Cartilage is a dense, specialized connective tissue that lines the ends of bones within joints, providing a smooth surface for movement. Its primary function is to act as a shock absorber, distributing mechanical loads across the joint and reducing friction between bone surfaces. Composed of a matrix of collagen and proteoglycans, this resilient tissue has the strength and flexibility to withstand decades of use. Biologically, its capacity for self-healing after an injury is generally minimal or absent.
Why Cartilage Struggles to Repair Itself
The limited ability of cartilage to mend after damage is rooted in its unique biological structure. Unlike most tissues, articular cartilage does not possess a direct blood supply, a condition known as avascularity. This lack of blood vessels means that the necessary inflammatory cells, growth factors, and nutrients required for a robust healing response cannot easily reach the injury site.
The specialized cells responsible for maintaining the tissue, called chondrocytes, are suspended within the dense matrix and have a very low metabolic rate. Chondrocytes rely on the slow process of diffusion from the surrounding synovial fluid for nourishment and waste disposal. This slow nutrient exchange severely limits the cells’ ability to multiply quickly and synthesize the new matrix needed to fill a defect.
Cartilage is also aneural, meaning it lacks nerve endings, which explains why damage often does not cause immediate pain. Furthermore, it does not contain lymphatic vessels. The absence of lymphatic drainage impedes the clearance of debris and the initiation of a proper repair cascade.
Differentiating Injury: Minor Damage Versus Full-Thickness Tears
The potential for natural repair depends heavily on the depth and extent of the initial damage. Injuries that are partial-thickness or superficial are contained entirely within the avascular cartilage. Since this damage does not penetrate the underlying bone, it fails to access any source of healing cells or blood supply. Consequently, these minor defects typically do not heal and remain as permanent irregularities on the joint surface.
A full-thickness tear presents a paradoxical situation where a more severe injury can initiate a limited repair attempt. This occurs only when the damage extends through the cartilage layer and breaches the subchondral bone underneath. Penetrating the bone allows blood, bone marrow cells, and mesenchymal stem cells to spill into the defect area. This inflow of biological material forms a clot, which serves as a scaffold for new tissue growth.
The tissue that forms in response to this injury is not the original, highly resilient hyaline cartilage. Instead, the body produces fibrocartilage, a mechanically inferior, scar-like tissue. While fibrocartilage temporarily fills the defect, it is less durable and more prone to wear and tear than native hyaline tissue. Even when a healing response occurs, the resulting repair is structurally compromised.
Treatment Options When Natural Repair Fails
Given the tissue’s poor capacity for self-repair, medical intervention is often necessary to manage symptoms and prevent the progression of joint damage. Conservative management options are typically the first line of defense, aiming to reduce pain and inflammation rather than directly repairing the defect. Physical therapy is a primary approach, focusing on strengthening the muscles surrounding the joint to improve stability and reduce the load placed on the damaged cartilage.
Non-Surgical Injections
Injections are a common non-surgical intervention used to manage symptoms caused by cartilage defects.
- Corticosteroid injections provide temporary relief by reducing joint inflammation and associated pain.
- Viscosupplementation involves injecting hyaluronic acid, a substance naturally found in healthy joint fluid, to improve lubrication and shock absorption.
- Biological therapies, such as platelet-rich plasma (PRP) and stem cell injections, utilize the patient’s own concentrated healing factors to reduce inflammation and promote a beneficial joint environment.
Surgical Repair and Replacement
When non-surgical methods are insufficient, several surgical procedures exist to stimulate a repair response or replace the damaged tissue. Microfracture surgery is a technique where a surgeon creates small holes in the exposed subchondral bone to encourage the release of blood and marrow elements into the defect. This procedure aims to generate the previously mentioned fibrocartilage scar tissue to cover the exposed bone surface.
For larger defects, tissue transfer or cell implantation techniques may be employed to restore the joint surface. Procedures like Osteochondral Autograft Transfer System (OATS) involve harvesting small plugs of healthy cartilage and bone from a less critical area of the joint and transplanting them into the defect. Alternatively, Matrix-induced Autologous Chondrocyte Implantation (MACI) is a two-step procedure where a patient’s own cartilage cells are harvested, grown in a lab, and then implanted into the damaged area to regenerate a more hyaline-like tissue. These surgical options are typically reserved for active patients with specific, isolated cartilage lesions.