Articular cartilage is a highly specialized type of connective tissue primarily located within the synovial joints. This tissue forms a smooth, resilient layer that caps the ends of the bones where they meet, such as in the knee, hip, and shoulder. Its structure is finely tuned to handle mechanical stress, providing an interface for movement. This covering provides durable mechanical support while ensuring fluid, unrestricted motion between the articulating bone surfaces. Without this tissue, the rigid surfaces of bone would grind against each other, quickly causing damage and immobility.
Structure and Composition
Articular cartilage is a form of hyaline cartilage, and in large joints, its thickness typically ranges from 2 millimeters to 4 millimeters. The tissue is primarily composed of an extracellular matrix, which is produced and maintained by specialized cells called chondrocytes. Water is the most abundant component, accounting for up to 80% of the tissue’s wet weight, a proportion that slightly decreases from the surface to the deeper layers.
The remaining matrix consists of a dense network of collagen fibers and proteoglycans. Collagen, mostly Type II, provides the tensile strength and framework for the tissue, making up approximately 60% of the dry weight. Proteoglycans, particularly aggrecan, are highly hydrophilic, meaning they strongly attract and trap water within the matrix. This unique, water-filled structure gives the cartilage its incompressible quality, allowing it to withstand compressive forces.
Essential Functions in Joint Movement
The structural components of articular cartilage combine to perform two primary mechanical functions: minimizing friction and distributing applied loads. The remarkably smooth, water-saturated surface creates one of the most efficient tribological systems in the body. This efficiency results in an ultralow coefficient of friction, which has been measured under physiological conditions to be as low as 0.001 to 0.03.
This incredibly low friction allows the opposing bone ends to glide over one another with minimal energy loss and wear, preventing heat and damage. The trapped water within the proteoglycan matrix plays a direct role in this lubrication process. As pressure is applied during movement, a thin layer of fluid is exuded onto the surface, creating a film that separates the two cartilage surfaces.
The viscoelastic nature of the tissue enables its second function: the distribution and absorption of mechanical shock. When a load is placed on a joint, such as during walking or jumping, the cartilage compresses slowly, acting like a spring. This compression allows the tissue to spread the force over a wide area of the underlying bone, dramatically reducing stress concentration. By temporarily deforming and then slowly returning to its original shape, the cartilage effectively dampens impacts and protects the subchondral bone.
Limitations in Self-Repair
Articular cartilage has a profound limitation in self-repair following injury. This poor regenerative capacity stems from the tissue’s avascular nature, meaning it lacks a direct blood supply. Nutrients and oxygen must diffuse slowly through the dense matrix from the surrounding joint fluid.
This slow, indirect delivery system severely restricts the metabolic activity of the chondrocytes, the cells responsible for maintaining the matrix. Chondrocytes are also largely immobile and sparsely distributed throughout the matrix, making it difficult for them to migrate to and repair large defects. Once damage penetrates the surface, the cells are often unable to produce enough new matrix components to bridge the gap effectively.
Furthermore, the tissue is aneural, meaning it lacks nerve endings, so damage often goes unnoticed until it has progressed significantly. This lack of initial warning allows minor damage to worsen under continued mechanical stress. The combination of low cellularity, low metabolic rate, and the absence of a direct repair pipeline leads to chronic, persistent defects that the body cannot naturally resolve.
Major Causes of Cartilage Degradation
Damage to articular cartilage generally occurs through two distinct mechanisms: acute traumatic injury and chronic mechanical wear. Traumatic injury involves a sudden, high-force event, such as a sports accident or a fall, which can cause immediate, localized damage. This acute impact can result in chondral fractures, where a piece of the cartilage breaks off, or focal lesions, which are deep tears in the surface.
The second, and far more common, cause of degradation is the progressive breakdown known as wear and tear, which leads to the development of osteoarthritis. This chronic process involves repetitive stress over many years, which gradually fatigues the collagen network and washes out the water-trapping proteoglycans. Joint instability, genetic predisposition, and advancing age often accelerate this degenerative thinning of the cartilage layer. As the matrix structure breaks down, the tissue loses its ability to distribute load and reduce friction effectively, creating a vicious cycle that leads to pain and joint stiffness.