Ma Jianjun, Shen Jian, Smith Beth Paterson, Ritting Andrew, Smith Thomas L, Koman L Andrew
Department of Orthopaedic Surgery, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
J Bone Joint Surg Am. 2007 Oct;89(10):2241-9. doi: 10.2106/JBJS.D.03054.
Tendon-repair techniques have evolved to increase the construct strength of the repair site in order to permit early active range of motion without tendon gap or rupture. The present study evaluated the hypothesis that the injection of botulinum neurotoxin type-A (BoNT-A) into the gastrocnemius muscle will reduce the active force production of that muscle below the force required to rupture the associated, repaired Achilles tendon.
Seventy-nine rat Achilles tendons were surgically bisected and were repaired with use of a two-strand core suture with a running epitenon repair. After the repair, the animals were treated with unilateral intramuscular (gastrocnemius) injections of either BoNT-A (6 U/kg body weight) (thirty-seven rats) or saline solution (forty-two rats). Operatively treated ankles were fixed in the neutral position with a percutaneous pin for the first two days after surgery. Unrestricted ankle motion and weight-bearing were allowed after the second postoperative day. An assessment of gap formation or rupture at the repair site, electrophysiologic measurements of force applied to the tendon, and an assessment of the strength of the repaired tendon were performed.
Intramuscular BoNT-A injections produced a significant, reversible reduction in active muscle force (p < 0.007). Twitch and tetanus contractions decreased to approximately 25% of the values for the control side within one week, remained at <50% of the values for the control side at one month, and returned to normal levels by six months. The tetanic force capability of the muscles that had been injected with BoNT-A was fivefold to tenfold less than the force required to rupture the associated Achilles tendon for as long as four weeks after tendon repair. The spontaneous Achilles tendon rupture rate of repaired tendons in the BoNT-A group was three times lower than that in the saline solution group at one week, and the tendon rupture force was significantly higher in the BoNT-A group between one and three weeks after repair (p < 0.007). There was no significant difference in tendon rupture force between the two groups after three weeks.
Intramuscular gastrocnemius BoNT-A injections were associated with a significant reduction in force-generating potential, such that the muscle was incapable of actively producing enough force to rupture the repaired Achilles tendon in this rat model of tendon repair.
肌腱修复技术不断发展,旨在增强修复部位的结构强度,以便在不出现肌腱间隙或断裂的情况下实现早期主动活动范围。本研究评估了以下假设:向腓肠肌注射A型肉毒杆菌神经毒素(BoNT-A)会使该肌肉的主动力产生降低至低于相关修复的跟腱断裂所需的力。
79条大鼠跟腱被手术切断,采用双股核心缝线加连续腱周修复进行修复。修复后,动物接受单侧肌肉内(腓肠肌)注射BoNT-A(6 U/kg体重)(37只大鼠)或生理盐水(42只大鼠)。术后前两天,手术治疗的踝关节用经皮钢针固定于中立位。术后第二天后允许踝关节自由活动和负重。对修复部位的间隙形成或断裂进行评估,对施加于肌腱的力进行电生理测量,并对修复肌腱的强度进行评估。
肌肉内注射BoNT-A使主动肌肉力量显著且可逆地降低(p < 0.007)。单收缩和强直收缩在一周内降至对照侧值的约25%,在一个月时仍低于对照侧值的50%,并在六个月时恢复至正常水平。在肌腱修复后的长达四周内,注射BoNT-A的肌肉的强直力能力比相关跟腱断裂所需的力小五至十倍。在一周时,BoNT-A组修复肌腱的自发性跟腱断裂率比生理盐水组低三倍,并且在修复后一至三周内,BoNT-A组的肌腱断裂力显著更高(p < 0.007)。三周后两组之间的肌腱断裂力无显著差异。
在该大鼠肌腱修复模型中,肌肉内注射腓肠肌BoNT-A与产生力量的潜力显著降低相关,以至于该肌肉无法主动产生足够的力来使修复的跟腱断裂。