Abstract
PurposeAn anterior cruciate ligament (ACL) injury is often combined with injury to the lateral extra-articular structures, which may cause a combined anterior and rotational laxity. It was hypothesised that addition of a ‘monoloop’ lateral extra-articular tenodesis (mLET) to an ACL reconstruction would restore anteroposterior, internal rotation and pivot-shift laxities better than isolated ACL reconstruction in combined injuries.MethodTwelve cadaveric knees were tested, using an optical tracking system to record the kinematics through 0°–100° of knee flexion with no load, anterior and posterior translational forces (90 N), internal and external rotational torques (5 Nm), and a combination of an anterior translational (90 N) plus internal rotational load (5 Nm). They were tested intact, after sectioning the ACL, sectioning anterolateral ligament (ALL), iliotibial band (ITB) graft harvest, releasing deep ITB fibres, hamstrings tendon ACL reconstruction, mLET combined with ACL reconstruction, and isolated mLET. Two-way repeated-measures ANOVA compared laxity data across knee states and flexion angles. When differences were found, paired t tests with Bonferroni correction were performed.ResultsIn the ACL-deficient knee, cutting the ALL significantly increased anterior laxity only at 20°–30°, and only significantly increased internal rotation at 50°. Additional deep ITB release significantly increased anterior laxity at 40°–90° and caused a large increase of internal rotation at 20°–100°. Isolated ACL reconstruction restored anterior drawer, but significant differences remained in internal rotation at 30°–100°. After adding an mLET there were no remaining differences with anterior translation or internal rotation compared to the intact knee. With the combined injury, isolated mLET allowed abnormal anterior translation and rotation to persist.ConclusionsCutting the deep fibres of the ITB caused large increases in tibial internal rotation laxity across the range of knee flexion, while cutting the ALL alone did not. With ACL deficiency combined with anterolateral deficiency, ACL reconstruction alone was insufficient to restore native knee rotational laxity. However, combining a ‘monoloop’ lateral extra-articular tenodesis with ACL reconstruction did restore native knee laxity.
Highlights
Anterior cruciate ligament (ACL) injury causes a ‘pivotshift’ instability, which is a combination of increased anterior translation and internal rotation of the tibia [4, 26]
The effect of ACL, anterolateral ligament and iliotibial band (ITB) sectioning on tibial anterior translation laxity
Cutting the ACL significantly increased anterior translation laxity by a mean of 4–7 mm compared to the intact knee at all flexion angles (p < 0.01 from 0° to 90°, p = 0.013 at 100°). (Fig. 4, Table 1)
Summary
Anterior cruciate ligament (ACL) injury causes a ‘pivotshift’ instability, which is a combination of increased anterior translation and internal rotation of the tibia [4, 26]. Among ACL-injured knees there is a range of the amount of rotational instability, which is believed to be caused by additional injury to the anterolateral soft tissue structures [27, 37, 38]. This view is supported by radiological findings of the Segond fracture and concomitant injury to the anterolateral soft tissues at the time of injury [14, 24, 41]. Focus has been on the anterolateral ligament for controlling rotational laxity [27] It is not well understood how this compares to the superficial and deep fibres of the ITB, which are important structures regarding the control of rotational laxity [21, 39, 42]. A recent robotic sectioning study found that sectioning the Kaplan fibres had a greater impact on rotational laxity when compared with ALL sectioning [11]
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