Biomechanical rationale for the pathology of rheumatoid arthritis in the craniovertebral junction

Abstract

Study design: A finite-element model of the craniovertebral junction was developed and used to determine whether a biomechanical mechanism, in addition to inflammatory synovitis, is involved in the progression of rheumatoid arthritis in this region of the spine.

Objectives: To determine specific structure involvement during the progression of rheumatoid arthritis and to evaluate these structures in terms of their effect on clinically observed erosive changes associated with the disease by assessing changes in loading patterns and degree of anterior atlantoaxial subluxation.

Summary of background data: Rheumatoid arthritis involvement of the occipito-atlantoaxial (C0-C1-C2) complex is commonly seen. However, the biomechanical contribution to the development and progression of the disease is neither well understood nor quantified. Although previous cadaver studies have elucidated information on kinematic motion and fusion techniques, the modeling of progressive disease states is not easily accomplished using these methods. The finite-element method is well suited for studying progressive disease states caused by the gradual changes in material properties that can be modeled.

Methods: A ligamentous, nonlinear, sliding-contact, three-dimensional finite-element model of the C0-C1-C2 complex was generated from 0.5 mm thick serial computed tomography scans. Validation of the model was accomplished by comparing baseline kinematic predictions with experimental data. Transverse, alar, and capsular ligament stiffness were reduced sequentially by 50%, 75%, and 100% (removal) of their intact values. All models were subjected to flexion moments replicating the clinical diagnosis of rheumatoid arthritis using full flexion lateral plane radiographs. Stress profiles at the transverse ligament-odontoid process junction were monitored. Changes in loading profiles through the C0-C1 and C1-C2 lateral articulations and their associated capsular ligaments were calculated. Anterior and posterior atlantodental interval values were calculated to correlate ligamentous destruction with advancement of atlantoaxial subluxation.

Results: Model predictions (at 0.3 Nm) fell within one standard deviation of experimental means, and range of motion data agreed with published in vitro and in vivo values. The model predicted that stresses at the posterior base of the odontoid process were greatly reduced with transverse ligament compromise beyond 75%. Decreases through the lateral C0-C1 and C1-C2 articulations were compensated by their capsular ligaments. Anterior and posterior atlantodental interval values indicate that the transverse ligament stiffness decreases beyond 75% had the greatest effect on atlantoaxial subluxation during the early stages of the disease (no alar and capsular ligament damage). Subsequent involvement of the alar and capsular ligaments produced advanced atlantoaxial subluxation, for which surgical intervention may be warranted.

Conclusions: To the best of the authors' knowledge, this is the first report of a validated, three-dimensional model of the C0-C1-C2 complex with application to rheumatoid arthritis. The data indicate that there may be a mechanical component (in addition to enzymatic degradation) associated with the osseous resorption observed during rheumatoid arthritis. Specifically, erosion of the odontoid base may involve Wolff's law of unloading considerations. Changes through the lateral aspects of the atlas suggest that this same mechanism may be partially responsible for the erosive changes seen during progressive rheumatoid arthritis. Anterior and posterior atlantodental interval values indicate that complete destruction of the transverse ligament coupled with alar and/or capsular ligament compromise is requisite if advanced levels of atlantoaxial subluxation are present.