A chondral defect is a localized area of damage to the articular cartilage, the specialized tissue covering the ends of bones within a joint. This damage is typically focal, affecting a specific spot while the surrounding cartilage remains otherwise healthy. The primary role of this smooth, resilient covering is to facilitate low-friction movement and absorb mechanical shock across the joint surfaces. When compromised, this protective layer leads to pain and impaired joint function.
The Role and Structure of Articular Cartilage
Articular cartilage is a highly specialized connective tissue. Its unique structure is composed of specialized cells called chondrocytes, which are embedded within a dense extracellular matrix primarily made up of water (70-85% of its weight), collagen, and proteoglycans.
The collagen, predominantly type II, provides the tissue’s tensile strength, while proteoglycans attract and retain water, giving the cartilage its ability to resist compressive forces. This composition creates a lubricated, wear-resistant surface that allows bones to glide past one another with minimal friction.
A significant challenge in treating chondral defects stems from the cartilage’s biological limitations. Articular cartilage is aneural, avascular, and alymphatic, meaning it lacks a blood supply, nerves, and lymphatic drainage. This absence prevents necessary healing factors and cells from reaching an injury site, severely limiting the tissue’s intrinsic capacity for self-repair. Once damaged, the cartilage cannot regenerate its original hyaline structure.
Causes and Categorization of Chondral Defects
Chondral defects arise from two main mechanisms: acute traumatic injury or chronic degenerative changes. Acute trauma often involves a direct blow, a sudden twisting motion, or a dislocation, which can shear off or compress the cartilage. These acute injuries are common in young, active individuals and may occur alongside other joint damage, such as ligament tears.
Degenerative causes relate to the gradual breakdown of the cartilage matrix over time, a process seen in conditions like osteoarthritis or due to repetitive stress. Factors such as joint instability, limb misalignment, or obesity can accelerate this wear and tear, leading to progressive cartilage thinning and fragmentation.
The severity of a chondral defect is systematically assessed using classification systems, most commonly the Outerbridge Classification. This classification grades the damage from Grade I (softening and swelling of the cartilage surface) to Grade IV (which signifies the most advanced stage).
Outerbridge Classification Grades
Grade II lesions feature partial-thickness defects with surface fissures or fraying that do not extend down to the underlying bone. A Grade III defect involves deep fissures that penetrate more than half the cartilage thickness. Grade IV is a full-thickness defect where the subchondral bone is completely exposed.
Recognizing the Signs and Confirmation Methods
The presence of a chondral defect manifests through mechanical and discomfort-related symptoms in the affected joint. Patients often report pain that worsens with activity, particularly weight-bearing movements like walking or climbing stairs. Intermittent swelling, known as an effusion, is also a common complaint, frequently caused by loose fragments of cartilage floating within the joint space.
Mechanical symptoms are highly suggestive of a joint surface problem. These include clicking, catching, or a grinding sensation, which occur as the damaged, uneven cartilage surfaces articulate. The joint may intermittently lock or suddenly give way due to an unstable cartilage flap or a loose body impeding normal movement.
Initial diagnosis involves a physical examination to assess range of motion, stability, and tenderness. Imaging techniques are then used for confirmation and detailed mapping of the defect. Standard X-rays are useful for ruling out underlying bone fractures or advanced joint space narrowing, though they cannot visualize the cartilage itself.
Magnetic Resonance Imaging (MRI) is the primary non-invasive tool, providing detailed images of the soft tissues to assess the size, depth, and exact location of the lesion. Arthroscopy, a minimally invasive surgical procedure using a small camera, remains the gold standard for directly visualizing the defect, confirming its grade, and planning the appropriate intervention.
Current Treatment Pathways for Cartilage Repair
Treatment for a chondral defect begins with conservative measures focused on symptom relief and joint protection. These non-operative strategies include rest, physical therapy to strengthen surrounding muscles, and the use of non-steroidal anti-inflammatory drugs (NSAIDs). Injections of hyaluronic acid or corticosteroids may manage pain and temporary inflammation, but they do not result in true cartilage repair or regeneration.
When symptoms persist or the defect is large and symptomatic, surgical intervention becomes necessary. The choice of procedure depends heavily on the defect’s size, the patient’s age, and activity level.
Microfracture
Microfracture is a common initial surgical treatment, typically reserved for smaller lesions (less than two to four square centimeters). This arthroscopic technique involves creating tiny holes in the subchondral bone beneath the defect, allowing blood and bone marrow cells to form a clot. The resulting tissue is fibrocartilage, which is biomechanically inferior to the original hyaline cartilage but provides a functional, temporary surface.
Advanced Restoration Techniques
For larger or full-thickness defects, advanced cartilage restoration techniques are preferred, as microfracture outcomes often deteriorate over time. The Osteochondral Autograft Transfer System (OATS), also known as mosaicplasty, is a single-stage procedure. It involves transplanting small cylindrical plugs of healthy bone and cartilage harvested from a less weight-bearing area into the defect, immediately restoring the area with native hyaline cartilage.
Autologous Chondrocyte Implantation (ACI) is a two-stage procedure. The first stage involves arthroscopic harvesting of a small sample of healthy cartilage cells (chondrocytes), which are cultured and multiplied in a laboratory over several weeks. In the second stage, these cultured cells are implanted back into the defect under a membrane or scaffold, where they mature into a more durable, hyaline-like repair tissue.
The optimal treatment pathway is individualized, weighing the ease and cost of microfracture against the potential for a more durable, hyaline-based repair offered by OATS or ACI.