There is a major controversy whether spinal trauma with vertebral endplate fractures can result in posttraumatic disc degeneration. Intervertebral discs, which are adjacent to burst endplates, are frequently removed and an intercorporal spondylodesis is performed. In any case, the biological effects within the discs following endplate factures are poorly elucidated to date. The aim of our investigations was therefore to establish a novel disc/endplate trauma culture model to reproducibly induce endplate fractures and investigate concurrent disc changes in vitro. This model is based on a full-organ disc/endplate culture system, which has been validated by the authors before. Intervertebral disc/endplate specimens were isolated from Burgundy rabbits and cultured in standard media (DMEM/ F12, 10%FCS). Burst endplate fractures were induced in half of the specimens with a custom-made fracture device and subsequently cultured for 9 days. The biological effects such as necrotic or apoptotic cell death and the expression of pro-apoptotic genes and other genes involved in organ degeneration, e.g. matrix metalloproteinases (MMPs) were analyzed. Cell damage was assessed by quantification of the lactate dehydrogenase (LDH) activity in the supernatant. The expression of genes involved in the cellular apoptotic pathway (caspase 3) and the pro-apoptotic proteins FasL and TNF-a were monitored. The results demonstrate that LDH levels increased significantly post trauma compared to the control and remained elevated for 3 days. Furthermore, a constant up-regulation of the caspase 3 gene in both disc compartments was present. The pro-apoptotic proteins FasL and TNF-a were up regulated predominantly in the nucleus whereas the MMP-1 and -13 transcripts (collagenases) were increased in both disc structures. From this study we can conclude that endplate burst fractures result in both necrotic and apoptotic cell death in nucleus and annulus tissue. Moreover, FasL and TNF-a expression by nucleus cells may lead to continued apoptosis induced by Fas-and TNF-a receptor bearing cells. In addition TNF-a over-expression has potentially deleterious effects on disc metabolism such as overexpression of matrix proteinases. Taken together, the short term biological response of the disc following endplate fracture exhibits characteristics, which may initiate the degeneration of the organ.
It is concluded that all implants achieved osseointegration with similar degrees of BIC and BVD; however, titanium implants showed a higher resistance to removal torque, probably due to higher surface roughness.
The goal of non-fusion stabilization is to reduce the mobility of the spine segment to less than that of the intact spine specimen, while retaining some residual motion. Several in vitro studies have been conducted on a dynamic system currently available for clinical use (Dynesys). Under pure moment loading, a dependency of the biomechanical performance on spacer length has been demonstrated; this variability in implant properties is removed with a modular concept incorporating a discrete flexible element. An in vitro study was performed to compare the kinematic and stabilizing properties of a modular dynamic lumbar stabilization system with those of Dynesys, under the influence of an axial preload. Six human cadaver spine specimens (L1-S1) were tested in a spine loading apparatus. Flexibility measurements were performed by applying pure bending moments of 8 Nm, about each of the three principal anatomical axes, with a simultaneously applied axial preload of 400 N. Specimens were tested intact, and following creation of a defect at L3-L4, with the Dynesys implant, with the modular implant and, after removal of the hardware, the injury state. Segmental range of motion (ROM) was reduced for flexion-extension and lateral bending with both implants. Motion in flexion was reduced to less than 20% of the intact level, in extension to approximately 40% and in lateral bending a motion reduction to less than 40% was measured. In torsion, the total ROM was not significantly different from that of the intact level. The expectations for a flexible posterior stabilizing implant are not fulfilled. The assumption that a device which is particularly compliant in bending allows substantial intersegmental motion cannot be fully supported when one considers that such devices are placed at a location far removed from the natural rotation center of the intervertebral joint.
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