Articular cartilage is the specialized, smooth, white tissue that covers the ends of bones in a joint. This tissue, typically only two to four millimeters thick, plays a fundamental role in joint mechanics by providing a low-friction surface for movement and absorbing compressive forces. It allows bones to glide effortlessly over one another, ensuring smooth articulation, but it lacks blood vessels, nerves, and a direct blood supply, which limits its ability to heal. Full thickness cartilage loss represents the most severe degree of damage to this protective layer, signifying a complete erosion of the tissue.
Understanding Cartilage Loss Severity
Cartilage damage is categorized on a spectrum, which helps clinicians understand the extent of the injury and determine the appropriate treatment path. Classification systems, such as the International Cartilage Repair Society (ICRS) or the Outerbridge system, grade the severity of these lesions. Full thickness loss is universally defined as the highest grade, often designated as Grade 4.
Full thickness loss means the entire layer of articular cartilage has been worn away, exposing the underlying bone tissue, known as the subchondral bone. When this protective, smooth barrier is lost, it leads to direct contact between the ends of the opposing bones. This condition is commonly referred to as “bone-on-bone” and results in significant friction, pain, and restricted joint function.
Primary Causes of Full Thickness Loss
The most frequent origin of full thickness cartilage loss is the progressive, degenerative disease known as osteoarthritis (OA). This condition involves the long-term, chronic wear and tear on the joint surfaces, which gradually thins and degrades the cartilage over many years. Osteoarthritis is particularly common in weight-bearing joints like the knee and hip, and its prevalence increases significantly with age.
Acute traumatic injuries are another significant cause, often leading to immediate and catastrophic damage. A severe fall, a sports injury, or a joint dislocation can generate enough force to fracture the underlying bone or tear a segment of cartilage completely away from the joint surface. Such trauma typically causes a focal defect, meaning the loss is localized to a specific spot rather than spread across the entire joint surface.
Mechanical misalignment of the joint contributes to accelerating degradation. Repetitive stress from certain occupations or sports can also lead to overuse injuries that wear down the tissue faster. Furthermore, inflammatory conditions such as rheumatoid arthritis can create a hostile environment within the joint, causing the body’s own immune response to damage the cartilage matrix.
Identifying the Condition Through Imaging
Diagnosis of full thickness cartilage loss relies heavily on medical imaging, as the cartilage itself cannot be directly felt or seen during a standard physical exam. Conventional X-rays are often the first step, providing an indirect assessment of the cartilage’s integrity. Since cartilage is not visible on an X-ray, its loss is inferred by measuring the distance between the two bones in the joint.
A significant reduction in this space, known as joint space narrowing, is the classic X-ray finding that indicates advanced cartilage deterioration and bone-on-bone contact. While X-rays are useful for assessing the end-stage condition, they are insensitive to minor or early cartilage damage. Magnetic Resonance Imaging (MRI) is considered the gold standard for visualizing soft tissues and precisely assessing the extent of damage.
The detailed soft-tissue contrast provided by an MRI allows physicians to accurately measure the depth of the lesion, confirming the defect penetrates the entire thickness of the cartilage. This imaging modality also evaluates the condition of the subchondral bone and surrounding structures. Visualizing the full depth of the lesion provides a comprehensive picture of the joint’s health, which is crucial for treatment planning.
Managing and Treating Full Thickness Loss
The management of full thickness cartilage loss begins with conservative strategies aimed at reducing pain and improving function without surgery. These non-surgical options include physical therapy to strengthen the muscles surrounding the joint, which can help stabilize it and absorb some of the mechanical load. Weight management is also emphasized, as reduced body weight directly lowers the stress placed on the damaged joint surface.
Medications often include nonsteroidal anti-inflammatory drugs (NSAIDs) to manage pain and reduce inflammation in the joint. Injections may also be used to provide temporary relief from severe symptoms. Corticosteroid injections deliver a potent anti-inflammatory agent directly into the joint, while hyaluronic acid injections, known as viscosupplementation, aim to improve the joint’s lubrication.
When conservative methods no longer provide adequate relief, surgical interventions become the necessary next step, particularly because full thickness defects have a limited capacity to heal naturally.
Surgical Interventions
##### #### Cartilage Repair Techniques
For younger patients with a small, localized defect, cartilage repair techniques may be considered. Microfracture is a procedure where small holes are made in the exposed bone to stimulate a healing response. This encourages the formation of new scar tissue to fill the defect.
##### #### Autologous Chondrocyte Implantation (ACI)
Another option for specific defects is ACI, which involves harvesting a patient’s own healthy cartilage cells. These cells are cultured in a lab and then reimplanted into the defect.
##### #### Osteotomy
In cases where the joint’s alignment is contributing to the wear, an osteotomy may be performed. This procedure surgically realigns the bone to shift the weight-bearing load away from the damaged area.
##### #### Joint Replacement
For widespread, irreversible full thickness loss, particularly in older patients, the definitive treatment is often joint resurfacing or replacement. Examples include total knee or hip arthroplasty.