- See: Chondral Injuries:
Nourishment
- Discussion:
-
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;
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Original Articles: 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.
