Rinchen Phuntsok, Benjamin J. Ellis, Michael R. Herron, Chase W. Provost, Andrew T. Dailey and Douglas L. Brockmeyer
There is contradictory evidence regarding the relative contribution of the key stabilizing ligaments of the occipitoatlantal (OA) joint. Cadaveric studies are limited by the nature and the number of injury scenarios that can be tested to identify OA stabilizing ligaments. Finite element (FE) analysis can overcome these limitations and provide valuable data in this area. The authors completed an FE analysis of 5 subject-specific craniocervical junction (CCJ) models to investigate the biomechanics of the OA joint and identify the ligamentous structures essential for stability.
Isolated and combined injury scenarios were simulated under physiological loads for 5 validated CCJ FE models to assess the relative role of key ligamentous structures on OA joint stability. Each model was tested in flexion-extension, axial rotation, and lateral bending in various injury scenarios. Isolated ligamentous injury scenarios consisted of either decreasing the stiffness of the OA capsular ligaments (OACLs) or completely removing the transverse ligament (TL), tectorial membrane (TM), or alar ligaments (ALs). Combination scenarios were also evaluated.
An isolated OACL injury resulted in the largest percentage increase in all ranges of motion (ROMs) at the OA joint compared with the other isolated injuries. Flexion, extension, lateral bending, and axial rotation significantly increased by 12.4% ± 7.4%, 11.1% ± 10.3%, 83.6% ± 14.4%, and 81.9% ± 9.4%, respectively (p ≤ 0.05 for all). Among combination injuries, OACL+TM+TL injury resulted in the most consistent significant increases in ROM for both the OA joint and the CCJ during all loading scenarios. OACL+AL injury caused the most significant percentage increase for OA joint axial rotation.
These results demonstrate that the OACLs are the key stabilizing ligamentous structures of the OA joint. Injury of these primary stabilizing ligaments is necessary to cause OA instability. Isolated injuries of TL, TM, or AL are unlikely to result in appreciable instability at the OA joint.
Rinchen Phuntsok, Chase W. Provost, Andrew T. Dailey, Douglas L. Brockmeyer and Benjamin J. Ellis
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.
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.
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.
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.