The pathomechanism of spondylolytic spondylolisthesis in immature primate lumbar spines in vitro and finite element assessments.

STUDY DESIGN: Immature Chacma baboon (Papio ursinus) spine specimens were used to determine load-displacement behavior as related to disc injury. This was accomplished through the application of A-P shear force until failure of FSUs with pars defects. Several finite element models (FEMs) of the FSU were developed to study the mechanism of slippage in immature baboon lumbar spines. OBJECTIVES: The purpose was to show that spondylolisthesis (olisthesis) always occurs through the growth plate using a model similar to immature human lumbar spines. Using FEMs, the roles of facet orientation, pars interarticularis thickness, and a weak growth-plate in producing slippage were examined. SUMMARY OF BACKGROUND DATA: Progression from spondylolysis (lysis) to olisthesis occurs, most often, during the adolescent growth spurt. The biomechanical literature dealing with the slippage mechanism in the immature lumbar spine does not provide a clear understanding and is sparse. METHODS: Several groups of FSUs were subjected to A-P shear force until failure. The results provided displacement at failure as a function of disc injury and flexion-extension fatigue. A bilateral pars defect was created in each specimen prior to application of A-P shear force using an MTS machine. Failure sites were assessed radiographically and histologically. A nonlinear 3-D FEM of the intact L4-L5 was created from CT scans. The model was modified to predict the effects of a pars fracture, a thin pars, a weak growth plate, and facet orientation on the shear load through the growth plate and stresses in the pars. RESULTS: Experimentally, failures always occurred through the growth-plate in the disc intact and disc-incised groups. In the intact FEM, the growth plate carried21% of the applied A-P shear force. The load increased when the facets were more sagittally oriented. The effect of thin pars and/or weaker growth plate was an increase in stresses in the pars. Changes in the load through the growth plate were minimal. CONCLUSIONS: The weakest link in immature baboon lumbar functional spinal units (FSUs) with lysis during an A-P shear load was the growth plate, between the cartilaginous and osseous end plates. Surgeons may assess this lesion on MRI views, thereby predicting the possible development and preventing progression of olisthesis. Finite element model results predict that more sagittally orientated facets and/or a pars fracture are prerequisites for olisthesis to occur.

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

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.

Stability analysis of an enhanced load sharing posterior fixation device and its equivalent conventional device in a calf spine model.

STUDY DESIGN: An in vitro test of calf spine lumbar segments to compare biomechanical stabilization of a rigid versus a dynamic posterior fixation device. OBJECTIVES: To compare flexibility of a dynamic pedicle screw fixation device with an equivalent rigid device. SUMMARY OF BACKGROUND DATA: Dynamic pedicle screw device studies are not as prevalent in the literature as studies of rigid devices. These devices contain the potential to enhance load sharing and optimize fusion potential while maintaining stability similar to that of rigid systems. METHODS: Load-displacement tests were performed on intact and stabilized calf spines for the dynamic and rigid devices. Stability across a destabilized L3-L4 segment was restored by insertion of either a 6 mm x 40 mm dynamic or rigid pedicle screw fixation device across the L2-L4 segment. The screws then were removed, 7 mm x 45 mm pedicle screws of the opposite type were inserted, and the construct then was re-tested. Axial pull-out tests were performed to assess the likely effects of pedicle screw replacement on the load-displacement data. RESULTS: Results indicated a 65% reduction in motion in flexion-extension and a 90% reduction in lateral bending across the destabilized level for both devices, compared with intact spine values. Reduction in axial rotation motion was much smaller than in other modes. Axial pull-out tests showed no weakening of the bone-screw interface. CONCLUSIONS: Both devices provided significant stability of similar magnitudes in flexion, extension, and lateral bending. In axial rotation, the devices only could restore stability to levels similar to those in an intact spine. The dynamic device offers a design that may enhance load sharing without sacrificing construct stability.

Neurocentral synchondrosis fracture in immature spines associated with pedicle screw type fixation devices.

The purpose of this study is to clarify the weak point in immature lumbar vertebrae associated with pedicle screw instrumentation. Ten immature thoracic and lumbar vertebrae were collected from calf spines. After installation of 6- and 7-mm-diameter pedicle screws into the pedicles of each specimen, pullout force was applied to the screw using the uniaxial MTS system until failure. Tightening torque during installation was measured. From the load-displacement curve, failure load was calculated and failure site was confirmed by radiographs. Inner pedicle diameters were measured after the pullout test, and percent fills of the pedicle screw were calculated. Mean tightening torque was 1.4 or 2.1 (Nm), mean failure load was 852.5 or 1,015.0 (N), and mean percent fill was 81.4 or 93.5% for 6- or 7-mm screws, respectively. Tightening torque and percent fill in 7-mm screws were significantly (p < 0.01) greater than that in 6-mm screws; however, failure load showed no significant difference (p = 0.10) between the two screw groups. Failure by screw pullout occurred at the screw-bone interface or through the neurocentral synchondrosis (NS). NS fractures were observed in 20% of 6-mm screws, 60% of 7-mm screws, and 40% overall, whereas interface failures occurred in 80% of 6-mm screws, 40% of 7-mm screws, and 60% overall. In NS fracture group, tightening torque (p < 0.05) and percent fill (p < 0.01) were significantly greater than in the interface failure group. The results led us to conclude that the mechanism of the NS fracture is unclear. However, NS fracture could be one of the conceivable complications associated with pedicle screw fixation in the immature spine.

Uncinate processes and Luschka joints influence the biomechanics of the cervical spine: quantification using a finite element model of the C5-C6 segment.

A fully three-dimensional finite element model of a C5-C6 motion segment of the human spine was developed and validated for the purpose of investigating the biomechanical significance of uncinate processes and Luschka joints. The original intact cervical model was modified to create two additional models. The first simulated the absence of Luschka joints by replacing the fissures with continuous annulus fibrosus and leaving the uncinate processes intact. The second model simulated a surgical resection of the uncinate processes, while leaving the Luschka joints intact. The results of these two models were compared with the intact model, which served as a baseline; thus, the relative contributions of these two structures to cervical motion were established. With use of our model, it was possible, for the first time, to provide quantitative data concerning the source of coupled motions in the lower cervical spine. In principle, the results from this model support the hypothesis of Penning and Wilmink. Our results indicate that the facet joints and Luschka joints are the major contributors to coupled motion in the lower cervical spine and that the uncinate processes effectively reduce motion coupling and primary cervical motion (motion in the same direction as load application), especially in response to axial rotation and lateral bending loads. Luschka joints appear to increase primary cervical motion, showing an effect on cervical motion opposite to that of the uncinate processes. Surgeons should be aware of the increase in motion accompanied by resection of the uncinate processes.