SOFT-TISSUE IMPINGEMENT IN DUAL MOBILITY COMPONENTS: A PROPOSED MECHANISM OF INTRAPROSTHETIC DISLOCATION USING CADAVER MODELS AND RETRIEVALS

Introduction The large diameter mobile polyethylene liner of the dual mobility implant provides increased resistance to hip dislocation. However, a problem specific to the dual mobility system is intra-prosthetic dislocation (IPD), secondary to loss of the retentive rim, causing the inner head to dissociate from the polyethylene liner. We hypothesized that impingement of the polyethylene liner with the surrounding soft-tissue inhibits liner motion, thereby facilitating load transfer from the femoral neck to the liner and leading to loss of retentive rim over time. This mechanism of soft-tissue impingement with the liner was evaluated via cadaver experiments, and retrievals were used to assess polyethylene rim damage. Methods Total hip arthroplasty was performed on 10 cadaver hips using 3D printed dual mobility components. A metal wire was sutured to the posterior surface (underside) of the iliopsoas, and metal wires were embedded into grooves on the outer surface of the liner and inner head to identify these structures under fluoroscopy. Tension was applied to the iliopsoas to move the femur from maximum hyperextension to 90° of flexion for the purpose of visualizing the iliopsoas and capsule interaction with the mobile liner. The interaction of the mobile liner with the iliopsoas was studied using fluoroscopy and direct visual observation. Fifteen retrieved dual mobility liners were assessed for rim edge and rim chamfer damage. Rim edge damage was defined as any evidence of contact, and rim chamfer damage was classified into six categories: impact ribs on the chamfer surface, loss of machining marks, scratching or pitting, rim deformation causing a raised lip, a rounded rim edge, or embedded metal debris. Results Manipulation of the cadaver specimens through full range of motion showed liner impingement with the iliopsoas tendon in low flexion angles, which impeded liner motion. At high flexion angles (beyond 30°), the iliopsoas tendon moved away from the liner and impingement was not observed. The fluoroscopy tests using the embedded metal wires confirmed what was observed during manual manipulation of the specimen. When observing the hip during maximum hyperextension, 0°, 15°, and 30° of flexion, there was obvious tenting of the iliopsoas. All retrieved components showed damage on the rim and the chamfer surface. The most common damage seen was scratching/ pitting. There was no association between presence of damage and time in vivo controlling for age and Body Mass Index (p≥0.255). Discussion The cadaver studies showed that the mobile liner motion could be impeded by impingement with the iliopsoas tendon and hip capsule. Visual and fluoroscopic observation showed impingement of iliopsoas and hip capsule with the distal portion of the mobile liner, particularly during low flexion angles. All retrieved liners showed damage despite their limited time in vivo and despite being retrieved for reasons other than IPD. This suggests that soft-tissue impingement may inhibit liner motion routinely in vivo , resulting in load transfer from the femoral neck on to the rim of the liner. This may be an important mechanism for IPD.