Spinal kinematics and facet load transmission after total disc replacement.

STUDY DESIGN: In vitro human cadaveric biomechanical study. OBJECTIVE: The objectives were to determine the effect of total disc replacement (TDR) on kinematics, especially range of motion (ROM), helical axis of motion (HAM), and facet joint contact force. SUMMARY OF BACKGROUND DATA: Ball-and-socket type artificial discs are designed to mimic normal motion, but the biomechanical effect on kinematics has not been thoroughly clarified. METHODS: Fourteen human cadaveric L4-L5 units were tested before and after TDR. In 7 specimens, facet contact forces were directly measured with thin-film piezoresistive load transducers inserted in the facet joints. In the other 7 specimens, the facet joint capsules were kept intact. Moments (±7.5 Nm) were applied in flexion/extension, lateral bending, and axial rotation motion, with and without an axial compressive preload of 400 N. Three-dimensional motion was recorded, and each angular ROM and HAM were calculated. RESULTS: Without axial compressive preload, the TDR did not produce significant differences in ROMs in all cases. However, under compressive preload, the TDR produced significantly larger ROMs for flexion (4.0° and 8.7°) and lateral bending (2.4° and 5.6°) (intact state and TDR, respectively). The TDR did not alter the HAM significantly except the location in lateral bending without compressive preload and the orientation in flexion/extension against horizontal plane. The location of HAM was slightly shifted caudally by the compressive preload in intact and TDR states. Despite the increased ROMs, the facet contact forces were not significantly altered by the TDR either with or without compressive preload (26 N and 27 N in extension, 41 N and 41 N in lateral bending, 117 N and 126 N in axial rotation). CONCLUSION: TDR using a ball-and-socket type artificial disc significantly increased ROM under axial load and maintained the HAM with similar facet contact forces to the intact state.

Action of fibroblast growth factor-2 on the intervertebral disc.

INTRODUCTION: Fibroblast growth factor 2 (FGF2) is a growth factor that is immediately released after cartilage injury and plays a pivotal role in cartilage homeostasis. In human adult articular cartilage, FGF2 mediates anti-anabolic and potentially catabolic effects via the suppression of proteoglycan (PG) production along with the upregulation of matrix-degrading enzyme activity. The aim of the present study was to determine the biological effects of FGF2 in spine disc cells and to elucidate the complex biochemical pathways utilized by FGF2 in bovine intervertebral disc (IVD) cells in an attempt to further understand the pathophysiologic processes involved in disc degeneration. METHODS: We studied the effect of FGF2 on IVD tissue homeostasis by assessing MMP-13 expression (potent matrix-degrading enzyme), PG accumulation, and PG synthesis in the bovine spine IVD, as well as evaluating whether FGF2 counteracts known anabolic factors such as BMP7. To understand the molecular mechanisms by which FGF2 antagonizes BMP7 activity, we also investigated the signaling pathways utilized by FGF2 in bovine disc tissue. RESULTS: The primary receptor expressed in bovine nucleus pulposus cartilage is FGFR1, and this receptor is upregulated in degenerative human IVD tissue compared with normal IVD tissue. Stimulation of bovine nucleus pulposus cells cultured in monolayer with FGF2 augmented the production of MMP-13 at the transcriptional and translational level in a dose-dependent manner. Stimulation of bovine nucleus pulposus cells cultured in alginate beads for 21 days with FGF2 resulted in a dose-dependent decrease in PG accumulation, due at least in part to the inhibition of PG synthesis. Further studies demonstrate that FGF2 (10 ng/ml) antagonizes BMP7-mediated acceleration of PG production in bovine nucleus pulposus cells via the upregulation of noggin, an inhibitor of the transforming growth factor beta/bone morphogenetic protein signaling pathway. Chemical inhibitor studies showed that FGF2 utilizes the mitogen-activated protein kinase and NF-kappaB pathways to upregulate noggin, serving as one potential mechanism for its anti-anabolic effects. CONCLUSION: FGF2 is anti-anabolic in bovine spine disc cells, revealing the potential of FGF2 antagonists as unique biologic treatments for both prevention and reversal of IVD degeneration.