退变性腰椎侧凸演变过程及相关生物力学机制的有限元分析
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摘要
目的：探讨退变性腰椎侧凸的演变过程及其侧凸形成的相关生物力学机制。
方法：通过腰椎连续薄层CT平扫获取二维影像数据，利用Simpleware三维建模软件分别构建腰椎正常模型、退变模型、侧凸模拟模型以及临床退变性腰椎侧凸模型，进行全腰椎模型的生物力学分析，分析比较正常腰椎、退变腰椎以及退变性侧凸腰椎各结构承载变化和应力分布特点，观察腰椎侧凸演变过程中是否存在负荷和应力的转移过程，从而探讨退变性腰椎侧凸的演变过程及其促进侧凸形成的生物力学机制，为临床退变性腰椎侧凸的预防和手术治疗提供科学的依据。
结果：（1）正常腰椎承载时椎间盘髓核受压变形将轴向载荷传递至骨性终板和椎体中央，关节突关节承载较小。腰椎应力分布为髓核压应力最高、纤维环和关节突关节应力较低。（2）椎间盘退变后髓核高度降低，主要由外周纤维环承载轴向载荷，纤维环受压变形将轴向载荷传递至椎体外缘，关节突关节等后部结构应力增大、后部结构轴向负载增加，髓核压应力减小、髓核和中央终板承载较小。腰椎应力分布为纤维环、椎体外缘和小关节突较高，中央髓核则较低。（3）退变性腰椎侧凸形成后，前柱承载减少、后部结构承载增加，凹侧椎体和后部结构应力增加，椎体倾斜与楔形变增加了滑移剪力，关节突关节压缩、变形、内聚则减弱了对椎体旋转和侧移的限制作用，导致椎体向主凸侧侧移和旋转脱位，承载力线偏离中线向主凸侧移位，退变性腰椎侧凸力学失衡而不断进展恶化。
结论：退变性腰椎侧凸的形成存在明显的退变演变过程，侧凸始于腰椎间盘不对称退变，应力是始动因素也是决定因素。在正常情况下，髓核起主要承载作用，通过变形将大部分压缩载荷传递给中央终板和椎体，同时向外周膨胀将剩余载荷传递给纤维环。单侧椎间盘应力集中引起了局部椎间盘组织损害、纤维的交叉连接断裂、纤维环基质变化、椎间盘内产基质细胞凋亡等一系列变化，椎间盘出现单侧不对称退变和类似固体样的生物力学行为。椎间盘退变后，髓核脱水纤维化，其承载能力下降，椎间盘主要承载功能转移至外周纤维环；腰椎承载部位由椎体中央转移至外缘，并向后部结构转移。侧凸腰椎在偏心应力作用下，凹侧椎体受压楔形变，凸侧关节突关节受压变形、增生内聚，关节间隙增大导致椎间侧向活动范围增加，关节突关节对椎体旋转和侧移的限制作用减弱，腰椎负重后由于剪力作用椎体向凸侧旋转半脱位且侧向移位，力线偏离骶骨中垂线向主凸侧移位导致腰椎不对称性负载，腰椎出现力学失衡。由于下段L4/5、L5/S1椎间活动度较大，单侧（主凸侧）椎间盘受压易形成局部反向侧弯而部分代偿近侧原发的腰椎侧弯。若L1上终板与L5下终板平行则腰椎力线恢复平衡，侧凸代偿完全；若不平行则腰椎力线不平衡，侧凸代偿不完全。由于力学失衡，腰椎则通过神经肌肉调节、椎间盘变形、椎体楔形变、椎体旋转侧移等自身多种平衡调节机制，最终改变腰椎结构和形态重新获得腰椎力线平衡。在扭转和侧移等剪力联合作用下重建腰椎平衡，势必加剧椎间盘撕裂破坏、关节突变形内聚、椎体严重畸形，腰椎结构严重不对称变形使得退变性腰椎侧凸不断进展。因此，“应力集中-不对称退变-负载不平衡-应力损伤-腰椎结构变形破坏-腰椎平衡重建”周而复始的恶性循环形成了DDS基本演变过程的生物力学机制。
严重畸形和异常的腰椎活动导致神经通路狭窄、肌肉力学失衡、椎间盘撕裂损伤、关节突关节炎，临床表现为患者顽固的腰腿痛和神经性跛行。患者术后疗效一般较好，手术治疗的关键是彻底神经减压、通过旋转技术重建腰椎前凸、尽量纠正椎体侧移与侧凸畸形、稳定椎体并恢复腰椎正常承载的垂直力线。
Objective: To investigate the evolution and the related biomechanical mechanism ofdegenerative lumbar scoliosis via finite element analysis.
Methods: To acquire image data of the lumbar by CT scan, then to utilize Simpleware toconstruct the healthy lumbar model, the degenerative lumbar model, the lumbar scoliosissimulation model and the degenerative lumbar scoliosis model.Given800N axial load or800N axial load combined with10N.m moment on the superior end plate of L1vertebrae,to observe the stress distribution and load on the part of the lumbar,then to seewheather there is a progress that load or stress is transferred from the anterior column tothe posterior structures.By contrast,we identify the difference of the stress distributionand load transmission of the lumbar to understand the biomechanical mechanism of thedegeneration lumbar scoliosis.Through the method, we can provide a scientific basis forthe prevention and surgical treatment of clinical degenerative lumbar scoliosis.
Results:(1) The nucleus pulposus play an important role of bearing weight in healthylumbar due to high intervertebral disc pressure which can transfer axial load to the centerof the adjacent endplate and vertebrae, the contact froce of the facet joints is low. Thepressure stress in the nucleus pulposus is high,but the von mises stress is very low inannulus fibrosus or facet joints.(2) With the disc degeneration, the character of lumbarloading changed, axial load is transmitted mainly by the annulus fibrosus and is inclined tobe transfered to the rear of the vertebrae, outer edge of the vertebrae and the facet joints.Stress increases in the posterior structures obviously,and pressure stress decreases in thenucleus pulposus followed by the decline in weight-bearing capability and the endpatebearing less weight. The stress is much higher in annulus fibrosus, outer edge of thevertebrae,facet joints, but lower in nucleus pulposus. So the endplate and the intervertebraldisc bear less weight and the contact force of facet joints increases.(3) After the formationof degenerative lumbar scoliosis, loading decreases in the anterior column,and the stressincreases in the posterior structures such as facet joints.The deformation of the facet jointsdue to compression keep itself out of capability of limitting rotation and blocking listhesis.Conclusion: The evolution of the degenerative lumbar scoliosis began with lumbar discasymmetric degeneration, stress is the initiatial and determined factors. In the health, thenucleus pulposus play an important role in weight bearing, transfering the most axial loadto the central endplate, while the remaining load is transfered by the annulus fibrous.Theasymmetric degeneration in the disc caused stress concentration,fiber cross-link broken, annulus ground substance changed,and produced a lot of cells apoptosis.So the asymmetricdisc degeneration makes it similar to the solid biomechanical behavior. In degeneration,the nucleus pulposus is dehydrated, its loading capability declines and the main load istransferred to the peripheral annulus fibrous.So the spinal loading site is transfered to theouter edge of the vertebrae and posterior structures. With the eccentric compressive stress,the vertebral wedging deformation appears on the concave side and facet compressivedeformation appears on the convex side, and it decreases in the effect of the facet joints ofthe convex side to limit the vertebral rotation and listhesis due to the shear forces act whenloaded, the vertebrae had rotatory subluxation and translation to the convex side.So thespine was imbalanced by asymmetric load, and the weight bearing line of force would beoffsetted by lumbar itself. The facet joints was in subluxation and translation with seriousimbalance due to the shear forces, the destructed disc has exacerbated severely asymmetricdeformity of the lumbar structures in the continuous progress of the degenerative lumbarscoliosis. Lumbar imbalance would be offsetted to reconstruct the lumbar balance byvertebral hyperplasia deformation,vertebral rotatory dislocation and decompensation of theinferior segmental reverse scoliosis.Therefore, the vicious cycle of " stressconcentration,asymmetric degeneration,imbalanced loading,stress injury, structuraldeformation of lumbar spine, lumbar balance reconstruct " was in the evolution ofdegenerative lumbar scoliosis. Severe deformities and abnormalities of the lumbar activityleads to stenosis of spinal neural pathways, mechanical imbalance of themuscle,osteoarthritis of facet joints. The patients had low back pain and neurogenicclaudication. Generally, postoperative efficacy is satisfying and much better via surgicaltreatment. The key point is thorough nerve decompression, to reconstruct the lumbarlordosis via the rotatory technology,to correct the vertebral rotation and listhesis withscoliosis deformity, to stabilize lumbar vertebrae, to restore lumbar spinal capability ofweight-bearing and to make it vertical the loading line.
方法：通过腰椎连续薄层CT平扫获取二维影像数据，利用Simpleware三维建模软件分别构建腰椎正常模型、退变模型、侧凸模拟模型以及临床退变性腰椎侧凸模型，进行全腰椎模型的生物力学分析，分析比较正常腰椎、退变腰椎以及退变性侧凸腰椎各结构承载变化和应力分布特点，观察腰椎侧凸演变过程中是否存在负荷和应力的转移过程，从而探讨退变性腰椎侧凸的演变过程及其促进侧凸形成的生物力学机制，为临床退变性腰椎侧凸的预防和手术治疗提供科学的依据。
结果：（1）正常腰椎承载时椎间盘髓核受压变形将轴向载荷传递至骨性终板和椎体中央，关节突关节承载较小。腰椎应力分布为髓核压应力最高、纤维环和关节突关节应力较低。（2）椎间盘退变后髓核高度降低，主要由外周纤维环承载轴向载荷，纤维环受压变形将轴向载荷传递至椎体外缘，关节突关节等后部结构应力增大、后部结构轴向负载增加，髓核压应力减小、髓核和中央终板承载较小。腰椎应力分布为纤维环、椎体外缘和小关节突较高，中央髓核则较低。（3）退变性腰椎侧凸形成后，前柱承载减少、后部结构承载增加，凹侧椎体和后部结构应力增加，椎体倾斜与楔形变增加了滑移剪力，关节突关节压缩、变形、内聚则减弱了对椎体旋转和侧移的限制作用，导致椎体向主凸侧侧移和旋转脱位，承载力线偏离中线向主凸侧移位，退变性腰椎侧凸力学失衡而不断进展恶化。
结论：退变性腰椎侧凸的形成存在明显的退变演变过程，侧凸始于腰椎间盘不对称退变，应力是始动因素也是决定因素。在正常情况下，髓核起主要承载作用，通过变形将大部分压缩载荷传递给中央终板和椎体，同时向外周膨胀将剩余载荷传递给纤维环。单侧椎间盘应力集中引起了局部椎间盘组织损害、纤维的交叉连接断裂、纤维环基质变化、椎间盘内产基质细胞凋亡等一系列变化，椎间盘出现单侧不对称退变和类似固体样的生物力学行为。椎间盘退变后，髓核脱水纤维化，其承载能力下降，椎间盘主要承载功能转移至外周纤维环；腰椎承载部位由椎体中央转移至外缘，并向后部结构转移。侧凸腰椎在偏心应力作用下，凹侧椎体受压楔形变，凸侧关节突关节受压变形、增生内聚，关节间隙增大导致椎间侧向活动范围增加，关节突关节对椎体旋转和侧移的限制作用减弱，腰椎负重后由于剪力作用椎体向凸侧旋转半脱位且侧向移位，力线偏离骶骨中垂线向主凸侧移位导致腰椎不对称性负载，腰椎出现力学失衡。由于下段L4/5、L5/S1椎间活动度较大，单侧（主凸侧）椎间盘受压易形成局部反向侧弯而部分代偿近侧原发的腰椎侧弯。若L1上终板与L5下终板平行则腰椎力线恢复平衡，侧凸代偿完全；若不平行则腰椎力线不平衡，侧凸代偿不完全。由于力学失衡，腰椎则通过神经肌肉调节、椎间盘变形、椎体楔形变、椎体旋转侧移等自身多种平衡调节机制，最终改变腰椎结构和形态重新获得腰椎力线平衡。在扭转和侧移等剪力联合作用下重建腰椎平衡，势必加剧椎间盘撕裂破坏、关节突变形内聚、椎体严重畸形，腰椎结构严重不对称变形使得退变性腰椎侧凸不断进展。因此，“应力集中-不对称退变-负载不平衡-应力损伤-腰椎结构变形破坏-腰椎平衡重建”周而复始的恶性循环形成了DDS基本演变过程的生物力学机制。
严重畸形和异常的腰椎活动导致神经通路狭窄、肌肉力学失衡、椎间盘撕裂损伤、关节突关节炎，临床表现为患者顽固的腰腿痛和神经性跛行。患者术后疗效一般较好，手术治疗的关键是彻底神经减压、通过旋转技术重建腰椎前凸、尽量纠正椎体侧移与侧凸畸形、稳定椎体并恢复腰椎正常承载的垂直力线。
Objective: To investigate the evolution and the related biomechanical mechanism ofdegenerative lumbar scoliosis via finite element analysis.
Methods: To acquire image data of the lumbar by CT scan, then to utilize Simpleware toconstruct the healthy lumbar model, the degenerative lumbar model, the lumbar scoliosissimulation model and the degenerative lumbar scoliosis model.Given800N axial load or800N axial load combined with10N.m moment on the superior end plate of L1vertebrae,to observe the stress distribution and load on the part of the lumbar,then to seewheather there is a progress that load or stress is transferred from the anterior column tothe posterior structures.By contrast,we identify the difference of the stress distributionand load transmission of the lumbar to understand the biomechanical mechanism of thedegeneration lumbar scoliosis.Through the method, we can provide a scientific basis forthe prevention and surgical treatment of clinical degenerative lumbar scoliosis.
Results:(1) The nucleus pulposus play an important role of bearing weight in healthylumbar due to high intervertebral disc pressure which can transfer axial load to the centerof the adjacent endplate and vertebrae, the contact froce of the facet joints is low. Thepressure stress in the nucleus pulposus is high,but the von mises stress is very low inannulus fibrosus or facet joints.(2) With the disc degeneration, the character of lumbarloading changed, axial load is transmitted mainly by the annulus fibrosus and is inclined tobe transfered to the rear of the vertebrae, outer edge of the vertebrae and the facet joints.Stress increases in the posterior structures obviously,and pressure stress decreases in thenucleus pulposus followed by the decline in weight-bearing capability and the endpatebearing less weight. The stress is much higher in annulus fibrosus, outer edge of thevertebrae,facet joints, but lower in nucleus pulposus. So the endplate and the intervertebraldisc bear less weight and the contact force of facet joints increases.(3) After the formationof degenerative lumbar scoliosis, loading decreases in the anterior column,and the stressincreases in the posterior structures such as facet joints.The deformation of the facet jointsdue to compression keep itself out of capability of limitting rotation and blocking listhesis.Conclusion: The evolution of the degenerative lumbar scoliosis began with lumbar discasymmetric degeneration, stress is the initiatial and determined factors. In the health, thenucleus pulposus play an important role in weight bearing, transfering the most axial loadto the central endplate, while the remaining load is transfered by the annulus fibrous.Theasymmetric degeneration in the disc caused stress concentration,fiber cross-link broken, annulus ground substance changed,and produced a lot of cells apoptosis.So the asymmetricdisc degeneration makes it similar to the solid biomechanical behavior. In degeneration,the nucleus pulposus is dehydrated, its loading capability declines and the main load istransferred to the peripheral annulus fibrous.So the spinal loading site is transfered to theouter edge of the vertebrae and posterior structures. With the eccentric compressive stress,the vertebral wedging deformation appears on the concave side and facet compressivedeformation appears on the convex side, and it decreases in the effect of the facet joints ofthe convex side to limit the vertebral rotation and listhesis due to the shear forces act whenloaded, the vertebrae had rotatory subluxation and translation to the convex side.So thespine was imbalanced by asymmetric load, and the weight bearing line of force would beoffsetted by lumbar itself. The facet joints was in subluxation and translation with seriousimbalance due to the shear forces, the destructed disc has exacerbated severely asymmetricdeformity of the lumbar structures in the continuous progress of the degenerative lumbarscoliosis. Lumbar imbalance would be offsetted to reconstruct the lumbar balance byvertebral hyperplasia deformation,vertebral rotatory dislocation and decompensation of theinferior segmental reverse scoliosis.Therefore, the vicious cycle of " stressconcentration,asymmetric degeneration,imbalanced loading,stress injury, structuraldeformation of lumbar spine, lumbar balance reconstruct " was in the evolution ofdegenerative lumbar scoliosis. Severe deformities and abnormalities of the lumbar activityleads to stenosis of spinal neural pathways, mechanical imbalance of themuscle,osteoarthritis of facet joints. The patients had low back pain and neurogenicclaudication. Generally, postoperative efficacy is satisfying and much better via surgicaltreatment. The key point is thorough nerve decompression, to reconstruct the lumbarlordosis via the rotatory technology,to correct the vertebral rotation and listhesis withscoliosis deformity, to stabilize lumbar vertebrae, to restore lumbar spinal capability ofweight-bearing and to make it vertical the loading line.
引文
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[3] Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: Correlation with age, sex, andspine level in600autopsy specimens.[J]Spine,1988,13:173-178
[4] Battie MC, Videman T, Gill K, et al.Smoking and lumbar intervertebral disc degeneration: AnMRI study of identical twins.[J]Spine,1991,16:1015-1021
[5] Battle MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc degeneration. A studyrelating lifetime exposures and magnetic resonance imaging findings in identical twins.[J]Spine,1995,20:2601-2612
[6] IVlonnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen indiabetes mellitus.[J]Proc Nat Acad Sci U S A,1984,81:583-87
[7] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[8] Nachemson A: Lumbar intradisca] pressure.Experimental studies on postmortem material.[J]Acta Orthop Scand Suppl,1960,43:1-104
[9] Rand N, Juliao S, Spengler D, et al: Static Hydrostatic Loading Induces Apoptosis in Humanlntervertebral Disc Cells. Orthopaedic Research Societ3.5Orlando, FL,2000
[10] Horst M,Brinckmann P. Measurement of the distribution of axial stress on the end-plate of thevertebralbody.[J]Spine,1981,6(3):217–32
[11] McNally DS,Adams MA.Internal disc mechanics as revealed by stress proflometry.[J]Spine,1992,17:66–73
[12] Adams MA,McNally DS,Dolan P.‘Stress’ distributions inside intervertebral discs:the effects ofage and degeneration.[J]Bone Joint Surg,1996,78B(6):965–72.
[13] Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for lowback pain.[J]Spine,1984,9(6):557–65
[14] ILissette M.Ruberte′et al.Infuence of single-level lumbar degenerative disc disease on thebehavior of the adjacentsegments—A fnite element model study.[J]Journal of Biomechanics2009,42:341–348
[1]Kebaish,KM.Degenerative(De Novo) Adult Scoliosis,[J] Semin Spine Surg,2009,21(1):7-15
[2] Jacob M, Buchowski..Adult Scoliosis:Etiology and Classifcation.[J]Semin Spine Surg，2009,21:2-6
[3] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[4] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[1] Salminen JJ, Erkintalo MO, Pentti J, et al: Recurrent low back pain and early disc degenerationin the young.[J]Spine,1999,24:1316-1321,
[2] Lyons H, Jones E, Quinn FE, et al: Changes in the protein-polysaccharide fractions of nucleuspulposus from human intervertebral disc with age and disc herniation.[J] Lab ClinMed,1966,68:930-939
[3] Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: Correlation with age, sex, andspine level in600autopsy specimens.[J]Spine,1988,13:173-178
[4] Battie MC, Videman T, Gill K, et al.Smoking and lumbar intervertebral disc degeneration: AnMRI study of identical twins.[J]Spine,1991,16:1015-1021
[5] Battle MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc degeneration. A studyrelating lifetime exposures and magnetic resonance imaging findings in identical twins.[J]Spine,1995,20:2601-2612
[6] Rand N, Juliao S, Spengler D, et al: Static Hydrostatic Loading Induces Apoptosis in Humanlntervertebral Disc Cells. Orthopaedic Research Societ3.5Orlando, FL,2000
[7] IVlonnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen indiabetes mellitus.[J]Proc Nat Acad Sci U S A,1984,81:583-87
[8] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[9] Nachemson A: Lumbar intradisca] pressure.Experimental studies on postmortem material.[J]Acta Orthop Scand Suppl,1960,43:1-104
[10] Horst M,Brinckmann P. Measurement of the distribution of axial stress on the end-plate of thevertebralbody.[J]Spine,1981,6(3):217–32
[11] McNally DS,Adams MA.Internal disc mechanics as revealed by stress proflometry.[J]Spine,1992,17:66–73
[12] Adams MA,McNally DS,Dolan P.‘Stress’ distributions inside intervertebral discs:the effects ofage and degeneration.[J]Bone Joint Surg,1996,78B(6):965–72.
[13] Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for lowback pain.[J]Spine,1984,9(6):557–65
[14] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[15] Ashton IK, Ashton BA, Gibson SJ, et al.Morphological basis for back pain: The demonstrationof nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentumflavum.[J]Orthop Res,1992,10:72-78,
[1]Khaled M.Kebaish,MD.Degenerative (De novo) adult scoliosis.Semi Spine Surg,2009,21:7-15
[2]Epstein JA, Epstein BS,Jones MD.Syptomatic lumbar scoliosis with degenerative changes inelderly.Spine,1979,4:542-47
[3]Schwab FJ,Smith VA,Biserni M,et a1. Adult scoliosis: a quantitative radio-graphic and clinicalanalysis.[J]Spine,2002,27(4):387-92
[4] Glassman SD, Berven S, Bridwell K, et al. Correlation of radiographic parameters and clinicalsymptoms in adult scoliosis.Spine,2005,30:682-88
[5]Jackson RP,Simmons EH,Stripinis D.Coronal and sagittal plane spinal deformities correlatingwith back pain and pulmonary fuction in adult idiopathic scoliosis. Spine,1989,14:1391-97
[6] Crandall DG, Revella J. Transforaminal lumbar interbody fusion versus anterior lumbarinterbody fusion as an adjunct to posterior instrumented correction of degenerative lumbarscoliosis:three year clinical and radiographic outcomes. Spine,2009,34:2126-33
[7]Hsieh PC, Koski TR,et al.Anterior lumbar interbody fusion in comparison with transforaminallumbar interbody fusion:implications for the restoration of foraminal height,local disc angle,lumbarlordosis,and sagittal balance.J Neurosurg Spine2007,7:379-86
[8]Birknes JK,White TJ,shaffrey. Adult degenerative scoliosis: a review. Neurosurgery,2008,63(3suppl):94-103
[9] Polly Jr DW,Klemme WR,Cunningham BW,et al.The biomechanical significance of anteriorcolumn support in a simulated single-level spinal fusion.J Spinal Disord,2000,13:58-62
[10]Nash CL,Goldstein JM,Wilham MR.Seletion of lumbar fusion levels in adult idiopathicscoliosis patients.Presented at the Annual Meeting of the Scoliosis Research Society, Amsterdam,1989
[11]Yang SH,Chen PQ.Proximal kyphosis after short posterior fusion for thoracolumbarscoliosis.Clin Orthop Relat Res2003,411:152-58
[12]Anant D Tambe, Antony Louis Rex Michael. Adult degenerative scoliosis. Mini symposium:Spinal deformity.2011,413-424
[1]Kebaish,KM.Degenerative(De Novo) Adult Scoliosis.[J] Semin Spine Surg,2009,21(1):7-15
[2] Schwab FJ,Smith VA,Biserni M,et a1. Adult scoliosis： a quan titative radiographic and clinicalanalysis.[J]Spine，2002,27(4)：387-92
[3] Ploumis A,Transfledt E,Denis F.Degenerative lumbar scoliosis associated with spinalstenosis[J].Spine,2007.7(4):428—436．
[4]Vanderpool DW, JamesJIP, Wynne-Davies R.Scoliosis in the elderly.[J] Bone JointSurg,1969,51:446-455,
[5] Benner B, Ehni G.Degenerative lumbarscoliosis.[J] Spine,1979,4:548
[6] Perennou U, Marcelli C, Harrison C, et al.Adult lumbarscoliosis: Epidemiologicaspects in alow-hack-pain population.[J] Spine,1994,19:123
[7] Bridwell，KH.Degenerative Scoliosis..Philadelphia,PA:Lippincott-Raven,1977,pp733-775
[8]Thevenon A,PollezB,CantegritF,etal.Relationship between kyphosis, scoliosis,and osteoporosis in theelderly population.[J]Spine,1987,12:744-745
[9] Robin GC,Span Y,Steinberg R,etal:Scoliosis in the elderly:A follow-up study.[J]Spine,1982,7:355-359
[10] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[11] Jacob M, Buchowski..Adult Scoliosis:Etiology and Classifcation.[J]Semin Spine Surg，2009,21:2-6
[12] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation to determineextent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[13]Ezequiel H,Cassinelli, James D,etal. Curent Undersdanding of Lumbar Disk Degeneration.[J]Operative Tech,2000,(10) pp:254-262
[14] Buckwalter J.The fine structure of the human intervertebral disc in White A, Gordon S (eds):AAOS Symposium on Idiopathic Low Back Pain. St. Louis, MO, CV Mosby,1982, pp:108-143
[15] Yoshizawa H, O'Brien JP, Smith WT, et al.The neuropathology of intervertebral discs removed forlow-back pain.[J] Pathol,1980,132:95-104
[16] Ashton IK, Ashton BA, Gibson SJ, et al.Morphological basis for back pain: The demonstration ofnerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum.[J]Orthop Res,1992,10:72-78,
[17] Ohshima H, Urban JP, Bergel DH: Effect of static load on matrix synthesis rates in theintervertebral disc measured in vitro by a new perfusion technique.[J]Orthop Res,1995,13:22-29
[18] Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance scans of the lumbar spine inasymptomatic subjects. A prospective investigation.[J]Bone Joint Surg,1990,72:403-408,
[19] Salminen JJ, Erkintalo MO, Pentti J, et al: Recurrent low back pain and early disc degeneration inthe young.[J]Spine,1999,24:1316-1321,
[20] Lyons H, Jones E, Quinn FE, et al: Changes in the protein-polysaccharide fractions of nucleuspulposus from human intervertebral disc with age and disc herniation.[J] Lab ClinMed,1966,68:930-939
[21] Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: Correlation with age, sex, and spinelevel in600autopsy specimens.[J]Spine,1988,13:173-178
[22] Battie MC, Videman T, Gill K, et al.Smoking and lumbar intervertebral disc degeneration: An MRIstudy of identical twins.[J]Spine,1991,16:1015-1021
[23] Battle MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc degeneration. A studyrelating lifetime exposures and magnetic resonance imaging findings in identical twins.[J]Spine,1995,20:2601-2612
[24] IVlonnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen indiabetes mellitus.[J]Proc Nat Acad Sci U S A,1984,81:583-87
[25] Nachemson A: Lumbar intradisca] pressure.Experimental studies on postmortem material.[J]ActaOrthop Scand Suppl,1960,43:1-104
[26]Liu YK,Njus G,Buckwalter J,etal.Fatigue response of lumbar intervertebral joints under axial cyclicloading.[J]Spine,1983,8:857-865
[27] Adams MA, Hutton WC: The relevance of torsion to the mechanical derangement of the lumbarspine.[J]Spine,1981,6:241-248,
[28] Rand N, Juliao S, Spengler D, et al: Static Hydrostatic Loading Induces Apoptosis in Humanlntervertebral Disc Cells. Orthopaedic Research Societ3.5Orlando, FL,2000
[29] Horst M,Brinckmann P. Measurement of the distribution of axial stress on the end-plate of thevertebralbody.[J]Spine,1981,6(3):217–32
[30] McNally DS,Adams MA.Internal disc mechanics as revealed by stress proflometry.[J]Spine,1992,17:66–73
[31] Adams MA,McNally DS,Dolan P.‘Stress’ distributions inside intervertebral discs:the effects of ageand degeneration.[J]Bone Joint Surg,1996,78B(6):965–72.
[32] Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for lowback pain.[J]Spine,1984,9(6):557–65
[33] Christina A,Thomas R.Oxland,PhD. Degenerative mechanics of the lumbar spine.[J]TheSpineJournal,2004,4:202–208
[2] Robin GC, Span Y, Steinberg R, Makin M, Menczel J. Scoliosis in the elderly: a follow-upstudy. Spine，1982,7(4):355-359
[3] Thevenon A, Pollez B, Cantegrit F,et al. Relationship between kyphosis, scoliosis, andosteoporosis in the elderly population. Spine,1987,12(8):744-745
[4] Kebaish KM.Degenerative (De Novo) Adult Scoliosis. Semi Spine Surg,2009,21:7-15
[5] Goto M, Kawakami N, Azegami H, et al. Buckling and bone modeling as factors in thedevelopment of idiopathic scoliosis. Spine2003,28(4):364-370
[6] Gignac D, Aubin CE, Dansereau J,et al.Optimization method for3D bracing correction ofscoliosis using a finite element model. Eur Spine J,2000,9(3):185-190
[7] Lim TH, Kim JG, Fujiwara A,et al.Biomechanical evaluation of diagonal fixation in pediclescrew instrumentation. Spine,2001,26(22):2498-2503
[8]刘耀升，陈其昕，廖胜辉，等.椎间盘高度降低及退变对腰椎生物力学影响的有限元分析[J].中国临床解剖学杂志，2006,24（5）：566-570
[9]马辉，赵杰，连小峰，等.腰椎滑脱后路不同融合术式的有限元研究[J].中华骨科杂志，2007,27（4）：282-286
[10]张美超，程立明，李义凯，等.三维有限元在正常与后凸畸形胸腰椎体力学性能比较中的应用[J].中国康复医学杂志，2003,18（11）：653-655
[11]余列道，杨国敬，张力成，等.胸腰段三维非线性有限元建模及临床意义[J].浙江创伤外科，2002,7（5）：281-283
[1]关海山，韩来春，马迅，等．有限元研究肌肉力对胸腰椎节段椎体应力的影像[J]．中国药物与临床，2007，7（12）：904-907
[2]王永福.Lenke5型青少年特发性脊柱侧凸有限元模型的建立及手术矫形的生物力学研究．[博士学位论文]，广州：中南大学，2010
[3] Buckwalter J.The fine structure of the human intervertebral disc in White A, Gordon S(eds).AAOS Symposium on Idiopathic Low Back Pain. St. Louis, MO, CV Mosby,1982, pp:108-143
[4]White AA,Panjabi MM.Clinical biomechanics of the spine..2nded.Philadelphia:Lippincott,1990.
[5] Yoshizawa H, O'Brien JP, Smith WT, et al.The neuropathology of intervertebral discs removedfor low-back pain.[J] Pathol,1980,132:95-104
[6] Ashton IK, Ashton BA, Gibson SJ, et al.Morphological basis for back pain: The demonstrationof nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum.[J]Orthop Res,1992,10:72-78,
[7]Ohshima H, Urban JP, Bergel DH: Effect of static load on matrix synthesis rates in theintervertebral disc measured in vitro by a new perfusion technique.[J]Orthop Res,1995,13:22-29
[8]杜东鹏，于进祥，葛宝丰.腰椎间盘膨隆的有限元分析.[J]．颈腰痛杂志，2000，21（1）：904-907：6-7
[9]Nachemson A.Lumbar intradiscal pressure.[J] Acta Ortho Scand，1960;43(suppl):1–104.
[10]Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for low-back pain.[J]Spine，1984，9(6):557–65.
[11]Nachemson A.The load on lumbar discs in different positions of the body.[J] ClinOrthop,1966，45:107–22.
[12]Shirazi-Adl A.Finite-element simulation of changes in the fuid content of human lumbar discs:mechanical and clinical implications.[J]Spine,1992,17(2):206–12
[1] Salminen JJ, Erkintalo MO, Pentti J, et al: Recurrent low back pain and early disc degenerationin the young.[J]Spine,1999,24:1316-1321,
[2] Lyons H, Jones E, Quinn FE, et al: Changes in the protein-polysaccharide fractions of nucleuspulposus from human intervertebral disc with age and disc herniation.[J] Lab ClinMed,1966,68:930-939
[3] Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: Correlation with age, sex, andspine level in600autopsy specimens.[J]Spine,1988,13:173-178
[4] Battie MC, Videman T, Gill K, et al.Smoking and lumbar intervertebral disc degeneration: AnMRI study of identical twins.[J]Spine,1991,16:1015-1021
[5] Battle MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc degeneration. A studyrelating lifetime exposures and magnetic resonance imaging findings in identical twins.[J]Spine,1995,20:2601-2612
[6] IVlonnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen indiabetes mellitus.[J]Proc Nat Acad Sci U S A,1984,81:583-87
[7] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[8] Nachemson A: Lumbar intradisca] pressure.Experimental studies on postmortem material.[J]Acta Orthop Scand Suppl,1960,43:1-104
[9] Rand N, Juliao S, Spengler D, et al: Static Hydrostatic Loading Induces Apoptosis in Humanlntervertebral Disc Cells. Orthopaedic Research Societ3.5Orlando, FL,2000
[10] Horst M,Brinckmann P. Measurement of the distribution of axial stress on the end-plate of thevertebralbody.[J]Spine,1981,6(3):217–32
[11] McNally DS,Adams MA.Internal disc mechanics as revealed by stress proflometry.[J]Spine,1992,17:66–73
[12] Adams MA,McNally DS,Dolan P.‘Stress’ distributions inside intervertebral discs:the effects ofage and degeneration.[J]Bone Joint Surg,1996,78B(6):965–72.
[13] Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for lowback pain.[J]Spine,1984,9(6):557–65
[14] ILissette M.Ruberte′et al.Infuence of single-level lumbar degenerative disc disease on thebehavior of the adjacentsegments—A fnite element model study.[J]Journal of Biomechanics2009,42:341–348
[1]Kebaish,KM.Degenerative(De Novo) Adult Scoliosis,[J] Semin Spine Surg,2009,21(1):7-15
[2] Jacob M, Buchowski..Adult Scoliosis:Etiology and Classifcation.[J]Semin Spine Surg，2009,21:2-6
[3] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[4] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[1] Salminen JJ, Erkintalo MO, Pentti J, et al: Recurrent low back pain and early disc degenerationin the young.[J]Spine,1999,24:1316-1321,
[2] Lyons H, Jones E, Quinn FE, et al: Changes in the protein-polysaccharide fractions of nucleuspulposus from human intervertebral disc with age and disc herniation.[J] Lab ClinMed,1966,68:930-939
[3] Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: Correlation with age, sex, andspine level in600autopsy specimens.[J]Spine,1988,13:173-178
[4] Battie MC, Videman T, Gill K, et al.Smoking and lumbar intervertebral disc degeneration: AnMRI study of identical twins.[J]Spine,1991,16:1015-1021
[5] Battle MC, Videman T, Gibbons LE, et al. Determinants of lumbar disc degeneration. A studyrelating lifetime exposures and magnetic resonance imaging findings in identical twins.[J]Spine,1995,20:2601-2612
[6] Rand N, Juliao S, Spengler D, et al: Static Hydrostatic Loading Induces Apoptosis in Humanlntervertebral Disc Cells. Orthopaedic Research Societ3.5Orlando, FL,2000
[7] IVlonnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen indiabetes mellitus.[J]Proc Nat Acad Sci U S A,1984,81:583-87
[8] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation todetermine extent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[9] Nachemson A: Lumbar intradisca] pressure.Experimental studies on postmortem material.[J]Acta Orthop Scand Suppl,1960,43:1-104
[10] Horst M,Brinckmann P. Measurement of the distribution of axial stress on the end-plate of thevertebralbody.[J]Spine,1981,6(3):217–32
[11] McNally DS,Adams MA.Internal disc mechanics as revealed by stress proflometry.[J]Spine,1992,17:66–73
[12] Adams MA,McNally DS,Dolan P.‘Stress’ distributions inside intervertebral discs:the effects ofage and degeneration.[J]Bone Joint Surg,1996,78B(6):965–72.
[13] Yang KH,KingAI. Mechanism of facet load transmission as a hypothesis for lowback pain.[J]Spine,1984,9(6):557–65
[14] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[15] Ashton IK, Ashton BA, Gibson SJ, et al.Morphological basis for back pain: The demonstrationof nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentumflavum.[J]Orthop Res,1992,10:72-78,
[1]Khaled M.Kebaish,MD.Degenerative (De novo) adult scoliosis.Semi Spine Surg,2009,21:7-15
[2]Epstein JA, Epstein BS,Jones MD.Syptomatic lumbar scoliosis with degenerative changes inelderly.Spine,1979,4:542-47
[3]Schwab FJ,Smith VA,Biserni M,et a1. Adult scoliosis: a quantitative radio-graphic and clinicalanalysis.[J]Spine,2002,27(4):387-92
[4] Glassman SD, Berven S, Bridwell K, et al. Correlation of radiographic parameters and clinicalsymptoms in adult scoliosis.Spine,2005,30:682-88
[5]Jackson RP,Simmons EH,Stripinis D.Coronal and sagittal plane spinal deformities correlatingwith back pain and pulmonary fuction in adult idiopathic scoliosis. Spine,1989,14:1391-97
[6] Crandall DG, Revella J. Transforaminal lumbar interbody fusion versus anterior lumbarinterbody fusion as an adjunct to posterior instrumented correction of degenerative lumbarscoliosis:three year clinical and radiographic outcomes. Spine,2009,34:2126-33
[7]Hsieh PC, Koski TR,et al.Anterior lumbar interbody fusion in comparison with transforaminallumbar interbody fusion:implications for the restoration of foraminal height,local disc angle,lumbarlordosis,and sagittal balance.J Neurosurg Spine2007,7:379-86
[8]Birknes JK,White TJ,shaffrey. Adult degenerative scoliosis: a review. Neurosurgery,2008,63(3suppl):94-103
[9] Polly Jr DW,Klemme WR,Cunningham BW,et al.The biomechanical significance of anteriorcolumn support in a simulated single-level spinal fusion.J Spinal Disord,2000,13:58-62
[10]Nash CL,Goldstein JM,Wilham MR.Seletion of lumbar fusion levels in adult idiopathicscoliosis patients.Presented at the Annual Meeting of the Scoliosis Research Society, Amsterdam,1989
[11]Yang SH,Chen PQ.Proximal kyphosis after short posterior fusion for thoracolumbarscoliosis.Clin Orthop Relat Res2003,411:152-58
[12]Anant D Tambe, Antony Louis Rex Michael. Adult degenerative scoliosis. Mini symposium:Spinal deformity.2011,413-424
[1]Kebaish,KM.Degenerative(De Novo) Adult Scoliosis.[J] Semin Spine Surg,2009,21(1):7-15
[2] Schwab FJ,Smith VA,Biserni M,et a1. Adult scoliosis： a quan titative radiographic and clinicalanalysis.[J]Spine，2002,27(4)：387-92
[3] Ploumis A,Transfledt E,Denis F.Degenerative lumbar scoliosis associated with spinalstenosis[J].Spine,2007.7(4):428—436．
[4]Vanderpool DW, JamesJIP, Wynne-Davies R.Scoliosis in the elderly.[J] Bone JointSurg,1969,51:446-455,
[5] Benner B, Ehni G.Degenerative lumbarscoliosis.[J] Spine,1979,4:548
[6] Perennou U, Marcelli C, Harrison C, et al.Adult lumbarscoliosis: Epidemiologicaspects in alow-hack-pain population.[J] Spine,1994,19:123
[7] Bridwell，KH.Degenerative Scoliosis..Philadelphia,PA:Lippincott-Raven,1977,pp733-775
[8]Thevenon A,PollezB,CantegritF,etal.Relationship between kyphosis, scoliosis,and osteoporosis in theelderly population.[J]Spine,1987,12:744-745
[9] Robin GC,Span Y,Steinberg R,etal:Scoliosis in the elderly:A follow-up study.[J]Spine,1982,7:355-359
[10] Pritchett JW,Bortel DT.Degenerative symptomatic lumbar scoliosis.[J] Spine,1993,18:700-703
[11] Jacob M, Buchowski..Adult Scoliosis:Etiology and Classifcation.[J]Semin Spine Surg，2009,21:2-6
[12] Lenke LG,Betz RR,HarmsJ,etal.Adolescent idiopathic scoliosis:A new classifcation to determineextent of spinal arthrodesis.[J] Bone Joint Surg,2001,83:1169-1181
[13]Ezequiel H,Cassinelli, James D,etal. Curent Undersdanding of Lumbar Disk Degeneration.[J]Operative Tech,2000,(10) pp:254-262
[14] Buckwalter J.The fine structure of the human intervertebral disc in White A, Gordon S (eds):AAOS Symposium on Idiopathic Low Back Pain. St. Louis, MO, CV Mosby,1982, pp:108-143
[15] Yoshizawa H, O'Brien JP, Smith WT, et al.The neuropathology of intervertebral discs removed forlow-back pain.[J] Pathol,1980,132:95-104
[16] Ashton IK, Ashton BA, Gibson SJ, et al.Morphological basis for back pain: The demonstration ofnerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum.[J]Orthop Res,1992,10:72-78,
[17] Ohshima H, Urban JP, Bergel DH: Effect of static load on matrix synthesis rates in theintervertebral disc measured in vitro by a new perfusion technique.[J]Orthop Res,1995,13:22-29
[18] Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance scans of the lumbar spine inasymptomatic subjects. A prospective investigation.[J]Bone Joint Surg,1990,72:403-408,
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