While hip arthroscopy utilization continues to increase, capsular management remains a controversial topic. Therefore the purpose of this research was to investigate the biomechanical effect of capsulotomy and capsular repair techniques on hip joint kinematics in varying combinations of sagittal and coronal joint positions. Eight fresh-frozen hemipelvises (4 left, 6 male) were dissected of all overlying soft tissue, with the exception of the hip joint capsule. The femur was potted and attached to a load cell, while the pelvis was secured to a custom-designed fixture allowing static alteration of the flexion/extension arc. Optotrak markers were rigidly attached to the femur and pelvis to track motion of the femoral head with respect to the acetabulum. Following specimen preparation, seven conditions were tested: i) intact, ii) after portal placement (anterolateral and mid-anterior), iii) interportal capsulotomy (IPC) [35 mm in length], iv) IPC repair, v)T-capsulotomy [15 mm longitudinal incision], vi) partial T-repair (vertical limb), vii) full T-repair. All conditions were tested in 15° of extension (−15˚), 0°, 30°, 60° and 90° of flexion. Additionally, all flexion angles were tested in neutral, as well as maximum abduction and adduction, resulting in 15 testing positions. 3Nm internal and external rotation moments were manually applied to the femur via the load cell at each position. Rotational range of motion and joint kinematics were recorded. IPC and T-capsulotomies increased rotational ROM and mediolateral (ML) joint translation in several different joint configurations, most notably from 0–30˚ in neutral abduction/adduction. Complete capsular repair restored near native joint kinematics, with no significant differences between any complete capsular repair groups and the intact state, regardless of joint position. An unrepaired IPC resulted in increased rotational ROM, but no other adverse translational kinematics. However, an unrepaired or partially repaired T-capsulotomy resulted in increased rotational ROM and ML translation. The results of this study show that complete capsular repair following interportal or T-capsulotomy adequately restores rotational ROM and joint translation to near intact levels. Where feasible, complete capsular closure should be performed, especially following T-capsulotomy. However, further clinical evaluation is required to determine if adverse kinematics of an unrepaired capsule are associated with patient reported outcomes.
Previous studies have identified the anterolateral complex (ALC) as having an important role in controlling anterolateral rotatory laxity following anterior cruciate ligament injury and subsequent reconstruction. In particular, injury to the iliotibial band (ITB) and its component deep (dITB) and capsulo-osseous (coITB) layers, have been shown to significantly correlate with different grades of the pivot-shift test in patients with acute ACL injuries. However, the kinematic properties of the capsulo-osseous layer of the ITB, throughout knee range of motion, are not fully understood. The purpose of this study was to quantify the kinematic behaviour of the capsulo-osseous layer of the ITB through various degrees of knee flexion. Ten fresh-frozen cadaveric knee specimens were dissected to expose the capsulo-osseous layer of the iliotibial band. Radiopaque beads were embedded, at standardized increments (12.5%, 25%, 50% and 75% of total length from proximal to distal), into the tissue and fluoroscopic images were taken from 0o to 105o of knee flexion in 15° increments. The positions of the beads were identified in each image and the length, width, and area changes of the capsulo-osseous layer were calculated. Comparisons of the total length of the anterior and posterior borders of the coITB through knee ROM were conducted using a two-way (8 knee angles by 2 borders) repeated measures analysis of variance (rm-ANOVA), whereas the effect of knee angle on isometry and total area changes was assessed using one-way rm-ANOVAs (α=0.05) There was a significant increase in the length of the anterior capsulo-osseous layer at flexion angles greater than 15o and on the posterior border at angles greater than 75 o with changes occurring primarily at 12.5 % of the total length. In addition, at all flexion angles the length changes were significantly larger in the anterior border compared to the posterior border. Meanwhile, non-homogenous decreases in width and area were found with increasing flexion angle. The distance between the capsulo-osseous layer insertion on the distal femur and proximal tibia significantly increased from 60o-105o, maximal changes occurred at 105o (9.64 [4.12] %, p = 0.003). The primary finding of this study was that the coITB behaved in a non-isometric fashion, with significant increases in length occurring at flexion angles greater than 15o. Moreover, these changes in length were non-homogenous across the different regions of the coITB that were investigated, with the greatest changes occurring in the proximal segments (0–25%). The data presented here suggest that coITB in flexion angles from 0o to 105o behaves in a non-isometric fashion, with the majority of its length change occurring in its proximal segment. Further quantification of the pathway that the coITB takes with respect to osseous landmarks may result in improvements in ALC procedures as an augmentation to ACL reconstruction, thereby potentially improving rotational stability and clinical outcomes.
Ligament reconstruction following knee soft tissue injuries, such as posterior cruciate ligament (PCL) tears, aim to restore normal joint function and motion; however, persistant pathomechanical joint behavior indicates that there is room for improvement in current reconstruction techniques. Increased attention is being directed towards the roles of secondary knee stabilizers, in an attempt to better understand their contributions to kinematics of knees. The objective of this study is to characterize the relative biomechanical contributions of the posterior oblique ligament (POL) and the deep medial collateral ligament (dMCL) in PCL-deficient knees. We hypothesized that, compared with the POL, the dMCL would have a more substantial role in stabilizing the medial side of the knee, especially in flexion (slack POL). Seven fresh-frozen cadaveric knees were used in this study (age 40–62, 4 female, 3). Specimens were potted and mounted onto a VIVO joint motion simulator (AMTI). Once installed, specimens were flexed from 0 to 90 degrees with a 10 N axial load and all remaining degrees of freedom unconstrained. This was repeated with (a) a 67 N posterior load, (b) a 2.5 Nm internal or external rotational moment and (c) a 50 N posterior load and 2.5 Nm internal rotational moment applied to the tibia. During each resulting knee motion, the relative AP kinematics of the dMCL tibial insertion (approximated as the most medial point of the proximal tibia) with respect to the flexion axis of the femur (the geometric center axis, based on the posterior femoral condyles) were calculated at 0, 30, 60 and 90 degrees of flexion. These motions were repeated following dissection of the PCL and then further dissection of either medial ligament (4 POL, 3 dMCL). The changes in AP kinematics due to ligament dissection were analyzed using three-way repeated-measures ANOVA with a significance value of 0.05.Introduction
Methods
Injury to the anterolateral ligament (ALL) has been reported to contribute to high-grade anterolateral laxity following anterior cruciate ligament (ACL) injury. Failure to address ALL injury has been suggested as a cause of persistent rotational laxity following ACL reconstruction. However, lateral meniscus posterior root (LMPR) tears have also has been shown to cause increased internal rotation and anterior translation of the knee. Due to the anatomic relationship of the ALL and the lateral meniscus, we hypothesise that the ALL and lateral meniscus work synergistically, and that a tear to the LMPR will have the same effect on anterolateral laxity as an ALL tear in the ACL deficient knee. Sixteen fresh frozen cadaveric knee specimens were potted into a hip simulator(femur) and a six degree-of-freedom load cell (tibia). Two rigid optical trackers were inserted into the proximal femur and distal tibia, allowing for the motion of the tibia with respect to the femur to be tracked during biomechanical tests. A series of points on the femur and tibia were digitised to create bone coordinate systems that were used to calculate the kinematic variables. Biomechanical testing involved applying a 5Nm internal rotation moment to the tibia while the knee was in full extension and tested sequentially in the following three conditions: i) ACLintact; ii) Partial ACL injury (ACLam) – anteromedial bundle sectioned; iii) Full ACL injury (ACLfull). The specimens were then randomised to either have the ALL sectioned first (ALLsec) followed by the LMPRsec or vice versa. Internal rotation and anterior translation of the tibia with respect to the femur were calculated. A mixed two-way (serial sectioning by ALL section order) repeated measures ANOVA (alpha = 0.05). Compared to the ACLintact condition, internal rotation was found to be 1.78° (p=0.06), 3.74° (p=0.001), and 3.84° (p=0.001) greater following ACLfull, LMPRsec and ALLsec respectively. LMPRsec and the ALLsec resulted in approximately 20 of additional internal rotation (p=0.004 and p=0.01, respectively) compared with the ACL deficient knee (ACLfull). No difference was observed between the ALL and LMPR sectioned states, or whether the ALL was sectioned before or after the LMPR (p=0.160). A trend of increasing anterior translation was observed when the 5Nm internal rotation moment was applied up until the ACL was fully sectioned; however, these differences were not significant (p=0.070). The ALL and LMPR seem to have a synergistic relationship in aiding the ACL in controlling anterolateral rotational laxity. High-grade anterolateral laxity following ACL injury may be attributed to injuries of the ALL and/or the LMPR. We suggest that the lateral meniscus should be thought of as part of the anterolateral capsulomeniscal complex (i.e., LM, ITB, and ALL) that acts as a stabiliser of anterolateral rotation in conjunction with the ACL.