The surfaces of synovial joints are lined
with a smooth, glistening material called articular cartilage
that provides for almost friction free motion with only minimal
fluid for lubrication. The articular cartilage is only a few millimeters
thick and consists of cells, called chondrocytes, and a matrix
of proteoglycans and collagen. The chondrocytes make up only 5%
of the articular cartilage and are themselves embedded within
the matrix in small lacunae. These cells are small chemical factories
that produce the matrix. There are no blood vessels or lymphatics
so the chondrocytes derive their nutrition by diffusion of substances
from the synovial fluid normally present in the joint.
Mature chondrocytes are normally incapable of cell division(reproduction) and because the chondrocytes are trapped within the lacunae and cannot migrate into an area of injury, articular cartilage has only limited abilities to repair itself. As a result of this, the cartilage around a defect accepts more weight, becoming larger, leading to progressive deterioration of the joint and ultimately degenerative arthritis.
Smooth, friction free and painless motion is what we all expect from our joints. In fact, for most of us the act of walking involves no conscious effort and joint motion is almost imperceptible. However, once injury or degeneration of the articular cartilage occurs, the joint develops heat with motion and produces fluid in a vain attempt to lubricate itself, thus , the pain, noise, warmth and fluid usually associated with chondromalacia (bad cartilage) and arthritis.
Over the years many different methods have evolved to treat chondromalacia. These include shaving of the loose fragments, drilling of the underlying bone, in attempt to form a layer of fibrous cartilage in the defect, and grafting. None of these methods have been satisfactory because in order to restore the articular surface, one must repair it with hyaline cartilage or some other material with similar biological and mechanical properties. Mere debridement only temporarily alleviates some of the mechanical symptoms and the fibrocartilage that forms after drilling is neither durable nor does it provide for low friction.
In 1987 Dr. Peterson and his staff, in Goteborg Sweden, began to use autologous chondrocyte transplantation to treat full thickness articular cartilage defects in the knees of patients. The initial results of the treatment of the first 23 patients was reported in the New England Journal of Medicine in 1994. 14 of 16 patients with femoral condylar implants had good and excellent results and biopsies of the treated areas showed that 11 of 15 femoral implants had the appearance of hyaline cartilage. This represented a watershed event in the treatment of chondromalacia because for the first time in history a potentially reliable way to restore articular cartilage exists. The young otherwise active individual that was previously essentially untreatable now has some hope of return to an active lifestyle. As of this writing almost three hundred cases have been done worldwide. More than 95,000 total knee replacements are performed each year in the United States of America. If early treatment of articular cartilage injuries can prevent the development of osteoarthritis the need for joint replacement may be postponed or possibly, with further refinements, eliminated.
If a patient meets the clinical criteria, an initial Arthroscopic evaluation is performed and, if appropriate, a small biopsy of healthy articular cartilage from a non-weight bearing portion of the joint is obtained. This tissue is then processed by the Genzyme laboratory in Cambridge, Massachusetts where the cells are separated from the matrix and then placed in a nutrient broth. In a carefully controlled environment the cells divide and replicate. The whole procedure is monitored for sterility and is performed in a special clean air room by trained laboratory technicians. After three weeks the process is complete and 12 million chondrocytes are returned for implantation. A second open procedure is then required to implant the chondrocytes, which are injected under a thin sheet of tissue that is sewn over the defect. The patient is usually hospitalized for 48 hours for observation and initiation of physical therapy. Exercises, including range of motion and strengthening, are started immediately but no weight bearing is permitted for the first 8 weeks. Usually light jogging can begin at 4-6 months and full return to sports by 12 months.
This procedure is currently limited to articular cartilage defects smaller than 10 square centimeters on the femur or patella in patients under 50 years of age. It is not indicated when there has been prior total meniscectomy, degenerative arthritis or inflammatory arthritis such as gout, rheumatoid arthritis or prior infection.
Another new option is known as mosaicplasty
or the OATS (OsteoArticular Transplantation) procedure. This procedure
involves taking cores of cartilage and bone from an area of the
knee that is non-weight bearing and transferring it into the articular
cartilage defect. This procedure can be safely accomplished with
just an overnight stay in the hospital followed by 8 weeks on
crutches and then a period of rehabilitation. Long term followup
is not available for this procedure.