for repair. Posterior condyle lesions and the less common patella and tibial plateau lesions are particularly difficult to fix arthroscopically and an arthrotomy should be used in order to ensure precise access, exposure, reduction, and fixation of the lesion. A 30-degree arthroscope is generally utilized and standard inferomedial and inferolateral arthroscopic portals are established. It may be beneficial to establish the arthroscopic viewing portal first (viewing from the portal opposite the OCD lesion) and then use a spinal needle to localize direct access to the OCD lesion before establishing the working portal on the same side of the knee as the defect. Anterior synovitis and hypertrophic fat pads should be excised with a shaver in order to allow adequate visualization of and access to the OCD lesion. The OCD lesion is then probed for stability, which will dictate the method of treatment. The meniscus of the affected compartment should be carefully examined for injury and stability. Likewise the surrounding cartilage on the tibial and femoral sides should be examined and probed for defects, flaps, and evidence of softening. If loose bodies are encountered, every attempt should be made to remove them intact, as they could possibly be salvaged and utilized to repair the osteochondral defect.
Treatment of Stable Lesions
Operative treatment for stable or intact lesions with normal articular cartilage involves drilling of the subchondral bone with the intention of stimulating vascular ingrowth and subchondral bone healing. Retrograde techniques (defined as methods that avoid articular cartilage disruption using a transosseous approach) have given way to arthroscopically assisted antegrade (transchondral) methods that have proven to be highly efficacious in skeletally immature patients. In general, drilling is more effective in promoting healing in skeletally immature patients than in older patients, but is still worth attempting in all patients with a persistently symptomatic lesion with intact articular cartilage.
Arthroscopically assisted antegrade drilling may be performed with a 0.062-in. Kirschner wire to a minimum
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depth of 1.5 cm to stimulate vascular ingrowth and subchondral bone healing (Fig. 56-4A,B). Care should be taken not to make a stable lesion unstable by creating too many drill holes. This technique should be performed under fluoroscopic guidance in patients whose physes are still open, to avoid drilling across the physis. Antegrade drilling, although easier, is associated with the disadvantage of drilling through and perforating areas of otherwise intact cartilage.
Fig. 56-4. Treatment of Guhl type I OCD lesion. A: Guhl type I OCD lesion with intact but softened overlying articular cartilage. B: Antegrade (transchondral) drilling of Guhl type I OCD lesion with 0.062 in. Kirschner wire.
Alternatively, for patients with closed physes, retrograde (transosseous) drilling may be performed under fluoroscopic guidance using a similar size Kirschner wire. In cases where there is unbreached or intact overlying articular cartilage but a significant loss of underlying osteochondral bone, transosseous drilling with a larger drill bit (3 or 4 mm) may be performed, followed by bone grafting retrograde through the drill holes. This technique may be performed under arthroscopic visualization to ensure that the articular cartilage is not violated. We have found that the use of an ACL drill guide, with the tip placed over the cartilage of the OCD lesion, greatly facilitates accurate placement of the drill tunnels for bone grafting. The use of a cannulated coring reamer for drilling the tunnel down to the defect may yield enough bone graft to pack the OCD lesion.
Treatment of Unstable Lesions
Though effective in eliminating mechanical symptoms, simple removal of a loose or detached fragment is rarely considered the optimal management for OCD, aside from cases where the fragment is macerated and irreparable. In cases where simple transchondral drilling has failed, or when the lesion is hinged, loose, or displaced, the objective is to restore the articular congruency by stimulating subchondral bone repair by curettage of underlying fibrous tissue, compression of the fragment with adequate fixation, and bone grafting when necessary. In this manner, the osseous portion of the fragment may heal and create a stable base for the overlying articular cartilage, with the goal being to reduce the risk of degenerative arthritis due to the loss of congruity of the articular cartilage.
Discrepancy between the size of a lesion and displaced fragments due to fragment overgrowth, loss of fragment substance due to mechanical damage, or craterization of the donor site have been described, and may present a significant technical challenge to the repair of displaced or even partially attached fragments. When the fragment-crater interface is relatively congruent, the lesion may often be treated arthroscopically. In this method, the partially attached fragment is reflected or temporarily removed to allow inspection of the osseous surfaces and removal of fibrocartilage from the opposing subchondral interface. Cancellous bone graft obtained from the proximal tibia, femoral condyle, or iliac crest (using a coring device) may be placed arthroscopically and packed in the base of the OCD lesion to obliterate step-off between the fragment and the surrounding cartilage. The use of an arthroscopic cannula will facilitate bone grafting and fragment fixation.
There are a variety of fixation methods utilized for fixation of OCD fragments. These include the use of 0.062-in threaded pins for antegrade or retrograde fixation of the lesion, cannulated headless screws, bioabsorbable screws or pins, headed cannulated screws, bone pegs, and osteochondral plugs. A subsequent procedure is often recommended to remove metal hardware. This is usually performed
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arthroscopically, with low morbidity, and provides an opportunity to directly assess healing and cartilage integrity. However, metal hardware fixation devices have also been associated with several complications including wire migration, adjacent cartilage damage, and implant fracture. Biodegradable implants (Fig. 56-5A,B,C,D) have the advantage of not requiring removal, but also have drawbacks due to occasional sterile abscess formation, synovitis, and loss of fixation.Compressive metal or bioabsorbable screws provide the advantage of compressing and loading the articular fracture, while pins and wires do not. In general, metallic devices are more optimal in cases where the lesion is larger (more than 2 cm2), if bone grafting of the crater is necessary, or if the OCD fragment is large or deformed. Bioabsorbable devices may be more appropriate for the fixation of smaller lesions (<2 cm2) not requiring bone grafting, with a more viable and thinner OCD fragment.
Fig. 56-5. Arthroscopic internal fixation of an unstable OCD lesion. A: Preoperative MRI of unstable OCD lesion of lateral femoral condyle. B: Intraoperative arthroscopic picture unstable OCD lesion. Fibrous tissue at base of crater is being débrided. C: Arthroscopic fixation of unstable OCD fragment. D: OCD fragment after fixation.
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When poor congruency of the fragment-donor interface exists, a technique similar to that described by Anderson et al.19 may be employed. In this method, the lesion is evaluated arthroscopically, followed by open curettage, grafting, reduction, and fixation (Fig. 56-6A,B,C,D,E). This is done by reflecting a partially attached fragment or removing it temporarily and to allow inspection of the osseous surfaces and removal of fibrocartilage from the opposing subchondral interface. The ensuing fragment/crater mismatch can then be grafted with autogenous bone (tibial metaphysis or iliac crest) prior to compression screw fixation of the osteochondral fragment. For fixation of osteochondral fragments, we have used cannulated Acutrak, mini-Acutrak headless screws, or a 4.0-mm cannulated headed screw. A supplemental Kirschner wire may be placed through the fragment in order to prevent rotation of the fragment in the crater during screw fixation. It is also important to place the fixation device so that it is perpendicular to the fragment when fixing it in order to achieve maximal compression. This may require the creation of an additional portal or even a
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transpatellar tendon portal. Screw heads should be countersunk 1 to 2 mm below the cartilage surface in order to avoid secondary articular cartilage abrasion on the opposing surface. Hardware may be removed arthroscopically after a period of 6 to 12 weeks following a period of strict non–weight bearing, when clinical and radiographic signs of healing are demonstrated.
Fig. 56-6. Surgical open reduction and internal fixation of an unstable OCD injury. A: Pre-op radiograph of an 18-year-old male with locking, catching, and swelling of the knee. OCD in the classic location of the medial femoral condyle at the insertion of the PCL with loose and fragmented lesion. B: Intraoperative photo of the lesion exposed with loose/unattached articular cartilage extension demarcated using a marking pen. C: Articular cartilage lesion being elevated after fibrocartilage débrided from the bed and prior to bone grafting. D: Knee after bone grafting and fixation with two compression screws and absorbable pins. E: Postoperative radiograph of the same knee after open reduction and internal fixation.
More recently, small osteochondral autologous plugs have been harvested from the notch or non–weight-bearing area of the proximal lateral femoral condyle and used as fixation devices for unstable lesions. Yoshizumi20 describes successful union by 6 months in three cases of “adult” OCD using the technique of Berlet. In the technique of Berlet et al.,21 the OCD lesion is essentially fixed in situ by applying autologous osteochondral plugs around the periphery of the lesion. The crater of the lesion is debrided, the osteochondral fragment placed anatomically in its crater, and the unstable cartilage edges are secured with 4.5-mm autograft osteochondral plugs harvested and transplanted using a mosaicplasty system.
Technical Alternatives/ Salvage Procedures
OCD lesions without a replaceable fragment may be treated in a variety of ways. Several techniques for salvage of full thickness defects of articular cartilage including curettage and microfracture, autologous chondrocyte implantation, mosaicplasty, and osteochondral allograft have been advocated. An algorithm for approaching this type of injury is outlined in a recent review article by Browne and Branch.22 Their algorithm for treating full-thickness cartilage injuries may also be applied to cartilage injuries sustained as a result of osteochondritis dissecans.
Curettage
Curettage or abrasion arthroplasty with the addition of microfracture for OCD lesions may be appropriate for small lesions or lesion in non–weight-bearing areas where the growth of fibrocartilage may be adequate treatment. Microfracture techniques should be carried out as described by Steadman et al.,23,24 with debridement of all loose or marginally attached cartilage around the defect, followed by curettage, to remove the calcified cartilage layer over the underlying bone. Arthroscopic awls are then utilized to create 3- to 4-mm deep microfracture holes separated by approximately 3 to 4 mm, taking care not to damage the subchondral plate between holes. The microfracture holes are placed starting peripherally next to the stable surrounding cartilage and then working centrally. The problem with microfracture techniques in OCD lesions is the bone loss that accompanies this condition.
Osteochondral Autografts
Some surgeons have advocated using autologous osteochondral autografts for filling empty craters to decrease edge loading. Osteochondral autograft transplantation involves the open or arthroscopic harvesting of cylindrical plugs ranging from 4.5 to 12 mm in diameter from the superolateral ridge of the femoral condyles above the sulcus terminalis or in the perimeter of the intercondylar notch. The harvested plugs are then transplanted directly into the osteochondral defect, with care taken to insert the plug in the proper orientation in order to restore cartilage congruency. Excessive countersinking or prominence of even 0.5 mm may result increased contact pressures and possibly early failure or opposing surface cartilage damage.25,26,27 The advantages of osteochondral autograft transfer techniques include the fact that only one surgical procedure is required, cartilage plugs are readily available (with no risk of disease transmission), and plug transfer involves the direct transfer of intact hyaline cartilage, the subchondral plate, and bone. Disadvantages include limitations on graft availability, particularly in attempting to treat larger lesions >2 cm2, concerns over donor site insult or morbidity, the technical challenge of restoring a congruent surface, and the unclear outcome of mismatched split lines (surface orientation) of the articular cartilage.26,27 Case reports have indicated generally favorable results for these procedures but contain limited follow-up.
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Autologous Chondrocyte Implantation
In larger lesions of osteochondral defects, surgical resurfacing using autograft transfer can be a significant challenge due to graft availability. Restoration of articular surface in lesions greater than 2.5 to 3 cm2 and up to 10 to 15 cm2 can be accomplished by autologous chondrocyte implantation (ACI).28 The procedure requires a two-stage approach in which the articular cartilage cells are first arthroscopically harvested and expanded ex vivo in cell culture. Then via arthrotomy, the cultured chondrocytes are implanted under an autologous periosteal tissue flap. The advantages of autologous chondrocyte implantation include the potential to treat larger lesions, use of autologous tissue, and reliability of obtaining hyalinelike tissue at outcome. Disadvantages are the high cost of the procedure, the need for a second staged surgery, and an arthrotomy for reimplantation as well as the possibility that the resultant repair tissue may be a combination of bone, fibrous, fibrocartilaginous, and hyaline tissue.
The essential steps of autologous chondrocyte implantation include an initial chondral biopsy for autologous chondrocyte cell culture. In cases where the bony depth of the defect exceeds 7 to 8 mm, a bone grafting procedure is performed either at the time of the original chondrocyte cell harvesting procedure, as a separate procedure, or at the time of implantation of the cells. The harvested cells are then expanded ex vivo in cell culture. The second surgery or implantation procedure consists of an arthrotomy, which allows adequate exposure of the defect, defect preparation, periosteal procurement from the proximal tibia, fixation of the periosteal tissue, securing a watertight seal with fibrin glue, and implantation of the chondrocytes.
Osteochondral Allograft
In cases in which larger lesions are noted (>2.5 cm2) or where significant concerns exist regarding the morbidity associated with donor site issues or staged surgical procedures, osteochondral allograft transfer provides a valuable treatment option. Osteochondral allografts have the advantage of providing fully formed articular cartilage without specific limitations with respect to size of the defect (Fig. 56-7A,B,C,D). A disadvantage of osteochondral allograft is the concern for disease transmission and immunologic rejection and problems with storage and sterilization, resulting in decreased chondrocyte viability.
The procedure begins with templating the lesion in order to obtain an allograft that matches the size and contour of the defect to be treated. Although multiple methods have been described for allograft sizing, plain radiographs of the recipient’s knee joint are commonly utilized. After correcting for magnification errors on radiographs, the size of the recipient’s knee bone can be measured and the appropriately sized allograft may be procured.
Surgical exposure is routinely made via a medial or lateral arthrotomy, depending on the involved side. If the lesion is on the anterior femur, a mini-arthrotomy often affords adequate access to the defect. The OCD defect base is prepared by removing any sclerotic bone or fibrous tissue, creating a vascular base to allow the allograft to heal. The recipient defect area is sized and then either a single large circular dowel is harvested from the donor allograft, which will fill the entire defect, or multiple plugs are harvested in order to perform an allograft mosaicplasty. The allograft is typically 8 to 10 mm in bone depth, which allows just enough bone to allow the graft heal to the host. Deeper grafts are not recommended, as the immunogenicity and healing time of the graft will be increased. If the host defect depth is more than 1 cm, autograft bone should be used to fill to the desired depth. The allograft should be in direct contact with recipient bone at the base, and the plug surface should be flush with the adjacent articular cartilage. If the allograft is countersunk, it will not function adequately. If left even 0.5 mm proud, articular cartilage damage or increased contact pressures may result.26,27
Pitfalls
Potential complications of repair of an OCD fragment or salvages procedures for OCD lesions include failure of healing, hardware complications, and joint surface incongruity. Therefore, optimal outcome is usually associated with adequate crater-base debridement to remove fibrous tissue, appropriate bone grafting, and achieving secure fixation and compression across the fragment-crater interface with the appropriate implant. Small or comminuted fragments that cannot be rigidly fixed are best removed. Careful attention should be paid to bone grafting and ensuring proper fit and fixation of the fragment or graft in the crater so that there is no residual incongruity or edge loading between the cartilage surface of the fragment/graft and surrounding articular cartilage, which will lead to early failure or opposing surface cartilage damage.26,27 Patients should be carefully followed postoperatively to watch for signs of hardware complications, including wire migration, adjacent cartilage damage due to proud implants, implant failure, loss of fixation, or synovitis. A second surgery to remove fixation devices may be required 6 to 12 weeks (based on clinical and radiographic signs of healing) after surgery prior to allowing the patient to bear weight, especially when metal implants are utilized for fixation.
Rehabilitation
Postoperative rehabilitation depends on the treatment technique utilized and should be individualized to the patient and procedure. In general, early motion in an unlocked hinged brace is encouraged for all treatment methods. Immediate range of motion including use of a
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continuous passive motion machine is started with touchdown or non–weight bearing for up to 6 to 8 weeks depending on the size, site, and security of fixation achieved. After satisfactory evidence of healing on radiographs, weight bearing may be progressed. If a metallic fixation device is used, then limited weight bearing may be delayed until the hardware is removed. Chronic OCD lesions or lesions requiring bone grafting may require a more extended healing time for chondral and bony consolidation. Graft healing is assessed both clinically and by serial cartilage-specific MRI scans. Patients should only be allowed to return to full sporting activities after MRI evidence of full healing has been obtained. Similar protocols should be utilized for OCD salvage procedures such as osteochondral autograft, osteochondral allograft, and autologous chondrocyte implantation.
Fig. 56-7. Salvage treatment of an OCD crater using an osteochondral allograft. A: Arthroscopic view of osteochondral defect of the lateral aspect of the medial femoral condyle. B: View of the OCD crater after mini-arthrotomy. C: Osteochondral allograft after press-fit fixation. D: Second-look arthroscopy of osteochondral allograft, 6 months post-op.
Outcomes and Future Directions
The outcome of the treatment of OCD lesions is dependent on the age at presentation, extent of surface restoration, underlying healing, and perimeter integration. Lateral femoral condyle lesions and patellar lesions may also be associated with a poorer prognosis. Linden3,29 and Twyman et al.30 are the only authors to publish long-term follow-up on the treatment of OCD lesions without surgical fixation of fragments. Linden showed that young patients did well long term regardless of treatment, whereas adults tended to develop arthritis after an approximately 20-year latency period. Twyman et al. reported on long-term results of skeletally immature patients diagnosed with OCD lesions and noted that 32% of the patients later developed moderate or severe osteoarthritis.
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Conversely, short-term functional results for patients treated with fragment takedown, curettage, grafting, and stabilization have been good to excellent in 80% to 90% of patients.31,32,33 Unfortunately, long-term results for patients treated by this method are not available at this time and are a subject for further follow-up.
Our knowledge of the etiology and natural history of OCD of the knee continues to grow. Two principal factors, the degree of skeletal maturity at symptom onset and the integrity of the subchondral bone and cartilage surface, remain the most important determinants in choosing the method of treatment. Dissecting and defining the different subtypes of OCD, the potential of each for spontaneous healing or progression, and improving opportunities and techniques for intervention to maintain and restore joint integrity remain significant challenges for the orthopedic community.
References
1. Paré A. Oeuvres completes. Vol. 3. 1840–1841, Paris, France: JB Bulliere.
2. Smillie I. Treatment of osteochondritis dissecans. J Bone Joint Surg Br. 1957;39B:248–260.
3. Linden B. The incidence of osteochondritis dissecans in the condyles of the femur. Acta Orthop Scand. 1976;47:664–667.
4. Bradley J, Dandy D. Osteochondritis dissecans and other lesions of the femoral condyles. J Bone Joint Surg Br. 1989;71:518–522.
5. Cahill B. Osteochondritis dissecans of the knee: treatment of juvenile and adult forms. Journal of American Academy of Orthopaedic Surgeons 1995;3(4):237–247.
6. Hefti F. Osteochondritis dissecans: a multicenter study of the European Pediatric Orthopedic Society. J Pediatric Orthop. 1999;8B:231–245.
7. Shigehito Y, Takaaki I, Hiroaki T, et al. Osteochondritis dissecans of the femoral condyle in the growth stage. Clin Orthop. 1998; 346:162–170.
8. König F. Ueber freie Korper in den Glenken. Zeiteschr Chir. 1888;27:90–109.
9. Mubarak S, Carrol M. Familial osteochondritis dissecans of the knee. Clin Orthop. 1979;140:130–136.
10. Paletta G, Bednarz P, Stanitski C, et al. The prognostic value of quantitative bone scan in knee osteochondritis dissecans. Am J Sports Med. 1998;26(1):7–14.
11. Berndt A, Harty M. Transcondylar fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am. 1959;41A:988–1020.
12. Cahill B, Berg B. 99m-technetium phosphate compound scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles. Am J Sports Med. 1983;11:329–335.
13. DiPaola J, Nelson D, Colville M. Characterizing osteochondritis dissecans lesion by magnetic resonance imaging. Arthroscopy. 1991;7:101–104.
14. Kramer J, Stiglbauer R, Engel A, et al. MR contrast arthrography (MRA) in osteochondritis dissecans. J Comput Assist Tomog. 1992;16:254–260.
15. O’Connor M, Palaniappan M, Kahn N, et al. Osteochondritis dissecans of the knee in children: a comparison of MRI and arthroscopic findings. J Bone Joint Surg Br. 2002;84B(2):258–262.
16. Guhl, F. Arthroscopic treatment of osteochondritis dissecans. Clin Orthop. 1982;167:65–74.
17. Rosenberg T, Paulos L, Parker R, et al. The forty-five-degree posteroanterior flexion weight-bearing radiograph of the knee. J Bone Joint Surg Am. 1988;70(10):1479–1483.
18. Caffey J, Madell S, Royer C, et al. Ossification of the distal femoral physis. J Bone Joint Surg Am. 1958;40A(3):647–654.
19. Anderson A, Lipscomb A, Coulam C. Antegrade curettement, bone grafting and pinning of osteochondritis dissecans in the skeletally mature knee. Am J Sports Med. 1990;18:254–261.
20. Yoshizumi Y. Cylindrical osteochondral graft for osteochondritis dissecans of the knee. Am J Sports Med. 2002;30(3):441–445.
21. Berlet G, Mascia A, Miniaci A. Treatment of unstable osteochondritis dissecans lesions of the knee using autogenous osteochondral grafts (mosaicplasty). Arthroscopy. 1999;15:312–316.
22. Browne J, Branch T. Surgical alternatives for treatment of articular cartilage lesions. J AAOS 2000;8(3):180–189.
23. Steadman J, Rodkey W, Singleton S, et al. Microfracture technique for full-thickness chondral defects: technique and clinical results. Oper Tech Orthop. 1997;7:300–304.
24. Steadman J, Briggs K, Rodrigo J, et al. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477–484.
25. Hangody L, Kish G, Karpati L. Mosaicplasty for the treatment of articular cartilage defects: application in clinical practice. Orthopedics. 1998;21:751–756.
26. Pearce S, Hurtig M, Clarnette R, et al. An investigation of 2 techniques for optimizing joint surface congruency using multiple cylindrical osteochondral autografts. Arthroscopy. 2000;17: 50–55.
27. Koh J, Wirsing K, Lautenschlager E, et al. The effect of graft height mismatch on contact pressure following osteochondral grafting. Am J Sports Med. 2004;32:317–320.
28. Peterson L, Minas T, Brittberg M, et al. Two- to 9-year outcome of autologous chondrocyte transplantation of the knee. Clin Orthop. 2000;374:212–234.
29. Linden, B. Osteochondritis dissecans of the femoral condyles. J Bone Joint Surg Am. 1977;59A:769–776.
30. Twyman R, Desai K, Aichroth P. Osteochondritis dissecans of the knee. A long-term study. J Bone Joint Surg Br. 1991;73B: 461–464.
31. Zuniga J, Sagastibelza J, Lopez-Blasco J, et al. Arthroscopic use of the Herbert screw in osteochondritis dissecans of the knee. Arthroscopy. 1993;9:668–670.
32. Thomson, N. Osteochondritis dissecans and osteochondral fragments managed by Herbert compression screw fixation. Clin Orthop. 1987;224:71–78.
33. Cugat R, Garcia M, Cusco X, et al. OCD: a historical review and treatment with cannulated screws. Arthroscopy. 1993;9(6):675–684.