Li Yue, Zhang Jin, Song Guanyang, Li Xu, Feng Hua
Sports Medicine Service, Beijing Jishuitan Hospital, Beijing, China.
Asia Pac J Sports Med Arthrosc Rehabil Technol. 2016 Jan 21;3:13-18. doi: 10.1016/j.asmart.2015.12.001. eCollection 2016 Jan.
The residual laxity after transtibial posterior cruciate ligament (PCL) reconstruction has been reported by several authors. The sharp angle where the graft exits the tibial tunnel, which is known as "killer turn", is believed to be the main reason. The purpose of this study was to reveal the mechanism of "killer turn" and its effect on both graft and tunnel inlet.
A total of 60 New Zealand white rabbits were included. All transtibial PCL reconstructions were performed using Achilles tendon autograft. The cyclic loading tests were conducted when reconstructed knees were subjected to 1500 cycles of tensile force of 50 N with the angle of pull at 45° to the tibial plateau. The tunnel inlet enlargement, graft elongation, stiffness, graft displacement, load to failure, and failure site were all recorded and analysed.
Fifty-eight New Zealand white rabbits were available for biomechanical evaluation. The subjects had significant graft elongation and tunnel enlargement. The graft displacement increased by a mean of 0.92 ± 0.36 mm (16.70%). At the 1500 cycle, the grafts were significantly elongated by 5.59 ± 4.98%, and the tunnel inlet diameter was also significantly enlarged by 12.08 ± 4.31%. There was a linear correlation between total graft displacement and the two variables (R2 = 0.402, F = 18.515, < 0.001). The coefficient for tunnel inlet enlargement was 0.419 ( = 0.006), and for graft elongation was 0.583 ( = 0.002). At the load-to-failure test, the failure load was 81.19 ± 20.13 N. Of the 58 grafts, 31 (53.45%) failed at the "killer turn", 13 (22.41%) for the para-tunnel fracture, seven (12.07%) for the graft pull-out, and the remaining seven (12.07%) for the rupture at the mounting site.
The mechanism of "killer turn" compromising posterior stability was that the repetitive friction between graft and tunnel inlet not only attenuated the graft, but also enlarged the tunnel inlet, leading to the displacement of the graft.
多位作者报道了经胫骨后交叉韧带（PCL）重建术后的残余松弛情况。移植物穿出胫骨隧道处的锐角，即所谓的“致命转角”，被认为是主要原因。本研究的目的是揭示“致命转角”的机制及其对移植物和隧道入口的影响。
共纳入60只新西兰白兔。所有经胫骨PCL重建均采用自体跟腱移植。当重建膝关节在与胫骨平台呈45°角的拉力下承受1500次50 N的循环加载试验时，记录并分析隧道入口扩大、移植物伸长、刚度、移植物位移、破坏载荷和破坏部位。
58只新西兰白兔可用于生物力学评估。实验对象出现了明显的移植物伸长和隧道扩大。移植物位移平均增加了0.92±0.36 mm（16.70%）。在1500次循环时，移植物显著伸长了5.59±4.98%，隧道入口直径也显著扩大了12.08±4.31%。移植物总位移与这两个变量之间存在线性相关性（R2 = 0.402，F = 18.515，P < 0.001）。隧道入口扩大的系数为0.419（P = 0.006），移植物伸长的系数为0.583（P = 0.002）。在破坏载荷试验中，破坏载荷为81.19±20.13 N。在58个移植物中，31个（53.45%）在“致命转角”处失败，13个（22.41%）发生隧道旁骨折，7个（12.07%）为移植物拔出，其余7个（12.07%）在固定部位断裂。
“致命转角”影响后稳定性的机制是移植物与隧道入口之间的反复摩擦不仅使移植物变弱，还扩大了隧道入口，导致移植物移位。
