退变性腰椎侧凸病因和发展因素分析及手术治疗策略
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摘要
1.TNF-α基因单核苷酸多态性及血清水平与退变性腰椎侧凸的相关性研究
目的：探讨肿瘤坏死因子-α基因单核苷酸多态性和血清中TNF-α水平与退变性腰椎侧凸的相关性,为临床分析退变性腰椎侧凸的病因及预防提供依据。
方法：选取2009年12月至2011年12月于河北医科大学第三医院脊柱外科门诊及病房收治的40例退变性腰椎侧凸患者作为研究对象,均行腰椎正侧位X线及腰椎MRI检查,选取同时期于该院进行健康体检者40例作为正常对照组,两组研究对象在性别、年龄、体重指数与病例组相匹配。收集两组患者的外周新鲜血液,用小量全血基因组DNA快速提取试剂盒提取DNA,应用聚合酶链反应(PCR)技术对两组研究对象DNA标本TNF-α基因启动子区特异性片段进行扩增,再应用限制性内切酶长度多态性(RFLP)技术对扩增的特异性片段用Ncol进行酶切,产物用2%琼脂糖凝胶电泳的方法进行检测,分析其基因型及等位基因频率的分布。用酶联免疫吸附测定技术(ELISA),对两组研究对象血清TNF-a蛋白水平进行检测。利用Adobe Photoshop6.0软件,测量病例组MRI图像中顶椎间盘及其上下椎间盘内髓核与脑脊液T2加权像的相对信号强度,同时测量病例组正位X线片上的Cobb角。应用SPSS17.0统计软件对数据进行统计分析,性别、体重指数、血清TNF-α含量比较采用t检验或方差分析。年龄、基因型及等位基因频率等计数资料比较采用χ2或Fisher精确概率法检验,血清TNF-α含量与椎间盘退变程度及Cobb角相关分析采用Linear correlate分析。
结果：两组研究对象的年龄、性别、体重指数比较差异无统计学意义(P>0.05)。TNF-a-308所在片段经PCR扩增后目的片段的长度为107bp,酶切后有3种基因型,G/G基因型(87bp、20bp2条带),G/A基因型(107bp、87bp、20bp3条带),A/A基因型(107bp1条带)。两组研究对象各基因型频率分布符合Hardy-Weinberg遗传平衡定律,研究对象具有代表性。TNF-a308多态性位点G/G、G/A和A/A基因型频率在病例组分别为70.0%、22.5%和7.5%,对照组为77.5%、17.5%和5.0%,两组基因型频率差异无统计学意义(P>0.05)。G/G基因型频率与非G/G基因型频率(G/A、A/A)及等位基因G、A频率在病例组为分别为70.0%、30.0%和81.3%、18.7%,对照组为77.5%、22.5%和86.2%、13.8%,两组比较差异均无统计学意义(P>0.05)。细胞因子TNF-α清浓度,病例组172.15±33.51ng/L,对照组53.75±3.84ng/L,两组之间差异有统计学意义(P<0.05),且病例组显著高于对照组。TNF-α血清浓度与髓核相对信号强度呈负相关,与Cobb's角呈正相关。将病例组根据椎间盘退变等级分组,各组之间差异有统计学意义(P<0.05)。
结论：退变性腰椎侧凸患者血清中TNF-α浓度比正常人群血清水平明显增高,血清中TNF-α浓度与侧凸角呈正相关,与退变性腰椎侧凸椎间盘髓核信号强度呈负相关,血清TNF-α浓度越高,椎间盘退变程度越重,TNF-a是退变性腰椎侧凸发生发展的危险因素。TNF-α-308多态性与退变性腰椎侧凸无明显相关。
2.退变性腰椎侧凸椎体终板MRI T1和T2信号改变及相关因素分析
目的：在腰椎退变性疾病中,椎体终板信号改变(vertebral endplate signal changes, vESC)在MRI T1和T2加权像上较为常见,在一定程度上是椎体终板损伤、炎症及退变在影像学上的表现形式。本研究通过观察退变性腰椎侧凸患者的椎体终板信号改变及分布情况,探讨其相关影响因素。
方法：回顾分析2005年3月～2010年3月经我院诊治的120例原发性退变性腰椎侧凸患者的影像学资料做为病例组,选取同时期、同年龄段及同性别比诊断为腰椎退变性疾病并除外腰椎侧凸的89例患者的影像学资料做为对照组,所有患者均行腰椎X线及MRI检查。观察两组中vESC的发生率、类型(Modic分型)及分布特点；分析vESC与椎间盘退变、腰椎侧凸角、体重指数及吸烟等因素的关系。
结果：病例组中120例患者的1440个终板中,71例(59.2%)124(17.2%)个终板存在vESC;对照组中89例患者的1068个终板中,21例(23.6%)49(4.6%)个终板存在vESC;两组的发生率比较有显著性差异(P<0.01)。病例组中,终板凹侧的vESC发生率(12.1%)与凸侧(1.5%)和双侧(3.6%)比较均有显著性差异(P<0.01),以L2/3、L4/5和L5/S1节段多发,且与主弯和代偿弯顶椎的好发节段相一致；对照组中,终板双侧的vESC发生率(2.9%)与左侧(0.7%)和右侧(1.0%)比较均有显著性差异(P<0.01),且主要发生在L4/5和L5/S1节段。按Modic分型,病例组中以Modic II型多见,而对照中以Modic I型更常见。相对危险度分析显示,椎间盘退变、腰椎侧凸、体重及吸烟是vESC的危险因素。经Multinomial Logistic逐步回归分析得出回归方程：logitY=-0.82+1.27D+0.55S+1.77D*S(Y为终板退变,D为椎间盘退变,S为腰椎侧凸角,D*S为椎间盘退变与腰椎侧凸角的交互作用)。
结论：退变性腰椎侧凸椎体终板信号改变发生率较高,多发生于靠近顶椎区域的L2/3、L4/5和L5/S1节段的凹侧,呈不对称分布,以Modic Ⅱ型多见；终板退变与椎间盘退变、腰椎侧凸及二者的交互作用呈正相关,超重和吸烟是危险因素。
3.后路有限减压、固定、融合治疗退变性腰椎侧凸合并椎管狭窄症
目的：成人退行性腰椎侧凸的患者同时合并腰椎管狭窄症的发生率很高,这种情况多因腰椎不稳引起椎间盘变性突出、小关节骨质增生以及关节囊肥大、黄韧带增生钙化等而导致椎间孔及椎管有效空间减小,压迫神经出现根性疼痛或间歇性跛行。本文通过探讨采用后路有限减压、固定、融合手术治疗退变性腰椎侧凸合并椎管狭窄症的疗效,为退变性腰椎侧凸合并椎管狭窄症的合理治疗提供理论依据。
方法：2001年1月至2008年1月我科收治退变性腰椎侧凸合并椎管狭窄症患者36例,男2例,女34例；年龄51-76岁,平均62.3±9.4岁；病程10个月-7年,平均37个月。所有患者术前均行X线、CT及MR检查,5例患者行脊髓造影。术前Cobb角为24.0°±10.2°,腰椎前凸角22.6°±11.2°。铅垂线(C7PL)与S1椎体后上缘距离(SVA)(7.8±6.6)cm,C7PL与骶正中线距离(CSVL)(6.9±5.8)cm。根据查体及影像学资料确定手术节段,采用后路有限减压、固定、融合进行手术治疗。术后随访采用VAS、SF-36评分系统评估神经功能恢复及症状改善情况。Cobb角、腰椎前凸角的变化评估矫形效果。
结果：所有患者均获得随访,随访时间1.2-4年,平均2.4年。患者术后、末次随访平均Cobb角(10.6±8.5)°、(8.9°±5.3)。,腰椎前凸角(25.6±14.3)°、(31.8±13.4)。,SVA(0.5±3.4)cm、(-1.2±2.7)cm,CSVL(2.9±1.4)cm.(1.7±1.2)cm,较术前均具有显著性差异。术后仅1例患者发生矫正丢失,无一例发生椎间隙塌陷、神经损伤、钉棒断裂等并发症。
结论：后路有限减压、固定、融合手术在减压的基础上最大程度的保留了脊柱的骨性结构,维持了术后脊柱的稳定性,是治疗退变性腰椎侧凸合并椎管狭窄症的有效手段。
4.退变性腰椎侧凸椎间盘退变程度以及骨密度与侧凸角度的关联性研究
目的：退变性腰椎侧凸的确切病因不明,一般认为可能与骨质疏松、椎间盘退变等因素有关。退变性腰椎侧凸和骨质疏松症这两种疾病的发病人群基本一致,其中老年、女性患者的发病率比较高,但是两者是否存在相关性一直存在争议。本文旨在探讨退变性腰椎侧凸患者椎间盘的不对称指数、腰椎间盘退变程度以及骨密度降低对侧凸角度的影响。
方法：采用回顾性研究的方法,选取2001年1月至2010年8月,共96例退变性腰椎侧凸患者为研究对象(侧凸组)；2001年1月至2010年8月确诊为腰椎管狭窄症并且资料齐全的患者96例为对照组；两组间性别、年龄、体质量指数匹配。侧凸组：在腰椎正位x线片上测量凸凹侧顶椎间盘及其上下椎间盘的高度和顶椎及其上下椎体的高度,利用Adobe Photoshop6.0软件,测量MRI图像T2WI顶椎及其上下椎间盘内髓核与脑脊液的相对信号强度。对照组：取L2-3,L3-4,L4-5这3个椎间盘为研究对象测定上述指标。应用双能x线吸收法测定两组患者腰椎(L2-4)及股骨颈、股骨粗隆和Ward's三角的T值。
结果：侧凸组凸侧椎间盘高度和为(40±7)mm高于凹侧的(28±7)mm(P<0.01),凸侧椎体高度和为(76±12)mm高于凹侧的(72±10)mm(P=0.016)；两组之间的椎间盘退变程度差异有统计学差异(P=0.003)；两组之间骨密度T值的平均值和骨质疏松的发生率差异有统计学意义(均P<0.01)。通过多元线性回归分析结果显示患者椎间盘的不对称指数、椎间盘的退变程度、骨密度T值影响退变性腰椎侧凸角度.
结论：退变性腰椎侧凸常伴有凸凹两侧椎间盘高度以及椎体高度不对称。侧凸角度与椎间盘的不对称指数、椎间盘的退变程度呈正相关,与骨密度值T值呈负相关。
1.Correlation between the gene single-nucleotide polymorphism and serum concentration of tumor necrosis factor-alpha and degenerative lumbar scoliosis
Objective:This study aims to investigate the correlation between tumor necrosis factor-alpha(TNF-α) gene single-nucleotide polymorphism and serum concentrations levels in degenerative lumbar scoliosis, which explore etiology of degenerative lumbar scoliosis from genetic and molecular level and provide the basis for analyzing the etiology and prevention of degenerative lumbar scoliosis.
Methods:40patients with degenerative lumbar scoliosis were selected as patient group, they were out-patient or in the wards of the Third Hospital of He Bei Medical University from December2009to December2011, the DLS group were all undertaken lumbar spine X-ray and MRI.40cases of healthy persons were selected as normal control. The two groups matched with gender, age, body mass index. Fresh peripheral blood of the two groups were collected. DNA was extracted by the small amount of whole blood Genomic DNA extraction reagent kit, specific fragments in TNF-a gene promoter region were amplified by polymerase chain reaction (PCR) technology, and then the amplified specific fragments were digested using Ncol by restriction fragment length polymorphism (RFLP) technology, finally the products were detected with a2%agarose gel electrophoresis and cases'genotype and allele frequency distribution were analyzed. Serum TNF-a levels were determined by Enzyme-linked immunosorbent assay technique (ELISA). Using Adobe Photoshop6.0software, in DLS group the relative signal intensity of apical vertebra and the upper and lower vertebral disc's nucleus pulposus and cerebrospinal fluid in T2-weighted MRI images were measured. Cobb angles were measured on the antero-posterior lumbar spine X-ray films. All the data were analyzed by Statistic Package for Social Science (SPSS)17.0. Gender, body mass index and serum TNF-a levels were compared using the t-test or analysis of variance. The count data, such as age, genotype and allele frequency were compared using the χ2or Fisher exact test. Correlation between serum TNF-αa levels and vertebral disc'degeneration and correlation between serum TNF-α levels and Cobb angles were made by Linear Correlation Analysis.
Results:The comparison of the two groups'age, gender distribution and body mass index did not show statistical difference, The amplification TNF-a-308fragments was107bp by polymerase chain reaction and there were three genotypes after digested by incision enzyme, including G/G genotype, G/A genotype, A/A genotype. On the electropherogram G/G genotype had two bright bars(87bp,20bp), G/A genotype had three bright bars(107bp,87bp,20bp), and A/A genotype had one bright bars(107bp). Three genotypes frequencies of the two groups are in accordance with Hardy-Weinberg equilibrium. In DLS group, the frequencies of GIG genotype, G/A genotype and A/A genotype were70.0%、22.5%and7.5%, in the control group the frequencies of the three genotypes were77.5%、17.5%and5.0%. The three genotypes frequencies of the two groups are of no significant differences. In DLS group the frequencies of G/G genotype and non-G/G (G/A、A/A) genotype and the frequencies of allele G and A were70.0%、30.0%and81.3%、18.7%, in the control group were77.5%,22.5%and86.2%、13.8%. The comparison of two groups are of no significant difference. Cytokine TNF-a serum concentration in DLS group was172.15±33.51ng/L and in control group was53.75±3.84ng/L, The concentration of DLS group was significantly higher than that of control group, and there was significant difference, and the patient group was significantly higher. Serum TNF-a concentration has a negative correlation with the RSI and a positive correlation with the Cobb angle. According to the disc degeneration grade, DLS group was divided, there were significant differences between different groups.
Conclusion:Serum TNF-α concentration in degenerative lumbar scoliosis patients were significantly increased. Serum TNF-a concentration has a negative correlation with the RSI and a positive correlation with the Cobb angle. The higher serum TNF-a concentration is, the more severe disc degeneration occur. TNF-a may play an important role in the degeneration of degenerative lumbar scoliosis.TNF-a-308polymorphism was of no significant correlation with degenerative lumbar scoliosis.
2.Vertebral endplate signal changes on MRI T1and T2in degenerative lumbar scoliosis and its associated factors analysis
Objective:Vertebral endplate signal changes (vESC) is common in degenerative lumbar disease, it is the characteristic of injury of endplate and degeneration of lumbar endplate, we do the work to investigate the vertebral endplate signal changes on MRI and explore its associated factors in degenerative lumbar scoliosis(DLS).
Methods:The image data of120patients who were diagnosed primary DLS in our hospital from march2005to march2011were retrospectively reviewed as the case group. The image data of89patients who were diagnosed degenerative lumbar diseases(DLD) without scoliosis were selected as the control group. The prevalence, type and distribution of vESC in two groups was observed and compared. Intervertebral disc degeneration, lumbar scoliosis Cobb's angle, body mass index(BMI) and status of smoking et al were recorded in DLS, and the relationship of vESC with these influential factors was analyzed.
Results:Of1440endplate from120patients in case group,247(17.2%) from71(59.2%) patients were found to have vESC. Contrasting to the control group, of1068endplate from89patients,49(4.5%) from21(23.6%) patients were found to have vESC. The prevalence of vESC in two groups had a significantly statistical difference (P<0.01). Modic type II was more common in case group but Modic type I was more common in control group. The prevalence of vESC on concave side(12.1%) was significantly different with on convex(1.5%) and both sides(3.6%) in case group(P<0.01), While in control group, the prevalence of vESC on both sides(2.9%) was significantly significantly different with on right(1.0%) or left sides(0.7%, P<0.01). vESC were more common at L4/5and L5/S1in control group, but in case group, vESC mainly occured at L2/3, L4/5and L5/S1which were accordance with the common levels of apex vertebrae. Intervertebral disc degeneration, lumbar scoliosis, overweight and heavy smoking were considered as risk factors to vESC. By Multinomial Logistic Regression analysis with these factors, the regression function was obtained:log Y=-0.82+1.27D+0.55S+1.77D*S (Y for endplate degeneration, D for intervertebral disc degeneration, S for scoliosis Cobb's angle and D*S for interaction of disc degeneration and scoliosis Cobb's angle).
Conclusion:vESC positively correlate with intervertebral disc degeneration, scoliosis Cobb's angle and their interaction in DLS. its prevalence is relatively higher, most of them are type II and mostly locate on the concave side of L2/3, L4/5and L5/S1. Overweight and heavy smoking are probably its risk factors.
3.Limited decompression, fixation,and fusion for degenerative scoliosis with vertebral stenosis
Objective:Patients with degenerative lumbar scoliosis always suffered from vertebral stenosis, this may be induced by the lumbar disc herniation,atrophy of articular process or calcification of yellow ligaments. Patients always complained of leg pain, which is caused by the compression of the nerve root or spinal cord. We do the work to evaluated the efficiency of limited decompression, fixation, and fusion for degenerative scoliosis with vertebral stenosis.
Method:From January,2001to January2008,36patients with degenerative scoliosis with vertebral stenosis were treated in our hospital. There were2males and34females. The age was from51to76years with an average of62.3years. X-ray, CT, MR examination were performed preoperatively for all the cases,5cases underwent myelography. Preoperative Cobb angle, focal lordosis, the distance between C7plumb line (C7PL) and upper edge of S1vertebral body(SVA), and the distance between C7PL and center sacral vertical line (CSVL) were24.0°±10.2°,22.6°±11.2°,(7.8±6.6)cm and (6.9±5.8)cm respectively. Limited decompression, pedicle screw internal fixation and fusion were carried out for patients, VAS and SF-36scored system were used to evaluate surgery effects.
Result:The mean follow-up period was2.4years (range,1.2-4years) and no patients were lost during follow-up. The mean surgery time was130min (range,115-164min) with an average bleeding amount of625ml (range,450-870ml). compared to pre-operation, Cobb angle (10.6°±8.5°,8.9°±5.3°), focal lordosis (25.6°±14.3°,31.8°±13.4°), SVA [(0.5±3.4) m,-1.2±2.7) cm] and CSVL [(2.9±1.4)cm,(1.7±1.2)cm] were significantly improved at post-operation and final follow-up through statistics of SPSS13.0software. Loss of correction happened in one case. No collapse of the disc height occurred, neither did never root injures nor fracture of the fixation system.
Conclusion:Limited decompression, pedicle screw fixation are testified efficient for degenerative scoliosis with vertebral stenosis, individualized surgery design should be made according to clinical symptoms, signs and imaging features to expect a satisfactory result.
4.1ntervertebral disc degeneration and bone density in degenerative lumbar scoliosis:a comparative study between patients with degenerative lumbar scoliosis and patients with lumbar stenosis
Objective:Degenerative lumbar scoliosis is common in old patients. Decreased bone density and the degeneration of intervertebral discs are considered to be correlated with degenerative lumbar scoliosis. A means of quantifying the relative signal intensity for degenerative disc disease has not been previously discussed. The purpose of this study was to compare bone mineral density and intervertebral disc degeneration between degenerative lumbar scoliosis and lumbar spinal stenosis patients and explore the relationship among disc degeneration and scoliotic angle.
Methods:From January2001to August2010,96patients with degenerative lumbar scoliosis were retrospectively enrolled and96patients with lumbar spinal stenosis were selected as controls. Cobb angle, height of the apical disc and the contiguous disc superiorly and inferiorly on convex and concave sides, the height of the convex and concave side of the apical and the contiguous vertebral body superiorly and inferiorly were measured in the scoliosis group. The height of L2/L3, L3/L4, L4/L5discs and the height of L2/L4vertebral body was measured in the control group. The grade of intervertebral disc degeneration was evaluated using T2WI sagittal images in both groups. The bone density of lumbar vertebrae was measured with dual-energy X-ray.
Results:In scoliosis group, the intervertebral disc height on the convex side was greater than the height on the concave side (P<0.001). The vertebral body height on the convex side was greater than the height on the concave side (P=0.016). There was a significant difference between the scoliosis group and the control group (P=0.003), and between T-value and the rate of osteoporosis between the two groups (both P<0.001). Results were verified using multiple linear regression analysis.
Conclusion:Degenerative lumbar scoliosis is accompanied by height asymmetry between the intervertebral disc and vertebral body regarding the convex and concave surfaces.There is a positive correlation between the angle of scoliosis and the disc index, the degree of degeneration of the intervertebral disc, and a negative correlation between the angle of scoliosis and bone density.
目的：探讨肿瘤坏死因子-α基因单核苷酸多态性和血清中TNF-α水平与退变性腰椎侧凸的相关性,为临床分析退变性腰椎侧凸的病因及预防提供依据。
方法：选取2009年12月至2011年12月于河北医科大学第三医院脊柱外科门诊及病房收治的40例退变性腰椎侧凸患者作为研究对象,均行腰椎正侧位X线及腰椎MRI检查,选取同时期于该院进行健康体检者40例作为正常对照组,两组研究对象在性别、年龄、体重指数与病例组相匹配。收集两组患者的外周新鲜血液,用小量全血基因组DNA快速提取试剂盒提取DNA,应用聚合酶链反应(PCR)技术对两组研究对象DNA标本TNF-α基因启动子区特异性片段进行扩增,再应用限制性内切酶长度多态性(RFLP)技术对扩增的特异性片段用Ncol进行酶切,产物用2%琼脂糖凝胶电泳的方法进行检测,分析其基因型及等位基因频率的分布。用酶联免疫吸附测定技术(ELISA),对两组研究对象血清TNF-a蛋白水平进行检测。利用Adobe Photoshop6.0软件,测量病例组MRI图像中顶椎间盘及其上下椎间盘内髓核与脑脊液T2加权像的相对信号强度,同时测量病例组正位X线片上的Cobb角。应用SPSS17.0统计软件对数据进行统计分析,性别、体重指数、血清TNF-α含量比较采用t检验或方差分析。年龄、基因型及等位基因频率等计数资料比较采用χ2或Fisher精确概率法检验,血清TNF-α含量与椎间盘退变程度及Cobb角相关分析采用Linear correlate分析。
结果：两组研究对象的年龄、性别、体重指数比较差异无统计学意义(P>0.05)。TNF-a-308所在片段经PCR扩增后目的片段的长度为107bp,酶切后有3种基因型,G/G基因型(87bp、20bp2条带),G/A基因型(107bp、87bp、20bp3条带),A/A基因型(107bp1条带)。两组研究对象各基因型频率分布符合Hardy-Weinberg遗传平衡定律,研究对象具有代表性。TNF-a308多态性位点G/G、G/A和A/A基因型频率在病例组分别为70.0%、22.5%和7.5%,对照组为77.5%、17.5%和5.0%,两组基因型频率差异无统计学意义(P>0.05)。G/G基因型频率与非G/G基因型频率(G/A、A/A)及等位基因G、A频率在病例组为分别为70.0%、30.0%和81.3%、18.7%,对照组为77.5%、22.5%和86.2%、13.8%,两组比较差异均无统计学意义(P>0.05)。细胞因子TNF-α清浓度,病例组172.15±33.51ng/L,对照组53.75±3.84ng/L,两组之间差异有统计学意义(P<0.05),且病例组显著高于对照组。TNF-α血清浓度与髓核相对信号强度呈负相关,与Cobb's角呈正相关。将病例组根据椎间盘退变等级分组,各组之间差异有统计学意义(P<0.05)。
结论：退变性腰椎侧凸患者血清中TNF-α浓度比正常人群血清水平明显增高,血清中TNF-α浓度与侧凸角呈正相关,与退变性腰椎侧凸椎间盘髓核信号强度呈负相关,血清TNF-α浓度越高,椎间盘退变程度越重,TNF-a是退变性腰椎侧凸发生发展的危险因素。TNF-α-308多态性与退变性腰椎侧凸无明显相关。
2.退变性腰椎侧凸椎体终板MRI T1和T2信号改变及相关因素分析
目的：在腰椎退变性疾病中,椎体终板信号改变(vertebral endplate signal changes, vESC)在MRI T1和T2加权像上较为常见,在一定程度上是椎体终板损伤、炎症及退变在影像学上的表现形式。本研究通过观察退变性腰椎侧凸患者的椎体终板信号改变及分布情况,探讨其相关影响因素。
方法：回顾分析2005年3月～2010年3月经我院诊治的120例原发性退变性腰椎侧凸患者的影像学资料做为病例组,选取同时期、同年龄段及同性别比诊断为腰椎退变性疾病并除外腰椎侧凸的89例患者的影像学资料做为对照组,所有患者均行腰椎X线及MRI检查。观察两组中vESC的发生率、类型(Modic分型)及分布特点；分析vESC与椎间盘退变、腰椎侧凸角、体重指数及吸烟等因素的关系。
结果：病例组中120例患者的1440个终板中,71例(59.2%)124(17.2%)个终板存在vESC;对照组中89例患者的1068个终板中,21例(23.6%)49(4.6%)个终板存在vESC;两组的发生率比较有显著性差异(P<0.01)。病例组中,终板凹侧的vESC发生率(12.1%)与凸侧(1.5%)和双侧(3.6%)比较均有显著性差异(P<0.01),以L2/3、L4/5和L5/S1节段多发,且与主弯和代偿弯顶椎的好发节段相一致；对照组中,终板双侧的vESC发生率(2.9%)与左侧(0.7%)和右侧(1.0%)比较均有显著性差异(P<0.01),且主要发生在L4/5和L5/S1节段。按Modic分型,病例组中以Modic II型多见,而对照中以Modic I型更常见。相对危险度分析显示,椎间盘退变、腰椎侧凸、体重及吸烟是vESC的危险因素。经Multinomial Logistic逐步回归分析得出回归方程：logitY=-0.82+1.27D+0.55S+1.77D*S(Y为终板退变,D为椎间盘退变,S为腰椎侧凸角,D*S为椎间盘退变与腰椎侧凸角的交互作用)。
结论：退变性腰椎侧凸椎体终板信号改变发生率较高,多发生于靠近顶椎区域的L2/3、L4/5和L5/S1节段的凹侧,呈不对称分布,以Modic Ⅱ型多见；终板退变与椎间盘退变、腰椎侧凸及二者的交互作用呈正相关,超重和吸烟是危险因素。
3.后路有限减压、固定、融合治疗退变性腰椎侧凸合并椎管狭窄症
目的：成人退行性腰椎侧凸的患者同时合并腰椎管狭窄症的发生率很高,这种情况多因腰椎不稳引起椎间盘变性突出、小关节骨质增生以及关节囊肥大、黄韧带增生钙化等而导致椎间孔及椎管有效空间减小,压迫神经出现根性疼痛或间歇性跛行。本文通过探讨采用后路有限减压、固定、融合手术治疗退变性腰椎侧凸合并椎管狭窄症的疗效,为退变性腰椎侧凸合并椎管狭窄症的合理治疗提供理论依据。
方法：2001年1月至2008年1月我科收治退变性腰椎侧凸合并椎管狭窄症患者36例,男2例,女34例；年龄51-76岁,平均62.3±9.4岁；病程10个月-7年,平均37个月。所有患者术前均行X线、CT及MR检查,5例患者行脊髓造影。术前Cobb角为24.0°±10.2°,腰椎前凸角22.6°±11.2°。铅垂线(C7PL)与S1椎体后上缘距离(SVA)(7.8±6.6)cm,C7PL与骶正中线距离(CSVL)(6.9±5.8)cm。根据查体及影像学资料确定手术节段,采用后路有限减压、固定、融合进行手术治疗。术后随访采用VAS、SF-36评分系统评估神经功能恢复及症状改善情况。Cobb角、腰椎前凸角的变化评估矫形效果。
结果：所有患者均获得随访,随访时间1.2-4年,平均2.4年。患者术后、末次随访平均Cobb角(10.6±8.5)°、(8.9°±5.3)。,腰椎前凸角(25.6±14.3)°、(31.8±13.4)。,SVA(0.5±3.4)cm、(-1.2±2.7)cm,CSVL(2.9±1.4)cm.(1.7±1.2)cm,较术前均具有显著性差异。术后仅1例患者发生矫正丢失,无一例发生椎间隙塌陷、神经损伤、钉棒断裂等并发症。
结论：后路有限减压、固定、融合手术在减压的基础上最大程度的保留了脊柱的骨性结构,维持了术后脊柱的稳定性,是治疗退变性腰椎侧凸合并椎管狭窄症的有效手段。
4.退变性腰椎侧凸椎间盘退变程度以及骨密度与侧凸角度的关联性研究
目的：退变性腰椎侧凸的确切病因不明,一般认为可能与骨质疏松、椎间盘退变等因素有关。退变性腰椎侧凸和骨质疏松症这两种疾病的发病人群基本一致,其中老年、女性患者的发病率比较高,但是两者是否存在相关性一直存在争议。本文旨在探讨退变性腰椎侧凸患者椎间盘的不对称指数、腰椎间盘退变程度以及骨密度降低对侧凸角度的影响。
方法：采用回顾性研究的方法,选取2001年1月至2010年8月,共96例退变性腰椎侧凸患者为研究对象(侧凸组)；2001年1月至2010年8月确诊为腰椎管狭窄症并且资料齐全的患者96例为对照组；两组间性别、年龄、体质量指数匹配。侧凸组：在腰椎正位x线片上测量凸凹侧顶椎间盘及其上下椎间盘的高度和顶椎及其上下椎体的高度,利用Adobe Photoshop6.0软件,测量MRI图像T2WI顶椎及其上下椎间盘内髓核与脑脊液的相对信号强度。对照组：取L2-3,L3-4,L4-5这3个椎间盘为研究对象测定上述指标。应用双能x线吸收法测定两组患者腰椎(L2-4)及股骨颈、股骨粗隆和Ward's三角的T值。
结果：侧凸组凸侧椎间盘高度和为(40±7)mm高于凹侧的(28±7)mm(P<0.01),凸侧椎体高度和为(76±12)mm高于凹侧的(72±10)mm(P=0.016)；两组之间的椎间盘退变程度差异有统计学差异(P=0.003)；两组之间骨密度T值的平均值和骨质疏松的发生率差异有统计学意义(均P<0.01)。通过多元线性回归分析结果显示患者椎间盘的不对称指数、椎间盘的退变程度、骨密度T值影响退变性腰椎侧凸角度.
结论：退变性腰椎侧凸常伴有凸凹两侧椎间盘高度以及椎体高度不对称。侧凸角度与椎间盘的不对称指数、椎间盘的退变程度呈正相关,与骨密度值T值呈负相关。
1.Correlation between the gene single-nucleotide polymorphism and serum concentration of tumor necrosis factor-alpha and degenerative lumbar scoliosis
Objective:This study aims to investigate the correlation between tumor necrosis factor-alpha(TNF-α) gene single-nucleotide polymorphism and serum concentrations levels in degenerative lumbar scoliosis, which explore etiology of degenerative lumbar scoliosis from genetic and molecular level and provide the basis for analyzing the etiology and prevention of degenerative lumbar scoliosis.
Methods:40patients with degenerative lumbar scoliosis were selected as patient group, they were out-patient or in the wards of the Third Hospital of He Bei Medical University from December2009to December2011, the DLS group were all undertaken lumbar spine X-ray and MRI.40cases of healthy persons were selected as normal control. The two groups matched with gender, age, body mass index. Fresh peripheral blood of the two groups were collected. DNA was extracted by the small amount of whole blood Genomic DNA extraction reagent kit, specific fragments in TNF-a gene promoter region were amplified by polymerase chain reaction (PCR) technology, and then the amplified specific fragments were digested using Ncol by restriction fragment length polymorphism (RFLP) technology, finally the products were detected with a2%agarose gel electrophoresis and cases'genotype and allele frequency distribution were analyzed. Serum TNF-a levels were determined by Enzyme-linked immunosorbent assay technique (ELISA). Using Adobe Photoshop6.0software, in DLS group the relative signal intensity of apical vertebra and the upper and lower vertebral disc's nucleus pulposus and cerebrospinal fluid in T2-weighted MRI images were measured. Cobb angles were measured on the antero-posterior lumbar spine X-ray films. All the data were analyzed by Statistic Package for Social Science (SPSS)17.0. Gender, body mass index and serum TNF-a levels were compared using the t-test or analysis of variance. The count data, such as age, genotype and allele frequency were compared using the χ2or Fisher exact test. Correlation between serum TNF-αa levels and vertebral disc'degeneration and correlation between serum TNF-α levels and Cobb angles were made by Linear Correlation Analysis.
Results:The comparison of the two groups'age, gender distribution and body mass index did not show statistical difference, The amplification TNF-a-308fragments was107bp by polymerase chain reaction and there were three genotypes after digested by incision enzyme, including G/G genotype, G/A genotype, A/A genotype. On the electropherogram G/G genotype had two bright bars(87bp,20bp), G/A genotype had three bright bars(107bp,87bp,20bp), and A/A genotype had one bright bars(107bp). Three genotypes frequencies of the two groups are in accordance with Hardy-Weinberg equilibrium. In DLS group, the frequencies of GIG genotype, G/A genotype and A/A genotype were70.0%、22.5%and7.5%, in the control group the frequencies of the three genotypes were77.5%、17.5%and5.0%. The three genotypes frequencies of the two groups are of no significant differences. In DLS group the frequencies of G/G genotype and non-G/G (G/A、A/A) genotype and the frequencies of allele G and A were70.0%、30.0%and81.3%、18.7%, in the control group were77.5%,22.5%and86.2%、13.8%. The comparison of two groups are of no significant difference. Cytokine TNF-a serum concentration in DLS group was172.15±33.51ng/L and in control group was53.75±3.84ng/L, The concentration of DLS group was significantly higher than that of control group, and there was significant difference, and the patient group was significantly higher. Serum TNF-a concentration has a negative correlation with the RSI and a positive correlation with the Cobb angle. According to the disc degeneration grade, DLS group was divided, there were significant differences between different groups.
Conclusion:Serum TNF-α concentration in degenerative lumbar scoliosis patients were significantly increased. Serum TNF-a concentration has a negative correlation with the RSI and a positive correlation with the Cobb angle. The higher serum TNF-a concentration is, the more severe disc degeneration occur. TNF-a may play an important role in the degeneration of degenerative lumbar scoliosis.TNF-a-308polymorphism was of no significant correlation with degenerative lumbar scoliosis.
2.Vertebral endplate signal changes on MRI T1and T2in degenerative lumbar scoliosis and its associated factors analysis
Objective:Vertebral endplate signal changes (vESC) is common in degenerative lumbar disease, it is the characteristic of injury of endplate and degeneration of lumbar endplate, we do the work to investigate the vertebral endplate signal changes on MRI and explore its associated factors in degenerative lumbar scoliosis(DLS).
Methods:The image data of120patients who were diagnosed primary DLS in our hospital from march2005to march2011were retrospectively reviewed as the case group. The image data of89patients who were diagnosed degenerative lumbar diseases(DLD) without scoliosis were selected as the control group. The prevalence, type and distribution of vESC in two groups was observed and compared. Intervertebral disc degeneration, lumbar scoliosis Cobb's angle, body mass index(BMI) and status of smoking et al were recorded in DLS, and the relationship of vESC with these influential factors was analyzed.
Results:Of1440endplate from120patients in case group,247(17.2%) from71(59.2%) patients were found to have vESC. Contrasting to the control group, of1068endplate from89patients,49(4.5%) from21(23.6%) patients were found to have vESC. The prevalence of vESC in two groups had a significantly statistical difference (P<0.01). Modic type II was more common in case group but Modic type I was more common in control group. The prevalence of vESC on concave side(12.1%) was significantly different with on convex(1.5%) and both sides(3.6%) in case group(P<0.01), While in control group, the prevalence of vESC on both sides(2.9%) was significantly significantly different with on right(1.0%) or left sides(0.7%, P<0.01). vESC were more common at L4/5and L5/S1in control group, but in case group, vESC mainly occured at L2/3, L4/5and L5/S1which were accordance with the common levels of apex vertebrae. Intervertebral disc degeneration, lumbar scoliosis, overweight and heavy smoking were considered as risk factors to vESC. By Multinomial Logistic Regression analysis with these factors, the regression function was obtained:log Y=-0.82+1.27D+0.55S+1.77D*S (Y for endplate degeneration, D for intervertebral disc degeneration, S for scoliosis Cobb's angle and D*S for interaction of disc degeneration and scoliosis Cobb's angle).
Conclusion:vESC positively correlate with intervertebral disc degeneration, scoliosis Cobb's angle and their interaction in DLS. its prevalence is relatively higher, most of them are type II and mostly locate on the concave side of L2/3, L4/5and L5/S1. Overweight and heavy smoking are probably its risk factors.
3.Limited decompression, fixation,and fusion for degenerative scoliosis with vertebral stenosis
Objective:Patients with degenerative lumbar scoliosis always suffered from vertebral stenosis, this may be induced by the lumbar disc herniation,atrophy of articular process or calcification of yellow ligaments. Patients always complained of leg pain, which is caused by the compression of the nerve root or spinal cord. We do the work to evaluated the efficiency of limited decompression, fixation, and fusion for degenerative scoliosis with vertebral stenosis.
Method:From January,2001to January2008,36patients with degenerative scoliosis with vertebral stenosis were treated in our hospital. There were2males and34females. The age was from51to76years with an average of62.3years. X-ray, CT, MR examination were performed preoperatively for all the cases,5cases underwent myelography. Preoperative Cobb angle, focal lordosis, the distance between C7plumb line (C7PL) and upper edge of S1vertebral body(SVA), and the distance between C7PL and center sacral vertical line (CSVL) were24.0°±10.2°,22.6°±11.2°,(7.8±6.6)cm and (6.9±5.8)cm respectively. Limited decompression, pedicle screw internal fixation and fusion were carried out for patients, VAS and SF-36scored system were used to evaluate surgery effects.
Result:The mean follow-up period was2.4years (range,1.2-4years) and no patients were lost during follow-up. The mean surgery time was130min (range,115-164min) with an average bleeding amount of625ml (range,450-870ml). compared to pre-operation, Cobb angle (10.6°±8.5°,8.9°±5.3°), focal lordosis (25.6°±14.3°,31.8°±13.4°), SVA [(0.5±3.4) m,-1.2±2.7) cm] and CSVL [(2.9±1.4)cm,(1.7±1.2)cm] were significantly improved at post-operation and final follow-up through statistics of SPSS13.0software. Loss of correction happened in one case. No collapse of the disc height occurred, neither did never root injures nor fracture of the fixation system.
Conclusion:Limited decompression, pedicle screw fixation are testified efficient for degenerative scoliosis with vertebral stenosis, individualized surgery design should be made according to clinical symptoms, signs and imaging features to expect a satisfactory result.
4.1ntervertebral disc degeneration and bone density in degenerative lumbar scoliosis:a comparative study between patients with degenerative lumbar scoliosis and patients with lumbar stenosis
Objective:Degenerative lumbar scoliosis is common in old patients. Decreased bone density and the degeneration of intervertebral discs are considered to be correlated with degenerative lumbar scoliosis. A means of quantifying the relative signal intensity for degenerative disc disease has not been previously discussed. The purpose of this study was to compare bone mineral density and intervertebral disc degeneration between degenerative lumbar scoliosis and lumbar spinal stenosis patients and explore the relationship among disc degeneration and scoliotic angle.
Methods:From January2001to August2010,96patients with degenerative lumbar scoliosis were retrospectively enrolled and96patients with lumbar spinal stenosis were selected as controls. Cobb angle, height of the apical disc and the contiguous disc superiorly and inferiorly on convex and concave sides, the height of the convex and concave side of the apical and the contiguous vertebral body superiorly and inferiorly were measured in the scoliosis group. The height of L2/L3, L3/L4, L4/L5discs and the height of L2/L4vertebral body was measured in the control group. The grade of intervertebral disc degeneration was evaluated using T2WI sagittal images in both groups. The bone density of lumbar vertebrae was measured with dual-energy X-ray.
Results:In scoliosis group, the intervertebral disc height on the convex side was greater than the height on the concave side (P<0.001). The vertebral body height on the convex side was greater than the height on the concave side (P=0.016). There was a significant difference between the scoliosis group and the control group (P=0.003), and between T-value and the rate of osteoporosis between the two groups (both P<0.001). Results were verified using multiple linear regression analysis.
Conclusion:Degenerative lumbar scoliosis is accompanied by height asymmetry between the intervertebral disc and vertebral body regarding the convex and concave surfaces.There is a positive correlation between the angle of scoliosis and the disc index, the degree of degeneration of the intervertebral disc, and a negative correlation between the angle of scoliosis and bone density.
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9 Wheelhouse NM, Chan YS, Gillies SE, et al. TNF-alpha induced DNA damage in primary murine hepatocytes. Int J Mol Med.2003,12(6): 889-894
10 Ahn SH, Cho YW, Ahn MW, et al. mRNA expression of cytokines and chemokines in herniated lumbar intervertebral discs. Spine,2002,27(9): 911-17
11 Igarashi T, Kikuchi S, Shubayev V, et al.2000 Volvo Award Winner in basic science studies:Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats. Spine,2000,25(23):2975-2980
12 Nerlich AG, Weiler C, Zipperer J, et al. Immunolocalization of phagocytic cells in normal and degenerated intervertebral discs. Spine,2002, 27(22):2484-2490
13 Seguin CA, Bojarski M, Pilliar RM, et al. Differential regulation of matrix degrading enzymes in a TNF-alpha-induced model of nucleus pulposus tissue degeneration. Matrix Biol,2006,25(7):409-418
14 Antoniou J, Steffen T, Nelson F, et al. The human lumbar intervertebral disc:evidence for changes in the biosynthesis and denaturation of the extracellular matrix with growth, maturation, ageing, and degeneration. J Clin Invest,1996,98(4):996-1003
15 Valdes AM, Hassett G, Hart DJ, et al. Radiographic progression of lumbar spine disc degeneration is influenced by variation at inflammatory genes:a candidate SNP association study in the Chingford cohort. Spine,2005, 30(21):2445-2451
16Kawaguchi S, Yamashita T, Katahira G, et al. Chemokine profile of herniated intervertebral discs infiltrated with monocytes and macrophages. Spine,2002,27(14):1511-1516
17Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-3-dependent generation of a macrophage chemoattractant in a model of herniated disc resorption. J Clin Invest,2000,105(2):133-141
18Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-7-depenndent realease of tumar necrosis factor-alpha in a model of herniated disc resorption. J Clin Invest,2000,105(2):143-150
19 Roberts S, Evans H, Menage J, et al. TNF alpha-stimulated gene product (TSG-6) and its binding protein, Ialphal, in the human intervertebral disc: new molecules for the disc. Eur spine,2005,14(1):36-42
20胡绪江,邵增务.外源性肿瘤坏死因子-α对腰椎间盘退变影响的实验研究.中国脊柱脊髓杂志,2006,16(7)：541-544
21 Takebayashi T, Cavanaugh JM, Cuneyt Ozaktay A, et al. Effect of nucleus pulposus on the neural activity of dorsal root ganglion. Spine,2001,26(8): 940-945
22 Onda A, Hamba M, Yabuki S, et al. Exogenous tumor necrosis factor-alpha induces abnormal discharges in rat dorsal horn neurons. Spine, 2002,27(15):1618-1624
23 Rand N, Reichert F, Floman Y, et al. Murine nucleus pulposus-derived cells secrete interleukins-1-beta,-6, and-10 and granulocyte-macrophage colony-stimulating factor in cell culture. Spine,1997,22 (22):2598-2601
24 Viviani B, Corsini E, Galli CL, et al. Glia increase degeneration of hippocampal neurons through release of tumor necrosis factor-alpha. Toxicol Appl Pharmacol,1998,150(2):271-276
25 Sasaki N, Kikuchi S, Konno S, et al. Anti-TNF-alpha antibody reduces pain-behavioral changes induced by epidural application of nucleus pulposus in a rat model depending on the timing of administration. Spine, 2007,32(4):413-416
26 Kroeger KM, Carville KS, Abraham LJ, et al. The -308 tumor necrosis factor-alpha promoter polymorphism effects transcription. Mol Immunol, 1997,34 (5):391-399
1 de Roos A, Kressel H, Spritzer C, et al. MR imaging of marrow changes adjacent to end plates in degenerative lumbar disk disease. AJR Am J Roentgegenol,1987; 149:531-534
2 Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: Assessment of changes invertebral body marrow with MR imaging. Radiology,1988,166:193-199
3 Modic MT, Masaryk TJ, Ross JS, et al. Imaging of degenerative disk disease. Radiology,1988; 168:177-186
4 Kokkonen SM, Kurunlahti M, Tervonen O, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine:correlation with pain provocation and disc changes observed on computed tomography discography. Spine,2002,27:2274-2278
5 Jones A,Clarke A, Freeman BJ et al. The Modic classification:inter-and intraobserver error in clinical practice. Spine,2005.30:1867-1869
6 Pfirrmaann CWA, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine,2001, 26:1873-1878
7孟昭恒,王远琴,宋庆伟,等.国内外10种肥胖判定标准的比较[J].中国公共卫生,2006,11：147-150
8 Jensen TS, Kjaer P, Korsholm L, et al. Predictors of new vertebral endplate signal (Modic) changes in the general population. Eur Spine, 2010; 19:129-35
9 Modic MT. Modic type 1 and type 2 changes. J Neurosurg Spine,2007; 6:150-151
10 Karchevsdy M, Schweitzer ME, Carrino JA, et al. Reactive endplate marrow changes:a systematic morphologic and epidemiologic evaluation. Skeletal Radiol,2005; 34:125-129
11 Adams MA, Freeman BJ, Morrison HP, et al. Mechanical initiation of intervertebral disc degeneration. Spine,2000; 25:1625-1636
12 Nizard RS, Wybier M, Laredo JD. Radiologic assessment of lumbar intervertebral instabiliby and degenerative spondylolisthesis. Radiol Clin North Am,2001; 39:55-71
13 Kaapa E, Luoma K,Pitkaniemi J, et al. Correlation of size and type of Modic type 1 and 2 lesion with clinical symptoms:a descriptive study in a subgroup of chronic low back pain patients based on a university hospital patient sample. Spine 2011;14:ahead publish
1 Schwab F, Dubey A, Gamez L'et al. Adult scoliosis:prevalence, SF-36. and nutritional parameters in an elderly volunteer population. Spine (Phila Pa 1976),2005,30(9):1082-1085
2 Shufflebarger H, Suk SI, Mardjetko S. Debate:determining the upper instrumented vertebra in the management of adult degenerative scoliosis:stopping at T10 versus L1. Spine(Phila Pa 1976),2006,31(19 Suppl):S185-194
3 Bridwell KH. Degenerative scoliosis//Bridwell KH. The textbook of spinal surgery. Philadelphia:JB Lippineott,1997:728-741
4 Jenkinson C, Wrisht L, Coulter A. Criterion validity and reliability of SF-36 in a population sample. Qual Life Res,1994,3(1):7-12
5 Leon GR. Koscheyev VS, Stone EA. Visual analog scales for sessment of thermal perception in different environments. Aviat Space Environ Med,2008,79(8):784-786
6 Oskouian RJ Jr, Shaffrey CI. Degenerative lumbar scoliosis. Neurosurg Clin N Am,2006,17(3):299-315
7 Weideubaum M. Considerations for focused surgical intervention in the presence of adult spinal deformity. Spine(Phila Pa 1976),2006,31(19 Suppl):S139-143
8 Lowe T, Berven SH, Schwab FJ, et al.111e SRS classification for adult spinal deformity:building on the King/Moe and Lenke classification systems. Spine(Phila Pa 1976),2006,31(19 Suppl):S119.125
9邱勇,王斌,朱锋,等.退变性腰椎侧凸的冠状面失衡分型及对截骨矫形术式选择的意义.中华骨科杂志,2009,29(5)：418-423
10 DeWald CJ, Stanley T. Instrumentation-related complications of multilevel fusions for adult spinal deformity patients over age 65: surgical considerations and treatment options in patients with poor bone quality. Spine(Phila Pa 1976),2006.31(19 Suppl):S144-151
11 Tan JS, Kwan BK, Dvorak MF, et al. Pedicle screw motion in the osteoporotic spine after augmentation with laminar hooks, sublaminar wires, or calcium phosphate cement:a comparative analysis. Spine(Phila Pa 1976),2004,29(16):1723-1730
12 Glassman SD. Hamill CL,Bridwell KH, et al. The impact of perioperative complications on clinical outcome in adult deformity surgery. Spine(Phila Pa 1976),2007,32(24):2764-2770
13曾岩,陈仲强,郭昭庆,等.腰椎管狭窄症伴退变性腰椎侧凸患者的影像学表现与临床特点.中国脊柱脊髓杂志,2007,17(10)：753-756
14 Aebi M. ne adult scoliosis. Eur Spine J,2005,14(10):925-948
15 Edwards CC 2nd, Bridwell KH, Patel A, et al. Long adult deformity fusions to L5 and the sacrum; a matched cohort analysis. Spine(Phila Pa 1976),2004,29(18):1996-2005
1 Kobayashi T, Atsuta Y, Takemitsu M, et al. A prospective study of de novo scoliosis in a community based cohort.Spine 2006; 31:178-182
2楼才俊,陈其昕,李方才,等.腰椎间盘髓核退变的MRI表现与病理学的相关性研究.中华骨科杂志,2003,23：531-535
3 Benner B, Ehni G. Degenerative lumbar scoliosis. Spine 1979; 4:548-552
4 Tribus CB. Degenerative lumbar scoliosis evaluation and management. J Am Acad Orthop Surg 2003; 11:174-183
5王乃国,王以朋,邱贵兴,等,短节段融合对退变性腰椎侧凸邻近节段椎间角的影响.中华外科杂志,2010,48：506-510
6 Murata Y, Takahashi K, Hanaoka E. Changes in scoliotic curvature and lordotic angle during the early phase of degenerative lumbar scoliosis. Spine 2002; 27:2268-2273
7 Akhtar S, Davies JR, Caterson B. Ultrastructural localization and distribution of proteogly can in normal and scoliotic lumbar disc. Spine 2005; 30:1303-1309
8 Bertram H, Steck E, Zimmerman G, et al. Accelerated intervertebral disc degeneration in scoliosis versus physiological aging develops against a background of enhanced anabolic gene expression. Biochem Biophys Res Commun 2006; 342:963-972
9 Aebi M. The adult scoliosis. Eur Spine J 2005; 14:925-948
10 Matsumura A, Namikawa T, Terai H, et al. The influence of approach side on facet preservation in microscopic bilateral decompression via a unilateral approach for degenerative lumbar scoliosis. J Neurosurg Spine 2010; 13:758-765
11 Cho KJ, Suk SI, Park SR, et al. Risk factors of sagittal decompensation after long posterior instrumentation and fusion for degenerative lumbar scoliosis. Spine 2010; 35:1595-1601
12 Routh RH, Rumancik S, Pathak RD,et al. The relationship between bone mineral density and biomechanics in patients with osteoporosis and scoliosis. Osteoporos Int 2005; 16:1857-1863
13 Sarikaya S,Ozdolap S,Acikguz G,et al. Pregnancy-associated osteoporosis with vertebrae fractures and scoliosis. Joint Bone Spine,2004,71:84-85
1 Kobayashi T, Atsuta Y, Takemitsu M, et al.A prospective study of de novo scoliosis in a community based cohort [J].Spine,2006,31(2):178-182
2 Sengupta DK,Herkowitz HN. Lumbar spinal stenosis:treatment strategies and indications for surgery [J].Orthop Clin North AM,2003,34(2):281-295
3 Sigurd H.Berven, Vedat Deviren,Brian Mitchell,et al.Operative management of degenerative scoliosis:an evidence-based approach to surgical strategies based on clinical and radiographic outcomes. Neurosurg Clin N AM,2007,18(3):261-272
4 Pritchett JW, Bortel DT. Degenerative symptomatic lumbar scoliosis.Spine,993,18(5):700-703
5 Murata Y, Takahashi K, Hanaoka E, et al. Changes in scoliotic curvature and lordotic angle during the early phase of degenerative lumbar scoliosis[J]. Spine,2002,27(20):2268-2273
6 Faldini C, Pagkrati S, Grandi G, et al. Degenerative lumbar scoliosis:features and surgical treatment [J].J Orthop Traumatol,2006, 7(2):67-71
7 Daffner SD, Vaccaro AR. Adult degenerative lumbar scoliosis[J].Am J Orthop,2003,32(2):77-82
8 Tribus CB. Degenerative lumbar scoliosis:evaluation and management. J Am Acad Orthop Surg,2003.11(3):174-183
9 Robin GC, Span Y, Steinberg R, et al. Scoliosis in the elderly:a follow-up study. Spine,1982,7:355-359
10 Grubb S A,Lipscomb H J,Coonrad R W. Degenerative adult scoliosis[J].Spine,1988,13(3):241-245
11 Max Aebi:The adult scoliosis. Eur Spine J,2005,14(10):925-948
12 Schwab F, Farcy JP, Bridwell K, et al.A clinical impact classification of scoliosis in the adult. Spine,2006 31(18):2109-2114
13 Simmons ED. Surgical treatment of patients with lumbar spinal stenosis with associated scoliosis [J].Clin Orthop Relat Res,2001,384:45-53
14 Avraam Ploumis, Ensor E, Tr.ansfledt,ea tl. Degenerative lumbar scoliosis associated with spinal stenosis[J].Spine J,2007,7(4):428-436
15 John K. Birknes,Andrew P. White, Todd J. Albert,et al. Adult degenerative scoliosis:a review[J].Neurosurgery,2008,63:A94-A103
16 Kuklo TR, Bridwell KH, Lewis SJ,et al:Minimum 2-year analysis of sacropelvic fixation and L5-S1 fusion using S1 and iliac screws[J]. Spine, 2001,26(18):1976-1983
17宋海峰.退变性脊柱侧凸的临床特点与影像学分析[J].中国脊柱脊髓杂志.2008,18(3)：201-205
18 Daubs MD, Lenke LG, Cheh G, et al. Adult spinal deformity surgery: complications and outcomes in patients over age 60[J].Spine,2007,32(20): 2238-2244
19 Auerbach AD,Goldman L.Beta-Blockers and reduction of cardiac events in noncardiac surgery:Clinical applications. JAMA,2002,287:1445-1447
20 Hansraj KK, O'Leary PF, Cammisa FP Jr, et al. Decompression, fusion,and instrumentation surgery for complex lumbar spinal stenosis.Clin Ortthop,2001,384:18-25
21 Gupta MC. Degenerative scoliosis. Options for surgical management. Orthop Clin North Am,2003,34:269-79
22 Shufflebarger H, Suk S, Mardjetko S. Debate:determining the upper instrumented vertebra in the management of adult degenerative scoliosis [J]. Spine,2006,31(19):185-194
23 Bridwell KH, Edwards CC, Lenke LG, et al.The pros and consto saving the L5-S1 motion segment in a long scoliosis fusion construct[J]. Spine, 2003,28 (20):234-242
2 Beamer BA, Yen CJ, Andersen RE, et al. Association of the Pro12Ala variant in the peroxisome proliferator-activated receptor-gamma2 gene with obesity in two Caucasian populations. Diabetes,1998,47(11): 1806-1808
3 Luoma K, Vehmas T, Riihimaki H, et al. Disc height and signal intensity of the nucleus pulposus on magnetic resonance imaging as indicators of lumbar disc degeneration. Spine,2001,26(6):680-686
4 Daffner SD, Vaccaro AR. Adult degenerative lumbar scoliosis. Am J Orthop,2003,32(2):77-82
5史亚民,张光铂.如何掌握退变性脊柱侧凸的手术适应证.中国脊柱脊髓杂志,2006,16(3)：178-179
6 Kobayashi T, Atsuta Y, Takemitsu M, et al. A prospective study of de novo scoliosis in a community based cohort. Spine,2006,31(2):178-182
7 Allen RD. Polymorphism of the human TNF-alpha promoter-random variation or functional diversity? Mol Immunol,1999,36(15-16): 1017-1027
8魏茂提,韩众,何丽等.中国汉族人群TNF-α基因启动子区的多态性研究.中国免疫学杂志.2007,23(6)：518-521
9 Wheelhouse NM, Chan YS, Gillies SE, et al. TNF-alpha induced DNA damage in primary murine hepatocytes. Int J Mol Med.2003,12(6): 889-894
10 Ahn SH, Cho YW, Ahn MW, et al. mRNA expression of cytokines and chemokines in herniated lumbar intervertebral discs. Spine,2002,27(9): 911-17
11 Igarashi T, Kikuchi S, Shubayev V, et al.2000 Volvo Award Winner in basic science studies:Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats. Spine,2000,25(23):2975-2980
12 Nerlich AG, Weiler C, Zipperer J, et al. Immunolocalization of phagocytic cells in normal and degenerated intervertebral discs. Spine,2002, 27(22):2484-2490
13 Seguin CA, Bojarski M, Pilliar RM, et al. Differential regulation of matrix degrading enzymes in a TNF-alpha-induced model of nucleus pulposus tissue degeneration. Matrix Biol,2006,25(7):409-418
14 Antoniou J, Steffen T, Nelson F, et al. The human lumbar intervertebral disc:evidence for changes in the biosynthesis and denaturation of the extracellular matrix with growth, maturation, ageing, and degeneration. J Clin Invest,1996,98(4):996-1003
15 Valdes AM, Hassett G, Hart DJ, et al. Radiographic progression of lumbar spine disc degeneration is influenced by variation at inflammatory genes:a candidate SNP association study in the Chingford cohort. Spine,2005, 30(21):2445-2451
16Kawaguchi S, Yamashita T, Katahira G, et al. Chemokine profile of herniated intervertebral discs infiltrated with monocytes and macrophages. Spine,2002,27(14):1511-1516
17Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-3-dependent generation of a macrophage chemoattractant in a model of herniated disc resorption. J Clin Invest,2000,105(2):133-141
18Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-7-depenndent realease of tumar necrosis factor-alpha in a model of herniated disc resorption. J Clin Invest,2000,105(2):143-150
19 Roberts S, Evans H, Menage J, et al. TNF alpha-stimulated gene product (TSG-6) and its binding protein, Ialphal, in the human intervertebral disc: new molecules for the disc. Eur spine,2005,14(1):36-42
20胡绪江,邵增务.外源性肿瘤坏死因子-α对腰椎间盘退变影响的实验研究.中国脊柱脊髓杂志,2006,16(7)：541-544
21 Takebayashi T, Cavanaugh JM, Cuneyt Ozaktay A, et al. Effect of nucleus pulposus on the neural activity of dorsal root ganglion. Spine,2001,26(8): 940-945
22 Onda A, Hamba M, Yabuki S, et al. Exogenous tumor necrosis factor-alpha induces abnormal discharges in rat dorsal horn neurons. Spine, 2002,27(15):1618-1624
23 Rand N, Reichert F, Floman Y, et al. Murine nucleus pulposus-derived cells secrete interleukins-1-beta,-6, and-10 and granulocyte-macrophage colony-stimulating factor in cell culture. Spine,1997,22 (22):2598-2601
24 Viviani B, Corsini E, Galli CL, et al. Glia increase degeneration of hippocampal neurons through release of tumor necrosis factor-alpha. Toxicol Appl Pharmacol,1998,150(2):271-276
25 Sasaki N, Kikuchi S, Konno S, et al. Anti-TNF-alpha antibody reduces pain-behavioral changes induced by epidural application of nucleus pulposus in a rat model depending on the timing of administration. Spine, 2007,32(4):413-416
26 Kroeger KM, Carville KS, Abraham LJ, et al. The -308 tumor necrosis factor-alpha promoter polymorphism effects transcription. Mol Immunol, 1997,34 (5):391-399
1 de Roos A, Kressel H, Spritzer C, et al. MR imaging of marrow changes adjacent to end plates in degenerative lumbar disk disease. AJR Am J Roentgegenol,1987; 149:531-534
2 Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: Assessment of changes invertebral body marrow with MR imaging. Radiology,1988,166:193-199
3 Modic MT, Masaryk TJ, Ross JS, et al. Imaging of degenerative disk disease. Radiology,1988; 168:177-186
4 Kokkonen SM, Kurunlahti M, Tervonen O, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine:correlation with pain provocation and disc changes observed on computed tomography discography. Spine,2002,27:2274-2278
5 Jones A,Clarke A, Freeman BJ et al. The Modic classification:inter-and intraobserver error in clinical practice. Spine,2005.30:1867-1869
6 Pfirrmaann CWA, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine,2001, 26:1873-1878
7孟昭恒,王远琴,宋庆伟,等.国内外10种肥胖判定标准的比较[J].中国公共卫生,2006,11：147-150
8 Jensen TS, Kjaer P, Korsholm L, et al. Predictors of new vertebral endplate signal (Modic) changes in the general population. Eur Spine, 2010; 19:129-35
9 Modic MT. Modic type 1 and type 2 changes. J Neurosurg Spine,2007; 6:150-151
10 Karchevsdy M, Schweitzer ME, Carrino JA, et al. Reactive endplate marrow changes:a systematic morphologic and epidemiologic evaluation. Skeletal Radiol,2005; 34:125-129
11 Adams MA, Freeman BJ, Morrison HP, et al. Mechanical initiation of intervertebral disc degeneration. Spine,2000; 25:1625-1636
12 Nizard RS, Wybier M, Laredo JD. Radiologic assessment of lumbar intervertebral instabiliby and degenerative spondylolisthesis. Radiol Clin North Am,2001; 39:55-71
13 Kaapa E, Luoma K,Pitkaniemi J, et al. Correlation of size and type of Modic type 1 and 2 lesion with clinical symptoms:a descriptive study in a subgroup of chronic low back pain patients based on a university hospital patient sample. Spine 2011;14:ahead publish
1 Schwab F, Dubey A, Gamez L'et al. Adult scoliosis:prevalence, SF-36. and nutritional parameters in an elderly volunteer population. Spine (Phila Pa 1976),2005,30(9):1082-1085
2 Shufflebarger H, Suk SI, Mardjetko S. Debate:determining the upper instrumented vertebra in the management of adult degenerative scoliosis:stopping at T10 versus L1. Spine(Phila Pa 1976),2006,31(19 Suppl):S185-194
3 Bridwell KH. Degenerative scoliosis//Bridwell KH. The textbook of spinal surgery. Philadelphia:JB Lippineott,1997:728-741
4 Jenkinson C, Wrisht L, Coulter A. Criterion validity and reliability of SF-36 in a population sample. Qual Life Res,1994,3(1):7-12
5 Leon GR. Koscheyev VS, Stone EA. Visual analog scales for sessment of thermal perception in different environments. Aviat Space Environ Med,2008,79(8):784-786
6 Oskouian RJ Jr, Shaffrey CI. Degenerative lumbar scoliosis. Neurosurg Clin N Am,2006,17(3):299-315
7 Weideubaum M. Considerations for focused surgical intervention in the presence of adult spinal deformity. Spine(Phila Pa 1976),2006,31(19 Suppl):S139-143
8 Lowe T, Berven SH, Schwab FJ, et al.111e SRS classification for adult spinal deformity:building on the King/Moe and Lenke classification systems. Spine(Phila Pa 1976),2006,31(19 Suppl):S119.125
9邱勇,王斌,朱锋,等.退变性腰椎侧凸的冠状面失衡分型及对截骨矫形术式选择的意义.中华骨科杂志,2009,29(5)：418-423
10 DeWald CJ, Stanley T. Instrumentation-related complications of multilevel fusions for adult spinal deformity patients over age 65: surgical considerations and treatment options in patients with poor bone quality. Spine(Phila Pa 1976),2006.31(19 Suppl):S144-151
11 Tan JS, Kwan BK, Dvorak MF, et al. Pedicle screw motion in the osteoporotic spine after augmentation with laminar hooks, sublaminar wires, or calcium phosphate cement:a comparative analysis. Spine(Phila Pa 1976),2004,29(16):1723-1730
12 Glassman SD. Hamill CL,Bridwell KH, et al. The impact of perioperative complications on clinical outcome in adult deformity surgery. Spine(Phila Pa 1976),2007,32(24):2764-2770
13曾岩,陈仲强,郭昭庆,等.腰椎管狭窄症伴退变性腰椎侧凸患者的影像学表现与临床特点.中国脊柱脊髓杂志,2007,17(10)：753-756
14 Aebi M. ne adult scoliosis. Eur Spine J,2005,14(10):925-948
15 Edwards CC 2nd, Bridwell KH, Patel A, et al. Long adult deformity fusions to L5 and the sacrum; a matched cohort analysis. Spine(Phila Pa 1976),2004,29(18):1996-2005
1 Kobayashi T, Atsuta Y, Takemitsu M, et al. A prospective study of de novo scoliosis in a community based cohort.Spine 2006; 31:178-182
2楼才俊,陈其昕,李方才,等.腰椎间盘髓核退变的MRI表现与病理学的相关性研究.中华骨科杂志,2003,23：531-535
3 Benner B, Ehni G. Degenerative lumbar scoliosis. Spine 1979; 4:548-552
4 Tribus CB. Degenerative lumbar scoliosis evaluation and management. J Am Acad Orthop Surg 2003; 11:174-183
5王乃国,王以朋,邱贵兴,等,短节段融合对退变性腰椎侧凸邻近节段椎间角的影响.中华外科杂志,2010,48：506-510
6 Murata Y, Takahashi K, Hanaoka E. Changes in scoliotic curvature and lordotic angle during the early phase of degenerative lumbar scoliosis. Spine 2002; 27:2268-2273
7 Akhtar S, Davies JR, Caterson B. Ultrastructural localization and distribution of proteogly can in normal and scoliotic lumbar disc. Spine 2005; 30:1303-1309
8 Bertram H, Steck E, Zimmerman G, et al. Accelerated intervertebral disc degeneration in scoliosis versus physiological aging develops against a background of enhanced anabolic gene expression. Biochem Biophys Res Commun 2006; 342:963-972
9 Aebi M. The adult scoliosis. Eur Spine J 2005; 14:925-948
10 Matsumura A, Namikawa T, Terai H, et al. The influence of approach side on facet preservation in microscopic bilateral decompression via a unilateral approach for degenerative lumbar scoliosis. J Neurosurg Spine 2010; 13:758-765
11 Cho KJ, Suk SI, Park SR, et al. Risk factors of sagittal decompensation after long posterior instrumentation and fusion for degenerative lumbar scoliosis. Spine 2010; 35:1595-1601
12 Routh RH, Rumancik S, Pathak RD,et al. The relationship between bone mineral density and biomechanics in patients with osteoporosis and scoliosis. Osteoporos Int 2005; 16:1857-1863
13 Sarikaya S,Ozdolap S,Acikguz G,et al. Pregnancy-associated osteoporosis with vertebrae fractures and scoliosis. Joint Bone Spine,2004,71:84-85
1 Kobayashi T, Atsuta Y, Takemitsu M, et al.A prospective study of de novo scoliosis in a community based cohort [J].Spine,2006,31(2):178-182
2 Sengupta DK,Herkowitz HN. Lumbar spinal stenosis:treatment strategies and indications for surgery [J].Orthop Clin North AM,2003,34(2):281-295
3 Sigurd H.Berven, Vedat Deviren,Brian Mitchell,et al.Operative management of degenerative scoliosis:an evidence-based approach to surgical strategies based on clinical and radiographic outcomes. Neurosurg Clin N AM,2007,18(3):261-272
4 Pritchett JW, Bortel DT. Degenerative symptomatic lumbar scoliosis.Spine,993,18(5):700-703
5 Murata Y, Takahashi K, Hanaoka E, et al. Changes in scoliotic curvature and lordotic angle during the early phase of degenerative lumbar scoliosis[J]. Spine,2002,27(20):2268-2273
6 Faldini C, Pagkrati S, Grandi G, et al. Degenerative lumbar scoliosis:features and surgical treatment [J].J Orthop Traumatol,2006, 7(2):67-71
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