Background: Microfracture is a surgical procedure that is used to
treat focal articular cartilage defects. Although joint function improves
following microfracture, the procedure elicits incomplete repair. As blood
clot formation in the microfracture defect is an essential initiating event in
microfracture therapy, we hypothesized that the repair would be improved if
the microfracture defect were filled with a blood clot that was stabilized by
the incorporation of a thrombogenic and adhesive polymer, specifically,
chitosan. The objectives of the present study were to evaluate (1) blood clot
adhesion in fresh microfracture defects and (2) the quality of the repair, at
six months postoperatively, of microfracture defects that had been treated
with or without chitosan-glycerol phosphate/blood clot implants, using a sheep
model.
Methods: In eighteen sheep, two 1-cm2 full-thickness
chondral defects were created in the distal part of the femur and treated with
microfracture; one defect was made in the medial femoral condyle, and the
other defect was made in the trochlea. In four sheep, microfracture defects
were created bilaterally; the microfracture defects in one knee received no
further treatment, and the microfracture defects in the contralateral knee
were filled with chitosan-glycerol phosphate/autologous whole blood and the
implants were allowed to solidify. Fresh defects in these four sheep were
collected at one hour postoperatively to compare the retention of the
chitosan-glycerol phosphate/blood clot with that of the normal clot and to
define the histologic characteristics of these fresh defects. In the other
fourteen sheep, microfracture defects were made in only one knee and either
were left untreated (control group; six sheep) or were treated with
chitosan-glycerol phosphate/blood implant (treatment group; eight sheep), and
the quality of repair was assessed histologically, histomorphometrically, and
biochemically at six months postoperatively.
Results: In the defects that were examined one hour postoperatively,
chitosan-glycerol phosphate/blood clots showed increased adhesion to the walls
of the defects as compared with the blood clots in the untreated microfracture
defects. After histological processing, all blood clots in the control
microfracture defects had been lost, whereas chitosanglycerol phosphate/blood
clot adhered to and was partly retained on the surfaces of the defect. At six
months, defects that had been treated with chitosan-glycerol phosphate/blood
were filled with significantly more hyaline repair tissue (p < 0.05)
compared with control defects. Repair tissue from medial femoral condyle
defects that had been treated with chitosan-glycerol phosphate/blood contained
more cells and more collagen compared with control defects and showed complete
restoration of glycosaminoglycan levels.
Conclusions: Solidification of a chitosan-glycerol phosphate/blood
implant in microfracture defects improved cartilage repair compared with
microfracture alone by increasing the amount of tissue and improving its
biochemical composition and cellular organization.
Clinical Relevance: The use of chitosan-glycerol phosphate/blood
implants in conjunction with microfracture can improve the structural and
compositional properties of repaired cartilage. These effects may result in
better integration, improved biomechanical properties, and longer durability
of the repair tissue.