Ma Yong, Zhang Xin, Wang Jian, Liu Ping, Zhao Liheng, Zhou Chunyan, Ao Yingfang
Institute of Sports Medicine, Peking University Third Hospital, Hai Dian District, Beijing, China.
Am J Sports Med. 2009 Mar;37(3):599-609. doi: 10.1177/0363546508325960. Epub 2008 Dec 4.
The posterior cruciate ligament heals to some extent after injury. However, results after conservative treatment may diminish with long-term follow-up. Bone morphogenetic protein-12 can induce formation of ligament tissues.
Bone morphogenetic protein-12 gene transfer can improve the histologic and biomechanical properties of healing posterior cruciate ligaments.
Controlled laboratory study.
Bilateral posterior cruciate ligaments of 32 rabbits were injured. The cut ends in 1 limb received an injection containing 3 x 10(7) pfu recombinant bone morphogenetic protein-12 adenovirus, and the posterior cruciate ligament in the contralateral limb served as an untreated control. Eight rabbits were sacrificed at each time point of 3, 6, 12, and 26 weeks after the operation. In addition, 6 rabbits receiving a sham operation were used to obtain normal control data. The posterior cruciate ligament specimens were evaluated biomechanically and histologically.
The repair tissue of the treatment group at 26 weeks was similar to the normal posterior cruciate ligament in collagen arrangement, collagen formation, and mechanical properties. At weeks 6, 12, and 26, the ultimate load, stiffness, and energy absorbed at failure of the treatment group were significantly greater than those of the untreated group.
Adenovirus-mediated bone morphogenetic protein-12 gene transfer in a partial posterior cruciate ligament laceration rabbit model resulted in an obvious improvement of histologic properties, tensile strength, and stiffness of the repaired ligaments, indicating improved posterior cruciate ligament healing.
Bone morphogenetic protein-12 gene transfer is a potential future strategy to improve the repair of injured posterior cruciate ligaments.
后交叉韧带损伤后可在一定程度上愈合。然而,保守治疗的效果在长期随访后可能会减弱。骨形态发生蛋白-12可诱导韧带组织形成。
骨形态发生蛋白-12基因转移可改善后交叉韧带愈合的组织学和生物力学特性。
对照实验室研究。
对32只兔的双侧后交叉韧带进行损伤。一侧肢体的断端注射含3×10⁷ 个噬斑形成单位重组骨形态发生蛋白-12腺病毒,对侧肢体的后交叉韧带作为未处理对照。术后3、6、12和26周的每个时间点处死8只兔。此外,6只接受假手术的兔用于获取正常对照数据。对后交叉韧带标本进行生物力学和组织学评估。
治疗组26周时的修复组织在胶原排列、胶原形成和力学性能方面与正常后交叉韧带相似。在6周、12周和26周时,治疗组的极限负荷、刚度和失效时吸收的能量显著高于未处理组。
在部分后交叉韧带撕裂兔模型中,腺病毒介导的骨形态发生蛋白-12基因转移导致修复韧带的组织学特性、拉伸强度和刚度明显改善,表明后交叉韧带愈合得到改善。
骨形态发生蛋白-12基因转移是未来改善损伤后交叉韧带修复的一种潜在策略。