The mechanism of "killer turn" causing residual laxity after transtibial posterior cruciate ligament reconstruction.
The mechanism of "killer turn" causing residual laxity after transtibial posterior cruciate ligament reconstruction.
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DOI：
10.1016/j.asmart.2015.12.001
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发表时间：
2016-01
期刊：
影响因子：
--
通讯作者：
Feng H
中科院分区：
文献类型：
--
作者：
Li Y;Zhang J;Song G;Li X;Feng H
经胫后交叉韧带（PCL）重建后的残余松弛已被几位作者报道。移植物离开胫骨隧道的尖角，被称为“致命转弯”，被认为是主要原因。本研究的目的是揭示“杀手转弯”的机制及其对移植物和隧道入口的影响。实验共选取60只新西兰大白兔。所有经胫骨PCL重建均采用自体跟腱体外移植。重建膝关节在胫骨平台45°的拉力作用下，承受50 N的拉力1500次循环加载试验。记录并分析了隧道进水口扩大、接枝伸长率、刚度、接枝位移、破坏荷载及破坏部位。采用58只新西兰大白兔进行生物力学评价。受试者有明显的移植物伸长和隧道扩大。移植物位移平均增加0.92±0.36 mm（16.70%）。在第1500次循环时，移植物明显延长了5.59±4.98%，隧道入口直径也明显增大了12.08±4.31%。移植物总位移与两个变量呈线性相关（R2 = 0.402, F = 18.515, p < 0.001）。隧道入口增大系数为0.419 (p = 0.006)，接枝伸长系数为0.583 （p = 0.002）。加载-破坏载荷为81.19±20.13 n。在58个移植物中，31个（53.45%）在“致命转弯”处失败，13个（22.41%）在隧道旁断裂，7个（12.07%）在移植物拔出处破裂，其余7个（12.07%）在安装处破裂。“致命转弯”损害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减弱，而且使隧道入口扩大，导致移植物位移。
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 in vitro 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 1500th 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, p < 0.001). The coefficient for tunnel inlet enlargement was 0.419 (p = 0.006), and for graft elongation was 0.583 (p = 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.