Osteochondritis dissecans (OCD) is a joint condition primarily affecting adolescents and young adults. This disorder involves damage to the area where bone meets cartilage, often causing persistent joint discomfort. While the precise origin remains under investigation, current understanding points to a combination of physiological failure and external mechanical stress. Exploring these underlying mechanisms clarifies how this complex disorder develops in active young people.
Understanding Osteochondritis Dissecans
Osteochondritis dissecans is defined by a pathological change where a segment of subchondral bone (the bone directly beneath the joint cartilage) partially or fully separates from the surrounding tissue. This separation creates a lesion, which often includes the overlying articular cartilage that provides the smooth surface for joint movement. OCD most frequently occurs in the knee, particularly on the end of the femur, but the elbow and ankle are also common sites. It typically manifests in individuals between the ages of 10 and 20, especially those approaching the end of their growth period.
The physical result is a loose or partially attached fragment of bone and cartilage within the joint space. If the fragment remains unstable, it can interfere with normal joint function. This damage is distinct from common arthritis because the initial problem is a failure of the underlying bone, which then secondarily affects the integrity of the protective cartilage layer.
Blood Flow Interruption and Necrosis
The fundamental physiological problem in OCD is a localized loss of blood supply to a small section of the subchondral bone. This interruption leads to avascular necrosis, meaning the bone tissue dies from a lack of oxygen and nutrients. The tiny blood vessels supplying the bone become compromised, initiating cellular death in the affected area.
When the bone segment dies, it weakens significantly and can no longer provide adequate support to the overlying articular cartilage. This necrotic bone tissue begins to resorb, which destabilizes the joint surface structure. Under normal forces, the weakened bone collapses, causing the overlying cartilage to crack and the entire osteochondral fragment to loosen from the main bone. This mechanical failure results in the characteristic lesion of OCD.
Repetitive Stress and Predisposing Factors
While avascular necrosis causes bone death, repetitive mechanical stress is considered the primary trigger for the blood supply disruption. Activities involving repeated impact, such as jumping, running, or throwing motions, subject the joints to microtrauma. These small, repeated injuries can compress or damage the delicate vessels supplying the subchondral bone over time, leading to the interruption of blood flow.
The mechanical overload hypothesis is supported by the high incidence of OCD in young athletes participating in high-impact or overhead sports. For example, repeated overhead throwing motions are associated with OCD in the elbow, while high-impact landings affect the knee. Internal factors also contribute, including a genetic predisposition due to inherited structural or vascular vulnerabilities. Furthermore, rapid growth spurts during adolescence may temporarily outpace the blood supply to the growing bone tissue, making the area more susceptible to microtrauma.
Identifying the Condition (Symptoms and Diagnosis)
The underlying bone necrosis and cartilage instability manifest through several distinct symptoms that prompt medical evaluation. The most common complaint is persistent joint pain, which typically worsens during or after physical activity. The affected joint may also exhibit swelling and tenderness, particularly following intense exercise.
As the osteochondral fragment loosens, patients may experience mechanical symptoms. These include joint catching, clicking, or locking, which occur when the separated fragment interferes with smooth joint movement. Patients may also report a feeling that the joint is unstable or “giving way,” alongside a reduction in the joint’s range of motion.
Diagnosis begins with a clinical examination followed by specific imaging techniques. Standard X-rays are used initially to visualize the bone and detect the characteristic oval-shaped abnormality. Magnetic Resonance Imaging (MRI) is often used next, providing a detailed assessment of soft tissues, including the cartilage. The MRI helps determine the size of the lesion and its stability—whether the fragment is still attached or fully separated—which guides further management.