Hip Contact Force Magnitude and Regional Loading Patterns Are Altered in Those with Femoroacetabular Impingement Syndrome.

ABSTRACT

PURPOSE: The magnitude and location of hip contact force influence the local mechanical environment of the articular tissue, driving remodeling. We used a neuromusculoskeletal model to investigate hip contact force magnitudes and their regional loading patterns on the articular surfaces in those with femoroacetabular impingement (FAI) syndrome and controls during walking. METHODS: An EMG-assisted neuromusculoskeletal model was used to estimate hip contact forces in eligible participants with FAI syndrome ( n = 41) and controls ( n = 24), walking at self-selected speed. Hip contact forces were used to determine the average and spread of regional loading for femoral and acetabular articular surfaces. Hip contact force magnitude and region of loading were compared between groups using statistical parametric mapping and independent t -tests, respectively ( P < 0.05). RESULTS: All of the following findings are reported compared with controls. Those with FAI syndrome walked with lower-magnitude hip contact forces (mean difference, -0.7 N·BW -1 ; P < 0.001) during first and second halves of stance, and with lower anteroposterior, vertical, and mediolateral contact force vector components. Participants with FAI syndrome also had less between-participant variation in average regional loading, which was located more anteriorly (3.8°, P = 0.035) and laterally (2.2°, P = 0.01) on the acetabulum but more posteriorly (-4.8°, P = 0.01) on the femoral head. Participants with FAI syndrome had a smaller spread of regional loading across both the acetabulum (-1.9 mm, P = 0.049) and femoral head (1 mm, P < 0.001) during stance. CONCLUSIONS: Compared with controls, participants with FAI syndrome walked with lower-magnitude hip contact forces that were constrained to smaller regions on the acetabulum and femoral head. Differences in regional loading patterns might contribute to the mechanobiological processes driving cartilage maladaptation in those with FAI syndrome.