From a clinical point of view, there are two distinct goals for cartilage repair: (a) restoration of joint function, which includes pain relief, and (b) prevention of, or at least delay of, the onset of osteoarthritis.² These goals can potentially be achieved through replacement of damaged or lost articular cartilage with a substance capable of functioning under normal physiologic environments for an extended period. Screening of potential procedures for human clinical use had been done by preclinical studies. Restoration of a joint surface is assessed by its appearance anatomically, histologically, biologically, and mechanically relative to the original tissue, hyaline cartilage. Preclinical studies use animal models. The choice of animal models is one of the most frequently discussed and controversial issues in biomedical research, especially in orthopaedics. It has been stated that the key issue in the selection of the appropriate model is to match the model to the question being investigated and the hypothesis being tested.³

In 1929, August Krogh, a Danish physiologist, wrote, “for a large number of problems there will be some animals of choice, or a few such animals, in which it [the problem] can be most conveniently studied.”⁴ However, it has also been pointed out that the uncritical application of this principle could lead to inaccurate generalizations, because extrapolating findings from one species to another is not without flaws.⁵ The researcher must consider which animal model(s) most accurately represent(s) the human condition being investigated and to what extent the results obtained from these models might be extrapolated to humans.⁶ The obvious critical questions with regard to joint defect repair are (a) which animal model(s) most accurately represents the critical chondral defect in humans and (b) to what extent can preclinical research results in this model be extrapolated to humans.² The equine stifle (femoropatellar and femorotibial articulations) are comparable to the human knee, and this joint also suffers considerable naturally occurring clinical disease. Osteoarthritis with erosion of articular cartilage occurs naturally on the medial condyle of the femur. In addition, the femoral trochlear ridges are commonly affected with osteochondritis dissecans.

A study was done in the first author’s laboratory where histologic measurements of the thickness of noncalcified and calcified cartilage, as well as the subchondral bone plate in five locations on the femoral trochlea and medial femoral condyles of species used in preclinical studies of human articular cartilage were made and compared with those of the human knee.⁷ Cadaveric specimens were obtained of six human knees, as well as six equine, six goat, six dog, six sheep, and six rabbit stifle joints (the animal equivalent to the human knee). Specimens were taken from the lateral trochlear ridge, medial trochlear ridge, and medial femoral condyle of the femur. After histopathologic processing, the thickness of noncalcified and calcified cartilage layers, as well as the subchondral bone plate, was measured. Average articular cartilage thickness over five locations was 0.2 to 0.3 mm for the rabbit, 0.5 to 0.7 mm for the sheep, 0.5 to 0.8 mm for the dog, 0.6 to 1.5 mm for the goat, 1.8 to 2.2 mm for the horse; human femurs showed a range of 2.4 to 2.9 mm. It was concluded that the horse provided the closest approximation to humans in terms of articular cartilage thickness, and this approximation is considered relevant in preclinical studies of cartilage defects.⁷

The typical human lesion is a defect on the medial femoral condyles and the defect is limited to the articular cartilage. Hunziker⁸ has given an example of the difficulty of creating an articular cartilage defect only in such species as the rabbit. If one created a 3-mm deep lesion in rabbit articular cartilage (the majority of which would be in the bone), 93% to 95% of the volume of this defect would be ensheathed by bone, bone marrow space, and vasculature (yielding an abundance of different cell types, growth factors, and signaling substances) and only 5% to 7% of the defect volume would abut on cartilage. Because of the thickness of articular cartilage on the medial condyle of the femur of the horse, experimental defects can be made without compromising the subchondral bone plate, but at the same time, removal of the calcified cartilage layer can be assured. In addition, these defects can be made arthroscopically, and after surgery the horses can be exercised at an increasingly athletic level on a high-speed treadmill.

The use of microfracture, or micropicking, as it has been referred to in equine arthroscopy, has many of the advantages associated with subchondral drilling, including focal penetration of the dense subchondral plate to expose cartilage defects to the benefits of cellular and growth factor influx, as well as improving anchorage of the new tissue to the underlying subchondral bone, and to some extent, surrounding cartilage.^9,10,11 However, microfracture has the advantages over drilling in that there is no thermal necrosis, and the holes have rough edges, which seems to enhance clot adhesion. Additionally, the microfracture awls allow access to all areas of the joint, whereas some areas cannot be reached with drills. The simplicity of microfracture comes from the use of a tapered awl (Linvatec, Largo, FL; Arthrex, Naples, FL) that eliminates the need for powered instrumentation and gives accurate control. A tapered entry into the subchondral marrow space is achieved.

The first experimental study in the horse documented improvement in the quantity of tissue and the type II collagen content at 4 and 12 months after microfracture of full-thickness defects¹² (Fig. 16.1). The testing model was a 1-cm² defect made arthroscopically on the medial condyle of the femur. The medial femoral tibial joint is a separate
joint compartment. The arthroscope was placed into the joint from the lateral aspect. The anterior instrument portal allowed a curette to be used to debride the cartilage down to the subchondral bone plate. Evaluations were made at 4 and 12 months.