This is a very brief description of ACI in my own words. The knee contains two types of cartilage - meniscal and articular. The menisci (we have two, on both the inside [medial] area and outside [lateral] area of each knee) are semi-circular, thick pieces of cartilage located between the thigh bone (femur) and the bones of the lower leg (tibia and fibula). Articular cartilage directly lines the bones and is the last line of defense for the femur, thereby shielding the bone from direct shock absorption. You can get a first-hand look at articular cartilage when examining the end of a chicken thigh bone - the shiny, white lining is articular cartilage.
ACI is a technique for rebuilding damaged articular cartilage and is a two-part process. In the first stage, a biopsy of an individual's articular cartilage is taken from a relatively non weight-bearing area of the femur. This cartilage is then sent to a laboratory (Genzyme) where additional cartilage cells (chondrocytes) are cultured. These cells are the same as those manufactured by the patient's own body. The term autologous refers to the fact that the chondrocytes are derived from the individual's own cartilage. After six weeks, the new cells are ready for implantation into the defective areas.
This may seem odd, but I wasn't in much pain prior to this surgery. Over the summer of 1999, I took many bike rides, several up to 70 miles long and maintained a very-near normal weightlifting routine. I had also scheduled a two-week, late-August, backpacking trip into the Grand Canyon. Running was painful but I had recognized this as a limitation I might always have, even before my second ACL reconstruction, and I had come to accept it. However, hiking and backpacking had not been a problem before the second ACL, but as the date of the trip neared, I had reservations.
What I didn't have with my knee was confidence. In my weightlifting workouts, my quadricep routine was involved and fairly complete (leg extensions, seated adduction, seated abduction, leg curls) but was short of what it had been before the second ACL reconstruction. Over the past year, I had tried several times to perform front squats, regular squats, or leg presses but always with lighter weight than I used before the second ACL reconstruction. I never reached the point where I could use a weight that my quadriceps could handle because my knee didn't feel stable at higher weights. I also took one backpacking trip in late spring and while I came out of it OK, I never felt completely comfortable stabilizing the backpack's weight with my knee. This was most evident while crossing streams or while crossing rocky terrain. I even got the unstable sensation whenever I'd stand while bicycling.
I cancelled the Grand Canyon trip. It had now been over a year since my July, 1998 reconstruction/chondroplasty. If I were to heal, I should have by September, 1999. I returned to my surgeon for another look at my knee.
I knew that I had articular cartilage damage, the chondroplasty performed in July, 1998 was a possible fix but my surgeon had already warned me of a potentially troublesome future. Whether my activities over the period July, 1998 to August, 1999 had accelerated further damage I'll never know. There were minor incidents over the past year that may have contributed to the deterioration but there was no single incident that I recall as exceptional. This, from what I've come to understand, is not all that uncommon in articular cartilage deficiencies which can begin many years prior to reaching a noticeable level and accelerate rapidly once a certain threshold is crossed.
My surgeon prescribed an magnetic resonance imaging (MRI) scan. Although an MRI scan isn't a completely reliable diagnostic method for evaluating articular cartilage damage, it is the best of the non-invasive techniques. The scan was performed in September, 1999. In the follow-up visit with my surgeon, he pointed to strong evidence that there were articular cartilage defects; however, the image resolution of an MRI isn't fine enough to indicate the extent of the damage. We discussed options for repairing the defects - either the osteochondral autologous transfer system (OATS) procedure or ACI. The proper technique would be dictated by the size of the lesions which could not be determined without an arthroscopic evaluation. In mid-October, I scheduled the arthroscopic evaluation for November 9, 1999.
This is the question I'm asked most often from those who have visited this site. The simple answer is yes. Even though my knee is not 100% better, I cannot run, and I still have athletic limitations, I would again make the decision that I made in 1999 (to have the ACI). At that time, I was faced with the high likelihood of having a knee replacement before I turned 40 - an extremely unattractive scenario. The ACI was presented to me as an opportunity to at least delay, if not prevent, a knee replacement. I was told prior to the ACI procedure that it would not likely return me to uninhibited and unrestricted physical activity. Furthermore, the rehabilitation involved in ACI is longer and more demanding than with any surgery I had prior and even today I'm not sure what the overall health of my knee might be. However, the prognosis was that I could continue to remain as active as I had been over the period from 1996 to 1999 (weight training, biking, hiking/backpacking). The opportunity of remaining active while delaying, or avoiding, a knee replacement made my choice an easy one and I would make that same decision today.