Autologous chondrocyte implantation (ACI, ATC code M09AX02) is a biomedical treatment that repairs damages in articular cartilage. ACI provides pain relief while at the same time slowing down the progression or considerably delaying partial or total joint replacement (knee replacement) surgery. The goal of ACI is to allow people suffering from articular cartilage damage to return to their old lifestyle; regaining mobility, going back to work and even practicing sports again.
ACI procedures aim to provide complete hyaline repair tissues for articular cartilage repair. Over the last 20 years, the procedure has become more widespread and it is currently probably the most developed articular cartilage repair technique.
The surgical technique was first published on humans by Brittberg in 1984. He reported good and promising results with 23 patients for defects on the femoral condyles (Brittberg et al., 1984).The technique also seems promising with regard to long-term results.[1]
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This cell based articular cartilage repair procedure takes place in three stages. In a first stage, between 200 and 300 milligrams cartilage is sampled arthroscopically from a less weight bearing area from either the intercondylar notch or the superior ridge of the medial or lateral femoral condyle of the patient. The matrix is removed enzymatically and the chondrocytes isolated. These cells are grown in vitro in a specialised laboratory for approximately four to six weeks, until there are enough cells to reimplant on the damaged area of the articular cartilage. The patient then undergoes a second treatment, in which the chondrocyte cells are applied on the damaged area during an open-knee surgery (also called arthrotomy). These autologous cells should adapt themselves to their new environment by forming new cartilage. During the implantation, chondrocyte cells are applied on the damaged area in combination with a membrane (tibial periosteum or biomembrane) or pre-seeded in a scaffold matrix.
Knutsen and coworkers have published the 2-year[2] and 5-year[3] follow-up results after surgery in patients randomized for ACI or microfracture treatment of localized articular defects of the knee joint. At the two-year follow-up the authors concluded that: "Both methods had acceptable short-term clinical results. There was no significant difference in macroscopic or histological results between the two treatment groups and no association between the histological findings and the clinical outcome at the two-year time-point." At the five-year follow-up the conclusions were similar: "Both methods provided satisfactory results in 77% of the patients at five years. There was no significant difference in the clinical and radiographic results between the two treatment groups and no correlation between the histological findings and the clinical outcome. One-third of the patients had early radiographic signs of osteoarthritis five years after the surgery. Further long-term follow-up is needed to determine if one method is better than the other and to study the progression of osteoarthritis."
Saris et al. studied histologic results and clinical outcome in a similar randomized study and concluded that: "One year after treatment, characterized chondrocyte implantation was associated with a tissue regenerate that was superior to that after microfracture. Short-term clinical outcome was similar for both treatments. The superior structural outcome may result in improved long-term clinical benefit with characterized chondrocyte implantation. Long-term follow-up is needed to confirm these findings."[4]
At present it seems fair to conclude that the repair tissue formed by ACI is as good or possible slightly better than a less invasive and simpler surgical technique 1–2 years after the surgery. ACI has not yet been shown to give better clinical outcome than microfracture at short-term or medium-term follow-up.
Minas et al studied clinical outcome in a cohort study of 321 patients. They found that defects treated by ACI, which had a prior treatment with marrow stimulating techniques, such as microfracture, were three times more likely to fail than for defects treated by ACI, which did not have a prior marrow stimulating technique. They concluded that marrow stimulating techniques should be employed judiciously in larger cartilage defects that may require future treatment with ACI.[5]