Surgical Treatment of Osteochondritis Dissecans Lesions

Michael J. Salata, MD

Neal B. Naveen, BS

Taylor M. Southworth, BS

Ian J. Dempsey, MD, MBA

Brian J. Cole, MD, MBA

Dr. Salata or an immediate family member serves as a paid consultant to or is an employee of Stryker. Dr. Cole or an immediate family member has received royalties from Arthrex, Inc. and Elsevier Publishing; serves as a paid consultant to or is an employee of Arthrex, Inc. and Regentis; has stock or stock options held in Ossio and Regentis; has received research or institutional support from Aesculap/B. Braun, Arthrex, Inc., the National Institutes of Health (NIAMS & NICHD), and Regentis; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research-related funding (such as paid travel) from Athletico, JRF Ortho, and Smith & Nephew; and serves as a board member, owner, officer, or committee member of the Arthroscopy Association of North America and the International Cartilage Repair Society. None of the following authors or any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter: Mr. Naveen, Mr. Southworth, and Dr. Dempsey.

This chapter is adapted from Bajaj S, Salata MJ, Cole BJ: Surgical Treatment of Osteochondritis Dissecans Lesions in Flatow E, Colvin AC, eds: Atlas of Essential Orthopaedic Procedures. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2013, pp 85-94.

INTRODUCTION

Osteochondritis dissecans (OCD) is a pathologic joint disorder that affects the subchondral bone and the overlying articular cartilage.¹ The disease results in subchondral bone loss and destabilization of the overlying articular cartilage, leading to separation and increased susceptibility to stress and shear of the resultant fragment.² The true etiology is unknown, but this condition may be related to repetitive microtrauma, a single acute traumatic event, vascular ischemia, endocrinopathy, and/or a genetic predisposition.³ Regardless of the etiology, the end result is fragmentation of both cartilage and bone that can progress to early degenerative changes and loss of function in the affected area. Once identified, lesions can be stratified into four categories based upon MRI, radiographic, and arthroscopic findings.⁴^,⁵^,⁶ In its final stages, bipolar osteoarthritis can develop, leading to the need for noncartilage restoration interventions like arthroplasty.

The prevalence of OCD is estimated at 15 to 30 per 100,000, with most lesions occurring in the knee. Nearly 80% of the cases involve the medial femoral condyle (MFC), 15% involve the lateral femoral condyle, and 5% involve the patellofemoral region. More than 70% of all OCD lesions are found in the “classic” area of the lateral aspect of the MFC intersecting the intercondylar notch near the femoral footprint of the posterior cruciate ligament (PCL).⁷

The course of treatment for a lesion is largely contingent on its stability, which is most accurately assessed arthroscopically, as MRI findings revealed an overall accuracy of 53% in determining lesion stability.⁸ In the case of a stable lesion and a short duration of symptoms, nonsurgical management can be successful. In the past, these lesions have been treated with immobilization and weight-bearing limitations. However, published studies have shown that prolonged immobilization can be detrimental to the health of the knee joint; thus, currently employed nonsurgical management should focus on a hiatus from sporting and high-impact activities for 6 to 8 weeks with allowance for normal weight bearing in a compliant patient.⁹

Asking a patient to participate in “relative rest program” much like the treatment recommendations for stress fractures can maintain the health of the joint without compromising the healing potential of a symptomatic OCD lesion. The length of time required to render a patient asymptomatic and safe to return to high-level activities is highly variable and is a consideration when deciding to intervene with surgery.

In the case of failed nonsurgical management or in the setting of an unstable fragment, surgical intervention includes fragment removal, drilling (antegrade or retrograde), internal fixation,² marrow stimulation, autologous chondrocyte implantation (ACI), or osteochondral autograft/allograft transplantation to repair the lesion or supplement the area of cartilage loss. As a last resort, joint arthroplasty may be the only feasible solution in advanced cases.

SUBTLETIES IN DECISION MAKING

Unique to OCD is the fact that patients with this pathology can have very little in the way of symptoms until the fragment becomes destabilized based on the endogenous natural history of that lesion or through acute or repetitive trauma. It is appropriate to consider symptomatic OCD with fragment instability as an intra-articular atrophic fracture nonunion. This concept is important to recognize
because it relates to treatment decisions and the technical steps requisite to successful defect healing. Because the natural history of the isolated OCD lesion is not clarified in the body of existing literature nor in our contemporary experience, successful clinical treatment is often achieved through fragment removal, at least in the short and intermediate term. Although intuitively it is reasonable always to try to retain a viable fragment and provide rigid fixation to promote biologic union of any osteochondral fragment, the fact that many patients can clinically tolerate a concave, well-defined osteochondral defect is provocative to the extent that benign neglect following fragment removal remains a practical treatment option in some instances.

The resultant paucity of symptoms following fragment removal is explicable by the typical geometry and the relatively load-sparing location of these lesions, which allow the defect bed to become clinically silent simply because the surrounding osteoarticular environment can “shield” the lesion, rendering it less clinically relevant. The debate that remains is when to treat these lesions early with cartilage restoration procedures when initial fragment excision renders a patient clinically normal. Because no cartilage restoration procedure has been demonstrated to last “forever” nor been demonstrated to definitively prevent progression of osteoarthritis over time, decision making remains challenging for the patient presenting with the asymptomatic defect following fragment removal. This is especially true for the high-level competitive athlete who places a premium on the short-and intermediate-term maintenance of functional activity.

PATIENT SELECTION

A thorough history is mandatory and should emphasize any inciting events, any underlying metabolic or systemic conditions that may have contributed to the OCD, the duration of symptoms, and previous attempts at treatment (both nonsurgical and surgical). There are a number of risk factors linked to OCD, which should also be thoroughly explored in a patient’s history. Individuals who are male are four times more likely to develop an OCD. Those who are African American, have a discoid lateral meniscus, have a family history of OCD, or are active sports participants also are at an increased risk.¹⁰^,¹¹ The typical presentation of OCD in the knee includes pain and swelling related to activity.¹^,³ Instability is usually not reported, although mechanical symptoms such as catching or locking can occur if the fragment has become destabilized or completely detached and is acting as a loose body. On physical examination, patients typically have tenderness localized over the compartment where the OCD lesion is located.¹ The patient may walk with an antalgic gait or with the leg externally rotated (Wilson sign) to decrease pressure over the lesion. With external rotation, a lesion located on the MFC will not impinge with the medial tibial eminence, which decreases the pain associated with motion at the lesion interface. Joint effusion, decreased range of motion, loose-body symptoms, and quadriceps atrophy are variably present, depending on the extent and stage of the lesion and the duration of symptoms.

When contemplating surgical intervention, it is important to consider the site of the lesion. Certain sites, such as the classic location on the MFC, have a spontaneous resolution rate of less than 30%, whereas nonclassic locations are much more likely to heal in the adolescent population, with 88% to 100% healing rates reported with nonsurgical management.³

The ideal candidate for primary repair is an unstable lesion in an active, symptomatic patient.¹² The ideal patient is willing to comply with the postoperative weight-bearing limitations and activity restrictions and understands the likely need for a second procedure for hardware removal. Patients with open physes on radiographs and in whom nonsurgical therapy for a stable fragment fails to achieve symptomatic and radiographic improvement should be considered for retrograde or antegrade drilling. Arthroscopically stable, symptomatic lesions might benefit from bioabsorbable screw fixation, with the screw heads buried just below the level of the subchondral plate as an adjunct to drilling through an extra-articular or periarticular location. Arthroscopically unstable, symptomatic lesions with intact cartilage attached to viable bone benefit from débridement and marrow stimulation of the defect surface and metal screw fixation of the fragment, with the screw heads buried deep to the articular cartilage for later removal. Should these initial treatments fail to resolve symptoms, definitive cartilage restoration (osteochondral autografting, osteochondral allograft transplantation, or ACI) can be considered as a subsequent surgical intervention.

CONTRAINDICATIONS TO SURGICAL MANAGEMENT

Age, clinical symptoms, lesion characteristics, and skeletal maturity are several important factors that must be taken into account when considering surgical management of an OCD lesion. Physeal status is used to stratify OCD into either juvenile OCD (JOCD) or adult OCD (AOCD). Although most AOCDs develop from the progression of untreated JOCDs, the management of these two diseases differs greatly. In the case of JOCD, nonoperative management is recommended for stable lesions.¹³ By telling patients to reduce the level of symptom-producing activity, clinicians hope to mitigate patients’ symptoms as well as create an environment for spontaneous healing by reducing the load bearing on the defective side of the knee. Modification of activity may include weight-bearing restrictions and disallowing participation in sports or high-impact activities.¹⁴^,¹⁵ This strategy achieves good outcomes in juveniles because of their increased
regenerative capacity from chondrocytes and mesenchymal stem cells.¹⁶ In a large, European Pediatric multicenter study on 355 patients who were treated surgically and 154 who were treated conservatively, patients with a lesion < 2 cm² found in a classic location had improved prognoses, with no evidence of effusion or dissection on imaging.¹⁷

Primary surgical fixation is not recommended if the lesion is free-floating as a loose body and the underlying subchondral bone is compromised. An initial strategy in this patient population should include loose body removal and possible chondrocyte biopsy for subsequent ACI if the patient demonstrates persistent symptoms attributable to the resultant chondral defect. In such cases, primary marrow stimulation can also be considered on a case-by-case basis.

PREOPERATIVE IMAGING

Because the physical findings of OCD are often vague and nonspecific, a physical examination cannot be used in isolation to diagnose this type of pathology. Imaging is crucial in the evaluation of patients presenting with these symptoms and should include a plain radiographic series and often a subsequent MRI. Preliminary radiographs should be standard and include AP weight-bearing knee, weight-bearing 45° flexion PA, lateral, and Merchant views³ (Figure 1). The flexion weight-bearing PA view should be obtained in addition to standard AP because it allows for better visualization of lesions along the posterolateral aspect of the MFC. Open physes are a positive predictor for healing of an OCD lesion and should be noted on the plain radiographs.

FIGURE 1 Radiographic appearance of an osteochondritis dissecans (OCD) lesion. A, Weight-bearing AP radiograph of a left knee depicts an OCD lesion on the medial femoral condyle (MFC). B, Lateral view at 45° flexion. C, Merchant view. The area of lucency on the MFC can be best appreciated on the AP and lateral views.

MRI is often required in the diagnosis of OCD lesions because it is the most informative imaging modality. Specifically, an evaluation for the presence of bone edema, subchondral separation, cartilage breakdown, lesion size, and location can be assessed using MRI before treatment.⁴ The MRI scans are assessed based on the following criteria, in which meeting one of the four criteria offers up to 97% sensitivity and 100% specificity in predicting lesion stability² (Figure 2):

A thin, ill-defined, or well-demarcated line of high signal intensity, measuring 5 mm or more in length at the interface between the lesion and the underlying subchondral bone
A discrete, rounded area of homogeneous high signal intensity
A focal defect with a width of 5 mm or more in the articular surface of the lesion
A high signal intensity line traversing the articular cartilage and subchondral bone plate into the lesion

PROCEDURE

Most AOCD cases arise from established but untreated or asymptomatic JOCD. Spontaneous healing has been reported in such cases with nonsurgical treatment options. However, for lesions presenting in the classic location of the lateral aspect of the MFC or lesions that persist after adequate nonsurgical treatment, an array of surgical options are available.

The overall goal of surgical intervention is to enhance the healing potential of the subchondral bone, fix the unstable
fragment, or replace the abnormal cartilage and bone with implantable tissue.² The type and extent of surgery necessary for OCD depends on a myriad of factors, including patient age, lesion characteristics (the quality of the articular cartilage; the quality of the associated subchondral bone; and the size, shape, thickness, and location of the lesion), lesion stability, and surgeon preference (Figure 3).

FIGURE 2 MRI appearance of an osteochondritis dissecans (OCD) lesion. A, T1-weighted sagittal view. B, T2-weighted sagittal view. C, T2-weighted coronal view of an OCD lesion presenting concomitantly with compromised subchondral bone. An area of high signal intensity between the OCD lesion and the subchondral bone suggests instability.

Room Setup/Patient Positioning

A supine position, with the affected leg placed within an ACL leg holder, with the foot of the bed dropped, permits full extension, flexion including hyperflexion, valgus loading, and figure-of-4 position, allowing complete access to femoral condyle lesions to optimize arthroscopic lesion preparation and fixation. The contralateral extremity is secured in the lithotomy position using a leg holder with adequate padding around the peroneal nerve. The affected joint is draped to the proximal thigh, and a well-padded nonsterile pneumatic tourniquet is applied before draping. An examination under anesthesia is performed to assess range of motion and ligamentous stability. Depending on the lesion site and size, an arthroscopic or a mini-open technique is used. Lesions on the condyles are often easily accessed with the use of arthroscopic techniques and through satellite portal placement wherever needed. Patellofemoral and tibial lesions can be more difficult to access arthroscopically and may require an arthrotomy or mini-arthrotomy for adequate visualization and treatment.

Surgical Technique

A complete arthroscopic evaluation of each compartment and its structure is performed to determine all intra-articular sources of pain. A standard arthroscopic probe is used to assess the boundaries and the stability of the lesion (Figure 4). In the case of a lesion with intact articular cartilage, the lesion will be ballottable, and a “trampoline” effect will be appreciated when the lesion is probed. This clinical scenario is more common in very young patients who present with activity-related pain without effusions and with fluid behind the lesion on MRI. However, in many cases, there are fissures or fibrillations that mark a distinct transition from a firm to a soft segment of cartilage that can be appreciated as one moves the elbow of a probe from normal cartilage to the overlying cartilage of an OCD lesion. Often, for classic OCD of the MFC, access can occur at the leading edge of the femoral origin of the PCL using an electrocautery device and elevator to expose a fissure that enters the intercondylar notch in this area.

With the lesion identified and classified, the following surgical techniques can be used to alleviate a patient’s symptoms.

Reparative Procedures

The goal of a reparative procedure is to restore the integrity of the subchondral bone, improve blood supply, and ultimately restore and preserve the overlying articular cartilage surface. This generally is a primary reduction and fixation of the fragment. It is often accompanied by a removal of fibrocartilaginous scar at the interface between the lesion and underlying subchondral bone, coupled with restoration of blood flow to the lesion by marrow stimulation techniques such as microfracture or drilling of the host tissue bed. In the presence of cystic changes or attritional bone loss, local bone graft procedures that harvest cancellous bone from the Gerdy tubercle or the distal femur using a small-diameter osteochondral autograft harvesting tube are effective.

FIGURE 3 Surgical treatment algorithm for osteochondritis dissecans (OCD). The surgical goals should always incorporate an attempt to reestablish the joint surface using the least invasive procedure first. ACI = autologous chondrocyte implantation, OA graft = osteochondral allograft, OATS = osteochondral autograft transfer system

Drilling

In the setting of a stable lesion with intact articular cartilage that remains symptomatic despite appropriate nonsurgical management, retrograde or antegrade drilling can restore blood supply to the fragment. This technique serves to create vascular channels that can provide adequate blood flow to the affected region, allowing for healing.⁴ This technique is less likely to be successful with true fragment instability. Understanding that these lesions often hurt because of micromotion due to “fracture nonunion” principles can help surgeons avoid implementation of subtherapeutic treatment that might inevitably lead to repeated surgical intervention if the lesions become macroscopically unstable.

Antegrade drilling has been described as being performed from within the joint through the articular cartilage and into the subchondral bone. Lesions of the MFC can be drilled through an anterolateral or anteromedial portal, or from a nonarticular location. This is done by introducing a Kirschner (K-wire) percutaneously at the anterior aspect of the origin of the PCL.¹⁸ Lesions of the lateral femoral condyle are usually accessible through the anterolateral portal. If the lesion is not accessible via standard portals, accessory portals are created to obtain an orthogonal drilling angle. Holes are drilled uniformly using a K-wire, and blood and fat droplets from the drilled region are used to confirm the depth of the penetration.¹⁹ Anterograde drilling violates the articular cartilage surface, with the resultant gap filled in with fibrocartilage, tissue similar to the cartilage created with a microfracture. We prefer to avoid direct penetration of intact healthy articular cartilage overlying the fragment and drill just behind the lesion through the intercondylar notch or through the juxta-articular osseous surfaces, which is more analogous to retrograde drilling. In addition, consideration should be given to the use of third-generation small-diameter bioabsorbable, variably pitched screws (Bio-Compression Screw, Arthrex) placed directly through the lesion, which will essentially provide a combined approach of antegrade drilling with fracture fixation, even if the fragment is only “microscopically” unstable (Figure 5). Surgeons must consider that, despite being bioabsorbable, these
devices will remain intact for up to several years; therefore, their heads must be advanced to or beyond the subchondral plate to avoid inadvertent damage to opposing articular surfaces either primarily or following potential fragment subsidence over time.

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