- Author: Grant Cooper, MD; Chief Editor: Thomas M DeBerardino, MD more...
The name osteochondritis dissecans (OCD) is a misnomer. In 1888, Konig coined the term when he sought to describe the pathologic process that led to atraumatic loose bodies of femoral origin in the knee and hip joints. Believing that an underlying inflammatory reaction of bone and cartilage was a major component of this process, he selected the terms osteochondritis, to refer to the inflammation of the osteochondral joint surface, and dissecans, derived from the Latin word dissec, which means to separate. However, investigators have failed to identify inflammatory cells in histologic sections of excised osteochondral loose bodies. Nevertheless, the name has persisted.
Images depicting osteochondritis dissecans are provided below:
OCD may occur in the kneed, elbow, or ankle. See also Knee Osteochondritis Dissecans. For patient education information, see the First Aid and Injuries Center, as well as Knee Pain, Knee Injury, BrokenElbow, and Ankle Fracture.
History of the Procedure
In osteochondritis dissecans, a fragment of cartilage and subchondral bone separates from an articular surface. In 1840, Pare was first to describe the surgical removal of loose bodies, presumably osteochondral fragments, from joints.
For many years, the treatment of choice for OCD remained either arthrotomy with removal of the loose osteochondral fragment or conservative, nonoperative management. The latter option remains the treatment of choice for patients with early disease and open physes. In contrast, surgical options have traditionally included drilling of the site of the defect, removing the loose body, fixing the loose body to the site of separation, and placing osteochondral grafts. Current operative methods include fixation of the lesion, drilling of the site of the defect with removal of loose bodies, and autologous osteochondral mosaicplasty and autologous chondrocyte transplantation.[1, 2]
Osteochondritis dissecans is characterized by separation of an osteochondral fragment from the articular surface. The underlying bone from which the fragment separates has normal vascularity. This characteristic distinguishes OCD from osteonecrosis, in which the underlying bone is avascular.
OCD affects 2 distinct populations of patients differentiated by the status of their physes. Patients aged 5-15 years who have open physes have the juvenile form of the disease. Older adolescents and adults who have closed physes have the adult form of the disease. Symptoms of OCD depend on the stage of the lesion. If left untreated, OCD may lead to early degenerative changes with chronic pain and functional impairment.
In the United States, the overall prevalence of osteochondritis dissecans is not known. However, in the femoral condyles, OCD has a prevalence of approximately 6 cases per 10,000 men and 3 cases per 10,000 women.
OCD occurs in the knee 75% of the time, the elbow 6% of the time, and the ankle 4% of the time. In the knee, OCD occurs in the medial femoral condyle 75% of the time, on the weight-bearing surface of the medial condyle 10% of the time, on the weight-bearing surface of the lateral condyle 10% of the time, and in the anterior intercondylar groove or patella 5% of the time. In the ankle, OCD occurs in the posteromedial aspect of the talus 56% of the time and in the anterolateral aspect of the talus 44% of the time.
OCD has a male predominance, with a male-to-female ratio of 2-3 to 1.
The average age at presentation of juvenile OCD in the knee is 11.3-13.4 years. The average age at presentation of adult OCD in the knee is 17-36 years, but this form can occur in adults of any age. The average age at presentation of OCD in the ankle is 15-35 years. The average age at presentation of OCD in the elbow is 12-21 years.
The true etiology of osteochondritis dissecans has been the source of enthusiastic debate for decades. The etiology has been described as traumatic, ischemic, idiopathic, and hereditary. The debate continues, but most authors now believe that OCD is a result of multifactorial elements.
Trauma has been described as a potential etiology of OCD. In the knee, direct trauma could create a transchondral fracture; however, the predilection of OCD for the posterolateral portion of the medial femoral condyle suggests indirect trauma as a more likely cause. Repetitive impingement of the tibial spine on the lateral aspect of the medial femoral condyle during internal rotation of the tibia has also been suggested as a contributing factor.
In the ankle, traumatic insult is more widely accepted as the etiology of OCD, although not without controversy. Tibiotalar subluxation results in impingement of the talus on the tibia or fibula. Cadaveric studies have revealed that posteromedial talar lesions may result from ankle inversion while in plantar flexion so that the talus impacts and torques the posterior aspect of the tibial plafond. Anterolateral talar lesions may result from impaction of the talus on the fibula in inversion with the ankle in dorsiflexion. Occasionally, however, medial talar lesions are not associated with trauma. Many authors believe that while lateral lesions are the result of trauma, medial lesions may be more multifactorial.
Although the exact cause of elbow OCD is unclear, most authors agree that repetitive microtrauma plays an important role. Occasionally, a single traumatic insult to the elbow may be identified as a potential etiology. Overhead motions, such as pitching in baseball, produce an abnormal valgus stress on the elbow. The tensile stress placed on the medial aspect of the elbow during throwing results in compressive forces between the radial head and the capitellum, potentially leading to osteochondrotic changes. One group reviewed 18 cases of elbow OCD and noted that each lesion was related to repetitive throwing or repeated engagement in racquet sports.
Ischemia has been investigated as a potential etiology for OCD. Enneking reported that the vascular supply to the subchondral bone was akin to that of the bowel mesentery, with poor anastomoses to surrounding arterioles. This propensity towards ischemia would naturally lead subchondral bone to form sequestra, making it particularly vulnerable to traumatic insult, resultant fracture, and potential separation. However, Enneking's report on the vasculature contradicts the findings of Rogers and Gladstone, who studied the vascularity of the distal part of the femur and found numerous anastomoses to intramedullary cancellous bone. Further refuting the ischemic hypothesis, Chiroff and Cooke found no signs of avascular necrosis in sections of excised osteochondral loose bodies.
Several authors have investigated a potential genetic link for OCD. Petrie reviewed the evidence and found no definite genetic etiology for OCD. However, at least 8 other authors have reported a hereditary influence for OCD. Ultimately, the link for most patients, if present, is probably minor.
Once a lesion is present, it typically progresses through 4 stages unless appropriately treated.
Stage I consists of a small area of compression of subchondral bone.
Stage II consists of a partially detached osteochondral fragment. A radiograph of the bone may reveal a well-circumscribed area of sclerotic subchondral bone separated from the remainder of the epiphysis by a radiolucent line.
Stage III lesions are the most common and consist of a completely detached fragment that remains within the underlying crater bed.
Stage IV lesions consist of a completely detached fragment that is completely displaced from the crater bed. This is also termed a loose body.
The symptoms of OCD vary with the stage of the lesion. In the knee, lesions early in their course are associated with vague and poorly defined symptoms, including variable amounts of pain and swelling. As the lesion progresses, symptoms such as catching, locking, and giving-way are often noted. These symptoms are often intermittent and associated with exertion.
Patients should be questioned as to how often they experience symptoms. Symptoms that are constant and severe are typically associated with loose bodies within the knee. Symptoms that are increasing in frequency may indicate progression of the lesion. In addition, patients with loose bodies within the joint may note locking and be able to palpate a loose body in the affected joint.
Differentiating OCD from osteonecrosis is difficult, but the most significant clue is the age of the patient. Younger patients tend to develop OCD, and older patients tend to develop osteonecrosis.
Physical examination of any patient who reports knee problems should begin with examination of the patient's gait. In a patient with OCD of the knee, the affected leg may be externally rotated during gait in an attempt to avoid impingement of the tibial spine on the lateral aspect of the condyle. Patients with OCD in the knee may have quadriceps weakness, not gluteus maximus weakness; however, this does not lead to a lack of patellar tracking.
Next, check for atrophy or weakness of the quadriceps muscle. An effusion may be noted. During range-of-motion testing, the patient may lack full knee extension on the affected side. Upon palpation, the lesion is often tender. The Wilson test may be useful. In this test, the examiner is to first flex the affected knee to 90° then internally rotate the tibia and slowly extend the knee. As the knee is extended to approximately 30° of flexion, the tibial spine abuts the OCD lesion on the medial femoral condyle, causing pain. External rotation eliminates the pain by taking the tibial spine away from the OCD lesion. Therefore, this test is only valid for OCD on the medial femoral condyle, which is the most common area in the knee for OCD.
Patients with OCD of the ankle report ankle swelling and symptoms of catching with walking or with active ankle motion. Approximately 90% of patients reveal a clear history of previous trauma to the affected ankle. Patients may or may not report pain, depending on the stage of the lesion.
Physical examination of a patient with ankle OCD may reveal joint effusion, crepitus, and diffuse or localized tenderness. As the lesion progresses, the symptoms become more severe and localized. Pain with compression of the tibiotalar joint and crepitus with dorsiflexion or plantar flexion are common. Lateral lesions may cause more pain and tenderness than medial lesions.
Patients with OCD of the elbow often report an insidious onset of generalized joint pain, swelling, and intermittent limitation of their range of motion. Patients' symptoms are usually intermittent and related to exertion. Patients almost always reveal a history of overuse injury, and some patients recall an additional single traumatic insult to the elbow. Most patients have a history of throwing activities or play a racquet sport. Junior-level (eg, Little League) and high-school athletes are particularly vulnerable to OCD of the elbow. Chronic valgus compression from their sports, combined with their immature articular surfaces, predisposes them to capitellar lesions. Patients with loose body lesions may report catching, locking, and giving-way.
Upon physical examination of a patient with elbow OCD, joint effusion, crepitus, and generalized tenderness may be noted.
The age of the patient is critical to the determination of whether a patient with knee OCD requires surgical intervention and, if so, the timing of that operation. Operative intervention is warranted in a child with knee OCD if symptoms have persisted for 6-12 months, if radiographic indices predict inadequate healing with conservative measures, if skeletal maturity will occur within 6 months, or if loose bodies are present. Earlier operative intervention is considered appropriate in an adult with knee OCD. In an adult with knee OCD, the decision to operate should rely more heavily on history and physical examination findings. If the physician feels that nonoperative management is unlikely to be successful, surgical intervention should be pursued.
Surgery is indicated in all patients with ankle OCD who have lateral talar lesion fragments that are completely detached but remain within the underlying crater bed (stage III). Symptomatic patients with medial stage III talar lesions require surgery. Loose body lesions (stage IV lesions) on both the medial and lateral side require surgical intervention.
The natural history of elbow OCD is not well understood, and therefore, the indications for surgery are controversial. Progressive joint contracture, unresolved symptoms after conservative treatment, and fixed contracture of more than 10° with elbow pain are common indications for surgical intervention. Indications for surgery include locking or catching in the elbow associated with pain and swelling. Pain with locking is often noted.
Finally, all patients with symptomatic lesions in whom conservative management fails should be offered surgery. Of course, radiographic findings must be correlated with other clinical features. Old, asymptomatic OCD may be an incidental finding in a patient with another cause for the symptoms. In addition, asymptomatic patients with lesions in weight-bearing joints should be considered for surgery because these lesions may lead to early degenerative joint disease.
Relative contraindications for osteochondral autografts include age older than 45 years, obvious chondromalacia of the articular cartilage surrounding the defect, and abnormal mechanical alignment or instability of the affected joint.
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