Surface zone articular chondrocytes inhibit trauma induced cell death and matrix loss in wounded cartilage

Previous studies have shown that articular cartilage grows by
apposition from the articular surface that is driven by proliferation of surface
zone cells (1) and that these cells have an extended cell cycle time (2), both
suggestive of the presence of a population of chondroprogenitor cells resident
within the surface zone of articular cartilage. In recent years, autologous
chondrocyte transplantation has been increasingly used to repair articular
cartilge defects (3). These procedures inevitably lead to the formation of a
fibrocartilaginous plug of repair tissue within the wound that lacks the distinct
structural architecture of articular cartilage proper. This lack of a defined
structure eventually leads to repair failure due to the altered biomechanical
properties of the repair tissue compared with articular cartilage itself. The
reasons for both fibrocartilaginous plug formation and its eventual failure are
unclear but they may include the poor intrinsic reparative ability of cartilage
itself, the fact that full depth cartilage is used which contains chondrocytes at
different stages in the differentiation pathway and a lack of integration at the
wound margin; the so called zone of necrosis.

We have recently devised a method of isolating articular cartilage progenitor
cells from surface zone articular cartilage using differential adhesion to
fibronectin. The cells thus isolated have a high colony forming efficiency
from an initially low seeding density. Our aim was to use progenitor
chondrocytes isolated by differential adhesion in a pellet culture system and
characterise the pellets derived from surface middle and deep zone articular
cartilage. Additionally, pellets from surface, middle and deep zone cartilage
were used in an in vitro model of articular cartilage wounding to assess their
effects on wound responses.

Poster No: 0418