(see also: Chondral Injuries: Nourishment)
- articular cartilage is avascular & is prevented from mounting a vascular response when there is isolated cartilage injury;
- absence of vessels w/ in cartilage imposes limitations on healing potential;
- indeed, some traumatic defects in cartilage apparently never heal;
- chondrocytes in articular cartilage are capable of cell division & are also capable of increased proteoglycan synethesis;
- regeneration of cartilage is slow, & highest potential for growth occurs in the perichondrium which lies at the periphery of articular cartilage;
mechanisms of repair
- when articular cartilage is injured, the type of healing that will take place is influenced by the depth of the injury;
- extrinsic healing:
- dependent on a synovial reaction or subchondral bone being penetrated at the time of injury;
- w/ subchondral injury, capillary injury forms a fibrin clot, which is then replaced by granulation tissue and fibrocartilage;
- if defect is limited to cartilage, no blood vessels are disrupted, and inflammatory response is less intense than if injury extends through cartilage into subchondral bone, as occurs in intraarticular frx;
- intrinsic healing (isolated injury):
- dependent on chondrocytes to synthesize a new matrix;
- since cartilage is largely avascular, healing is dependent on diffusion of nutrients from synovial fluid;
- potential for intrinsic healing appears somewhat limited;
- isolated injuries to cartilage (which do not extend to subchondral bone heal slowly and incompletely;
Continuous Passive Motion:
- continuous passive motion can promote healing of articular cartilage;
- in joints treated w/ continuous passive motion, healed articular defects where as joints that were immobilized showed no healing
- Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation.
- Quantitation of chondrocyte performance in growth-plate cartilage during longitudinal bone growth.
- Elaboration of neutral proteoglycanase by growth-plate tissue cultures.
- The viability of articular cartilage in fresh osteochondral allografts after clinical transplantation.
- Characterization of aggregating proteoglycans from the proliferative, maturing, hypertrophic, and calcifying zones of the cartilaginous physis.
- The induction of neochondrogenesis in free intra-articular periosteal autografts under the influence of continuous passive motion. An experimental investigation in the rabbit.
- Passive motion: the dose effects on joint stiffness, muscle mass, bone density, and regional swelling. A study in an experimental model following intra-articular injury.
- Mesenchymal Cell-Based Repair of Large, Full-Thickness Defects of Articular Cartilage.