短节段固定融合术治疗退变性腰椎侧凸合并腰椎管狭窄疗效观察

目的探讨短节段固定融合术治疗退变性腰椎侧凸(DLS)合并腰椎管狭窄的手术策略、影像学及临床疗效。方法选择性减压、短节段固定融合术治疗68例DLS合并腰椎管狭窄患者,比较患者术前及末次随访时的Cobb角、腰椎前凸角、冠状面躯干偏移及矢状面躯干偏移。以Oswestry功能障碍指数(ODI)评估患者功能改善情况。结果患者均获得随访,时间36~60个月。Cobb角术前12°~28°(15.9°±4.6°),末次随访3.6°~9.8°(5.2°±3.1°);腰椎前凸角术前1.2°~3.3°(1.9°±2.9°),末次随访-28.1°~4.6°(-23.6°±3.7°);冠状面躯干偏移术前8.2~13.7(10.8±5.2)mm,末次随访2.8~5.6(4.3±1.8)mm;矢状面躯干偏移术前10.2~15.6(12.6±3.7)mm,末次随访3.1~6(4.6±2.2)mm;ODI评分术前25.2~29.8(27.6±2.1)分,末次随访2.1~4.2(3.6±1.3)分。以上各项指标末次随访与术前比较差异均有统计学意义(P0.05)。术后早期并发症发生率为7.3%。末次随访时未发现钉棒松动或断裂等情况。结论对于冠状面Cobb角30°且躯干失平衡较小的DLS合并腰椎管狭窄患者,行选择性减压、短节段固定融合可获得良好的中期临床疗效。     

MicroRNA-491-5p调控基质金属蛋白酶9参与退变性腰椎侧凸的发病机制

BACKGROUND: MicroRNAs are widely involved in the regulation of protein expression, and play a critical role in many physiological and pathological processes in the body. But microRNA expression profile in degenerative lumbar scoliosis is rarely reported and understood. OBJECTIVE: To compare the microRNA expression profile in the normal intervertebral disc and degenerative lumbar scoliosis and to identify degenerative lumbar scoliosis-specific microRNAs, followed by functional validation. METHODS: Total RNA samples were extracted from the nucleus pulposus tissues of 57 patients with degenerative lumbar scoliosis as experimental groups and the normal nucleus pulposus tissues of 42 patients with lumbar fractures as control group. An initial screening of differentially expressed microRNAs in the nucleus pulposus tissues by microRNA microarray was performed in 10 samples from each group. Subsequently, differentially expressed microRNAs were validated using real-time quantitative RCR. The level of differentially expressed microRNAs in the degenerative nucleus pulposus tissues was investigated. Then, the functional analysis of microRNAs in regulating collagen II expression was carried out. Western blot and luciferase reporter assay were also used to detect target genes. RESULTS AND CONCLUSION: We identified 22 microRNAs that were differentially expressed (17 upregulated and 5 downregulated) in degenerative lumbar scoliosis patients compared with the controls. Following real-time quantitative RCR confirmation, miR-491-5p was significantly down-regulated in degenerative nucleus pulposus tissues in comparison with the controls. Moreover, its level was closely correlated with the pathological grading of disc degeneration. Overexpression of miR-491-5p promoted type II collagen expression in nucleus pulposus cells. Bioinformatics target prediction identified matrix metalloproteinase-9 as a putative target of miR-491-5p. Furthermore, luciferase reporter assays demonstrated that miR-491-5p directly targeted matrix metalloproteinase-9 and affected its protein expression in nucleus pulposus cells. These results show that the downregulation of miR-491-5p induces type II collagen loss by directly targeting matrix metalloproteinase-9, thereby resulting in degeneration of the intervertebral disc and degenerative lumbar scoliosis. This study also underscores the potential of miR-491-5p as a novel therapeutic target in degenerative lumbar scoliosis.