A chondral defect represents a localized injury to the articular cartilage, the smooth, specialized tissue covering the ends of bones in a joint. This damage involves the cartilage layer only, without extending into the underlying bone, a distinction that greatly influences treatment. Articular cartilage is present in all synovial joints, but defects are most commonly identified and treated in the major load-bearing joints, such as the knee, ankle, and hip. Recognizing this damage is the first step in addressing the pain and limited mobility it can cause.
Understanding Articular Cartilage
Articular cartilage is specifically known as hyaline cartilage, which provides a low-friction, shock-absorbing surface for joint movement. This tissue is composed primarily of an extracellular matrix, consisting of water, collagen (predominantly type II), and proteoglycans. The primary cells within this matrix are chondrocytes, which are responsible for maintaining the matrix.
A defining feature of articular cartilage is its lack of a direct blood supply. Chondrocytes receive nourishment through the diffusion of nutrients from the surrounding synovial fluid, a process that limits the tissue’s ability to repair itself effectively after injury. Furthermore, articular cartilage is aneural, which explains why the cartilage itself does not register pain.
This biological structure accounts for the limited healing potential of chondral defects. When the damage extends through the cartilage layer and into the subchondral bone, it is classified as an osteochondral defect. The underlying bone possesses a blood supply, which allows for a different healing response compared to an isolated chondral defect.
Causes and Symptoms of Cartilage Damage
Chondral defects often arise from two main mechanisms: a single, acute traumatic event or the cumulative effect of repetitive stress over time. A direct blow to the joint can shear off or compress a portion of the cartilage. Sports involving pivoting, jumping, or high-impact contact, like football or soccer, carry a higher risk for this type of injury.
Repetitive microtrauma, common in high-level athletes or individuals with poor joint mechanics, leads to cartilage damage. Underlying conditions, such as osteochondritis dissecans, where a piece of bone and its overlying cartilage become damaged, can also lead to focal cartilage loss. Obesity increases the mechanical load on weight-bearing joints, accelerating this degenerative process.
The resulting symptoms are related to the disruption of the joint’s smooth gliding surface. The most common complaint is joint pain, which often worsens with activity and weight-bearing. Swelling and stiffness may also occur as the joint reacts to the damaged tissue fragments.
Patients frequently report mechanical symptoms, such as the joint catching, locking, or giving way during movement. Crepitus, a grinding sensation, can sometimes be felt or heard as the irregular joint surfaces move against each other.
Diagnosis and Severity Grading
Diagnosing a chondral defect begins with a physical examination and history of the patient’s symptoms. Initial imaging often involves standard X-rays, but these are insufficient for visualizing the cartilage itself. Articular cartilage is radiolucent, though X-rays can show bone alignment or signs of advanced joint space narrowing.
Magnetic Resonance Imaging (MRI) is the preferred non-invasive method for confirming the presence and extent of a chondral defect. The high-resolution images provided by MRI allow visualization of the cartilage layer and assessment of the lesion’s depth. Definitive assessment is often performed through arthroscopy, a minimally invasive surgical procedure that allows direct visual inspection of the joint.
During arthroscopy, the severity of the defect is commonly graded using a standardized classification system, such as the Outerbridge Classification. This scale grades the damage from Grade 0 (normal cartilage) to Grade IV (most severe damage).
Outerbridge Classification Grades
- Grade 0: Normal cartilage.
- Grade I: Softening and swelling of the cartilage.
- Grade II: Partial-thickness defects with fissures that do not reach the bone.
- Grade III: Fissures extending to the level of subchondral bone.
- Grade IV: Full-thickness cartilage erosion that exposes the underlying bone.
Treatment Options for Chondral Defects
The management of a chondral defect depends on the defect’s size, location, and severity grade. Initial treatment often focuses on conservative, non-surgical approaches. This includes activity modification, physical therapy to strengthen supporting muscles, and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) to manage pain and inflammation.
Injections may also be used, such as corticosteroid injections to reduce inflammation or viscosupplementation with hyaluronic acid to improve joint lubrication. These non-operative strategies aim to control symptoms and maintain joint function, but they do not repair the damaged cartilage tissue. If conservative treatment fails, or if the defect is large and symptomatic, surgical intervention is necessary.
Surgical treatments are broadly categorized as reparative or restorative. Microfracture involves creating small holes in the exposed subchondral bone. This stimulates a blood clot that introduces bone marrow cells to the defect, forming fibrocartilage, which is a durable but biomechanically inferior repair tissue. Microfracture is generally reserved for smaller defects, typically less than two to four square centimeters.
Restorative options aim to replace the damaged tissue with a more durable substance, ideally hyaline cartilage. OATS (Osteochondral Autograft Transfer System), or mosaicplasty, involves transplanting small plugs of healthy bone and cartilage from a non-weight-bearing area of the joint into the defect. This technique is limited by the size of the defect it can cover and can cause donor site morbidity. For larger lesions, a two-stage procedure called Autologous Chondrocyte Implantation (ACI) may be used. ACI involves harvesting the patient’s own cartilage cells, expanding them in a lab, and then re-implanting them into the defect under a cover or scaffold.