Articular cartilage is the specialized, smooth tissue that covers the ends of bones within a joint, such as the knee, enabling frictionless movement and absorbing mechanical shock. A full thickness cartilage defect represents a severe form of joint damage where the cartilage layer has been completely worn away or torn. This injury penetrates the entire depth of the tissue, reaching the underlying bone structure.
Understanding Cartilage and Full Thickness Damage
Articular cartilage is primarily composed of water and an extracellular matrix containing collagen and proteoglycans, maintained by specialized cells called chondrocytes. This unique composition makes the tissue remarkably resilient to compressive forces while providing a low-friction surface. Crucially, native hyaline cartilage is avascular (lacking a direct blood supply) and aneural (lacking nerves).
Because cartilage lacks a blood supply, it has a very limited capacity for self-repair after injury. A partial thickness defect involves damage that does not extend through the entire layer and typically does not heal spontaneously. Conversely, a full thickness defect is characterized by the complete loss of cartilage down to the subchondral bone, often classified as International Cartilage Repair Society (ICRS) Grade 4.
When the damage exposes the subchondral bone, it breaches a layer called the tidemark. This penetration allows blood and bone marrow elements, including mesenchymal progenitor cells, to enter the defect site. While this triggers a healing response, the resulting tissue is generally fibrocartilage, which is biomechanically inferior and less durable than the original hyaline cartilage.
Identifying the Causes and Symptoms
Full thickness defects can arise from mechanisms often categorized as traumatic or degenerative. Acute trauma, such as a direct blow to the joint, a hard twisting injury, or a joint dislocation, can cause a sudden, forceful tear or shear-off of the cartilage layer. This is frequently seen in athletes involved in high-impact or pivoting sports.
Repetitive stress and chronic overload on the joint can also lead to the gradual deterioration of the cartilage. Conditions like osteochondritis dissecans (OCD), where a segment of bone and its overlying cartilage separates from the main joint surface, are another common cause of focal full thickness lesions. Long-term wear and tear, eventually leading to osteoarthritis, is a progressive cause of extensive cartilage loss.
Symptoms stem from the underlying bone exposure and resulting joint inflammation. Localized pain is the most common complaint, often worsening with weight-bearing activities or prolonged movement. Patients frequently report intermittent swelling as a result of inflammatory fluid buildup within the joint.
Mechanical symptoms are also characteristic of these defects, resulting from the irregular joint surface or loose fragments of tissue. These include catching, popping, or locking. A feeling of instability or the joint giving way under pressure can also occur due to the compromised joint surface.
Surgical Intervention Methods
Because native cartilage cannot regenerate into a durable, functional tissue, surgical interventions are often required to manage full thickness defects and prevent the progression to arthritis. Treatment strategies generally fall into two categories: marrow stimulation and cartilage restoration/transplantation. The selection of the technique is typically guided by the patient’s age, activity level, and the specific size of the defect.
Marrow stimulation, most commonly performed as a microfracture procedure, involves creating tiny holes in the exposed subchondral bone beneath the defect, allowing blood and bone marrow contents to stream into the cartilage bed. The resulting blood clot forms a scaffold for the growth of new repair tissue, but microfracture is typically reserved for smaller lesions (usually less than two square centimeters) and is a relatively low-cost, single-stage procedure.
For defects of small to intermediate size, the Osteochondral Autograft Transfer System (OATS), sometimes called mosaicplasty, is used. This single-stage procedure involves harvesting one or more cylindrical plugs of healthy bone and cartilage from a non-weight-bearing area of the same joint. These plugs are then immediately transferred and press-fit into the prepared defect, effectively replacing the damaged area with the patient’s own native hyaline cartilage.
Cartilage restoration techniques are frequently employed for larger lesions, particularly in younger patients. Autologous Chondrocyte Implantation (ACI) is a two-stage process that begins with an initial surgery to harvest healthy chondrocytes from a low-stress joint area. These cells are then sent to a lab where they are cultured and expanded over several weeks.
In the second surgical stage, the expanded cells are implanted into the defect, often secured with a periosteal flap or a synthetic cover. A more modern variation, Matrix-Induced Autologous Chondrocyte Implantation (MACI), simplifies the second step by seeding the cultured cells onto a bioresorbable collagen membrane or scaffold. Both ACI and MACI aim to grow hyaline-like repair tissue, which is considered more durable than the fibrocartilage produced by microfracture.
Recovery and Long-Term Outlook
Recovery following surgical repair of a full thickness defect is a protracted process. Due to the inherent lack of blood supply in the cartilage and the time required for new tissue to mature, rehabilitation can span many months. Physical therapy is a mandatory component of post-operative care, focusing on controlled motion to nourish the joint and strengthening the surrounding muscles.
Weight-bearing restrictions are common, often necessitating the use of crutches for at least six weeks, though the exact timeline depends on the procedure and the location of the repair. The long-term success of the surgery is influenced by factors such as the original size of the defect, the patient’s compliance with rehabilitation, and the specific technique employed. While these procedures aim to restore function and relieve pain, the repaired tissue may never fully replicate the biomechanical properties of the original hyaline cartilage. If the repair fails or the defect is left untreated, the full thickness damage creates a predisposition for the joint to develop early-onset osteoarthritis.