Articular Cartilage's Struggle with Regeneration

Articular Cartilage Injuries 

Articular cartilage is an all-important tissue keeping our joints properly functioning everyday. As described earlier, unlike most tissues in the human body, cartilage lacks the ability to regenerate on its own. Abrupt movements during physical activity can easily lead to cartilage defects of which there are two types: partial and full thickness defects. These defects can grow worse over time leaving bony ends exposed causing joint stiffness, pain, and eventually bone damage. The protection provided by the tissue surrounding the bone is invaluable to proper function. 

Sports can Result in Cartilage Damage

The above photograph is of a full thickness defect site in the knee, as seen with an arthroscope (a camera inserted in the joint via a small cavity).

Football and rugby are the two sports in which articular cartilage is most frequently damaged. The injury often occurs in the knee from a forceful impact such as a tackle. Depending on the force of the impact, the thickness of the damage varies. One of the most common areas of injury to the knee is the meniscus. Each knee joint has two crescent-shaped cartilage menisci which cushion and support the knee. Twisting is also a common way to tear the meniscus. 

Partial Thickness Defects

The term “partial thickness defects” indicates damage of the zonal articular cartilage, without penetration into the underlying bone. This type of injury on the surface leaves the defect site inaccessible to the cell types that stimulate self-healing responses.  The macromolecules in articular cartilage (including proteoglycans) make the tissue surfaces anti-adhesive. While chondrocytes begin to synthesize extracellular matrix (ECM) immediately after the injury, not enough chondrocytes are able to migrate to the affected sites for full regeneration to occur. Self-healing activity gradually comes to a stop, resulting in progressive reduction of tissue function, initiating tissue degeneration.

Full Thickness Defects

The more severe case of cartilage defect is full thickness defect, penetrating into the bone, past the calcified zone (a layer of calcified cartilage covers the underlying bone). Unlike partial thickness defects, the site is accessible to blood cells, bone cells, and progenitor cells in bone morrow, all of which are involved in a spontaneous healing process. Upon injury, the defect site is immediately filled with a fibrin clot and an inflammatory response is activated. Mesenchymal stem stems located in the bone marrow move into the defect site, replacing the fibrin clot completely after approximately one week. These stem cells then differentiate into chondrocytes, due to the chondrocytes’ ability to secrete proteoglycan-rich extracellular matrix, helping repair the damaged cartilage tissue. However, healing is short-lived as the new tissue is of inferior quality.


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