Osteochondritis dissecans (OCD) can cause knee pain and dysfunction in children. The etiology of OCD remains unclear; theories on causes include inflammation, ischemia, ossification abnormalities, genetic factors, and repetitive microtrauma. Most OCD lesions in skeletally immature patients will heal with nonoperative treatment. The success of nonoperative treatment decreases once patients reach skeletal maturity. The goals of surgical treatment include maintenance of articular cartilage congruity, rigid fixation of unstable fragments, and repair of osteochondral defects with cells or tissues that can adequately replace lost or deficient cartilage. Unsalvageable OCD lesions can be treated with various surgical techniques.
Key points
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Osteochondritis dissecans (OCD) lesion of the knee is a relatively common cause of knee pain in pediatric patients.
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Most pediatric OCD lesions of the knee will heal with nonoperative treatment, which includes a period of rest or activity modification with or without immoblization.
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Surgical treatment is indicated for patients with closed physes or unstable or unsalvageable lesions.
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The goals of surgical treatment include maintenance of articular cartilage congruity, rigid fixation of unstable fragments, and repair of osteochondral defects with cells or tissue that can adequately replace lost or deficient cartilage.
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High-quality evidence for the optimal evaluation and management of pediatric OCD lesions remains sparse, and continued research is needed.
Introduction
Osteochondritis dissecans (OCD) of the knee can be a source of pain and dysfunction in pediatric patients. The estimated incidence of OCD ranges from 9.5 to 29 cases per 100,000 population. Boys have an approximately fourfold increased incidence of OCD of the knee compared with girls. Most lesions are found within the distal femur, and the most common site is the lateral aspect of the medial femoral condyle. OCD is an acquired condition of articular cartilage and subchondral bone that initially manifests itself as a softening of the overlying cartilage ( Fig. 1 ). Without treatment, this can progress to articular cartilage fissuring, separation, partial detachment, and eventually, osteochondral separation. OCD of the knee can be subcategorized based on the status of the distal femoral physis. Juvenile OCD occurs in patients with open physes and has a much better prognosis than adult OCD. Greater than 50% of juvenile OCD cases will show healing within 6 to 18 months with nonoperative treatment, whereas patients with adult OCD frequently require operative intervention.
Introduction
Osteochondritis dissecans (OCD) of the knee can be a source of pain and dysfunction in pediatric patients. The estimated incidence of OCD ranges from 9.5 to 29 cases per 100,000 population. Boys have an approximately fourfold increased incidence of OCD of the knee compared with girls. Most lesions are found within the distal femur, and the most common site is the lateral aspect of the medial femoral condyle. OCD is an acquired condition of articular cartilage and subchondral bone that initially manifests itself as a softening of the overlying cartilage ( Fig. 1 ). Without treatment, this can progress to articular cartilage fissuring, separation, partial detachment, and eventually, osteochondral separation. OCD of the knee can be subcategorized based on the status of the distal femoral physis. Juvenile OCD occurs in patients with open physes and has a much better prognosis than adult OCD. Greater than 50% of juvenile OCD cases will show healing within 6 to 18 months with nonoperative treatment, whereas patients with adult OCD frequently require operative intervention.
History and etiology
The etiology of OCD remains unclear, and no theory regarding its cause is universally accepted. Theories on etiology include inflammation, ischemia, ossification abnormalities, genetic factors, and repetitive microtrauma. In 1887, König suggested an inflammatory etiology, coining the term “osteochondritis dissecans.” Further study, however, did not support inflammation as the primary cause of OCD. Ribbing attributed abnormalities in ossification within the distal femoral epiphysis as a cause. A possible vascular etiology has been proposed, with relative ischemia and subsequent necrosis being important components in the development of OCD. Other studies, however, have failed to definitively identify avascular necrosis of the OCD fragment or find a relative ischemic watershed area of the lateral aspect of the medial femoral condyle (the most common location of OCD lesions). More recent research in the development of OCD lesions in animals has focused on the role that vascular architecture may play in the development of OCD. Both pigs and people develop OCD lesions in similar anatomic regions, and the vascular anatomy in both species demonstrates that both species have similar vascular architecture, which may predispose them to the development of OCD of the femoral condyles. This research suggests that vascularity may play a role in the development of OCD in people.
A genetic predisposition for the development of OCD has also been proposed. Several cases of monozygotic twins with OCD lesions have been described, as well as large reports of OCD lesions within the same family. Additionally, there are several genetic diseases that are associated with the development of OCD lesions. Patients with Stickler syndrome have been found to have multiple OCD lesions. OCD lesions are also commonly reported in association with dwarfism.
Mechanical factors such as malalignment or repetitive microtrauma have also been implicated in the development of OCD. The frequent occurrence of OCD lesions in patients who are involved in activities and sports with repetitive impact as well as the association with abnormal meniscal anatomy help support the concept of altered knee biomechanics as a cause of OCD. This theory holds that OCD occurs as a result of an initial stress reaction, which may then progress to a stress fracture of the underlying subchondral bone. With progressive repetitive loading, the stress fracture fails to heal, and the subchondral bone becomes necrotic, causing the fragment to eventually dissect and separate from the fracture bed.
Although the precise etiology of OCD is unclear, it is known that if these lesions are left untreated and fail to heal appropriately, they have a high potential of contributing to the development of future osteoarthritis.
Biology of articular cartilage and subchondral bone
Understanding the anatomy and morphology of subchondral bone is important to adequately evaluate and manage conditions that affect the subchondral bone such as OCD. The subchondral zone or the subchondral bone plate refers to the cortical endplate lying adjacent to the calcified zone of the articular cartilage with its accompanying subarticular spongiosa ( Fig. 2 ). The cement line separates the calcified zone from the subchondral bone plate, with the thickness of the subchondral bone plate varying depending on the joint.
The architecture of the subchondral bone plate consists of 2 mineralized layers, which together form a single unit, separating the articular cartilage from the bone marrow. There is a discrete band of calcified cartilage on the articular side of the subchondral bone plate. This band appears as the tidemark on hematoxylin and eosin histologic staining. The tidemark is a complex 3-dimensional structure. The tidemark is significant, because it represents the mineralization front and is a transition zone between 2 dissimilar regions of cartilage (see Fig. 2 ). The tidemark separates the type II collagen fibrils of the articular cartilage from the type I collagen found deeper (away from the joint surface). The tidemark has significant biomechanical functions and changes in response to microinjury. There is evidence that collagen fibrils cross the tidemark, resulting in a strong link between these 2 zones. This is clinically relevant, because meticulous removal of all calcified cartilage during articular cartilage repair procedures is important to allow for good attachment of any repair tissue to the subchondral bone plate.
The calcified cartilage extends further toward the marrow cavity, where it is remodeled and replaced by woven or lamellar bone, taking on the appearance of the supporting trabeculae. The dense cancellous bone underlying the calcified cartilage has a honeycomb appearance that looks like a solid mass of bone fenestrated by intercommunicating spaces. Deeper away from the articular cartilage surface is the subarticular spongiosa. No collagen fibers transverse the area between the calcified cartilage and the cortical endplate, making the osteochondral junction an area of regional weakness. This is in contrast to the tidemark that separates the calcified cartilage from the articular cartilage, which is crossed by collagen fibrils.
There are a high number of arterial and venous vessels as well as nerves, sending small branches into the calcified cartilage layer. The subchondral plate is fenestrated by hollow spaces, which may provide a direct connection between the unmineralized cartilage and the marrow cavity of the subarticular spongiosa. Blood vessels have the potential of reaching the overlying articular cartilage directly, such as during microfracture procedures, in which the calcified zone of cartilage is removed prior to surgically penetrating through to the subchondral bone plate into the subarticular spongiosa.
Evaluation and diagnosis
Clinical Presentation
The initial presentation in most children with knee OCD is relatively nonspecific. In stable lesions, knee aching and activity-related pain are the most common complaints. Symptoms may mimic patellofemoral pain due to chondromalacia patella or subtle patellofemoral malalignment. Knee instability or mechanical symptoms are unusual. On physical examination, children with stable lesions may walk with a slight limp. Palpation through varying degrees of knee flexion often reveals a point of maximal tenderness over the involved femoral condyle, typically the lateral aspect of the medial femoral condyle. In long-standing symptomatic lesions, quadriceps dysfunction may be noted. Knee effusion and crepitus are unusual in stable lesions; however, unstable lesions more commonly present with mechanical symptoms, effusion, limping, and crepitus, as the knee is taken through a range of motion. In younger patients with significant growth remaining, unstable lesions and associated mechanical symptoms are rare. Some stable lesions may develop symptomatic plica bands or synovial folds, which can produce some mechanical symptoms. Symptoms and examination of the contralateral knee should also be assessed, since lesions may be bilateral in 20% to 25% of cases.
Imaging
The ideal imaging modality for the evaluation of OCD lesions should be reliable, reproducible, and provide prognostic information on the lesion’s ability to heal with nonoperative management. Imaging begins with plain radiography and should include anterior-posterior (AP), lateral, and tunnel or notch views of the knee ( Fig. 3 ). A sunrise or Merchant view should also be obtained if there is suspicion for a trochlear or patellar lesion. Full-length, bilateral, lower extremity standing alignment films are useful to assess patients’ mechanical axis, particularly in those with uncommon lesion locations (ie, lateral femoral condyle lesions) ( Fig. 4 ). Plain radiography is useful to characterize lesion location, rule out other bony pathology, and evaluate skeletal maturity, which is prognostic of healing potential. Plain radiographs can also be used to longitudinally monitor lesion healing. In younger patients (typically <7 years old), the distal femoral epiphyseal ossification center may appear irregular and mimic the appearance of an OCD, making correlation with clinical findings important. Contralateral knee radiographs may also be considered to assess ossification irregularities as well as potential asymptomatic lesions. Important characteristics that can be noted on plain radiographs include lesion size, location, shape/contour, radiodensity, and fragmentation.
MRI has become a routine part of the evaluation of OCD lesions and is useful for determining lesion size, cartilage morphology, and condition of the underlying subchondral bone. MRI has also been shown to correlate well with histopathologic findings in juvenile OCD lesions and can be used to assess areas of increased T2 signal deep to the osteochondral fragment as well as the presence of loose bodies. De Smet and colleagues described MRI findings found on T2-weighted sequences that could be used to predict lesion stability ( Table 1 ). The authors found that a high signal line deep to the OCD fragment was most predictive of an unstable lesion ( Fig. 5 ). This high signal line may indicate the presence of either healing vascular granulation tissue or synovial fluid beneath the subchondral bone implying a break in the articular surface (when interpreted in conjunction with a breach in the articular surface as seen on T1-weighted images). It has been shown that patients with this finding on MRI are less likely to heal with nonoperative treatment. Additionally, lesion size as assessed on MRI has been shown to be predictive of healing potential. Despite the widespread use of MRI in the evaluation of pediatric OCD lesions, appearance on MRI does not always correlate with lesion stability. Kijowski and colleagues showed that although the sensitivity of MRI for diagnosing an unstable lesion in pediatric patients is 100%, the specificity was only 11% in their series. Heywood and colleagues had similar findings when correlating MRI findings with arthroscopy. Table 2 summarizes the MRI classification of OCD lesions. Based on current literature, smaller lesions with intact cartilage are more likely to heal with nonoperative management alone, especially in skeletally immature patients.
| Description | |
|---|---|
| 1 | Thin line of high signal intensity 5 mm or more in length at the interface between the OCD and underlying bone |
| 2 | Discrete, round area of homogenous high signal intensity 5 mm or more in diameter beneath the lesion |
| 3 | Focal defect with a width of 5 mm or more in the articular surface of the lesion |
| 4 | High signal intensity line traversing the articular cartilage and subchondral bone plate into the lesion |
| Stage | MRI Findings |
|---|---|
| I | Small change of signal without clear margins of fragment |
| II | Osteochondral fragment with clear margins but without fluid between fragment and underlying bone |
| III | Fluid is visible partially between fragment and underlying bone |
| IV | Fluid is completely surrounding the fragment, but the fragment remains in situ |
| V | Fragment is completely detached and displaced (loose body) |
Arthroscopic Appearance
Recently, the Research on Osteochondritis Dissecans of the Knee (ROCK) Study Group developed a knee arthroscopy classification system of OCD lesions. In this classification system, lesions are divided into 2 groups based on diagnostic arthroscopy: immobile or mobile. These groups are further subdivided into 3 categories within each group describing specific lesion characteristics ( Fig. 6 ). Intraclass correlation coefficients were used to measure intra- and inter-rater reliability during the development of the classification system, and very good to excellent reliability was found among orthopedic surgeon members of the ROCK group. This classification system will be useful for future radiograph and MRI validation studies and for facilitating multicenter OCD research.
