Osteochondritis dissecans (OCD or OD) is a joint disorder primarily of the subchondral bone in which cracks form in the articular cartilage and the underlying subchondral bone. OCD usually causes pain during and after sports. In later stages of the disorder there will be swelling of the affected joint that catches and locks during movement. Physical examination in the early stages does only show pain as symptom, in later stages there could be an effusion, tenderness, and a crackling sound with joint movement.
OCD is caused by blood deprivation of the secondary physes around the bone core of the femoral condyle. This happens to the epiphyseal vessels under the influence of repetitive overloading of the joint during running and jumping sports. During growth such chondronecrotic areas grow into the subchondral bone. There it will show as bone defect area under articular cartilage. The bone will then possibly heal to the surrounding condylar bone in 50% of the cases. Or it will develop into a pseudarthrosis between condylar bone core and osteochondritis flake leaving the articular cartilage it supports prone to damage. The damage is executed by ongoing sport overload. The result is fragmentation (dissection) of both cartilage and bone, and the free movement of these bone and cartilage fragments within the joint space, causing pain, blockage and further damage. OCD has a typical anamnesis with pain during and after sports without any history of trauma. Some symptoms of late stages of osteochondritis dissecans are found with other diseases like rheumatoid disease of children and meniscal ruptures. The disease can be confirmed by X-rays, computed tomography (CT) or magnetic resonance imaging (MRI) scans.
Non-surgical treatment is successful in 50% of the cases. If in late stages the lesion is unstable and the cartilage is damaged, surgical intervention is an option as the ability for articular cartilage to heal is limited. When possible, non-operative forms of management such as protected reduced or non-weight bearing and immobilization are used. Surgical treatment includes arthroscopic drilling of intact lesions, securing of cartilage flap lesions with pins or screws, drilling and replacement of cartilage plugs, stem cell transplantation, and in very difficult situation in adults joint replacement. After surgery rehabilitation is usually a two-stage process of unloading and physical therapy. Most rehabilitation programs combine efforts to protect the joint with muscle strengthening and range of motion. During an immobilization period, isotonic exercises, such as straight leg raises, are commonly used to restore muscle loss without disturbing the cartilage of the affected joint. Once the immobilization period has ended, physical therapy involves continuous passive motion (CPM) and/or low impact activities, such as walking or swimming.
OCD occurs in 15 to 30 people per 100,000 in the general population each year. Although rare, it is an important cause of joint pain in physically active children and adolescents. See introduction and discussion sections on incidence Because their bones are still growing, adolescents are more likely than adults to recover from OCD; recovery in adolescents can be attributed to the bone's ability to repair damaged or dead bone tissue and cartilage in a process called bone remodeling. While OCD may affect any joint, the knee tends to be the most commonly affected, and constitutes 75% of all cases. Franz König coined the term osteochondritis dissecans in 1887, describing it as an inflammation of the bone–cartilage interface. Many other conditions were once confused with OCD when attempting to describe how the disease affected the joint, including osteochondral fracture, osteonecrosis, accessory ossification center, osteochondrosis, and hereditary epiphyseal dysplasia. Some authors have used the terms osteochondrosis dissecans and osteochondral fragments as synonyms for OCD.
Signs and symptoms In osteochondritis dissecans, fragments of cartilage or bone become loose within a joint, leading to pain and inflammation. These fragments are sometimes referred to as joint mice. OCD is a type of osteochondrosis in which a lesion has formed within the cartilage layer itself, giving rise to secondary inflammation. OCD most commonly affects the knee, although it can affect other joints such as the ankle or the elbow.
People with OCD report activity-related pain that develops gradually. Individual complaints usually consist of mechanical symptoms including pain, swelling, catching, locking, popping noises, and buckling / giving way; the primary presenting symptom may be a restriction in the range of movement. Symptoms typically present within the initial weeks of stage I. The onset of stage II occurs within months and offers little time for diagnosis. The disease progresses rapidly beyond stage II, as OCD lesions quickly move from stable cysts or fissures to unstable fragments. Non-specific symptoms, caused by similar injuries such as sprains and strains, can delay a definitive diagnosis.
Physical examination typically reveals fluid in the joint, tenderness, and crepitus. The tenderness may initially spread, but often reverts to a well-defined focal point as the lesion progresses. Just as OCD shares symptoms with common maladies, acute osteochondral fracture has a similar presentation with tenderness in the affected joint, but is usually associated with a fatty hemarthrosis. Although there is no significant pathologic gait or characteristic alignment abnormality associated with OCD, the patient may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle of the femur.
Causes
Despite much research, the causes remain unclear but include repetitive physical trauma, ischemia (restriction of blood flow), hereditary and endocrine factors, avascular necrosis (loss of blood flow), rapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and problems of bone formation. Although the name "osteochondritis" implies inflammation, the lack of inflammatory cells in histological examination suggests a non-inflammatory cause. It is thought that repetitive microtrauma, which leads to microfractures and sometimes an interruption of blood supply to the subchondral bone, may cause subsequent localized loss of blood supply or alteration of growth.
Trauma, rather than avascular necrosis, is thought to cause osteochondritis dissecans in juveniles. In adults, trauma is thought to be the main or perhaps the sole cause, and may be endogenous, exogenous or both. The incidence of repetitive strain injury in young athletes is on the rise and accounts for a significant number of visits to primary care; this reinforces the theory that OCD may be associated with increased participation in sports and subsequent trauma. High-impact sports such as gymnastics, soccer, basketball, lacrosse, football, tennis, squash, baseball and weight lifting may put participants at a higher risk of OCD in stressed joints (knees, ankles and elbows).
Recent case reports suggest that some people may be genetically predisposed to OCD. Families with OCD may have mutations in the aggrecan gene. Studies in horses have implicated specific genetic defects.
Pathophysiology
Osteochondritis dissecans differs from "wear and tear" degenerative arthritis, which is primarily an articular surface problem. Instead, OCD is a problem of the bone underlying the cartilage, which may secondarily affect the articular cartilage. Left untreated, OCD can lead to the development of degenerative arthritis secondary to joint incongruity and abnormal wear patterns.
OCD occurs when a loose piece of bone or cartilage partially (or fully) separates from the end of the bone, often because of a loss of blood supply (osteonecrosis) and decalcification of the trabecular bone matrix. The loose piece may stay in place or slide around, making the joint stiff and unstable. OCD in humans most commonly affects the knees, ankles, and elbow but can affect any joint.
In skeletally immature individuals, the blood supply to the epiphyseal bone is good, supporting both osteogenesis and chondrogenesis. With disruption of the epiphyseal plate vessels, varying degrees and depth of necrosis occur, resulting in a cessation of growth to both osteocytes and chondrocytes. In turn, this pattern leads to disordered ossification of cartilage, resulting in subchondral avascular necrosis and consequently OCD.
Four minor stages of OCD have been identified after trauma. These include revascularization and formation of granulation (scar) tissue, absorption of necrotic fragments, intertrabecular osteoid deposition, and remodeling of new bone. With delay in the revascularization stage, an OCD lesion develops. A lesion can lead to articular-surface irregularities, which in turn may cause progressive arthritic deterioration.
Diagnosis To diagnose osteochondritis dissecans, an X-ray, CT scan or MRI scan can be performed to show necrosis of subchondral bone, formation of loose fragments, or both. Occasionally a nuclear medicine bone scan is used to assess the degree of loosening within the joint.
Physical examination Physical examination often begins with examination of the patient's gait. In OCD of the knee, people may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle of the femur.
Next, the examining physician may check for weakness of the quadriceps. This examination may reveal fluid in the joint, tenderness, and crepitus. The Wilson test is also useful in locating OCD lesions of the femoral condyle. The test is performed by slowly extending the knee from 90 degrees, maintaining internal rotation. Pain at 30 degrees of flexion and relief with tibial external rotation is indicative of OCD.
Physical examination of a patient with ankle OCD often returns symptoms of joint effusion, crepitus, and diffuse or localized tenderness. Examination often reveals symptoms of generalized joint pain, swelling, and times with limited range of motion. Some with loose body lesions may report catching, locking, or both. The possibility of microtrauma emphasizes a need for evaluation of biomechanical forces at the knee in a physical examination. As a result, the alignment and rotation of all major joints in the affected extremity is common, as are extrinsic and intrinsic abnormalities concerning the affected joint, including laxity.
Diagnostic imaging X-rays show lucency of the ossification on the anterior aspect of the knee in juvenile patients. In older people, the lesion typically appears as an area of osteosclerotic bone with a radiolucent line between the osteochondral defect and the epiphysis. The visibility of the lesion depends on its location and on the amount of knee flexion used. Harding described the lateral X-ray as a method to identify the site of an OCD lesion.
Magnetic resonance imaging (MRI) is useful for staging OCD lesions, evaluating the integrity of the joint surface, and distinguishing normal variants of bone formation from OCD by showing bone and cartilage edema in the area of the irregularity. MRI provides information regarding features of the articular cartilage and bone under the cartilage, including edema, fractures, fluid interfaces, articular surface integrity, and fragment displacement. A low T1 and high T2 signal at the fragment interface is seen in active lesions. This indicates an unstable lesion or recent microfractures. While MRI and arthroscopy have a close correlation, X-ray films tend to be less inductive of similar MRI results.