EVOLVING CONSIDERATIONS OF HIP CAPSULE MANAGEMENT IN PERIACETABULAR OSTEOTOMY: A CADAVERIC STUDY

Periacetabular osteotomy (PAO) aims to surgically correct hip dysplasia, restoring hip function by optimizing acetabular coverage. However, post-operative restrictions in range of motion (ROM) are being increasingly reported and likely stem from hip joint bony impingement and soft tissue constraints. Recently, the literature implicated the iliofemoral (IFL), ischiofemoral (ISFL), and pubofemoral (PFL) hip capsular ligaments as critical to the joint's structural alignment and positional effect on post-PAO ROM. Changes in acetabular positioning may alter tension forces on capsular ligaments, causing stretching or inappropriate relaxation. The functional impact of staged capsulotomy (capsular release) may improve these deficits and remains unknown. This study aimed to explore the biomechanical relationship of staged IFL capsulotomy following PAO and its influence on hip internal rotation (IR), external rotation (ER), and flexion. Radiographic markers were implanted into the medial and lateral arms of the IFL in six cadaveric hip joints. ROM and joint stability were assessed in maximum flexion and external/internal rotation (ER) of 90° until firm endpoints were discovered. Each hip underwent PAO, with preservation of capsular ligaments, and was retested. Following PAO, stepwise anterior capsulotomy of the IFL was performed preserving zona orbicularis and labrum. ROM was reassessed, and marker displacement analyzed with serial radiographs. Joint stability was verified via hip translation, distraction, and dislocation. Paired sample t-tests compared ROM in experimental settings (CI = 95%). Capsular tightening from PAO significantly restricted IR, independent of bony corrections. We observed a 12° decrease in IR at 90° of hip flexion after PAO (P = 0.0039), with non-significant decreases in ER and flexion (P > 0.05). T-capsulotomy restored IR (P = 0.0341) without significant losses in ER or hip flexion; rather, these non-significantly increased (P > 0.05). Full capsulectomy increased IR (20° +/− 3.2°, P = 0.0028), ER (50° +/− 3.2°, P = 0.0031), and flexion (111.25° +/− 8.3°, P = 0.006), but compromised stability. Examining radiographic markers, PAO positioned the hip center inferomedially, tensioning the posterior capsule and impairing IR. After PAO, markers displaced superolaterally with minimal anteroinferior movement, suggesting pulling forces from a taut ISFL. T-capsulotomy of the IFL alleviated this tension, indirectly restoring normal conformations to the ISFL and PFL, explaining increased ROM, not explained by iliofemoral contributions alone. In conclusion, post-PAO mobility deficits appear to be linked to soft tissue (capsular twist from acetabular reorientation) and bony constraints (femoroacetabular impingement, spherical defects of the femoral head, and acetabular over coverage and version). An unopened capsule after PAO can lead to overtightening, loss of functional ROM, and stiffness, culminating in impaired patient outcomes. Increased ROM may be beneficial if joint stability is not sacrificed. Therefore, if the post-operative hip has well-balanced anteversion on the femoral and acetabular side, and is well positioned to optimize coverage, the hip capsule can be left open after capsulotomy or loosely closed without risking iatrogenic instability. The hip capsule may act as a soft tissue constraint and barrier to mobility post-PAO and can be opened to free the hip capsular ligaments of iatrogenic tensioning.