颈椎前路融合术后螺钉周围骨密度变化及相邻椎间盘退变的实验研究
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摘要
研究目的
随着社会老龄化的加速和交通的日益发展和生活质量的渐高要求,因脊椎损伤、脊椎退变性疾病和脊柱畸形的就诊的病例数日益增加,需行钉板或钉棒内固定术者也越来越多,这也要求脊柱外科医生对颈椎内固定术后受固定脊椎有一深入的了解,从而有利于手术方法、手术器械和内固定技术的不断发展。研究表明颈前路内固定术后,颈椎螺钉的拔出力及最大扭力矩和颈椎体的骨密度密切相关,植入物上下椎板的塌陷和植入物的沉陷也与之密切相关。故有学者建议性颈前路植骨融合术前先测颈椎的骨密度。对于脊柱钉板或钉棒内固定术后其周围椎体骨密度情况目前尚缺乏研究。
近年来,随着内固定器械的日趋成熟,脊柱融合术的成功率明显提高,而脊柱融合术后邻近节段退变问题变得更突出。颈椎融合术后邻近节段退变的病理主要是颈椎病样改变,如颈椎前后方骨赘形成、椎间隙变窄、椎体滑移等,亦可发生椎间盘突出、黄韧带肥厚、椎管狭窄等,邻近节段退变多发生于融合的上方节段,颈椎前路椎体间融合术后邻近节段的发生率为6-60%。在退变椎间盘的基因治疗中,转化生长因子-β1(TGF-β1)和骨形态发生蛋白-7(BMP-7)是研究最多的目的基因。1991年Thompson等首先描述通过外源性转化生长因子(TGF-β1)转入犬椎间盘细胞能增加蛋白多糖的合成,开创了椎间盘基因治疗的先河。骨形态发生蛋白(BMP)是转化生长因子超家族的成员,BMP及其受体几乎遍及所有组织器官,在动物的生长发育中,功能涉及胚胎学、发育学、进化学、基因学和病理学多种学科。1990年发现BMP-7以来,越来越多的实验证明rhBMP-7能促进体外培养的兔髓核和纤维环细胞增加蛋白多糖的合成。An HS等在正常的低龄兔子腰椎内注入BMP-7后发现,注入BMP-7组相较于注入生理盐水组椎间盘长高高度增加和椎间盘内胶原和蛋白多糖增多,但据统计学分析,没有统计学上的差别,建议在往随年龄退变的人体椎间盘内注入合成代谢的细胞因子之前需进行反复的动物实验。选山羊为实验动物模型进行颈前路融合研究,其根据是山羊是颈椎前路椎间融合研究中最理想的实验动物。山羊具有头部直立、颈椎垂直负重等特点。脊椎融合的生物力学环境与人体相似,而且山羊的椎间盘和椎体的大小也与人的相似,能够有效地比较植入物在人体的情况。人们利用山羊进行了多方面的研究。如检测各种生长因子对融合的作用、比较不同的骨移植材料及不同椎间融合器械促进脊柱融合方面的作用。
文献报道,颈前路内固定融合术后,颈椎BMD、BMC与颈前路螺钉的拔出力和最大扭力矩有密切的线性相关。椎体的最大抗压缩力和刚度与BMD关系的研究也证明了密切的相关。颈椎椎体骨密度是预示颈椎终板力学性能的重要指标,其对终板力学强度有重要影响。另实验也证明了颈前路植骨融合钢板内固定术后,螺钉拔出力和最大扭力矩与固定前椎体的骨密度有密切的相关性。检测椎体骨密度对于预示植入物沉陷和颈前路螺钉的脱出、进而假关节的形成有一定意义。
椎间盘是脊柱运动功能单位中最关键的结构,生理老化和病理损害导致的椎间盘退变常使椎间盘破坏,其破坏后不但引起椎间盘源性疾病,而且将引起脊柱的生物力学紊乱。诸多实验证实了促代谢合成的细胞因子如BMP-7能有效刺激椎间盘内蛋白多糖和胶原的合成,有效保持其椎间盘高度;其在生物力学上的意义也得到了实验证实。美国FDA已经批准BMP-7进行了临床实验。促代谢合成的细胞因子如BMP-7如果经临床证实有延缓椎间盘退变意义,那将对脊柱外科学产生重要的影响,颈前路融合术后融合节段注入促代谢合成的细胞因子将成为一种常规,早期退变的椎间盘注入该种细胞因子后可能减轻或延缓其退变。目前对于BMP-7的研究多限于对创伤、退变等兔子腰椎间盘。
本试验建立颈椎前路融合术后动物模型,螺钉周围骨密度以及相邻椎间盘的变化,为指导临床治疗、康复提供理论依据。
研究方法:
1、体位:仰卧位,应用布代固定四肢于动物试验台上
2、建立静脉通道。
3、麻醉方式:插管静脉全麻。麻醉药物:氯胺酮
4、标本分组:
分三组,
Ⅰ正常组(N):无需手术等干预4只
Ⅱ:固定3个月组(F3) 5只
Ⅲ:固定6个月组(F6) 5只
5、手术:颈前路C4椎体切除+钛网植骨内固定术
术后处理:无需外固定,切口不拆线,抗生素应用5-7天
6、放养:分为3个月、6个月两组,自由进食,部分限制活动
7、取标本:
(1)处死方式:窒息
(2)选取椎间盘的节段:C2/3、C5/6
(3)选取部位:髓核、纤维环、椎体
(4)数量:每节段、每部位3个,一共(14×2×2×3)=168个
(5)保存方式:-80°低温冰箱
8、测试:
A:纤维环免疫组化测试项目:COL1、COL2、BMP-2/4阳性细胞,髓核测试项目:COL1、COL2、AGGRECAN(聚集蛋白聚糖)、BMP2、docorin、biglycan(双糖链蛋白多糖,二聚糖)、MMP-13、TIMP-1
B:骨密度测试,关键在于螺钉周围的骨密度
C:测试计分(Videman椎间盘半定量数字评估)
具体方法是:选择SE脉冲序列(为尽可能减小因主观因素所产生的偶然误差,要求由两个以上的专业人员)对每个椎间盘的前、中、后三部分退变程度进行主观评估,根据退变程度评定为四级:
Ⅰ级,椎间盘无退变征象,显示为高信号密度,评定为0分;
Ⅱ级,轻度退变,信号密度轻微的降低,1分;
Ⅲ级,中等程度退变,信号密度中等程度的降低,2分;
Ⅳ级,严重退变,信号缺失,评定为3分。
每个椎间盘退变分数为前、中、后三部分退变分数之和,变化范围0～9,0分无退变,9分退变最为严重。
D:PCR检测
检测的基因:1>TIMP-1(NM 001009319)
2>biglycan(NM_001009201)
3>BMP-4(NM_001114767)
内参基因:GAPDH(AF030943)
结果:1、成功制作羊颈椎前路融合术后的退变的模型,作为研究对象。2、在影像学的观察中,在实验组三个月后,在X光片上可以看到明确的骨质退变。在手术干预的情况下,时间越长,椎体退变在X线上的表现越明显。在MRI的评分中,实验组三个月后,在MRI上可以看到明确的椎间盘的退变。但是实验组三个月与六个月的椎间盘退变在MRI的表现上未见明显差异。3、骨密度的测试结果表明,在对照组的试验动物中,骨密度无明显变化。三个月的时间尚短,由内固定引起的骨密度改变的情况尚未发生。实验组六个月,由内固定引起的骨密度降低的情况已经发生。同时,钉道添塞骨屑对保持椎体的骨密度是有效的。手术融合后,固定的椎体的骨密度在六个月内的变化无差异。4、Ⅰ型胶原在纤维环中的含量较高,实验组三个月、六个月的Ⅰ型胶原的含量较对照组明显增高,说明在固定融合,椎体相邻节段椎间盘的纤维环发生退变。而融合椎体上位和下位椎间盘纤维环的退变在术后六个月的期限内尚未看到明显差异。内固定六个月组的BMP2/4阳性细胞的表达数量较对照组明显降低而对照组与实验组三个月的BMP2/4阳性细胞的表达数目的差异无显著性,这说明,在融合后六个月的时间,BMP2/4阳性细胞明显的消耗降低,这也是椎间盘退变的征相之一。Ⅱ型胶原的变化以及意义同BMP2/4阳性细胞。实验组三个月和六个月的MMP-13、TIMP-1的量较对照组明显升高,说明在内固定后,椎体相邻节段椎间盘的髓核发生退变。5、在PCR的试验中,观察3个月及6个月实验组比对照组Timp-1、Bmp-15和biglycan基因表达量均增加(p＜0.05),术后3月组与术后6个月组组比未见明显的统计学差异(p＞0.05)。说明,在手术干预的情况下,内固定术后三个月与六个月的椎间盘发生退变(较对照组),但是试验组3个月和6个月并无明显差异。
结论:建立颈椎前路融合的退变模型,通过检测骨密度、椎间盘的变化和说明:颈椎融合术后,相邻节段椎间盘较未行固定的椎间盘退变发生的要早而且程度严重。
Objective.In the world,people have higher quality on life.On the same time, the aged will be the main stream and the traffic is more developed than any other years.So the spine injury,spine degeneration diseases and spine deformations occur more equent than before which need to be treat with internal fixation.We must know more situation about the spine after internal fixations to make the surgery method,instruments and the internal fixation technology better than before.Some research shows that the BMD is related to the power of screws extraction and the collapse of the implants.People also suggest that we should test the BMD of the cervical before fixing on them.Now the BMD exchangment around the screws has not been investigated.
In these years,spine fusions have the higher achievement ratio which lead to the ASD occurring more often.The ASD of cervical spine after fusion is to show that osteophyma formation,narrow intervertebral space,vertebrae slippage, intervertebral disk hernia,spinal stenosis,flaval ligaments thickening and so on. ASD often occer on the upper segment of fusion and it has the rate of 6-60%after the cervical fusion.The TGF-β1 and the BMP-7 are researched as the treatment gene on intervertebral disk degeneration.Thompson described that the TGF-β1 can enhance the PG,which is the first describtion on gene treatment.BMP nearly is on all of the organs which contains the cyemology,auxanology and so on.After 1990,lots of tests showed that rhBMP-7 can enhance the PG of the rabbits. However AnHS got the contrast goal.Goat is the best animal as the model of anterior cervical fusions because it has the characteristic of rectal head and perpendicular weight loading.Besides,goat has the same size of intervertebral disk as person and the same biomechanics as people.The goat has been used to test the role of GF,bone graft,and so on.
After anterior cervical fusion,the BMD、BMC are related to the screws extraction.BMD is an important index on end-plate mechanics.The test of centrum vertebrae BMD is significant to precede the implant sinking,screws extraction and false articulation.
Intervertebral disk is the important structure in spine motion function. Retrogradation and injury are the main reasons to damage it,which can cause not only the intervertebral disk diseases,but also disturb the spine motion.Many researches showed the BMP-7's role on the biomechanics.Now,the research on BMP-7 is just on the rabbit about the injury and degeneration.
Our test will establish the animal model on anterior cervical fusions and research the bone density around the screws,biochemistry in intervertebral disks and the imageology variations.All of above are served for clinic treatment by providing the evidence.
Methods.
1 body position:dorsal position,with the extremities binded on the operation table
2 transfusion
3 anaesthesia:general anaesthesia with tracheal intubation
4 grouping:dividing into 3 groups
Ⅰ:normal 4 goats
Ⅱ:fixation 3 months 5 goats
Ⅲ:fixation 6 months 5 goats
5 operation:
6 post-operation:without external fixation,with antibiotics 5-7 days
7 breeding:foodintake freely
8 type of executing:asphyxiation
9 segment of intervertebral disks:C2/3 and C5/6
10 position:nucleus gelatinosus annular fibrosus centrum vertebrae
11 items of test:Immunohistochemistry BMD imageology PCR
Results.After establishing the models and researching all the data,we get the results as follows:(1)Degenerations on intervertebral discs appear more earlier and serious than the control.(2) The bone density around the screws are decreasing more earlier and serious than the control.(3)The MRI shows that Degenerations on intervertebral discs appear more earlier and serious than the control
Conclusion.Establishing the goat model of anterior cervical fusion and researching the bone density around the screws,biochemistry in intervertebral disks and the MRI variations,which show that ASD must have happened after operation.Our surgeons should consider it.
随着社会老龄化的加速和交通的日益发展和生活质量的渐高要求,因脊椎损伤、脊椎退变性疾病和脊柱畸形的就诊的病例数日益增加,需行钉板或钉棒内固定术者也越来越多,这也要求脊柱外科医生对颈椎内固定术后受固定脊椎有一深入的了解,从而有利于手术方法、手术器械和内固定技术的不断发展。研究表明颈前路内固定术后,颈椎螺钉的拔出力及最大扭力矩和颈椎体的骨密度密切相关,植入物上下椎板的塌陷和植入物的沉陷也与之密切相关。故有学者建议性颈前路植骨融合术前先测颈椎的骨密度。对于脊柱钉板或钉棒内固定术后其周围椎体骨密度情况目前尚缺乏研究。
近年来,随着内固定器械的日趋成熟,脊柱融合术的成功率明显提高,而脊柱融合术后邻近节段退变问题变得更突出。颈椎融合术后邻近节段退变的病理主要是颈椎病样改变,如颈椎前后方骨赘形成、椎间隙变窄、椎体滑移等,亦可发生椎间盘突出、黄韧带肥厚、椎管狭窄等,邻近节段退变多发生于融合的上方节段,颈椎前路椎体间融合术后邻近节段的发生率为6-60%。在退变椎间盘的基因治疗中,转化生长因子-β1(TGF-β1)和骨形态发生蛋白-7(BMP-7)是研究最多的目的基因。1991年Thompson等首先描述通过外源性转化生长因子(TGF-β1)转入犬椎间盘细胞能增加蛋白多糖的合成,开创了椎间盘基因治疗的先河。骨形态发生蛋白(BMP)是转化生长因子超家族的成员,BMP及其受体几乎遍及所有组织器官,在动物的生长发育中,功能涉及胚胎学、发育学、进化学、基因学和病理学多种学科。1990年发现BMP-7以来,越来越多的实验证明rhBMP-7能促进体外培养的兔髓核和纤维环细胞增加蛋白多糖的合成。An HS等在正常的低龄兔子腰椎内注入BMP-7后发现,注入BMP-7组相较于注入生理盐水组椎间盘长高高度增加和椎间盘内胶原和蛋白多糖增多,但据统计学分析,没有统计学上的差别,建议在往随年龄退变的人体椎间盘内注入合成代谢的细胞因子之前需进行反复的动物实验。选山羊为实验动物模型进行颈前路融合研究,其根据是山羊是颈椎前路椎间融合研究中最理想的实验动物。山羊具有头部直立、颈椎垂直负重等特点。脊椎融合的生物力学环境与人体相似,而且山羊的椎间盘和椎体的大小也与人的相似,能够有效地比较植入物在人体的情况。人们利用山羊进行了多方面的研究。如检测各种生长因子对融合的作用、比较不同的骨移植材料及不同椎间融合器械促进脊柱融合方面的作用。
文献报道,颈前路内固定融合术后,颈椎BMD、BMC与颈前路螺钉的拔出力和最大扭力矩有密切的线性相关。椎体的最大抗压缩力和刚度与BMD关系的研究也证明了密切的相关。颈椎椎体骨密度是预示颈椎终板力学性能的重要指标,其对终板力学强度有重要影响。另实验也证明了颈前路植骨融合钢板内固定术后,螺钉拔出力和最大扭力矩与固定前椎体的骨密度有密切的相关性。检测椎体骨密度对于预示植入物沉陷和颈前路螺钉的脱出、进而假关节的形成有一定意义。
椎间盘是脊柱运动功能单位中最关键的结构,生理老化和病理损害导致的椎间盘退变常使椎间盘破坏,其破坏后不但引起椎间盘源性疾病,而且将引起脊柱的生物力学紊乱。诸多实验证实了促代谢合成的细胞因子如BMP-7能有效刺激椎间盘内蛋白多糖和胶原的合成,有效保持其椎间盘高度;其在生物力学上的意义也得到了实验证实。美国FDA已经批准BMP-7进行了临床实验。促代谢合成的细胞因子如BMP-7如果经临床证实有延缓椎间盘退变意义,那将对脊柱外科学产生重要的影响,颈前路融合术后融合节段注入促代谢合成的细胞因子将成为一种常规,早期退变的椎间盘注入该种细胞因子后可能减轻或延缓其退变。目前对于BMP-7的研究多限于对创伤、退变等兔子腰椎间盘。
本试验建立颈椎前路融合术后动物模型,螺钉周围骨密度以及相邻椎间盘的变化,为指导临床治疗、康复提供理论依据。
研究方法:
1、体位:仰卧位,应用布代固定四肢于动物试验台上
2、建立静脉通道。
3、麻醉方式:插管静脉全麻。麻醉药物:氯胺酮
4、标本分组:
分三组,
Ⅰ正常组(N):无需手术等干预4只
Ⅱ:固定3个月组(F3) 5只
Ⅲ:固定6个月组(F6) 5只
5、手术:颈前路C4椎体切除+钛网植骨内固定术
术后处理:无需外固定,切口不拆线,抗生素应用5-7天
6、放养:分为3个月、6个月两组,自由进食,部分限制活动
7、取标本:
(1)处死方式:窒息
(2)选取椎间盘的节段:C2/3、C5/6
(3)选取部位:髓核、纤维环、椎体
(4)数量:每节段、每部位3个,一共(14×2×2×3)=168个
(5)保存方式:-80°低温冰箱
8、测试:
A:纤维环免疫组化测试项目:COL1、COL2、BMP-2/4阳性细胞,髓核测试项目:COL1、COL2、AGGRECAN(聚集蛋白聚糖)、BMP2、docorin、biglycan(双糖链蛋白多糖,二聚糖)、MMP-13、TIMP-1
B:骨密度测试,关键在于螺钉周围的骨密度
C:测试计分(Videman椎间盘半定量数字评估)
具体方法是:选择SE脉冲序列(为尽可能减小因主观因素所产生的偶然误差,要求由两个以上的专业人员)对每个椎间盘的前、中、后三部分退变程度进行主观评估,根据退变程度评定为四级:
Ⅰ级,椎间盘无退变征象,显示为高信号密度,评定为0分;
Ⅱ级,轻度退变,信号密度轻微的降低,1分;
Ⅲ级,中等程度退变,信号密度中等程度的降低,2分;
Ⅳ级,严重退变,信号缺失,评定为3分。
每个椎间盘退变分数为前、中、后三部分退变分数之和,变化范围0～9,0分无退变,9分退变最为严重。
D:PCR检测
检测的基因:1>TIMP-1(NM 001009319)
2>biglycan(NM_001009201)
3>BMP-4(NM_001114767)
内参基因:GAPDH(AF030943)
结果:1、成功制作羊颈椎前路融合术后的退变的模型,作为研究对象。2、在影像学的观察中,在实验组三个月后,在X光片上可以看到明确的骨质退变。在手术干预的情况下,时间越长,椎体退变在X线上的表现越明显。在MRI的评分中,实验组三个月后,在MRI上可以看到明确的椎间盘的退变。但是实验组三个月与六个月的椎间盘退变在MRI的表现上未见明显差异。3、骨密度的测试结果表明,在对照组的试验动物中,骨密度无明显变化。三个月的时间尚短,由内固定引起的骨密度改变的情况尚未发生。实验组六个月,由内固定引起的骨密度降低的情况已经发生。同时,钉道添塞骨屑对保持椎体的骨密度是有效的。手术融合后,固定的椎体的骨密度在六个月内的变化无差异。4、Ⅰ型胶原在纤维环中的含量较高,实验组三个月、六个月的Ⅰ型胶原的含量较对照组明显增高,说明在固定融合,椎体相邻节段椎间盘的纤维环发生退变。而融合椎体上位和下位椎间盘纤维环的退变在术后六个月的期限内尚未看到明显差异。内固定六个月组的BMP2/4阳性细胞的表达数量较对照组明显降低而对照组与实验组三个月的BMP2/4阳性细胞的表达数目的差异无显著性,这说明,在融合后六个月的时间,BMP2/4阳性细胞明显的消耗降低,这也是椎间盘退变的征相之一。Ⅱ型胶原的变化以及意义同BMP2/4阳性细胞。实验组三个月和六个月的MMP-13、TIMP-1的量较对照组明显升高,说明在内固定后,椎体相邻节段椎间盘的髓核发生退变。5、在PCR的试验中,观察3个月及6个月实验组比对照组Timp-1、Bmp-15和biglycan基因表达量均增加(p＜0.05),术后3月组与术后6个月组组比未见明显的统计学差异(p＞0.05)。说明,在手术干预的情况下,内固定术后三个月与六个月的椎间盘发生退变(较对照组),但是试验组3个月和6个月并无明显差异。
结论:建立颈椎前路融合的退变模型,通过检测骨密度、椎间盘的变化和说明:颈椎融合术后,相邻节段椎间盘较未行固定的椎间盘退变发生的要早而且程度严重。
Objective.In the world,people have higher quality on life.On the same time, the aged will be the main stream and the traffic is more developed than any other years.So the spine injury,spine degeneration diseases and spine deformations occur more equent than before which need to be treat with internal fixation.We must know more situation about the spine after internal fixations to make the surgery method,instruments and the internal fixation technology better than before.Some research shows that the BMD is related to the power of screws extraction and the collapse of the implants.People also suggest that we should test the BMD of the cervical before fixing on them.Now the BMD exchangment around the screws has not been investigated.
In these years,spine fusions have the higher achievement ratio which lead to the ASD occurring more often.The ASD of cervical spine after fusion is to show that osteophyma formation,narrow intervertebral space,vertebrae slippage, intervertebral disk hernia,spinal stenosis,flaval ligaments thickening and so on. ASD often occer on the upper segment of fusion and it has the rate of 6-60%after the cervical fusion.The TGF-β1 and the BMP-7 are researched as the treatment gene on intervertebral disk degeneration.Thompson described that the TGF-β1 can enhance the PG,which is the first describtion on gene treatment.BMP nearly is on all of the organs which contains the cyemology,auxanology and so on.After 1990,lots of tests showed that rhBMP-7 can enhance the PG of the rabbits. However AnHS got the contrast goal.Goat is the best animal as the model of anterior cervical fusions because it has the characteristic of rectal head and perpendicular weight loading.Besides,goat has the same size of intervertebral disk as person and the same biomechanics as people.The goat has been used to test the role of GF,bone graft,and so on.
After anterior cervical fusion,the BMD、BMC are related to the screws extraction.BMD is an important index on end-plate mechanics.The test of centrum vertebrae BMD is significant to precede the implant sinking,screws extraction and false articulation.
Intervertebral disk is the important structure in spine motion function. Retrogradation and injury are the main reasons to damage it,which can cause not only the intervertebral disk diseases,but also disturb the spine motion.Many researches showed the BMP-7's role on the biomechanics.Now,the research on BMP-7 is just on the rabbit about the injury and degeneration.
Our test will establish the animal model on anterior cervical fusions and research the bone density around the screws,biochemistry in intervertebral disks and the imageology variations.All of above are served for clinic treatment by providing the evidence.
Methods.
1 body position:dorsal position,with the extremities binded on the operation table
2 transfusion
3 anaesthesia:general anaesthesia with tracheal intubation
4 grouping:dividing into 3 groups
Ⅰ:normal 4 goats
Ⅱ:fixation 3 months 5 goats
Ⅲ:fixation 6 months 5 goats
5 operation:
6 post-operation:without external fixation,with antibiotics 5-7 days
7 breeding:foodintake freely
8 type of executing:asphyxiation
9 segment of intervertebral disks:C2/3 and C5/6
10 position:nucleus gelatinosus annular fibrosus centrum vertebrae
11 items of test:Immunohistochemistry BMD imageology PCR
Results.After establishing the models and researching all the data,we get the results as follows:(1)Degenerations on intervertebral discs appear more earlier and serious than the control.(2) The bone density around the screws are decreasing more earlier and serious than the control.(3)The MRI shows that Degenerations on intervertebral discs appear more earlier and serious than the control
Conclusion.Establishing the goat model of anterior cervical fusion and researching the bone density around the screws,biochemistry in intervertebral disks and the MRI variations,which show that ASD must have happened after operation.Our surgeons should consider it.
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6. Heim D, Herkert F, Hess P, Regazzni P. (1993) Surgical treatment of humeral shaft fracture: the Basel experience. J Trauma. 35:22632.
7. Heitemeyer U, Kemper F, Hierholzer G, Haines J. (1987) Severely comminuted femoral shaft fracture: treatment by bridging plate osteosynthesis. Arch Orthop Trauma Surg. 106: 327 30.
8. Helfet DL, Shonnard PY, Levine D, Borrelli Jr J. (1997) Minimally invasive plate osteosynthesis of distal fractures of the tibia. Injury. 28(Suppl 1):428.
9. Henle MB. In: Hansen ST, Swiontkowski MF, editors. (1993) Humeral shaft fracture. Orthopedic trauma protocols. New York: Raven Press, pp. 91 95.
10. JI Fang, YANG Tie-yi, WANG Ming-chun, et al. (2005) Anatomic analysis of MIPPO technique in treatment of humeral fractures: a preliminary clinic report. Chinese Journal of Orthopaedic Trauma. Dec, 7(12):1128-1131 .
11. Lau TW, Leung F, Chan CF, Chow SP. (2007) Epub 2006 Oct 11. Minimally invasive plate osteosynthesis in the treatment of proximal humeral fracture. Int Orthop. Oct;31(5):657-664.
12. Perren SM. (2002) The technology of minimally invasive percutaneous osteosynthesis (MIPO). Injury. Apr;33 Suppl 1:Ⅵ-Ⅶ.
13. Perren SM. (2002) Evolution of the internal fixation of long bone fractures. The scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg Br. Nov;84(8):1093-110.
14. Stoffel K, Dieter U, Stachowiak G, Gachter A, Kuster MS. (2003) Biomechanical testing of the LCP—how can stability in locked internal fixators be controlled?Injury. Nov;34 Suppl 2:B11-9.
15. Wagner M. (2003) General principles for the clinical use of the LCP.Injury. Nov;34 Suppl 2:B31-42.
16. Wagner M, Frenk A, Frigg R. (2004) New concepts for bone fracture treatment and the Locking Compression Plate. Surg Technol Int. 12:271-7.
17. Zhiquan A, Bingfang Z, Yeming W, Chi Z, Peiyan H. (2007) Minimally Invasive Plating Osteosynthesis (MIPO) of Middle and Distal Third Humeral Shaft Fractures. J Orthop Trauma. Oct:21(9):628-633.
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1: Bednarik J, Kadanka Z, Dusek L, Kerkovsky M, Vohanka S, Novotny O, Urbanek I, Kratochvilova D. Presymptomatic spondylotic cervical myelopathy: an updated predictive model.Eur Spine J. 2008 Jan 12; [Epub ahead of print]
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6: Lo YL. The role of electrophysiology in the diagnosis and management of cervical spondyloticmyelopathy. Ann Acad Med Singapore. 2007 Nov;36(11):886-8.
7: Fraix V, Delalande I, Parrache M, Derambure P, Cassim F. Action-induced clonus mimicking tremor. Mov Disord. 2008 Jan 30;23(2):285-8.
8: Kadanka Z, Kerkovsky M, Bednarik J, Jarkovsky J. Cross-sectional transverse area and hyperintensities on magnetic resonance imaging in relation to the clinical picture in cervical spondylotic myelopathy. Spine. 2007 Nov 1;32(23):2573-7.
9: Scheufler KM, Kirsch E. Percutaneous multilevel decompressive laminectomy, foraminotomy, and instrumented fusion for cervical spondylotic radiculopathy and myelopathy: assessment of feasibility and surgical technique. J Neurosurg Spine. 2007 Nov;7(5):514-20.
10: Amaral SH, Silva MN, Giraldi M, Viterbo MB, Pereira CA. Multiple cervical arcocristectomies for the treatment of cervical spondylotic myelopathy: surgical technique and results. J Neurosurg Spine. 2007 Nov;7(5):503-8.
11: Lu J, Wu X, Li Y, Kong X. Surgical results of anterior corpectomy in the aged patients with cervical myelopathy. Eur Spine J. 2008 Jan;17(1):129-35. Epub 2007 Oct 31.
12: Bruneau M, Cornelius JF, George B. Multilevel oblique corpectomies: surgical indications and technique. Neurosurgery. 2007 Sep;61(3 Suppl): 106-12; discussion 112. Review.
13: Alafifi T, Kern R, Fehlings M. Clinical and MRI predictors of outcome after surgical intervention for cervical spondylotic myelopathy. J Neuroimaging. 2007 Oct;17(4):315-22.
14: Tsuji T, Asazuma T, Masuoka K, Yasuoka H, Motosuneya T, Sakai T, Nemoto K. Retrospective cohort study between selective and standard C3-7 laminoplasty. Minimum 2-year follow-up study. Eur Spine J. 2007 Dec;16(12):2072-7. Epub 2007 Aug 29.
15: Yukawa Y, Kato F, Ito K, Horie Y, Hida T, Ito Z, Matsuyama Y. Laminoplasty and skip laminectomy for cervical compressive myelopathy: range of motion, postoperative neck pain, and surgical outcomes in a randomized prospective study. Spine. 2007 Aug 15;32(18):1980-5.
16: Rajshekhar V, Muliyil J. Patient perceived outcome after central corpectomy for cervical spondylotic myelopathy. Surg Neurol. 2007 Aug;68(2):185-90; discussion 190-1.
17: Gala VC, O'Toole JE, Voyadzis JM, Fessler RG. Posterior minimally invasive approaches for the cervical spine. Orthop Clin North Am. 2007 Jul;38(3):339-49; abstract v.
18: Li L, Wang H, Cui S.Effect of modified unilaterally-open expansive laminoplasty using bridge grafting and restructing posterior ligamentous complex methods on axial symptoms and cervical curvature change .2007 May;21(5):457-60. Chinese.
19: Koller H, Hempfing A, Ferraris L, Maier O, Hitzl W, Metz-Stavenhagen P. 4- and 5-level anterior fusions of the cervical spine: review of literature and clinical results. Eur Spine J. 2007 Dec;16(12):2055-71. Epub 2007 Jun 29. Review.
20: Holly LT, Dong Y, Albistegui-DuBois R, Marehbian J, Dobkin B. Cortical reorganization in patients with cervical spondylotic myelopathy. J Neurosurg Spine. 2007 Jun;6(6):544-51.
21: Pino Rivero V, Pantoja Hernandez CG, Mora Santos ME, Gonzalez Palomino A, Ambel Albarran A, Rodriguez Sanchez JA, Blasco Huelva A. Cervical hematoma after discectomy for spondylosis. An indication of urgent tracheotomy An Otorrinolaringol Ibero Am. 2007;34(2): 105-10. Spanish.
22: Iencean SM. Alternating cervical laminoplasty for cervical spondylotic myelopathy. J Bone Joint Surg Br. 2007 May;89(5):639-41.
23: Kawasaki M, Tani T, Ushida T, Ishida K. Anterolisthesis and retrolisthesis of the cervical spine in cervical spondylotic myelopathy in the elderly. J Orthop Sci. 2007 May;12(3):207-13. Epub 2007 May 31.
24: Aydogan M, Ozturk C, Mirzanli C, Karatoprak O, Tezer M, Hamzaoglu A. Treatment approach in tandem (concurrent) cervical and lumbar spinal stenosis. Acta Orthop Belg. 2007 Apr;73(2):234-7.
25: Lo YL, Tan YE, Dan YF, Leoh TH, Tan SB, Tan CT, Chan LL. Cutaneous silent periods in the evaluation of cord compression in cervical spondylosis. J Neurol. 2007 Jan;254(1):14-9. Epub 2007 Feb 14.
26: Yang S, Hu Y, Zhao J, He X, Liu Y, Xu W, Du J, Fu D. Follow-up study on the motion range after treatment of degenerative disc disease with the Bryan cervical disc prosthesis. J Huazhong Univ Sci Technolog Med Sci. 2007 Apr;27(2): 176-8.
27: Caroli E, Orlando ER, D'Andrea G, Ferrante L. Anterior cervical fusion with interbody titanium cage containing surgical bone site graft: our institution's experience in 103 consecutive cases of degenerative spondylosis. J Spinal Disord Tech. 2007 May;20(3):216-20.
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29: Ghogawala Z, Coumans JV, Benzel EC, Stabile LM, Barker FG 2nd. Ventral versus dorsal decompression for cervical spondylotic myelopathy: surgeons' assessment of eligibility for randomization in a proposed randomized controlled trial: results of a survey of the Cervical Spine Research Society. Spine. 2007 Feb 15;32(4):429-36.
30: Lim MR, Huang RC, Wu A, Girardi FP, Cammisa FP Jr. Evaluation of the elderly patient with an abnormal gait. J Am Acad Orthop Surg. 2007 Feb;15(2):107-17. Review.
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34: Nakama S, Ihara T, Sugamata M, Endo T, Ooyama M, Hoshino Y. An ultrastructural study on the ligamentum flavum of the cervical spine in patients with ossification of the posterior longitudinal ligament. Med Mol Morphol. 2006 Dec;39(4): 198-202. Epub 2006 Dec 21.
35: Steinmetz MP, Resnick DK. Cervical laminoplasty. Spine J. 2006 Nov-Dec;6(6 Suppl):274S-281S. Review.
36: Kim PK, Alexander JT. Indications for circumferential surgery for cervical spondylotic myelopathy. Spine J. 2006 Nov-Dec;6(6 Suppl):299S-307S. Review.
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38: Medow JE, Trost G, Sandin J. Surgical management of cervical myelopathy: indications and techniques for surgical corpectomy. Spine J. 2006 Nov-Dec;6(6 Suppl):233S-241S. Review.
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40: Dickerman RD, Reynolds AS, Morgan B. Comment on "Segmental instability in cervical spondylotic myelopathy with severe disc degeneration" (Spine 2006;31:1327-31).Spine. 2006 Oct 15;31(22):2638; author reply 2638-9. No abstract available.
41: Fujiwara Y, Tanaka N, Fujimoto Y, Nakanishi K, Kamei N, Ochi M. Surgical outcome of posterior decompression for cervical spondylosis with unilateral upper extremity amyotrophy. Spine. 2006 Sep 15;31(20):E728-32.
42: Kaplan L, Bronstein Y, Barzilay Y, Hasharoni A, Finkelstein J. Canal expansive laminoplasty in the management of cervical spondylotic myelopathy. Isr Med Assoc J. 2006 Aug;8(8):548-52.
43: Mori K, Yamamoto T, Nakao Y, Maeda M. Cervical spondylotic amyotrophy treated by anterior decompression. Three case reports. Neurol Med Chir (Tokyo). 2006 Jul;46(7):366-70.
44: Kuwazawa Y, Pope MH, Bashir W, Takahashi K, Smith FW. The length of the cervical cord: effects of postural changes in healthy volunteers using positional magnetic resonance imaging. Spine. 2006 Aug 1;31(17):E579-83.
45: Lee JY, Hilibrand AS, Lim MR, Zavatsky J, Zeiller S, Schwartz DM, Vaccaro AR, Anderson DG, Albert TJ. Characterization of neurophysiologic alerts during anterior cervical spine surgery. Spine. 2006 Aug 1;31(17):1916-22.
46: Kaneko K, Kato Y. Kojima T, Imajyo Y, Taguchi T. Epidurally recorded spinal cord evoked potentials in patients with cervical myelopathy and normal central motor conduction time measured by transcranial magnetic stimulation. Clin Neurophysiol. 2006 Jul;117(7):1467-73. Epub 2006 Jun 6.
47: Sakayama K, Kidani T, Sugawara Y, Masuno H, Matsuda Y, Yamamoto H. Elevated concentration of hyaluronan in the cerebrospinal fluid is a secondary marker of spinal disorders: hyaluronan in the cerebrospinal fluid in patients with spinal disorders.J Spinal Disord Tech. 2006 Jun;19(4):262-5.
1. Apivatthakakul T, Arpornchayanon O.(2005) Minimally invasive plate osteosynthesis (MIPO) combined with distraction osteogenesis in the treatment of bone defects. A new technique of bone transport: a report of two cases. Injury. Apr;36(4):530-8.
2. Fernandez Dell Oca AA. (2002) The principle of helical implants. Unusual ideas worth considering. Injury. Suppl 33: Al 27.
3. Frigg R. (2001) Locking compression plate (LCP): an osteosynthesis plate based on the dynamic compression plate and point contact f ixator (PCFix). Injury. 32 (Suppl 2) : 636.
4. Frigg R. (2003) Development of the Locking Compression Plate, Injury. Nov;34 Suppl 2:B6-10.
5. Gerwin M, Hotchkiss RN, Weiland AJ. (1996) Alternative operative exposures of the posterior aspect of the humeral diaphysis with reference to the radial nerve. J Bone Joint Surg Am . 78-A:1690 5.
6. Heim D, Herkert F, Hess P, Regazzni P. (1993) Surgical treatment of humeral shaft fracture: the Basel experience. J Trauma. 35:22632.
7. Heitemeyer U, Kemper F, Hierholzer G, Haines J. (1987) Severely comminuted femoral shaft fracture: treatment by bridging plate osteosynthesis. Arch Orthop Trauma Surg. 106: 327 30.
8. Helfet DL, Shonnard PY, Levine D, Borrelli Jr J. (1997) Minimally invasive plate osteosynthesis of distal fractures of the tibia. Injury. 28(Suppl 1):428.
9. Henle MB. In: Hansen ST, Swiontkowski MF, editors. (1993) Humeral shaft fracture. Orthopedic trauma protocols. New York: Raven Press, pp. 91 95.
10. JI Fang, YANG Tie-yi, WANG Ming-chun, et al. (2005) Anatomic analysis of MIPPO technique in treatment of humeral fractures: a preliminary clinic report. Chinese Journal of Orthopaedic Trauma. Dec, 7(12):1128-1131 .
11. Lau TW, Leung F, Chan CF, Chow SP. (2007) Epub 2006 Oct 11. Minimally invasive plate osteosynthesis in the treatment of proximal humeral fracture. Int Orthop. Oct;31(5):657-664.
12. Perren SM. (2002) The technology of minimally invasive percutaneous osteosynthesis (MIPO). Injury. Apr;33 Suppl 1:Ⅵ-Ⅶ.
13. Perren SM. (2002) Evolution of the internal fixation of long bone fractures. The scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg Br. Nov;84(8):1093-110.
14. Stoffel K, Dieter U, Stachowiak G, Gachter A, Kuster MS. (2003) Biomechanical testing of the LCP—how can stability in locked internal fixators be controlled?Injury. Nov;34 Suppl 2:B11-9.
15. Wagner M. (2003) General principles for the clinical use of the LCP.Injury. Nov;34 Suppl 2:B31-42.
16. Wagner M, Frenk A, Frigg R. (2004) New concepts for bone fracture treatment and the Locking Compression Plate. Surg Technol Int. 12:271-7.
17. Zhiquan A, Bingfang Z, Yeming W, Chi Z, Peiyan H. (2007) Minimally Invasive Plating Osteosynthesis (MIPO) of Middle and Distal Third Humeral Shaft Fractures. J Orthop Trauma. Oct:21(9):628-633.
1 蔡郑东.骨盆外科学.第1版。南京:江苏科学技术出版社,1999.169-205
2 钱齐荣,贾连顺,周伟明,等.坐位骶髂关节面应力分布的三维有限元研究.临床骨科杂志,2001,4(4):241-243.
3 许硕贵,张春才.骨科生物力学测试技术及其意义.生物医学工程与临床,2002,6(4):232-235.
4 Marvin Tile,Editor-in-Chief.Fractures of the Pelvic and Acetabulum.Third Edition.
5 Vrahas M,Hearn TC,D'AngeloD,et al.Ligamentous contribution to pelvic ring stiffness.Orthopedics 1995;18:271-274.
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