OBJECTIVE
Prior studies have provided conflicting evidence regarding the contribution of key ligamentous structures to atlantoaxial (AA) joint stability. Many of these studies employed cadaveric techniques that are hampered by the inherent difficulties of testing isolated-injury scenarios. Analysis with validated finite element (FE) models can overcome some of these limitations. In a previous study, the authors completed an FE analysis of 5 subject-specific craniocervical junction (CCJ) models to investigate the biomechanics of the occipitoatlantal joint and identify the ligamentous structures essential for its stability. Here, the authors use these same CCJ FE models to investigate the biomechanics of the AA joint and to identify the ligamentous structures essential for its stability.
METHODS
Five validated CCJ FE models were used to simulate isolated- and combined ligamentous–injury scenarios of the transverse ligament (TL), tectorial membrane (TM), alar ligament (AL), occipitoatlantal capsular ligament, and AA capsular ligament (AACL). All models were tested with rotational moments (flexion-extension, axial rotation, and lateral bending) and anterior translational loads (C2 constrained with anterior load applied to the occiput) to simulate physiological loading and to assess changes in the atlantodental interval (ADI), a key radiographic indicator of instability.
RESULTS
Isolated AACL injury significantly increased range of motion (ROM) under rotational moment at the AA joint for flexion, lateral bending, and axial rotation, which increased by means of 28.0% ± 10.2%, 43.2% ± 15.4%, and 159.1% ± 35.1%, respectively (p ≤ 0.05 for all). TL removal simulated under translational loads resulted in a significant increase in displacement at the AA joint by 89.3% ± 36.6% (p < 0.001), increasing the ADI from 2.7 mm to 4.5 mm. An AACL injury combined with an injury to any other ligament resulted in significant increases in ROM at the AA joint, except when combined with injuries to both the TM and the ALs. Similarly, injury to the TL combined with injury to any other CCJ ligament resulted in a significant increase in displacement at the AA joint (significantly increasing ADI) under translational loads.
CONCLUSIONS
Using FE modeling techniques, the authors showed a significant reliance of isolated- and combined ligamentous–injury scenarios on the AACLs and TL to restrain motion at the AA joint. Isolated injuries to other structures alone, including the AL and TM, did not result in significant increases in either AA joint ROM or anterior displacement.
