The operative treatment of full thickness cartilage defects in the knee joint with autologous chondrocyte transplantation

OBJECTIVE: The high clinical and socio-economical impact of cartilage defects and chondral degeneration is well-known. After trauma or without a known etiology, often young patients suffer from pain and a loss of function leading into a decrease of physical activity and, more severe, into long term disability and unemployment. The clinical use of autologous chondrocyte transplantation was introduced in 1994 reporting the data of a pilot study. The objective of this study is to evaluate the efficacy of this method of surgery.

METHODS: Autologous chondrocyte transplantation has been established in our department since 1995 for the treatment of large, full thickness cartilage defects which can be completely covered with hyaline-like cartilage without harming the subchondral bone plate. Our first patients (n=24) all showed Grade IV lesions and an average defect size of 6.27 cm2. All but 4 of the patients had at least 1 cartilage defect related operation on the knee.

RESULTS: The patients and the clinicians rating indicated an increase of a modified Cincinnati Knee score from 3.6 point pre-operation to 6.9 points after 6 months and 8.1 points at 12 months on a scale from 1 (bad) to 10 (excellent). These results support the data of an international multicenter study with almost 2000 patients. The 5 year results described by the originate authors are good to excellent in 85%-95% with an adverse event rate of 5%.

CONCLUSION: Autologous chondrocyte transplantation has to be considered a safe and effective method for the treatment of large full thickness cartilage defects. Alternative treatments are symptomatical: drilling, abrasion, lavage, chondroplasty, or osteotomies. The short term results are promising but a lot of patients have to be treated for osteoarthritis as a consequence of failure with total joint arthroplasty. Osteochondral transplantations have the disadvantage of limited harvesting sites and the impairment of the subchondral bone plate.