Articular cartilage is a specialized connective tissue that provides a smooth, lubricated surface on the ends of bones in joints, allowing for nearly frictionless movement. This tissue acts as a natural shock absorber, designed to withstand immense compressive forces. When this material is damaged, the body’s natural capacity to repair it is exceptionally limited, particularly in adult joints. This inability to regenerate the tissue effectively is the central challenge in treating joint injuries and chronic conditions like osteoarthritis.
The Structural Barrier to Natural Repair
The poor regenerative capacity of mature cartilage stems from its unique biological structure. Cartilage is an avascular tissue, meaning it contains no blood vessels to supply oxygen, nutrients, or the inflammatory cells required for a healing response. Instead, it relies on the slow process of diffusion from the surrounding synovial fluid and the underlying subchondral bone for sustenance.
The tissue’s resident cells, known as chondrocytes, are the only cells present and are encased within a dense, rigid extracellular matrix (ECM). Chondrocytes comprise only about one to five percent of the total tissue volume. Their primary role is to maintain the surrounding matrix of Type II collagen and proteoglycans, rather than to proliferate or migrate to an injury site.
When a defect occurs, the limited number of chondrocytes near the damage site cannot multiply quickly or move through the dense matrix to fill the void. The lack of blood flow also prevents the recruitment of mesenchymal stem cells or immune components that typically initiate tissue repair elsewhere. This combination of avascularity and low cellularity means that damaged cartilage often remains a permanent defect, with no significant natural repair occurring.
Distinguishing Types of Cartilage Damage
Understanding the nature of cartilage damage is fundamental because it dictates the potential for intervention and the necessary treatment strategy. Damage is broadly categorized into two types: traumatic focal defects and degenerative damage. Traumatic focal defects are isolated injuries to a specific area of the articular surface, often caused by an acute event like a sports injury or fall.
These focal lesions can be classified by their depth, sometimes extending completely through the cartilage layer to the subchondral bone. This damage typically appears in younger individuals with otherwise healthy joints. Since the surrounding cartilage remains intact, these defects are a more suitable target for localized tissue repair or replacement procedures.
In contrast, degenerative damage, most commonly recognized as osteoarthritis, is a chronic, progressive condition that affects the entire joint. This involves the gradual, widespread thinning and deterioration of the articular cartilage over time, often associated with aging, mechanical stress, or obesity. Osteoarthritis is a systemic joint disease, not just a localized defect, which complicates regenerative efforts because the entire joint environment is compromised.
Current Medical Strategies for Regeneration
Given the body’s inability to naturally repair cartilage, medical science has developed interventions that attempt to stimulate new tissue growth or replace the damaged area. One common surgical technique is microfracture, typically used for smaller, contained defects. This procedure involves creating tiny holes in the subchondral bone plate, allowing blood and bone marrow contents, including mesenchymal stem cells, to seep into the defect and form a clot.
Microfracture encourages new tissue formation, but the resulting repair tissue is generally fibrocartilage, which is biomechanically inferior to native hyaline cartilage. Fibrocartilage is less durable and may break down over time, making this technique a less ideal long-term solution, particularly for high-demand patients or larger lesions. For defects too large for microfracture, more advanced surgical options are employed to restore the hyaline cartilage surface.
The Osteochondral Autograft Transfer System (OATS), also called mosaicplasty, involves transplanting small plugs of healthy bone and overlying hyaline cartilage from a non-weight-bearing area of the joint to the damaged site. This method provides immediate coverage with durable, native hyaline cartilage. A limitation of OATS is the potential for morbidity at the donor site and the restriction on the size of the defect that can be treated due to limited availability of healthy tissue.
Another sophisticated cell-based approach is Autologous Chondrocyte Implantation (ACI), which has evolved into Matrix-Induced ACI (MACI). This two-stage procedure involves first harvesting a small sample of the patient’s healthy chondrocytes and expanding them in a laboratory. In the second stage, the expanded cells are implanted into the defect, often on a scaffold, to promote the growth of new hyaline-like cartilage. This technique is often reserved for larger defects and aims to create tissue with mechanical properties closer to the original cartilage.
Beyond surgery, non-surgical approaches focus primarily on supportive therapy and biological stimulation. Injections of platelet-rich plasma (PRP), which concentrates growth factors from a patient’s blood, are used to modulate the local inflammatory environment and potentially stimulate cellular activity. Similarly, mesenchymal stem cell (MSC) injections, often derived from bone marrow or adipose tissue, are emerging as a promising therapy, leveraging the cells’ ability to differentiate into cartilage-forming cells.
While these cell- and factor-based injections show promise, the long-term evidence for true, durable hyaline cartilage regeneration remains a topic of ongoing research. Other common injections, such as corticosteroids and hyaluronic acid, are considered supportive treatments that reduce inflammation or provide temporary joint lubrication, rather than actively regenerating lost tissue. The selection of the most appropriate treatment is highly individualized, depending on the patient’s age, the size and location of the defect, and the overall health of the joint.