What Is an Osteochondral Lesion and How Is It Treated?

An osteochondral lesion (OCL) describes damage that affects two distinct tissues within a joint: the articular cartilage and the underlying subchondral bone. This condition is a common orthopedic problem that can occur in any joint, but is most frequently found in those that bear significant weight and high stress. The lesion can range from minor cartilage softening to a complete separation of a bone and cartilage fragment into the joint space. OCL often leads to persistent pain and mechanical dysfunction, especially in active individuals.

Anatomy of Osteochondral Tissue

The term “osteochondral” refers to the two components of the injury: bone (“osteo”) and cartilage (“chondral”). Articular cartilage is a smooth, white connective tissue covering the ends of bones in a joint, acting as a shock absorber and providing a low-friction surface for movement. Beneath this layer lies the subchondral bone, which provides structural support and blood supply to the cartilage. Damage to this specific tissue interface is problematic because cartilage has a very limited capacity to heal itself, primarily due to its lack of blood vessels.

The location of these lesions often correlates with the highest stress points in the body’s major weight-bearing joints. In the ankle, the most common site is the talar dome, which is the upper part of the talus bone. For the knee, lesions frequently develop on the lateral aspect of the medial femoral condyle, which is a rounded prominence at the end of the thigh bone. Other joints, such as the elbow’s capitellum, can also be affected, especially in athletes involved in repetitive overhead activities.

Mechanisms of Lesion Development

Osteochondral lesions primarily form through two distinct mechanisms: acute trauma and chronic, non-traumatic processes. Acute trauma, such as a severe sprain, dislocation, or a direct impact, can cause a sudden fracture that shears off a piece of cartilage and the attached subchondral bone. This type of injury often occurs in sports and results from a single, high-energy event. The resulting fragment may be displaced into the joint space, where it can cause mechanical issues.

The second major cause involves chronic, repetitive stress or a disturbance in the bone’s blood supply, leading to a condition historically known as osteochondritis dissecans (OCD). In OCD, a localized area of the subchondral bone loses its blood flow and dies, leading to necrosis. This weakened area can fracture and separate from the surrounding healthy bone, taking the overlying cartilage with it. Repetitive microtrauma is thought to be the primary trigger for many non-traumatic lesions, leading to cumulative damage that eventually causes the fragment to detach.

Identifying Symptoms and Diagnosis

A patient with an osteochondral lesion typically presents with persistent, deep joint pain that often worsens with activity and weight-bearing. Swelling is a common symptom, especially after periods of increased activity. Many individuals also report mechanical symptoms, which are sensations related to the physical movement of the damaged tissue within the joint. These include feelings of clicking, catching, or joint locking, which can suggest that a fragment of bone or cartilage has become loose, sometimes referred to as a “joint mouse”.

Diagnosis requires a combination of clinical examination and advanced imaging to confirm the extent of the damage. A doctor will assess the joint for tenderness, stability, and range of motion. Standard X-rays are the initial imaging modality, useful for visualizing underlying bone abnormalities like a detached bone fragment or a cyst, but they cannot adequately visualize the cartilage itself. Magnetic Resonance Imaging (MRI) is the gold standard for full evaluation, providing detailed images of both the articular cartilage and the bone marrow. MRI is used to determine the lesion’s size, stability, and the presence of associated subchondral bone edema, which guides the treatment approach.

Treatment Approaches

The treatment for an osteochondral lesion is highly individualized, depending on the lesion’s size, its stability, the patient’s age, and their activity level. The initial approach for smaller, stable lesions, particularly in younger patients, is non-operative management. This conservative protocol typically involves a period of rest, protected weight-bearing using crutches or a brace, and physical therapy to maintain strength and range of motion. Non-steroidal anti-inflammatory drugs (NSAIDs) may be used to manage pain and swelling. This non-operative phase is generally pursued for a minimum of three to six months to allow for potential natural healing.

If conservative treatment fails, or if the lesion is large or unstable, surgical intervention becomes necessary. Arthroscopic debridement is a minimally invasive option where unstable cartilage is removed and the underlying bone is prepared.

Microfracture

Following debridement, a microfracture procedure is often performed, which involves creating small holes in the subchondral bone. This process releases bone marrow elements, including mesenchymal stem cells, into the defect, stimulating the formation of a repair tissue called fibrocartilage. This technique is best suited for smaller lesions, typically less than four square centimeters in size.

Restorative Grafting Procedures

For larger defects, more advanced restorative procedures are used to replace the damaged tissue with a more durable, hyaline-like cartilage. The Osteochondral Autograft Transfer System (OATS), also known as mosaicplasty, is a single-stage procedure that involves harvesting cylindrical plugs of healthy bone and cartilage from a less weight-bearing area of the joint and transferring them to the defect. Another option is Autologous Chondrocyte Implantation (ACI), a two-stage process where a sample of the patient’s own cartilage cells is harvested, grown in a laboratory, and then implanted into the defect during a second surgery. These grafting techniques aim to restore the joint surface with tissue that more closely resembles the original hyaline cartilage.