Articular Cartilage:
Properties and Optimal Healing Stimuli
In synovial joints, the articulating ends of the bone are covered with a layer of hyaline cartilage of varying thickness. This cartilage is designed to distribute load across the joint, and allow for movement with minimal friction and wear.
Mature chondrocytes account for a mere sprinkling of the cells in articular cartilage and furthermore have minimal capacity for proliferation and migration. These cells therefore are only able to affect a small and local area. Mature articular cartilage is also devoid of nerve supply, blood and lymphatic vessels, creating a low oxygen environment dependent on anaerobic metabolism.
The metabolic response of articular cartilage is affected by growth factors, interleukins, mechanical loads, hydrostatic pressure changes and electrical field changes. Nutrition is accomplished mostly via diffusion through the cartilage matrix in response to fluctuations in mechanical pressure.
Diffusion of nutrients in articular cartilage is dependent on proteoglycans. These cells are stimulated by compression/decompression and have a high affinity for water. As the proteoglycan aggregates in the joint are driven into the cartilage matrix, diffusion of nutrients and removal of waste occurs.
Cartilage gliding will reduce the viscosity of the synovial fluid which will further facilitate imbibition into the cartilage. Gliding will also distribute the synovial fluid over the joint surface which aids nutrition and prevents the build up of stagnant pools of hyaluronic acid.
Optimal Healing of Articular Cartilage therefore includes compression and decompression with gliding. Gliding of a joint is a process that occurs with normal movement and can also be applied passively to the joint surface.
Immobilization of a joint on the other hand, will remove the mechanical loads that allow nutrients to pump into the cartilage matrix. Immobilization will also decrease the amount of GAG, chondroitin sulfates and hyaluronic acid. Numerous other histologic changes also occur with immobilization, including distortion of normal cell alignment, decreased collagen content, decreased tendon strength, weakening of the ligament-bone complex, muscle deterioration, fatty tissue build up, and decreased metabolism.
Healing or regeneration of articular cartilage is dependent on the depth and nature of damage to the tissue. Regeneration usually results in fibrocartilage creation rather than hyaline cartilage. The articular cartilage tidemark is the layer in which blood vessels from the subchondral bone extend into the deep layer of cartilage to assist the healing process. Cartilage injuries that extend into this zone will create bleeding and a fibrin clot. This clot forms the meshwork for repair, but as stated above, the repair is typically of inferior quality to the original.
There are many factors of course that contribute to injury and degradation of articular cartilage. Aside from direct trauma, the activity level of the individual, joint mobility and alignment, muscle weakness, body weight, age, blood supply and genetics are all factors to consider when treating articular cartilage.
The concept of cyclic repetitive loading and gliding to articular cartilage is therefore dose dependent. Clinical decision making depends on the factors listed above, and the depth of injury to the cartilage itself. The goal of the clinician is to provide or encourage a high number of repetitions due to the avascularity of articular cartilage and its anaerobic metabolism.
Reference:
1. Grimsby O, Rivard J. Science, Theory and Clinical Application in Orthopaedic Manual Physical Therapy(2008). Academy of Graduate Physical Therapy, Taylorsville UT.