The therapeutic value of microfracture has been demonstrated in clinical patients. The rationale is that focal penetration of the dense subchondral plate exposes cartilage defects to the benefits of cellular and growth factor influx in addition to improving anchorage of the new tissue to the underlying subchondral bone and, to some extent, the surrounding cartilage. While functional outcomes have been reported, there is a paucity of data on the histological, biochemical, and molecular changes in human patients. This paper reviews 4 basic science studies of microfracture using an equine chondral defect model that gave some insight into possible mechanisms of action and also how the microfracture response could be augmented. In study I, microfracture of full-thickness chondral defects in exercised horses significantly increased the repair tissue volume in the defects at both 4 and 12 months. No adverse effects were seen. In study II, an investigation of the healing of full-thickness chondral defects during the first 8 weeks with or without microfracture demonstrated that microfracture significantly increased type II collagen expression as early as 8 weeks after treatment compared to controls; aggrecan expression was progressively increased during the first 8 weeks but was not significantly enhanced by microfracture. In study III, it was demonstrated that removal of the calcified cartilage layer provided optimal amount and attachment of repair tissue, emphasizing that careful removal of calcified layer is critical during debridement prior to microfracture. Study IV assessed the ability of IL-1ra/IGF-1 combination gene therapy to further modulate repair of microfractured chondral defects. The repair tissue in gene therapy–treated joints demonstrated increased proteoglycan and type II collagen content compared to microfracture alone.
Knee cartilage defects: association with early radiographic osteoarthritis, decreased cartilage volume, increased joint surface area and type II collagen breakdown
