Deep and large, crater-like osteochondral defects are not suitable for osteochondral autograft transplantation, mainly because of the limited availability of autologous osteochondral grafts. Also, it is difficult to reconstruct the subchondral bone and restore the contour of the defect area, and to cover the entire defect area with hyaline articular cartilage. The dead spaces between circular grafts, the lack of integration of donor and recipient hyaline cartilage, different orientation, thickness and mechanical properties of donor and recipient hyaline cartilage are further sources of clinical concern.
TruFit CB Plugs (Smith and Nephew, London, UK), are synthetic cylindrical biphasic absorbable scaffolds, based on PolyGraft Technology, designed to capture and retain bone marrow elements and encourage differentiation into articular cartilage and bone. Three-dimensional porous scaffold with interconnected pores (mean diameter of 250 μm) encourages tissue ingrowth and remodeling. This techinology is approved for use in UK. In the US this product is marketed by Smith & Nephew as , as Bone Graft Substitute for filling circular drill holes in bone, with the following disclaimer: "the safety and effectiveness of this device in osteochondral defects have not been established". This product is not intended for articular cartilage repair in the USA.
[A36] Puelacher WC, Mooney D, Langer R, et al: Design of nasoseptal cartilage replacements synthesized from biodegradable polymers and chondrocytes. Biomaterials 15:774-778, 1994.
From animal studies, corticosteroids have shown to produce a deleterious effect on cartilage metabolism. This is manifested by damage to, and death of, the chondrocytes. The chondrocytes are the cells that synthesize the components of cartilage, mainly the type II collagen and proteoglycans. Because chondrocytes decrease in number and function, collagen and proteoglycan synthesis decline. The net result of these effects is articular cartilage degeneration. The degenerated cartilage loses elasticity, making the joint more stiff. Ultimately, the cartilage thins and there is narrowing of the joint space as evidenced by X-ray. This narrowing is typical of osteoarthritis.
[A21] Puelacher WC, Kim SW, Vacanti JP, et al: Tissue engineered growth of cartilage: The effect of varying the concentration of chondrocytes seeded onto synthetic polymer matrices. Int J Oral Maxillofac Surg 23:49-53, 1994.
Using tritiated glycine (glycine 3H) as an indicator of amino acid incorporation in protein synthesis in cartilage matrices, Mankin and Conger injected hydrocortisone acetate into rabbit knees. Their data showed a rapid and profound decrease in glycine incorporation that appeared to depend on dosages. Maximum decline was seen six hours after the injection.28 They did a similar experiment using glycine 14C as the radiotracer, which showed a definite decrease in the rate of protein synthesis within two hours of the injection. They noted that the rate of the inhibitory effect of intraarticular hydrocortisone on cartilage protein synthesis was about twice that of the observed rate for corticosteroids given by intramuscular route.29 One year later, researchers injected hydrocortisone into normal rabbit knees and produced thinning of the cartilage, and the development of fissures and fibrillations in the articular cartilage. They also found multiple small white deposits within the substance of the articular cartilage, which were found to represent cystic areas of degeneration within the middle zone of the cartilage matrix. These effects were most marked in the animals which had the greatest number of injections.30 Deleterious effects of cortisone were reported by some researchers who noted that the drug inhibited the synthesis and deposition of chondroitin sulfate in cartilage.31-33
Early in the course of OA, the tissue mounts an attempt at repair. Chondrocytes proliferate with a resulting increase in matrix synthesis. However, in the face of chronic mechanical degenerative forces, degradative enzymes overwhelm the synthetic capability. The net result is too much degradation of cartilage and not enough repair. Traditional pharmacological treatments, including nonsteroidal anti-inflammatory drugs and corticosteroids shots, are typically used to not only decrease symptoms, but also to hopefully improve the physiology of the disease process. Unfortunately the preponderance of evidence shows that these treatments actually accelerate the osteoarthritic process.17,18 The rest of this paper will focus on the evidence that corticosteroids deteriorate normal and degenerated articular cartilage.
They noted that the rate of the inhibitory effect of intraarticular hydrocortisone on cartilage protein synthesis was about twice that of the observed rate for corticosteroids given by intramuscular route.
In selecting methods of restoring the damaged articular surface, it is important to distinguish articular cartilage repair from articular cartilage regeneration. Repair refers to the healing of injured tissues or replacement of lost tissues by cell proliferation and synthesis of new extracellular matrix. Unfortunately, repaired articular cartilage generally fails to replicate the structure, composition, and function of normal articular cartilage. Regeneration in this context refers to the formation of an entirely new articulating surface that essentially duplicates the original articular cartilage. Therefore, the best we can do at present is to repair chondral or osteochondral defects with functionally similar tissue.
In regard to the progression of OA, is the articular cartilage damage seen from the disease or from the steroid injection treatments? One research paper put it this way: “After administration of corticosteroids to patients suffering from arthritis, it is impossible to decide how much damage is due to the steroids and how much is due to the natural progress of the disease. To answer this question, these researchers devised a study to look at what happens to rabbit articular cartilage subjected to corticosteroid concentrations compatible with what we observed in human patients. They compared this group to normal control animals who received no injections. They also induced an artificial arthritis in one group of animals, used them as another control, and saw what happened to some of these animals if they also were subjected to low dose corticosteroids. Compared to the control groups, the corticosteroids caused severe deleterious effects on the articular cartilage. The articular cartilage became thin, the matrix near the surface lost its hyaline appearance and became fibrous, the surface fibrillated, and the arthritic cartilage lost its ability to repair itself. This last effect caused the researchers to state “It must be expected that corticosteroids can retard or prevent recovery in naturally occurring joint diseases. Administration of these drugs must therefore be considered with caution.”42 This last quote was written in 1973. For this review I purposely used “old” research to emphasize the point that the effects of corticosteroids have been known for years. Current research done in 2007 on rabbit cartilage continues to confirm that corticosteroid injections into the knee joints of rabbits causes cartilage necrosis.43
Although fibrocartilage fills and covers the defect, this is the right tissue from the biomechanical standpoint. The fibrocartilage is made to resist tension forces, while the hyaline cartilage is made to resist compression forces, to enable smooth articulation, and to withstand long-term variable cyclic load and shearing forces. Focal articular cartilage defects, often found in young adults, have been increasingly recognized as a cause of pain and functional problems.