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

Study Design. A finite-element model of the craniovertebral junction was de veloped and used to determine whether a biomechanical mechanism, in additio n to inflammatory synovitis, is involved in the progression of rheumatoid a rthritis in this region of the spine. Objectives, To determine specific structure involvement during the progress ion of rheumatoid arthritis and to evaluate these structures in terms of th eir effect on clinically observed erosive changes associated with the disea se by assessing changes in loading patterns and degree of anterior atlantoa xial subluxation. Summary of Background Data. Rheumatoid arthritis involvement of the occipit o-atlantoaxial (C0-C1-C2) complex is commonly seen. However, the biomechani cal contribution to the development and progression of the disease is neith er well understood nor quantified. Although previous cadaver studies have e lucidated information on kinematic motion and fusion techniques, the modeli ng of progressive disease states is not easily accomplished using these met hods. The finite-element method is well suited for studying progressive dis ease states caused by the gradual changes in material properties that can b e modeled. Methods. A ligamentous, nonlinear, sliding-contact, three-dimensional finit e-element model of the C0-C1-C2 complex was generated from 0.5 mm thick ser ial 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%, 7 5%, 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 trans verse ligament-odontoid process junction were monitored. Changes in loading profiles through the C0-C1 and C1-C2 lateral articulations and their assoc iated capsular ligaments were calculated. Anterior and posterior atlantoden tal interval Values were calculated to correlate ligamentous destruction wi th advancement of atlantoaxial subluxation. Results. Model predictions (at 0.3 Nm) fell within one standard deviation o f experimental means, and range of motion data agreed with published in vit ro and in viva values. The model predicted that stresses at the posterior b ase of the odontoid process were greatly reduced with transverse ligament c ompromise beyond 75%. Decreases through the lateral. C0-C1 and C1-C2 articu lations were compensated by their capsular ligaments. Anterior and posterio r atlantodental: Interval values:indicate that the transverse ligament stif fness decreases beyond 75% had the greatest effect on atlantoaxial subluxat ion 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 repor t of a validated, three-dimensional mode! of the C0-C1-C2 complex with appl ication to rheumatoid arthritis.:The data indicate that there may be a mech anical Component (in addition,to enzymatic degradation) associated with the osseous resorption observed during rheumatoid-arthritis; Specifically, ero sion of the odontoid base may involve Wolff's law of unloading consideratio ns. Changes through the lateral aspects of-the atlas suggest that this sa;m e:mechanism may be partially responsible for the erosive changes Seen durin g progressive rheumatoid arthritis. Anterior and posterior:atlantodental in terval values indicate that complete destruction of the transverse ligament coupled with alar and/or capsular ligament compromise is requisite:if adva nced levels inf atlantoaxial subluxation are present.