Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture.

The purpose of this study is to investigate cellular responses and histological changes of cartilaginous layers in human anterior cruciate ligament (ACL) tibial insertions after rupture compared with those in normal insertions. Fully 16 tibial insertions of ruptured ACLs were obtained during primary ACL reconstructions. We also obtained 16 normal ACL tibial insertions from cadavers. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) to detect apoptosis, proliferating cell nuclear antigen (PCNA) staining, and histological examination were performed. The percentage of TUNEL-positive chondrocytes in ruptured ACL insertions (30.2 +/- 15.6%) was higher than that in normal insertions (9.6 +/- 5.8%). The percentage of PCNA-positive chondrocytes was significantly different between ruptured ACL insertions (19.9 +/- 15.0%) and normal insertions (12.3 +/- 7.3%). The average thickness of the cartilage layer, the glycosaminoglycan-stained area, and the number of chondrocytes per millimeter in ruptured ACL insertions was smaller than those in normal insertions. The decrease in the number of chondrocytes owing to an imbalance between cell death and cell proliferation in the ACL insertions after rupture, as compared with normal insertions, may lead to histological changes of the cartilage layer in the insertions. An in-depth understanding of injured ACL insertion may help elucidate the etiology of histological changes and the function and significance of the existence of the cartilage layer of insertion. This understanding may help in developing optimal treatment protocols for ACL injuries if apoptosis and cell proliferation are controlled.