OBJECTIVE: To explore the mechanism of the "killer turn", which is reported to be a reason for postoperative residual laxity after transtibial posterior cruciate ligament (PCL) reconstruction, in a low bone mineral density (BMD) condition. METHODS: A total of 80 skeletally mature female New Zealand white rabbits were included for biomechanical evaluation after transtibial PCL reconstructions. The subjects were equally divided into low BMD (n = 40) and control groups (n = 40). Rabbits in the low BMD group were treated with surgery and drug injection to establish an osteoporotic model. Rabbits in the control group received sham surgeries and no injection. All assignments were conducted randomly according to random numbers generated by a computer. All grafts were then subjected to biomechanical testing with an MTS model-858 Mini Bionix servohydraulic materials testing machine (MTS Systems, Minneapolis, Minnesota, USA). The experimental outcomes were the increment of total graft displacement, tunnel inlet enlargement, graft elongation, stiffness and failure load of the two groups, and the comparison between them. RESULTS: Among the 80 subjects, 1 subject of the low BMD group failed at the 30th cycle by proximal tibial fracture and 1 subject of the control group failed at the 20th cycle for the same reason. As a result, 39 subjects of the low BMD group and 39 subjects of the control group survived the cyclic loading test. Compared with the control group, the low BMD group demonstrated significantly larger total graft displacement ( P = 0.006) and tunnel inlet enlargement ( P = 0.041) than the control group. The number of subjects with less than 10% enlargement was significantly greater (57.1%) in the control group than in the low BMD group ( P = 0.004). In the load-to-failure test, 26 (66.7%) subjects in the low BMD group failed by proximal tibial fracture (around the tunnel), 6 (15.4%) at the mounting site, 5 (12.8%) at the fixation site, and only 2 (5.1%) failed at the "killer turn." In the control group, 20 (51.3%) failed at the "killer turn," 9 (23.1%) at the proximal tibia (around the tunnel), 5 (12.8%) at the mounting site, and 5 (12.8%) at the fixation site. There were significantly fewer failures (10.0%) at the "killer turn" ( P = 0.000) and 155.6% more for the para-tunnel fracture ( P = 0.000) in the low BMD group compared with the control group. CONCLUSIONS: The low BMD group demonstrated an inferior biomechanical outcome to the control group with the transtibial technique. With low BMD, the "killer turn" effect compromises the posterior tibial cortex by enlarging the tunnel inlet.
OBJECTIVE: To explore the mechanism of the "killer turn", which is reported to be a reason for postoperative residual laxity after transtibial posterior cruciate ligament (PCL) reconstruction, in a low bone mineral density (BMD) condition. METHODS: A total of 80 skeletally mature female New Zealand white rabbits were included for biomechanical evaluation after transtibial PCL reconstructions. The subjects were equally divided into low BMD (n = 40) and control groups (n = 40). Rabbits in the low BMD group were treated with surgery and drug injection to establish an osteoporotic model. Rabbits in the control group received sham surgeries and no injection. All assignments were conducted randomly according to random numbers generated by a computer. All grafts were then subjected to biomechanical testing with an MTS model-858 Mini Bionix servohydraulic materials testing machine (MTS Systems, Minneapolis, Minnesota, USA). The experimental outcomes were the increment of total graft displacement, tunnel inlet enlargement, graft elongation, stiffness and failure load of the two groups, and the comparison between them. RESULTS: Among the 80 subjects, 1 subject of the low BMD group failed at the 30th cycle by proximal tibial fracture and 1 subject of the control group failed at the 20th cycle for the same reason. As a result, 39 subjects of the low BMD group and 39 subjects of the control group survived the cyclic loading test. Compared with the control group, the low BMD group demonstrated significantly larger total graft displacement ( P = 0.006) and tunnel inlet enlargement ( P = 0.041) than the control group. The number of subjects with less than 10% enlargement was significantly greater (57.1%) in the control group than in the low BMD group ( P = 0.004). In the load-to-failure test, 26 (66.7%) subjects in the low BMD group failed by proximal tibial fracture (around the tunnel), 6 (15.4%) at the mounting site, 5 (12.8%) at the fixation site, and only 2 (5.1%) failed at the "killer turn." In the control group, 20 (51.3%) failed at the "killer turn," 9 (23.1%) at the proximal tibia (around the tunnel), 5 (12.8%) at the mounting site, and 5 (12.8%) at the fixation site. There were significantly fewer failures (10.0%) at the "killer turn" ( P = 0.000) and 155.6% more for the para-tunnel fracture ( P = 0.000) in the low BMD group compared with the control group. CONCLUSIONS: The low BMD group demonstrated an inferior biomechanical outcome to the control group with the transtibial technique. With low BMD, the "killer turn" effect compromises the posterior tibial cortex by enlarging the tunnel inlet.