Does Capsular Laxity Lead to Microinstability of the Native Hip?

BACKGROUND: Hip "microinstability" is commonly cited as the cause of symptoms that occur in the presence of translation of the femoral head away from conformity with the acetabular fossa. However, there is still no consistent objective criteria defining its presence and biomechanical basis. One hypothesis is that abnormal motion of the articular surfaces occurs because of capsular laxity, ultimately leading to clinical symptoms.
PURPOSE: To determine the relationship between capsular laxity and abnormal rotation and translation of the hip. STUDY
DESIGN: Controlled laboratory study.
METHODS: Eight cadaveric hips were dissected down to the capsule and mounted in a customized multiaxial hip activity simulator. Each specimen was loaded with 5 N·m of internal and external rotational torque in full extension and 0°, 30°, 60°, and 90° of flexion. During testing, the relative position and rotation of the femur and the pelvis were monitored in real time with a 6-camera motion analysis system. The testing was repeated after capsular laxity was generated by placing a regular array of incisions ("pie crusting") in the iliofemoral, pubofemoral, and ischiofemoral ligaments. Joint rotation and femoral head translation were calculated with specimen-specific models. A hip microinstability index was defined as the ratio between the length of the locus of the femoral head center and the radius of the femoral head during rotation from extension to 90° of flexion.
RESULTS: In intact hips, the components of femoral head translation were within 0.5 mm in positions close to neutral (<30° of flexion). Capsular modification led to significant increases in internal and external rotation ( P < .01) and in the translation of the femoral head center at different positions ( P < .05). Compared with intact hips, the femoral head was inferiorly displaced during external rotation and anteroinferiorly during internal rotation. The length of the locus of the femoral head center increased from 3.61 ± 1.30 mm to 5.35 ± 1.83 mm for external rotation ( P < .05) and from 6.24 ± 1.48 mm to 8.21 ± 1.42 mm for internal rotation ( P < .01). The correlations between rotational laxity and the total translation of the femoral head were not significant, with coefficients of 0.093 and 0.006 in external and internal rotation, respectively. In addition, the hip microinstability index increased from 0.40 ± 0.08 for intact hips to 0.55 ± 0.09 for modified hips ( P < .01).
CONCLUSION: The native hip approximates a concentric ball-and-socket joint within 30° of flexion; however, beyond 30° of flexion, the femoral head translation reached as high as 4 mm. Capsular laxity leads to microinstability of the hip, as indicated by significantly increased joint rotations and femoral head translations and an abnormal movement path of the femoral head center. However, there was no correlation between rotational laxity and the increase in femoral head translation. CLINICAL RELEVANCE: Capsular laxity alters normal kinematics (joint rotation and femoral head translation) of the hip, potentially leading to abnormal femoral-acetabular contact and joint degeneration.