The purpose of this retrospective clinical series was to evaluate the benefits and complications of plate fixation for open-door laminoplasty in cervical spondylotic myelopathy with multilevel spinal stenosis compared with open-door laminoplasty without fixation. Forty-nine patients underwent open-door laminoplasty for cervical myelopathy with multilevel spinal stenosis with at least 13 months of follow-up. A plate was used as the sole method of fixation between the lateral mass and lamina with 3 screws. Computed tomography scans obtained pre- and postoperatively were assessed for plate complications and spinal canal enlargement. Pre- and postoperative neurological condition was assessed by the Japanese Orthopedic Association (JOA) myelopathy score. Overall cervical spine range of motion (ROM) was measured in full flexion and extension radiographs pre- and postoperatively. No restenosis due to door reclosure was noted, and no plates failed. No screws were backed out or broken. Almost all patients showed neurological improvement. The JOA score increased by 3.9±0.7 points in the suture group and 4.3±0.8 points in the plate group (P>.05). The postoperative increase in mean anteroposterior diameter of the spinal canal from C3 to C7 was 4.5±0.6 mm in the suture group and 5.1±0.5 mm in the plate group. The greater mean anteroposterior diameter increase in the plate group was statistically significant (P<.01). The mean cervical ROM decreased in the plate and suture groups postoperatively (P<.001). No significant difference was found in mean cervical ROM reduction between the groups (P>.05). No difference in axial symptoms was found between the 2 groups.
Intervertebral disc (IVD) degeneration is a strong etiological factor in chronic lower back pain. Stem cell migration toward the site of IVD degeneration for regeneration is restricted by avascularity and distance. Our previous study indicated that the expression of stromal cell‑derived factor‑1 (SDF‑1) and its receptor, C-X-C chemokine receptor type 4 (CXCR4) was upregulated in degenerated cartilage endplate (CEP) and nucleus pulposus (NP). In the present study, SDF‑1 increased CXCR4 mRNA and protein expression in human endplate chondrocytes in a dose‑dependent manner. The results of reverse transcription-quantitative polymerase chain reaction, western blotting and zymography indicated that SDF‑1 increased matrix metalloproteinase (MMP)‑1, ‑3 and ‑13 mRNA and protein expression in human endplate chondrocytes in a dose‑dependent manner. The results of zymography suggested that SDF‑1 also increased MMP‑2 and ‑9 protein expression in a dose‑dependent manner. The CXCR4‑specific chemical inhibitor AMD3100 significantly decreased the levels of MMP‑1, ‑2, ‑3, ‑9 and ‑13 expression. In a human cartilage explant culture model, SDF‑1 accelerated the degradation of extracellular matrix (ECM), and AMD3100 decreased cartilage cleavage. However, in a rat tail disc degeneration model, the injection of SDF‑1 into the NP resulted in the retention of dense areas of proteoglycan matrix and enhanced NP regeneration. These results suggest that SDF‑1, as an inflammatory cytokine, induces MMP expression in human endplate chondrocytes and that ECM remodeling in the CEP may be a favorable factor of endogenous stem cell homing into the NP for regeneration in vivo.
Selective segmental TLIF is helpful in correcting lumbar lordosis, segmental deformity, and translation, and thus obtaining satisfactory outcome in the treatment of degenerative lumbar scoliosis.
Objective: To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design: We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate nick-end labelling (TUNEL) and immunostaining for caspase-3, Bcl-2 and Bax. Methods: Experiments were conducted in male Sprague-Dawley rats (n=78) weighing 300~400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day 1 or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site (7.5 mm away from the lesion). Results: The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day 1, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 (Bcl-2)-associated X-protein (Bax), but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion: Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.
Duraplasty after decompression decreases the lesion size and scar formation, promoting better functional recovery, but the underlying mechanism has not been clarified. Here, we fabricated a series of poly(hydroxybutyrate‐co‐hydroxyvalerate)/polylactic acid/collagen (PHBV/PLA/Col) membranes and cultured them with VSC4.1 motor neurons. The material characteristics and in vitro biological characteristics were evaluated. In the subcutaneous implantation test, PHBV/PLA/COl scaffolds supported the cellular infiltration, microvasculature formation, and decreased CD86‐positive macrophage aggregation. Following contusion spinal cord injury at T10 in Sprague‐Dawley rats, durotomy was performed with allograft dura mater or PHBV/PLA or PHBV/PLA/Col membranes. At 3 days post‐injury, Western blot assay showed decreased the expression of the NLRP3, ASC, cleaved‐caspase‐1, IL‐1β, TNF‐α, and CD86 expression but increased the expression of CD206. Immunofluorescence demonstrated that duraplasty with PHBV/PLA/Col membranes reduced the infiltration of CD86‐positive macrophages in the lesion site, decreased the glial fibrillary acidic protein expression, and increased the expression of NF‐200. Moreover, duraplasty with PHBV/PLA/Col membranes improved locomotor functional recovery at 8 weeks post‐injury. Thus, duraplasty with PHBV/PLA/Col membranes decreased the glial scar formation and promoted axon growth by inhibiting inflammasome activation and modulating macrophage polarization in acute spinal cord injury.
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