Abstract
Objectives:
Experimental disruption of the labrum has been shown to compromise its sealing function and alter cartilage lubrication. However, it is not known whether pathological changes to the labrum secondary to femoro-acetabular impingement (FAI) have a similar impact on labral function. This study was performed to determine the effect of natural labral damage secondary to abnormal femoral morphology on the labral seal.
Methods:
Ten intact hip specimens were obtained from male donors (47.8 ± 1.5 yrs) for use in this study. CT reconstructions demonstrated that 6 specimens were of normal morphology, while 4 displayed morphology typical of cam-FAI. Specimens were dissected free of the overlying soft tissue, leaving the capsule and labrum intact. Each specimen was potted and placed in a loading apparatus (0.5 BW). Pressures developed within the central and peripheral compartments were monitored with miniature pressure transducers. The sealing capacity of the labrum was measured by introducing fluid into the central compartment at a constant rate until transport was detected from the central to the peripheral compartment. These measurements were performed in 10 functional positions simulating sequential stages of gait, stooping, and pivoting. During testing, the 3D motion of the femoral head in the acetabulum was measured with motion analysis combined with computer visualization. Peak pressures were compared between specimens with and without labral damage for each of the three activities (p < 0.05).
Results:
Visual observation following testing showed that each specimen with CAM morphology exhibited secondary damage of the labrum and the adjacent chondral surface, while specimens of normal morphology were undamaged. Average peak central compartment pressure was affected by the presence of labral damage secondary to impingement. The specimens with labral damage exhibited reduced peak central compartment pressure during pivot (15.2 ± 2.6 vs. 42.3 ± 7.7 kPa; p = 0.007) when compared to intact specimens. Conversely, no differences in peak pressure were detected between specimens with and without labral damage during simulated gait (21.1 ± 6.0 vs. 22.0 ± 4.2 kPA; p = 0.9) and stooping (8.6 ± 2.4 vs. 7.5 ± 2.6 kPa; p = 0.78).
Conclusions:
The acetabular seal, quantified by intra-articular pressure, was affected by the presence of labral damage secondary to impingement. The reduction in ultimate pressure occurred during pivoting; however, the seal was maintained during gait and stooping. These results are in contrast to previous studies which reported a complete negation of the seal in response to experimentally-created labral disruption. As degeneration is progressive with repetitive impingement, loss of the seal starts to be seen during pivoting and may progress from there, but at this time point (50 years), the seal remains intact during gait and stooping. Our study highlights the importance of using clinically relevant joint injury models to study labral function.
