To The Editor:
As the surgeon who performed the reconstruction and later retrieved the specimen discussed in "Observations on a Retrieved Patellar Tendon Autograft Used to Reconstruct the Anterior Cruciate Ligament. A Case Report" (2002;84:1433-8), by Delay et al., I believe that I can offer some helpful insight on the histological finding of an area of necrosis in the intra-articular portion of the graft just proximal to its insertion in the tibial tunnel. The authors speculated that the "over-the-top" placement of the autograft in the lateral femoral condyle was not isometric and may have created excess tension of the graft in extension. They also suggested that perhaps the graft was "overtensioned" at the time of the reconstruction. I have extensive experience with this procedure, and I always am careful to avoid overtensioning of the graft. I believe that the area of compromised vascularity was most likely caused by slight instability of the joint due to the combined effects of meniscal loss and changes in the contour of the tibial articular surface that were related to the creation of the tibial tunnel. The necrosis also may reflect either an inadequate notchplasty or regrowth of bone and fibrocartilage at the anterior articular surface of the femur. I noted a small cyclops lesion at the insertion of the graft into the tibial tunnel when we retrieved the graft. To me, this lesion indicates a reaction to compressive mechanical forces on the section of the graft that is most solidly fixed by the roof of the notch during maximal extension.
I would like to thank the family of the patient in this case report for giving me permission to retrieve the specimen for use in research that will contribute to the fund of knowledge in orthopaedics and will help us to improve patient care in the future.
B.S. Delay, B.E. McGrath, and E.R. Mindell reply:
In response to Dr. Olson's letter, it is unclear whether the area of necrosis in the autograft tendon was tissue that had never revascularized or had revascularized and then had become acellular over time. Dr. Olson suggested in his letter that "the area of compromised vascularity was most likely caused by slight instability of the joint due to the combined effects of meniscal loss and changes in the contour of the tibial articular surface that were related to the creation of the tibial tunnel." This suggestion may be correct. It is also possible, as we mentioned, that areas of necrosis may persist indefinitely in the center of a large tendon autograft, just as areas of necrosis persist indefinitely deep within cortical bone autografts.
Dr. Olson stated that the tendon autograft was not "overtensioned" during surgery. We have stated that this was a possible explanation for the region of acellularity. We appreciate Dr. Olson's comments on this possibility.
We wish to emphasize that the small, persistent areas of necrosis deep within the substance of the autograft tendon and autograft bone did not lead to any clinical problems.
Finally, we thank Dr. Olson for providing an autopsy specimen for research that hopefully will improve the fund of knowledge in orthopaedics.