New Horizons in Articular Cartilage Repair

Articular cartilage rarely reforms a functional hyaline surface after injury. Most simple cartilage lacerative injuries reach a benign nonhealing phase, which remains unchanged over time. Deeper cartilage lesions, which violate the tide-mark and extend into the subchondral bone plate, result in an improved healing response. This is largely because of the proliferation of undifferentiated mesenchymal cells from the deeper tissues. In horses, the progression in cartilage defects from granulation to fibrous tissue and, finally, fibrocartilage is slower than it is in rodents; the healing of defects in dogs tends to be somewhere between these extremes. The fibrous tissue undergoes progressive chondrification to form a fibrocartilaginous mass that is loosely attached to the original cartilage edges. The subchondral bony plate occasionally reforms to the same approximate level as the adjacent undamaged bone. Immediately above the reformed subchondral plate, areas of cartilage proliferation predominate. The deeper cartilage layers and surface fibrous tissue generally follow a pattern of decreasing cellularity as the defect matures. The phenomenon of matrix flow, an intrinsic repair mechanism, may also contribute to the healing of equine articular cartilage defects by forming overhanging lips of cartilage on the perimeter of the lesion that tend to migrate in a centripetal manner. In small defects, this can result in significant reduction in lesion size. In larger defects, matrix flow plays an insignificant role, compared with mesenchymal cell proliferation. Although depth of injury (full or partial thickness) is a critical determinant in healing, the size of the defect, its location in relation to weight-bearing or non-weight-bearing areas, and the age of the animal influence the repair rate and resiliency of new cartilage surfaces. Convery et al. showed that lesions in the equine femorotibial joint that were less than 3 mm in diameter healed with little residual deformity. More recently, Hurtig et al. determined that lesions larger than 15 mm in surface area tend to show reasonably good repair at 5 months but degenerate with increasing time. Given these and other studies, repair of full-thickness articular cartilage defects in the horse may not be as satisfactory or as complete as that documented in smaller animals. Metaplasia of fibrous tissue to fibrocartilage is not always evident and, depending on the time of examination, degeneration to fibrous tissue and later mechanical erosion of the repair tissue can occur. Repair tissue is biomechanically inferior to normal articular cartilage, even though the histological appearance is often fibrocartilage or even hyaline-like tissue. Repair tissue generally has significantly less proteoglycan and, to some extent, type II collagen than does normal cartilage. Additionally, the development of subchondral architecture and re-establishment of a tide-mark is often irregular and inconsistent. This creates susceptibility to cartilage deterioration with normal joint activity. Poor-quality, relatively short-lived repair cartilage has led to the development of pharmacologic and surgical methods to improve the repair process.