髋臼软骨冲击伤的实验研究
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摘要
第一部分髋臼软骨冲击伤实验动物模型的建立与冲击能的量化研究
目的初步探讨髋臼软骨冲击伤动物模型的建立和冲击能的量化研究。方法新西兰大白兔30只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高35cm和15cm处分别下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为高能组和低能组,另一组为对照组,每组10只。高能组和低能组的区分以软骨所受冲击能25Mpa为标准,并分别给予冲击能量化观察和统计学分析。在伤后6小时分别取材和收集标本,分别给予大体观察和组织学观察(HE染色和番红“O”染色)。结果高能组和低能组软骨所受总冲力平均值分别为203.910N和105.919N,分别和预实验30只兔在相同条件下得到的总冲击能平均值203.937N和105.849N相比,经统计学分析,均显示无统计学意义(P>0.05);平均总压强值分别为28.862Mpa和14.992Mpa,分别和预实验中得到的冲击能平均总压强值28.866Mpa和14.982Mpa相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现高能组软骨裂隙增大,软骨表面粗糙,损失程度重于低能组和对照组;在高能组细胞变扁、变宽,相对于低能组和对照组,细胞死亡增多。高能组和低能组番红“O”染色均轻度减弱,但高能组染色相对交淡;对照组染色正常。结论通过自制冲击器冲击兔右侧髋臼软骨,模拟冲击伤机制,初步建立髋臼软骨冲击伤实验动物模型并量化冲击能,通过统计学分析,大体和组织病理学检查,并与国外动物模型相比,本模型重复性和稳定性好,术式操作简单,创伤小,护理方便,易于推广,为研究活体动物髋臼软骨冲击后的短期和长期变化提供实验基础和依据。
第二部分髋臼软骨冲击致伤后的MRI影像学研究
目的初步探讨MRI对显示和诊断关节软骨冲击伤的最佳序列。方法新西兰大白兔20只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高35cm处下滑垂直冲击兔右侧髋臼软骨,给予冲击能量化观察并行统计学分析。在伤前和伤后6小时,对兔髋臼软骨冲击伤模型行MRI不同序列扫描,请三位资深放射科医师利用上述序列对髋臼软骨进行双盲读片,观察并评价各MRI序列对软骨成像情况。并以Collins病理诊断为标准,评价及不同序列对诊断软骨损伤的敏感度和特异度。对各种扫描序列的SNR和CNR结果使用描述统计评价。结果髋臼软骨所受总冲力平均值为203.944N,和预实验30只兔在相同条件下得到的总冲击能平均值203.937N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为28.867Mpa,和预实验中得到的冲击能平均总压强值28.866Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。在MRI各序列中,软骨呈弧状带表现。T1WI和STIR/T/FSE/PSAT序列上软骨为低信号,T1/C/FSE/C+造影序列上软骨为中等或低信号,但造影剂为高信号,软骨与造影剂对比明显;T2WI上软骨为中高信号,T2*/C/RF-FAST/VOL和T2*/T /FE/MTC/MAST上软骨为灰白信号;T2* / C/RF-FAST/VOL和T2*/T/FE/MTC/MAST信噪比最好,显示关节软骨图像最清晰。SNR结果良好的有T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;一般的有T1 WI、T2WI和T1/C/FSE/C+;较差的是STIR/T/FSE/PSAT。CNR测定结果中软骨对骨皮质的CNR“极佳”的有T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;“一般”的有T2WI;“差”的有T1WI、STIR/T/FSE/PSAT和T1/C/ FSE /C+。软骨对骨髓CNR“极佳”的T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;“良好”的有T1WI;其余皆为“一般”。软骨对脂肪CNR“极佳”的有T1WI、T2*/C/RF-FAST/VOL、T2*/T/FE/MTC/MAST和T1/C/ FSE /C+;“良好”的有T2WI;“一般”的有STIR / T/FSE/PSAT。软骨对肌肉CNR“良好”的有T2*/C/RF-FAST/VOL和T2*/T/ FE/ MTC/MAST;其余皆为“差”。以病理Collins诊断为标准,诊断能力中,敏感度T2*/ C/RF-FAST/VOL和T2*/T/FE/ MTC/MAST大致相同>T1/C/ FSE /C+>T2WI>T1WI>STIR/T/FSE/PSAT;特异度结果与敏感度大致相同。结论通过对兔髋臼软骨行FSE T1WI、T2WI、T2*/C/RF-FAST/ VOL、T2*/T/FE/ MTC/ MAST、STIR/T/FSE/PSAT和T1/C/FSE/C+等扫描序列的SNR、CNR、敏感度和特异度对比研究发现,FSE T1WI、T2WI可作为诊断髋臼软骨的常规序列。T2*/C/ RF- FAST/VOL和T2*/T/FE/MTC/MAST是诊断髋臼软骨损伤的最佳扫描序列。T1/C/ FSE /C+造影序列对关节软骨表面检查,尤其在诊断软骨表面缺损方面具有特殊性和潜在的临床价值。
第三部分髋臼软骨冲击致伤后的大体、组织病理学和细胞凋亡的研究
目的初步探讨不同能量的髋臼软骨冲击致伤后短期和长期的变化,软骨损伤的病理机制,以及软骨细胞凋亡和软骨退变的关系。方法新西兰大白兔54只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,分别沿导向杆从高35cm和15cm处下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为高能组和低能组,另一组为对照组,每组18只。高能组和低能组分别给予冲击能量化观察,并行统计学分析。在伤后6小时、4周和24周分别取材和收集标本,行大体、HE、番红“O”和甲苯胺蓝染色、透射、扫描电镜以及TUNEL标记法观察。将常规HE和番红“O”染色软骨病理切片采用双盲法阅片,按照Mankin评分法对软骨冲击伤的严重度给予组织评分。并采用双盲法观察软骨细胞凋亡率。结果髋臼软骨所受总冲力平均值分别为203.924N和105.853N,分别和预实验30只兔在相同条件下得到的总冲击能平均值203.937N和105.849N相比,经统计学分析,均显示无统计学意义(P>0.05);平均总压强值分别为28.864Mpa和14.983Mpa,分别和预实验中得到的冲击能平均总压强值28.866Mpa和14.982Mpa相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现随时间延长,高能组软骨裂隙增大,软骨表面粗糙,损失程度重于低能组和对照组;在高能组细胞变扁、变宽,相对于低能组和对照组,细胞死亡增多。高能组番红“O”和甲苯胺蓝染色逐渐减弱,低能组染色先轻度减弱,后又恢复正常;对照组染色正常。透射电镜中,高能组与低能组和正常组相比,细胞器逐渐减少,细胞死亡增多,染色质分布不均匀,有大量空泡形成。扫描电镜中,高能组于低能组和正常组相比,软骨表面裂隙更加扩大,大量胶原纤维裸露,排列紊乱,甚至有软骨下骨暴露。高能组的Mankin评分在伤后6小时、4周和24周,呈逐步增高趋势,与对照组在不同时间相比,经统计学分析,均显示有统计学意义(P<0.05)。低能组评分与对照组在伤后2天相比,经统计学分析,显示有统计学意义(P<0.05)。在伤后4周和24周与对照组相比,经统计学分析,均显示无统计学意义(P>0.05)。高能组在伤后6小时软骨浅表层和移行层出现凋亡细胞,至伤后4周和24周,凋亡细胞所占比率越大,伤后6小时、4周和24周的软骨细胞凋亡率与对照组相比,经统计学分析,均显示有统计学意义(P<0.05)。低能组在伤后6小时软骨的移行层出现凋亡细胞,细胞调亡率与对照组相比,经统计学分析,显示有统计学意义(P<0.05);伤后4周,软骨凋亡细胞明显减少,细胞调亡率与对照组相比,经统计学分析,显示无统计学意义(P>0.05),伤后24周软骨凋亡细胞逐渐恢复正常,细胞调亡率与对照组相比,经统计学分析,显示无统计学意义(P>0.05)。细胞凋亡率在高能组与低能组各时间组相比,经统计学分析,均显示有统计学意义(P<0.05)。结论根据实验研究观察,我们认为高能组在软骨损伤中的可能机制是通过对基质的破坏和引起胶原纤维网架断裂从而导致软骨的损伤和退变。而低能组是通过软骨细胞为始动因素,发生不同的改变,从而引起软骨的修复或损伤。软骨冲击能的大小与软骨细胞凋亡程度密切相关,而细胞凋亡程度和软骨损伤程度也密切相关。软骨细胞凋亡可能是软骨细胞早期损伤的反应之一。软骨细胞过度凋亡可能会引起软骨退变。
第四部分髋臼软骨冲击致伤后的MRI影像学和组织病理学的比较研究
目的初步探讨髋臼软骨冲击致伤后MRI信号改变的组织病理学基础,MRI与病理之间的关系,以及MRI早期诊断软骨损伤的可行性。方法新西兰大白兔30只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤的机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高30cm处下滑垂直冲击兔右侧髋臼软骨,给予冲击能量化观察并行统计学分析。通过对兔髋臼软骨模型分别在伤后6小时、4周和24周MRI扫描后,立即分别给予收集标本行大体观察和组织病理学检查。请三位资深放射科医师双盲读片,评价MRI对软骨显示情况,并给予诊断结果与病理对照研究分析。MRI分级采用Recht标准,组织病理学分级根据Collins标准。结果髋臼软骨所受总冲力平均值为262.735N,和预实验30只兔在相同条件下得到的总冲击能平均值262.748N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为27.323Mpa,和预实验中得到的冲击能平均总压强值27.324Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。MRI与病理对照结果显示,MRI的0级3例,其中2例病理分级1级;Ⅰ级9例,其中1例病理分级为2级;Ⅱ级8例,与病理分级一致;Ⅲ级8例,与病理分级一致;Ⅵ级2例,与病理分级一致。MRI分级组和病理分级组比较,经统计学分析,显示MRI检查关节软骨病变的结果和病理结果呈高度正相关(P< 0.05)。结论MRI检查关节软骨病变的结果和病理结果呈高度正相关,软骨损伤程度越重,MRI分级和病理分级一致性越高,反之越低。在早期软骨损伤中,当病理变化不足以引起信号改变时,MRI诊断软骨损伤的敏感性和准确性与组织病理学相比还有待于进一步提高。当软骨基质、蛋白多糖和含水量的改变足以引起信号改变时,MRI诊断软骨损伤的敏感性和正确性与组织病理学一致。通过MRI检查,诊断早期软骨损伤具有可行性。
第五部分关节腔内注射透明质酸钠对髋臼软骨高能冲击伤的影响
目的初步探讨关节腔内注射SH对髋臼软骨冲击致伤后的影响,为临床应用提供实验依据。方法新西兰大白兔24只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高45cm处下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为模型组和对照组,每组12只。模型组给予右侧髋关节腔注射SH,对照组给予生理盐水注射。在伤后4天和4周分别取材和收集标本,行大体、HE、番红“O”和甲苯胺蓝染色、透射、扫描电镜以及TUNEL标记法观察,并行冲击能量化观察和统计学分析。番红“O”染色切片,在图像分析仪内做图像分析,测得目标灰度值。TUNEL末端标记法中,采用双盲法观察软骨细胞凋亡率。目标灰度值和软骨细胞凋亡率均给予统计学分析。结果髋臼软骨所受总冲力平均值为153.331N,和预实验30只兔在相同条件下得到的总冲击能平均值153.327N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为31.254Mpa,和预实验中得到的冲击能平均总压强值31.253Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。模型组的冲击能和冲击能压强分别与对照组相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现随时间延长,模型组和对照组均有软骨裂隙,对照组软骨裂隙增大,软骨表面粗糙,损失程度严重;在对照组细胞变扁、变宽,相对于模型组,软骨细胞死亡增多。模型组和对照组番红“O”和甲苯胺蓝染色均逐渐减弱,但在相同时间,对照组染色相对淡。其中,模型组和对照组分别在伤后4天和4周,番红“O”染色均有不同程度减弱,但模型组目标灰度值均较对照组低,两组分别比较,经统计学分析,均显示有统计学意义(P<0.05)。透射电镜中,对照组和模型组相比,细胞器逐渐减少,软骨细胞死亡增多,染色质分布不均匀。扫描电镜中,对照组与模型组相比,软骨表面裂隙更加扩大,胶原纤维裸露相对较多,排列紊乱。模型组和对照组在伤后4天软骨出现凋亡细胞,至伤后4周,凋亡细胞所占比率均增大,伤后4天与4周的软骨细胞凋亡率分别与对照组相比,经统计学分析,均显示有统计学意义(P<0.05)。结论SH可以减少软骨细胞凋亡。SH在软骨冲击致伤后有修复作用,能够延缓软骨的损伤,但是在高能损伤中,由于软骨损伤程度严重,却无法阻止软骨的退变,从而达到根治目的。损伤能量的大小,对SH治疗髋臼软骨冲击伤的疗效有一定影响。临床上在髋臼软骨受到冲击致伤后,无论是否合并有髋臼骨折,在严格的无菌操作条件下,均应立即给予髋关节注射SH,并持续4周,每周1次髋关节注射,虽然可能无法治愈软骨损伤,但对损伤后的软骨有保护和修复作用,延缓软骨退变继发骨性关节炎的过程。
PartⅠEstablishment of experimental animal model forthe impactive Injury of acetabular cartilageand study of Quantifying the impactive energy
Objective To discusses the feasibility of establishing the animal model for the impactive injury of acetabular cartilage and quantify the energy. Methods Thirty New Zealand white rabbits were divided into high energy and low energy groups randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm and 15cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The another group was control group. Each group was 10,in which the distinguish standard of high and low energy group was that the impactive energy was 25Mpa for cartilage .The observation of quantifying the energy and the analysis of statistics were made for two model groups. The observation of macrography and histology (stained by HE and safarnin O) were made for three groups, which were killed postinjuriously at 6 hour. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 203.910N and 105.919N for the high and low energy group respectively. There was no statistical significance(P>0.05) through comparing the two model groups and the former groups in which the impactive average force was measured 203.937N and 105.849N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of two model groups (28.862Mpa and 14.992Mpa, respectively) and the former groups (28.866Mpa and 14.982Mpa, respectively).We found the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in high energy group. The staining of safarnin O was made mild in high energy and in low energy group and normal in control group. Conclusions The model had good duplicability and stability through the method of establishing the animal model in which the simple operative method,small wound and convenient nurse was obtained so easilyis that the animal model was spread easily.The study of the change of short and long period was made to provide the experimental base and reason through the animal model.
PartⅡThe study of MRI after the impactive Injury of acetabular cartilage
Objective To discuss the excellent sequence of MRI for displaying and diagnosing the impactive injury of acetabular cartilage. Methods Twenty New Zealand white rabbits were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The observation of quantifying the energy and the analysis of statistics were made for 20 rabbits. The observation and the evaluation of MRI with different sequence for the imaging of acetabular cartilage by three experienced doctors by which the MRI was read through double–blinded in radiative department at 6 hour before and after operation. The sensitivity and the especiality of chondral injury were evaluated through the diagnosis of different sequence according to the standard of Collins’pathological diagnosis. The results of SNR and CNR of different sequence were evaluated describly. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 203.944N for the experimental group. There was no statistical significance(P>0.05) through comparing the experimental group and the former group in which the impactive average force was measured 203.937N through 30 rabbits under the same circumstance. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (28.867Mpa) and the former group (28.866Mpa).The arc strap was showed for cartilage in different MRI sequence. The low signal was showed for cartilage in T1WI and STIR/T/FSE/PSAT. The middling or low signal was showed for cartilage in T1/C/FSE/C+, in which the arthrography was showed high signal. The middling or high signal was showed for cartilage in T2WI. The hoariness signal was showed for cartilage in T2*/C/RF-FAST/VOL and T2*/T /FE/MTC/MAST.The excellent SNR was obtained in T2* / C/RF-FAST/VOL and T2*/T/FE/MTC/MAST in which the MRI was most clear. Among the result of SNR, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST good, T1WI、T2WI and T1/C/FSE/C+ fair, STIR/T/FSE/PSAT bad. Among the result of CNR, comared cartilage with bone cortex, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST excellent , T2WI fair, T1WI、STIR/T/FSE/PSAT and T1/C/ FSE /C+ bad; comared cartilage with bone marrow, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST excel- lent, T1WI good,others fair; comared cartilage with fat, T1WI、T2*/C/RF-FAST /VOL、T2*/T/FE/MTC/MAST and T1/C/ FSE /C+ excellent, T2WI good, STIR /T/ FSE /PSAT fair and comared cartilage with muscle, T2*/C/RF-FAST/VOL and T2*/T/FE/ MTC/MAST good,others bad.To the sensitivity, T2*/ C/RF-FAST/VOL as the same as T2*/T/FE/ MTC/MAST probably>T1/C/ FSE /C+>T2WI>T1WI>STIR/T/FSE/PSAT and the especiality is as the same as the sensitivity probably according to the Collins’diagnostic standard. Conclusions FSE T1WI and T2WI were use as the routine sequence for diagnosing the chondral injury. T2*/C/RF-FAST/VOL and T2*/ T/FE /MTC/ MAST were used as the best sequence. T1/C/ FSE /C+ as arthrography was used as the examinatong of surface of articular cartilage and had particularity and potential clinical value in diagnosing the defects of the surface of cartilage.
PartⅢThe study of macrography, histology, pathology and apoptosis After the impactive injury of acetabular cartilage
Objective To discuss the change of short and long peoriod for the impactive injury of acetabular cartilage by using different energy,the pathological mechanism of chondral injury and the relation between chondrocyte apoptosis and cartilage degeneration. Methods fifty-four New Zealand white rabbits were divided into high energy and low energy groups randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm and 15cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The another group was control group. Each group was 18.The observation of quantifying the energy and the analysis of statistics were made for two model groups. The observation of macrography, histology (stained by HE, safarnin O and toluidine blue), transmission electron microscope, scanning electron microscope and the method of TUNEL were made for the three groups which were killed postope- ratively at 6 hour,4 week and 24 week. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg.The pathological sections were read by the double-blinded method for estimating the Mankin’s score after the impactive injury of acetabular cartilage and observing the chondrocytes apoptosis. Results The impactive average force was 203.924N and 105.853N for the high and low energy group respectively. There was no statistical significance(P>0.05) through comparing the two model groups and the former groups in which the impactive average force was measured 203.937N and 105.849N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of two model groups (28.864Mpa and 14.983Mpa, respectively) and the former groups (28.866 Mpa and 14.982Mpa, respectively).We found with time extending, the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in high energy group. The staining of safarnin O and toluidine blue was weaker in high energy group with time extending, mild in low energy group and normal in control group. Among transmission electron microscope, there were decreasing of cellar organ, the increasing of chond- rocyte, the increasing of asymmetry of chromatin and the forming of more vacuole in high energy group. Among scanning electron microscope, the increasing of the cranny of cartilage, the nudity of more collagen fibre that arrange turbulently, even the exposure of subchondral bone in high energy group. The differences of operative results between the Mankin’s score of high energy group and the one of control group at different times as well 6 hour, 4 week and 24 week were significant (P<0.05). The difference of operative results between the Mankin’s score of low energy group and the one of control group at 6 hour was significant (P<0.05). But at 4 week and 24 week, there was no statistical significance(P>0.05)between the Mankin’s score of low energy group and the one of control group. The differences of operative results between the rate of chondrocyte apoptosis of high energy group and the one of control group at different times as well 6 hour,4 week and 24 week were significant (P<0.05) through the method of TUNEL. The difference of operative results between the rate of chondrocyte apoptosis of low energy group and the one of control group at 6 hour was significant (P<0.05) through the method of TUNEL. But at 4 week and 24 week, there was no statistical significance(P>0.05)between the rate of chondrocyte apoptosis of low energy group and the one of control group through the method of TUNEL. The differences of operative results between the rate of chondrocyte apoptosis of high energy group and the one of low energy group at different times as well 6 hour,4 week and 24 week were significant (P<0.05)through the method of TUNEL. Conclusions We think there was different in the mechanism of the injury and the degen eration of cartilage between high energy group and low energy group. The mechanism of the injury and the degeneration in high energy group was caused by destroying the collagen fibre framework, but in low energy group by destroying chondrocyte .The severity of chondrocyte apoptosis was related with the severity of impactive energy and the injury of cartilage nearly. The chondrocyte apoptosis was the one of the early injury reaction of cartilage. The excessive chondrocyte apoptosis maybe caused the degeneration of cartilage.
PartⅣThe comparative study between MRI and pathology after the Impactive injury of acetabular cartilage
Objective To discuss the histological and pathological base of the change of MRI signal after the impactive injury of acetabular cartilage. Methods Thirty New Zealand white rabbits were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 30cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The observation of quantifying the energy and the analysis of statistics were made for 30 rabbits. The observation of macrography and histology (stained by HE, safarnin O and toluidine blue) were made for the experimental group which were killed postinjuriously at 6 hour,4 week and 24 week. The result which was compared with the result of patholoty and the evaluation of MRI for the imaging of acetabular cartilage by three experienced doctors by which the MRI was read through double–blinded in radiative department at 6 hour,4 week and 24 week postinjuriously. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg.The grade of MRI and pathology were according to Recht’s and Collins’standard. Results The impactive average force was 262.735N for the experimental group. There was no statistical significance(P>0.05) through comparing the exp- erimental group and the former group in which the impactive average force was measured 262.748N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (27.323Mpa) and the former group (27.324Mpa). Through the comparative result between MRI and pathology, 3 cases were Recht 0,in which 2 cases Collins 1; 9 cases were RechtⅠ,in which 1 cases Collins 2; 8 cases were RechtⅡas the same as Collins’grade; 8 cases were RechtⅢas the same as Collins’grade; 2 cases were RechtⅣas the same as Collins’grade;the difference were significant (P<0.05) between the result of MRI and pathology. Conclusions The result of MRI and pathology showed positive correlation highly.When the degree of injury of cartilage was severe,the more consistency was obtained between the grade of MRI and pathology,whereas,the less consistency was obtained between them.When the pathological change was not enough to cause the change of signal,the sensitivity and veracity of MRI for diagnosing the injury of cartilage need further improve,whereas,the more consistency in sensitivity and veracity was obtained between MRI and pathology.The diagnosis of early injury of cartilage is feasible through the examination of MRI.
PartⅤThe influence for impactive injury of high energy of acetabular Cartilage by injecting sodium hyaluronate to articular cavity
Objective To discuss the influence of impactive injury of high energy of acetabular cartiage by injecting SH to articular cavity. Methods Twenty–four New Zealand white rabbits were divided into model group and control group randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 45cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. Each group was 12.The model group was injected SH.The control group was injected NaCl solution. The observation of macrography, histology (stained by HE, safarnin O and toluidine blue), transmission electron microscope, scanning electron microscope and the method of TUNEL were made for the three groups that were killed postinjuriously at 4 day and 4 week. The observation of quantifying the energy and the analysis of statistics were made for two groups. The target ash value was measured through analyzing the imaging obtained by sections stained by safarnin O and the rate of chondrocyte apoptosis was observed through double-blinded method.The target ash value and the rate of chondrocyte apoptosis was analyzed by statistics.The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 153.331N for the experimental group. There was no statistical significance(P>0.05) through comparing the experimental group and the former group in which the impactive average force was measured 153.327N through 30 rabbits under the same circumstance. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (31.254Mpa) and the former group (31.253 Mpa). There was no statistical significance (P>0.05)between the impactive energy and the impactive pressure of the model group and the control group. We found with time extending, the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in the model group. The staining of safarnin O and toluidine blue was made weaker in both groups at 4 day and 4 week postinjuriously. But in both groups, the staining of safarnin O of control group was made weaker than that of the model group. The target ash value of the model group was lower than the control group. The difference was significant (P<0.05) between both groups. Among transm- ission electron microscope, there were decreasing of cellar organ, the increasing of chondrocyte and the increasing of asymmetry of chromatin in the control group. Among scanning electron microscope, the increasing of the cranny of cartilage and the nudity of more collagen fibre that arrange turbulently in the control group were showed. The difference was significant (P<0.05) between the rate of chondrocyte apoptosis of the model group and the control group at 4 day and 4 week respectively. Conclusions SH may decrease the chondrocyte apoptosis. SH which can’t prevent the degeneration of cartilage to heal the chondral injury can rehabilitate cartilage and stay the injury of high energy of cartilage. The severity of impactive energy had some influence on SH for the treatment of impactive injury of acetabular cartilage. The impactive injury of cartilage whether or not with the acetabular fracture should be treated by injecting SH to hip articular cavity under the circumstance of sterile operation immediately and once a week for four weeks. Though the method maybe did not heal the injury of cartilage, it can protect and rehabilitate cartilage after impactive injury for staying the degeneration of cartilage that could happen osteoarthritis.
目的初步探讨髋臼软骨冲击伤动物模型的建立和冲击能的量化研究。方法新西兰大白兔30只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高35cm和15cm处分别下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为高能组和低能组,另一组为对照组,每组10只。高能组和低能组的区分以软骨所受冲击能25Mpa为标准,并分别给予冲击能量化观察和统计学分析。在伤后6小时分别取材和收集标本,分别给予大体观察和组织学观察(HE染色和番红“O”染色)。结果高能组和低能组软骨所受总冲力平均值分别为203.910N和105.919N,分别和预实验30只兔在相同条件下得到的总冲击能平均值203.937N和105.849N相比,经统计学分析,均显示无统计学意义(P>0.05);平均总压强值分别为28.862Mpa和14.992Mpa,分别和预实验中得到的冲击能平均总压强值28.866Mpa和14.982Mpa相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现高能组软骨裂隙增大,软骨表面粗糙,损失程度重于低能组和对照组;在高能组细胞变扁、变宽,相对于低能组和对照组,细胞死亡增多。高能组和低能组番红“O”染色均轻度减弱,但高能组染色相对交淡;对照组染色正常。结论通过自制冲击器冲击兔右侧髋臼软骨,模拟冲击伤机制,初步建立髋臼软骨冲击伤实验动物模型并量化冲击能,通过统计学分析,大体和组织病理学检查,并与国外动物模型相比,本模型重复性和稳定性好,术式操作简单,创伤小,护理方便,易于推广,为研究活体动物髋臼软骨冲击后的短期和长期变化提供实验基础和依据。
第二部分髋臼软骨冲击致伤后的MRI影像学研究
目的初步探讨MRI对显示和诊断关节软骨冲击伤的最佳序列。方法新西兰大白兔20只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高35cm处下滑垂直冲击兔右侧髋臼软骨,给予冲击能量化观察并行统计学分析。在伤前和伤后6小时,对兔髋臼软骨冲击伤模型行MRI不同序列扫描,请三位资深放射科医师利用上述序列对髋臼软骨进行双盲读片,观察并评价各MRI序列对软骨成像情况。并以Collins病理诊断为标准,评价及不同序列对诊断软骨损伤的敏感度和特异度。对各种扫描序列的SNR和CNR结果使用描述统计评价。结果髋臼软骨所受总冲力平均值为203.944N,和预实验30只兔在相同条件下得到的总冲击能平均值203.937N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为28.867Mpa,和预实验中得到的冲击能平均总压强值28.866Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。在MRI各序列中,软骨呈弧状带表现。T1WI和STIR/T/FSE/PSAT序列上软骨为低信号,T1/C/FSE/C+造影序列上软骨为中等或低信号,但造影剂为高信号,软骨与造影剂对比明显;T2WI上软骨为中高信号,T2*/C/RF-FAST/VOL和T2*/T /FE/MTC/MAST上软骨为灰白信号;T2* / C/RF-FAST/VOL和T2*/T/FE/MTC/MAST信噪比最好,显示关节软骨图像最清晰。SNR结果良好的有T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;一般的有T1 WI、T2WI和T1/C/FSE/C+;较差的是STIR/T/FSE/PSAT。CNR测定结果中软骨对骨皮质的CNR“极佳”的有T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;“一般”的有T2WI;“差”的有T1WI、STIR/T/FSE/PSAT和T1/C/ FSE /C+。软骨对骨髓CNR“极佳”的T2*/C/RF-FAST/VOL和T2*/T/FE/MTC/MAST;“良好”的有T1WI;其余皆为“一般”。软骨对脂肪CNR“极佳”的有T1WI、T2*/C/RF-FAST/VOL、T2*/T/FE/MTC/MAST和T1/C/ FSE /C+;“良好”的有T2WI;“一般”的有STIR / T/FSE/PSAT。软骨对肌肉CNR“良好”的有T2*/C/RF-FAST/VOL和T2*/T/ FE/ MTC/MAST;其余皆为“差”。以病理Collins诊断为标准,诊断能力中,敏感度T2*/ C/RF-FAST/VOL和T2*/T/FE/ MTC/MAST大致相同>T1/C/ FSE /C+>T2WI>T1WI>STIR/T/FSE/PSAT;特异度结果与敏感度大致相同。结论通过对兔髋臼软骨行FSE T1WI、T2WI、T2*/C/RF-FAST/ VOL、T2*/T/FE/ MTC/ MAST、STIR/T/FSE/PSAT和T1/C/FSE/C+等扫描序列的SNR、CNR、敏感度和特异度对比研究发现,FSE T1WI、T2WI可作为诊断髋臼软骨的常规序列。T2*/C/ RF- FAST/VOL和T2*/T/FE/MTC/MAST是诊断髋臼软骨损伤的最佳扫描序列。T1/C/ FSE /C+造影序列对关节软骨表面检查,尤其在诊断软骨表面缺损方面具有特殊性和潜在的临床价值。
第三部分髋臼软骨冲击致伤后的大体、组织病理学和细胞凋亡的研究
目的初步探讨不同能量的髋臼软骨冲击致伤后短期和长期的变化,软骨损伤的病理机制,以及软骨细胞凋亡和软骨退变的关系。方法新西兰大白兔54只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,分别沿导向杆从高35cm和15cm处下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为高能组和低能组,另一组为对照组,每组18只。高能组和低能组分别给予冲击能量化观察,并行统计学分析。在伤后6小时、4周和24周分别取材和收集标本,行大体、HE、番红“O”和甲苯胺蓝染色、透射、扫描电镜以及TUNEL标记法观察。将常规HE和番红“O”染色软骨病理切片采用双盲法阅片,按照Mankin评分法对软骨冲击伤的严重度给予组织评分。并采用双盲法观察软骨细胞凋亡率。结果髋臼软骨所受总冲力平均值分别为203.924N和105.853N,分别和预实验30只兔在相同条件下得到的总冲击能平均值203.937N和105.849N相比,经统计学分析,均显示无统计学意义(P>0.05);平均总压强值分别为28.864Mpa和14.983Mpa,分别和预实验中得到的冲击能平均总压强值28.866Mpa和14.982Mpa相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现随时间延长,高能组软骨裂隙增大,软骨表面粗糙,损失程度重于低能组和对照组;在高能组细胞变扁、变宽,相对于低能组和对照组,细胞死亡增多。高能组番红“O”和甲苯胺蓝染色逐渐减弱,低能组染色先轻度减弱,后又恢复正常;对照组染色正常。透射电镜中,高能组与低能组和正常组相比,细胞器逐渐减少,细胞死亡增多,染色质分布不均匀,有大量空泡形成。扫描电镜中,高能组于低能组和正常组相比,软骨表面裂隙更加扩大,大量胶原纤维裸露,排列紊乱,甚至有软骨下骨暴露。高能组的Mankin评分在伤后6小时、4周和24周,呈逐步增高趋势,与对照组在不同时间相比,经统计学分析,均显示有统计学意义(P<0.05)。低能组评分与对照组在伤后2天相比,经统计学分析,显示有统计学意义(P<0.05)。在伤后4周和24周与对照组相比,经统计学分析,均显示无统计学意义(P>0.05)。高能组在伤后6小时软骨浅表层和移行层出现凋亡细胞,至伤后4周和24周,凋亡细胞所占比率越大,伤后6小时、4周和24周的软骨细胞凋亡率与对照组相比,经统计学分析,均显示有统计学意义(P<0.05)。低能组在伤后6小时软骨的移行层出现凋亡细胞,细胞调亡率与对照组相比,经统计学分析,显示有统计学意义(P<0.05);伤后4周,软骨凋亡细胞明显减少,细胞调亡率与对照组相比,经统计学分析,显示无统计学意义(P>0.05),伤后24周软骨凋亡细胞逐渐恢复正常,细胞调亡率与对照组相比,经统计学分析,显示无统计学意义(P>0.05)。细胞凋亡率在高能组与低能组各时间组相比,经统计学分析,均显示有统计学意义(P<0.05)。结论根据实验研究观察,我们认为高能组在软骨损伤中的可能机制是通过对基质的破坏和引起胶原纤维网架断裂从而导致软骨的损伤和退变。而低能组是通过软骨细胞为始动因素,发生不同的改变,从而引起软骨的修复或损伤。软骨冲击能的大小与软骨细胞凋亡程度密切相关,而细胞凋亡程度和软骨损伤程度也密切相关。软骨细胞凋亡可能是软骨细胞早期损伤的反应之一。软骨细胞过度凋亡可能会引起软骨退变。
第四部分髋臼软骨冲击致伤后的MRI影像学和组织病理学的比较研究
目的初步探讨髋臼软骨冲击致伤后MRI信号改变的组织病理学基础,MRI与病理之间的关系,以及MRI早期诊断软骨损伤的可行性。方法新西兰大白兔30只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤的机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高30cm处下滑垂直冲击兔右侧髋臼软骨,给予冲击能量化观察并行统计学分析。通过对兔髋臼软骨模型分别在伤后6小时、4周和24周MRI扫描后,立即分别给予收集标本行大体观察和组织病理学检查。请三位资深放射科医师双盲读片,评价MRI对软骨显示情况,并给予诊断结果与病理对照研究分析。MRI分级采用Recht标准,组织病理学分级根据Collins标准。结果髋臼软骨所受总冲力平均值为262.735N,和预实验30只兔在相同条件下得到的总冲击能平均值262.748N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为27.323Mpa,和预实验中得到的冲击能平均总压强值27.324Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。MRI与病理对照结果显示,MRI的0级3例,其中2例病理分级1级;Ⅰ级9例,其中1例病理分级为2级;Ⅱ级8例,与病理分级一致;Ⅲ级8例,与病理分级一致;Ⅵ级2例,与病理分级一致。MRI分级组和病理分级组比较,经统计学分析,显示MRI检查关节软骨病变的结果和病理结果呈高度正相关(P< 0.05)。结论MRI检查关节软骨病变的结果和病理结果呈高度正相关,软骨损伤程度越重,MRI分级和病理分级一致性越高,反之越低。在早期软骨损伤中,当病理变化不足以引起信号改变时,MRI诊断软骨损伤的敏感性和准确性与组织病理学相比还有待于进一步提高。当软骨基质、蛋白多糖和含水量的改变足以引起信号改变时,MRI诊断软骨损伤的敏感性和正确性与组织病理学一致。通过MRI检查,诊断早期软骨损伤具有可行性。
第五部分关节腔内注射透明质酸钠对髋臼软骨高能冲击伤的影响
目的初步探讨关节腔内注射SH对髋臼软骨冲击致伤后的影响,为临床应用提供实验依据。方法新西兰大白兔24只,平均年龄6个月,体重2.5±0.5kg,模拟人髋臼软骨冲击伤机制,采用自制冲击装置,用质量为0.400kg的重锤,沿导向杆从高45cm处下滑垂直冲击兔右侧髋臼软骨,建立兔髋臼软骨冲击伤模型,随机分为模型组和对照组,每组12只。模型组给予右侧髋关节腔注射SH,对照组给予生理盐水注射。在伤后4天和4周分别取材和收集标本,行大体、HE、番红“O”和甲苯胺蓝染色、透射、扫描电镜以及TUNEL标记法观察,并行冲击能量化观察和统计学分析。番红“O”染色切片,在图像分析仪内做图像分析,测得目标灰度值。TUNEL末端标记法中,采用双盲法观察软骨细胞凋亡率。目标灰度值和软骨细胞凋亡率均给予统计学分析。结果髋臼软骨所受总冲力平均值为153.331N,和预实验30只兔在相同条件下得到的总冲击能平均值153.327N相比,经统计学分析,显示无统计学意义(P>0.05);平均总压强值为31.254Mpa,和预实验中得到的冲击能平均总压强值31.253Mpa相比,经统计学分析,显示无统计学意义(P>0.05)。模型组的冲击能和冲击能压强分别与对照组相比,经统计学分析,均显示无统计学意义(P>0.05)。通过大体和组织学观察,发现随时间延长,模型组和对照组均有软骨裂隙,对照组软骨裂隙增大,软骨表面粗糙,损失程度严重;在对照组细胞变扁、变宽,相对于模型组,软骨细胞死亡增多。模型组和对照组番红“O”和甲苯胺蓝染色均逐渐减弱,但在相同时间,对照组染色相对淡。其中,模型组和对照组分别在伤后4天和4周,番红“O”染色均有不同程度减弱,但模型组目标灰度值均较对照组低,两组分别比较,经统计学分析,均显示有统计学意义(P<0.05)。透射电镜中,对照组和模型组相比,细胞器逐渐减少,软骨细胞死亡增多,染色质分布不均匀。扫描电镜中,对照组与模型组相比,软骨表面裂隙更加扩大,胶原纤维裸露相对较多,排列紊乱。模型组和对照组在伤后4天软骨出现凋亡细胞,至伤后4周,凋亡细胞所占比率均增大,伤后4天与4周的软骨细胞凋亡率分别与对照组相比,经统计学分析,均显示有统计学意义(P<0.05)。结论SH可以减少软骨细胞凋亡。SH在软骨冲击致伤后有修复作用,能够延缓软骨的损伤,但是在高能损伤中,由于软骨损伤程度严重,却无法阻止软骨的退变,从而达到根治目的。损伤能量的大小,对SH治疗髋臼软骨冲击伤的疗效有一定影响。临床上在髋臼软骨受到冲击致伤后,无论是否合并有髋臼骨折,在严格的无菌操作条件下,均应立即给予髋关节注射SH,并持续4周,每周1次髋关节注射,虽然可能无法治愈软骨损伤,但对损伤后的软骨有保护和修复作用,延缓软骨退变继发骨性关节炎的过程。
PartⅠEstablishment of experimental animal model forthe impactive Injury of acetabular cartilageand study of Quantifying the impactive energy
Objective To discusses the feasibility of establishing the animal model for the impactive injury of acetabular cartilage and quantify the energy. Methods Thirty New Zealand white rabbits were divided into high energy and low energy groups randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm and 15cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The another group was control group. Each group was 10,in which the distinguish standard of high and low energy group was that the impactive energy was 25Mpa for cartilage .The observation of quantifying the energy and the analysis of statistics were made for two model groups. The observation of macrography and histology (stained by HE and safarnin O) were made for three groups, which were killed postinjuriously at 6 hour. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 203.910N and 105.919N for the high and low energy group respectively. There was no statistical significance(P>0.05) through comparing the two model groups and the former groups in which the impactive average force was measured 203.937N and 105.849N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of two model groups (28.862Mpa and 14.992Mpa, respectively) and the former groups (28.866Mpa and 14.982Mpa, respectively).We found the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in high energy group. The staining of safarnin O was made mild in high energy and in low energy group and normal in control group. Conclusions The model had good duplicability and stability through the method of establishing the animal model in which the simple operative method,small wound and convenient nurse was obtained so easilyis that the animal model was spread easily.The study of the change of short and long period was made to provide the experimental base and reason through the animal model.
PartⅡThe study of MRI after the impactive Injury of acetabular cartilage
Objective To discuss the excellent sequence of MRI for displaying and diagnosing the impactive injury of acetabular cartilage. Methods Twenty New Zealand white rabbits were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The observation of quantifying the energy and the analysis of statistics were made for 20 rabbits. The observation and the evaluation of MRI with different sequence for the imaging of acetabular cartilage by three experienced doctors by which the MRI was read through double–blinded in radiative department at 6 hour before and after operation. The sensitivity and the especiality of chondral injury were evaluated through the diagnosis of different sequence according to the standard of Collins’pathological diagnosis. The results of SNR and CNR of different sequence were evaluated describly. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 203.944N for the experimental group. There was no statistical significance(P>0.05) through comparing the experimental group and the former group in which the impactive average force was measured 203.937N through 30 rabbits under the same circumstance. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (28.867Mpa) and the former group (28.866Mpa).The arc strap was showed for cartilage in different MRI sequence. The low signal was showed for cartilage in T1WI and STIR/T/FSE/PSAT. The middling or low signal was showed for cartilage in T1/C/FSE/C+, in which the arthrography was showed high signal. The middling or high signal was showed for cartilage in T2WI. The hoariness signal was showed for cartilage in T2*/C/RF-FAST/VOL and T2*/T /FE/MTC/MAST.The excellent SNR was obtained in T2* / C/RF-FAST/VOL and T2*/T/FE/MTC/MAST in which the MRI was most clear. Among the result of SNR, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST good, T1WI、T2WI and T1/C/FSE/C+ fair, STIR/T/FSE/PSAT bad. Among the result of CNR, comared cartilage with bone cortex, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST excellent , T2WI fair, T1WI、STIR/T/FSE/PSAT and T1/C/ FSE /C+ bad; comared cartilage with bone marrow, T2*/C/RF-FAST/VOL and T2*/T/FE/MTC/MAST excel- lent, T1WI good,others fair; comared cartilage with fat, T1WI、T2*/C/RF-FAST /VOL、T2*/T/FE/MTC/MAST and T1/C/ FSE /C+ excellent, T2WI good, STIR /T/ FSE /PSAT fair and comared cartilage with muscle, T2*/C/RF-FAST/VOL and T2*/T/FE/ MTC/MAST good,others bad.To the sensitivity, T2*/ C/RF-FAST/VOL as the same as T2*/T/FE/ MTC/MAST probably>T1/C/ FSE /C+>T2WI>T1WI>STIR/T/FSE/PSAT and the especiality is as the same as the sensitivity probably according to the Collins’diagnostic standard. Conclusions FSE T1WI and T2WI were use as the routine sequence for diagnosing the chondral injury. T2*/C/RF-FAST/VOL and T2*/ T/FE /MTC/ MAST were used as the best sequence. T1/C/ FSE /C+ as arthrography was used as the examinatong of surface of articular cartilage and had particularity and potential clinical value in diagnosing the defects of the surface of cartilage.
PartⅢThe study of macrography, histology, pathology and apoptosis After the impactive injury of acetabular cartilage
Objective To discuss the change of short and long peoriod for the impactive injury of acetabular cartilage by using different energy,the pathological mechanism of chondral injury and the relation between chondrocyte apoptosis and cartilage degeneration. Methods fifty-four New Zealand white rabbits were divided into high energy and low energy groups randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 35cm and 15cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The another group was control group. Each group was 18.The observation of quantifying the energy and the analysis of statistics were made for two model groups. The observation of macrography, histology (stained by HE, safarnin O and toluidine blue), transmission electron microscope, scanning electron microscope and the method of TUNEL were made for the three groups which were killed postope- ratively at 6 hour,4 week and 24 week. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg.The pathological sections were read by the double-blinded method for estimating the Mankin’s score after the impactive injury of acetabular cartilage and observing the chondrocytes apoptosis. Results The impactive average force was 203.924N and 105.853N for the high and low energy group respectively. There was no statistical significance(P>0.05) through comparing the two model groups and the former groups in which the impactive average force was measured 203.937N and 105.849N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of two model groups (28.864Mpa and 14.983Mpa, respectively) and the former groups (28.866 Mpa and 14.982Mpa, respectively).We found with time extending, the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in high energy group. The staining of safarnin O and toluidine blue was weaker in high energy group with time extending, mild in low energy group and normal in control group. Among transmission electron microscope, there were decreasing of cellar organ, the increasing of chond- rocyte, the increasing of asymmetry of chromatin and the forming of more vacuole in high energy group. Among scanning electron microscope, the increasing of the cranny of cartilage, the nudity of more collagen fibre that arrange turbulently, even the exposure of subchondral bone in high energy group. The differences of operative results between the Mankin’s score of high energy group and the one of control group at different times as well 6 hour, 4 week and 24 week were significant (P<0.05). The difference of operative results between the Mankin’s score of low energy group and the one of control group at 6 hour was significant (P<0.05). But at 4 week and 24 week, there was no statistical significance(P>0.05)between the Mankin’s score of low energy group and the one of control group. The differences of operative results between the rate of chondrocyte apoptosis of high energy group and the one of control group at different times as well 6 hour,4 week and 24 week were significant (P<0.05) through the method of TUNEL. The difference of operative results between the rate of chondrocyte apoptosis of low energy group and the one of control group at 6 hour was significant (P<0.05) through the method of TUNEL. But at 4 week and 24 week, there was no statistical significance(P>0.05)between the rate of chondrocyte apoptosis of low energy group and the one of control group through the method of TUNEL. The differences of operative results between the rate of chondrocyte apoptosis of high energy group and the one of low energy group at different times as well 6 hour,4 week and 24 week were significant (P<0.05)through the method of TUNEL. Conclusions We think there was different in the mechanism of the injury and the degen eration of cartilage between high energy group and low energy group. The mechanism of the injury and the degeneration in high energy group was caused by destroying the collagen fibre framework, but in low energy group by destroying chondrocyte .The severity of chondrocyte apoptosis was related with the severity of impactive energy and the injury of cartilage nearly. The chondrocyte apoptosis was the one of the early injury reaction of cartilage. The excessive chondrocyte apoptosis maybe caused the degeneration of cartilage.
PartⅣThe comparative study between MRI and pathology after the Impactive injury of acetabular cartilage
Objective To discuss the histological and pathological base of the change of MRI signal after the impactive injury of acetabular cartilage. Methods Thirty New Zealand white rabbits were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 30cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. The observation of quantifying the energy and the analysis of statistics were made for 30 rabbits. The observation of macrography and histology (stained by HE, safarnin O and toluidine blue) were made for the experimental group which were killed postinjuriously at 6 hour,4 week and 24 week. The result which was compared with the result of patholoty and the evaluation of MRI for the imaging of acetabular cartilage by three experienced doctors by which the MRI was read through double–blinded in radiative department at 6 hour,4 week and 24 week postinjuriously. The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg.The grade of MRI and pathology were according to Recht’s and Collins’standard. Results The impactive average force was 262.735N for the experimental group. There was no statistical significance(P>0.05) through comparing the exp- erimental group and the former group in which the impactive average force was measured 262.748N through 30 rabbits under the same circumstance respectively. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (27.323Mpa) and the former group (27.324Mpa). Through the comparative result between MRI and pathology, 3 cases were Recht 0,in which 2 cases Collins 1; 9 cases were RechtⅠ,in which 1 cases Collins 2; 8 cases were RechtⅡas the same as Collins’grade; 8 cases were RechtⅢas the same as Collins’grade; 2 cases were RechtⅣas the same as Collins’grade;the difference were significant (P<0.05) between the result of MRI and pathology. Conclusions The result of MRI and pathology showed positive correlation highly.When the degree of injury of cartilage was severe,the more consistency was obtained between the grade of MRI and pathology,whereas,the less consistency was obtained between them.When the pathological change was not enough to cause the change of signal,the sensitivity and veracity of MRI for diagnosing the injury of cartilage need further improve,whereas,the more consistency in sensitivity and veracity was obtained between MRI and pathology.The diagnosis of early injury of cartilage is feasible through the examination of MRI.
PartⅤThe influence for impactive injury of high energy of acetabular Cartilage by injecting sodium hyaluronate to articular cavity
Objective To discuss the influence of impactive injury of high energy of acetabular cartiage by injecting SH to articular cavity. Methods Twenty–four New Zealand white rabbits were divided into model group and control group randomly, of which the two groups which were made through the homemade impactive equipment by impacting the right acetabular cartilage of rabbit at 45cm with 0.400kg weight vertically and simulating the mechanism of impactive injury of human acetabular cartilage. Each group was 12.The model group was injected SH.The control group was injected NaCl solution. The observation of macrography, histology (stained by HE, safarnin O and toluidine blue), transmission electron microscope, scanning electron microscope and the method of TUNEL were made for the three groups that were killed postinjuriously at 4 day and 4 week. The observation of quantifying the energy and the analysis of statistics were made for two groups. The target ash value was measured through analyzing the imaging obtained by sections stained by safarnin O and the rate of chondrocyte apoptosis was observed through double-blinded method.The target ash value and the rate of chondrocyte apoptosis was analyzed by statistics.The average age and weight of these rabbits was 0.5 years old and 2.5±0.5kg. Results The impactive average force was 153.331N for the experimental group. There was no statistical significance(P>0.05) through comparing the experimental group and the former group in which the impactive average force was measured 153.327N through 30 rabbits under the same circumstance. There was no statistical significance(P>0.05)through comparing the pressure of experimental group (31.254Mpa) and the former group (31.253 Mpa). There was no statistical significance (P>0.05)between the impactive energy and the impactive pressure of the model group and the control group. We found with time extending, the increasing of the cranny of cartilage, the coarseness of chondral surface, the great severity of chondral injury, the increasing of the flat cells and the increasing of chondrocyte death in the model group. The staining of safarnin O and toluidine blue was made weaker in both groups at 4 day and 4 week postinjuriously. But in both groups, the staining of safarnin O of control group was made weaker than that of the model group. The target ash value of the model group was lower than the control group. The difference was significant (P<0.05) between both groups. Among transm- ission electron microscope, there were decreasing of cellar organ, the increasing of chondrocyte and the increasing of asymmetry of chromatin in the control group. Among scanning electron microscope, the increasing of the cranny of cartilage and the nudity of more collagen fibre that arrange turbulently in the control group were showed. The difference was significant (P<0.05) between the rate of chondrocyte apoptosis of the model group and the control group at 4 day and 4 week respectively. Conclusions SH may decrease the chondrocyte apoptosis. SH which can’t prevent the degeneration of cartilage to heal the chondral injury can rehabilitate cartilage and stay the injury of high energy of cartilage. The severity of impactive energy had some influence on SH for the treatment of impactive injury of acetabular cartilage. The impactive injury of cartilage whether or not with the acetabular fracture should be treated by injecting SH to hip articular cavity under the circumstance of sterile operation immediately and once a week for four weeks. Though the method maybe did not heal the injury of cartilage, it can protect and rehabilitate cartilage after impactive injury for staying the degeneration of cartilage that could happen osteoarthritis.
引文
1. Pantazopoulos T, Nicolopoulos CS, Babis GC, et al. Surgical treatment of acetabular posterior wall fractures. Injury, 1993, 24:319-323.
2. Moed BR, Wiuson Carr SE, Watson JT.Results of operative treatment of fractures of the posterior wall of the acetabulum .J Bone Joint Surg (Am), 2002,84:752-758.
3. Mears DC, Velyvis JH, Chang CP. Displaced acetabular fractures managed operatively: indicators of outcome. Clin Orthop Relat Res, 2003, (407): 173-186.
4. Giannoudis PV, Grotz MR. Operative treatment of displacedfractures of the acetabulum: a meta-analysis. J Bone Joint Surg(Am),2005,87-B(1): 2-9.
5. Alonso JE.A review of the treatment of hip dislocations associated with acetabular fractures. Clin Orthop Relat Res, 2000, (377): 32-43.
6. Saterbak AM, Marsh JL, Nepola JV, et al. Clinical failure after posterior wall acetabular fractures: the influence of initial fracture patterns. J Orthop Trauma, 2000,14:230-237.
7. Johnson EE, Matta JM, Mast JW, etal. Deloyed reconstruction of acetabular fractures 21～210 days following injury.Clin Orthop, 1994, 305:20-29.
8. Matta JM. Fractures of the acetabulum: accuracy of reduction and clinicalresults in patients managed operatively within three weeks after the injury. J Bone Joint Surg (Am), 1996,78:1632-1645.
9. Letournel E, Judet R. Fractures of the acetabulum. New York: Springer, 1981:21-4, 211-19, 311-15.
10. Wright R, Barrett K, Christie MJ, et al. Acetabular fractures: Long-term follow-up of open reduction and internal fixation. J Orthop Trauma, 1994, 8:397-403.
11. Borrelli J, William M, Ricci MD.Acute effects of cartilage impact. Clin Orthop Relat Res, 2004, (423): 33–39.
12. Repo RU, Finlay J. Survival of articular cartilage after controlledimpact. J Bone Joint Surg (Am), 1977,59:1068–1076.
13. Donohue J, Buss D, Oegema T, et al. The effects of indirect blunt trauma on adult canine articular cartilage . J Bone Joint Surg (Am), 1983, 65: 948-957.
14. Thompson JR, Oegema JT, Lewis JL, et al. Osteoarthrotic changes after acute transarticular load: An animal model. J Bone Joint Surg (Am), 1991,73: 990–1001.
15. Borrelli J, Burns ME, Ricci WM, et al. A method for delivering variable impact stresses to the articular cartilage of rabbit knees. J Orthop Trauma, 2002, 16:182-188.
16. Ewers BJ, Weaver BT, Sevensma ET, et al.Chronic changes in rabbit retropatellar cartilage and subchondral bone after blunt impact loading of the patellofemoral joint. J Orthop Res, 2002, 20:545–550.
17. Borrelli Jr J, Tinsley KW, Ricci WM, et al: Induction of chondrocyte apoptosis following impact load. J Orthop Trauma, 2003, 17:635-641.
18. Costouros JG, Dang AC, Kim HT. Comparison of chonrocyte apoptosis in vivo and in vitro following acute osteochondral injury . J Orthop Res, 2004, 22:678-683.
19. Disler D, Recht M, McCauley TR. MR imaging of articular cartilage. Skeletal Radiol, 2000,29:367-377.
20. Matsuno H, Yudoh K, Kondo M, etal. Biochemical effect of intra-articular injections of high molecular weight hyaluronate in rheumatoid arthritis patients . Inflamm Res, 1999,48(3): 154.
21.张鸿逵,王韶进,王永惕,等. SH关节腔内注射治疗膝骨关节炎.中国生化药物杂志, 1998,19(5): 231.
22. Dougados M, Nguyen M, Listrat V, et al. High molecular weight sodium hyaluronate (hylectin) in osteoarthritis of the knee: a year placebo controlled trial. J Osteoathritis and cartilage, 1993,1:97-103.
23. Letournel E, Judet R. Fractures of the acetabulum. Seconded. Berlin: Springer Verlag, 1998.
24. Asik, M, Eralp L, Cetik O, et al. Mid-to long-term resultsfor the surgical treatment of acetabulum fractures. J Bone Joint Surg (Br), 2001, 83 (Supp-II): 119.
25. Newberry WN, Garcia JJ, Mackenzie CD, et al. Analysis of acute mechanical insult in an animal model of post-traumatic osteoarthrosis. J Biomech Eng, 1998,120:704-709.
26. Vrahas MS, Smith GA, Rosler DM, et al. Method to impact in vivo rabbit femoral cartilage with blows of quantifiable stress. J Orthop Res, 1997,15:314–317.
27. Borrelli JJ, Ricci WM, Steger-May K, et al. Postoperative radiographic assessment of acetabular fractures: a comparison of plain radiographs and CT scans. J Orthop Trauma, 2005,19:299-304.
28. Jeffrey JE, Thomson LA, Aspden RM.Matrix loss and synthesis following a single impact load on articular cartilage in vitro. Biochim Biophys Acta, 1997,1334:223-232.
29. Torzilli PA, Grigiene R, Borrelli JJ, et al. Effect of impact load onarticular cartilage: Cell metabolism and viability, and matrix water content. J Biomech Eng, 1999,121:433–441.
30. Haut RC, Ide TM.Mechanical responses of the rabbit patellofemoral joint to blunt impact. J Biomech Eng, 1995,117:402-408.
31. Jeffrey JE, Gregory DW, Aspden RM.Matrix damage and chondrocyte viability following a single impact load on articular cartilage . Arch Biochem Biophys, 1995,322:87-96.
32. Zhang H, Vrahas MS, Baratta RV, et al. Damage to rabbit femoral articular cartilage following direct impacts of uniform stresses in vitro study.Clin Biomech,1999,14:543-548.
1. Missi MJ, Toyras J, Laasanen MS, et al. Proteoglycan and collagen sensitive MRI evaluation of normal and degenerated articular cartilage. J Orthop Res. 2004, 22(3): 557-564.
2. Graichen H, von ER, Vogl T, et al. Quantitative assessment of cartilage status in osteoarthritis by quantitative magnetic resonance imaging. Technical validation for use in analysis of cartilage volume and further morphological parameters . Arthritis Rheum, 2004,50:811-816.
3. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
4.雷新玮,尹建忠,倪红艳等.膝关节软骨退变的MRI与病理对照研究.中国临床医学影像杂志, 2003,14(6) :424-427.
5. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging. J Bone Joint Surg (Am), 1998,80:1276-1284.
6. Disler DG, McCauley TR, Kelman CG, et al. Fat-suppressed three dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: comparison with standard MR imaging and arthroscopy.Am J Roentgenol, 1996,67:127-132.
7. Woolf SD, Chesnick S, Frank JA, et al. Magnetization transfer contrasts: MR imaging of the knee. Radiology, 1991, 170:623-628.
8. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
9. Kim YJ, Iobst C, Millis MB, et al. Assessment of early osteoarthritis in hip dysplasia and pelvic osteotomy using delayed gadolinium enhanced MRI (dGEMRIC). Presented at the Tenth Scientific Meeting and Exhibition of the International Society of Magnetic Resonance in Medicine, 2002:18–24 .
10. Bacic G, Liu KJ, Goda F, etal. MRI contrast enhanced study of cartilage proteoglycan degradation in the rabbit knee.Magn Reson Imaging,1997,37:764 .
11. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivo assessment with delayed GD(DTPA)2- enhanced MR imaging.Radiology,1997,205:551
12.江浩,何国祥,陈克敏,等.骨与关节MRI [M] .第1版.上海:上海科学技术出版社,2000:249-312.
1. Repo RU, Finlay J. Survival of articular cartilage after controlled impact. J Bone Joint Surg (Am), 1977,59:1068–1076.
2. Jeffrey JE, Thomson LA, Aspden RM.Matrix loss and synthesis following a single impact load on articular cartilage in vitro. Biochim Biophys Acta, 1997, 1334:223-232.
3. Torzilli PA, Grigiene R, Borrelli JJ, et al. Effect of impact load on articular cartilage: Cell metabolism and viability, and matrix water content. J Biomech Eng, 1999,121:433–441.
4. Conrozier T.Death of articular chondrocyte, mechanisms and protection. Pressc Med, 1998,27(36): 1859-1861.
5. Kim HA, Lee YJ, Seong SC, et al. Apoptotic chondrocyte death in human osteoarthritis.J Rheum,2000,27(2):455-462.
6. Kouri JB, Agniera JM, Reyes J, etal. Apoptotic chondrocytes from osteoarthrotic human articular cartilage and abnormal calcification of subchondral . Bone, 2000, 27: 1005-1019.
7. Blaw FJ, Guistian R, Vazguez ME, et al. Osteoarthritis chondrocyte did by apoptosis : A possible pathway for osteoarthritis pathology Arthritis Rheum,1998,41(2): 284-289.
8. Mankin HJ. Current concepts review: The response of articular cartilage to mechanical injury. J Bone Joint Surg (Am), 1982,64:460-466.
9. Mankin HJ, Mow VC, Buckwalter JA, et al . Articular Cartilage Structure, composition and Function . In Buckwalter JA, Einhorn JA, Simon SR (eds). Orthopaedic Basic Science.Biology and Biomechanics of the Musculo- skeletal System . Rosemont, IL, American Academy of Orthopaedic Surgeons, 1999,443–470.
10. Blanco FJ, Ochs RL, Schwarz H, etal. Chondrocyte apoptosis induced by nitric oxide [J] . Am J Pathol, 1995, 146(1): 75-85.
11. Yatsugi N, Tsukazaki T, Osaki M, et al. Apoptosis of articular chondrocytes in reheumatoid arthritis and osteoarthritis: correlation of apoptosis with degree of cartilage destruction and expression of apoptosis-related proteins of p53 and c-myc [J]. J Orthop Sci, 2000, 5(2):150-156.
12. Blanco FJ, Guitian R, Vazquez-Martul E, et al. Osteoarthritis chondrocytes die by apoptosis: a possible pathway for osteoarthritis pathology. Arthritis Rheum 1998, 41:284-289.
13. Hashimoto S, Ochs RL, Komiya S, et al. Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis. Arthritis Rheum 1998,41:1632-1638.
14. Loening AM, James IE, Levenston ME, et al. Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis [J]. Archives of Biochemistry & Biophysics, 2000,381 (2): 205-212.
15. Chen CT, Burton WN, Borden C, et al. Chondrocyte necrosis and apoptosis in impact damaged articular cartilage [J]. Journal of Orthopaedic Res,2001,19(4):703-711.
1. McCauley TR, Disler DG.MR imaging of articular cartilage. Radiology,1998,209:629
2. Hargreaves BA, Gold GE, Beaulieu CF, et al. Comparison of new sequences for high-resolution cartilage imaging. Magn Reson Med, 2003,49:700 -709.
3. Nieminen MT, Rieppo J, Toyras J, et al. T2 relaxation reveals spatial collagen architecture in articular cartilage: a comparative quantitative MRI and polarized light microscopic study. Magn Reson Med, 2001, 46:487 -493.
4. Dahlberg L, Nyquist F, Olsson LE, et al. Biochemical analysis of proteoglycan content in biopsies of repaired human joint cartilage is in line with contrast enhanced MRI results. In: Orthopaedic Research Society.New Orleans, LA, 2003.
5. Konig H, Sauter R, Deimling M, et al. Cartilage disorders: comparison of spin echo,CHESS and FLASH sequence MR images.Radiology,1987,164:753 .
6. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
7.雷新玮,尹建忠,倪红艳等.膝关节软骨退变的MRI与病理对照研究.中国临床医学影像杂志, 2003,14(6) :424-427.
8. Goodwin DW, Dunn JF. High-resolution magnetic resonance imaging of articular cartilage: correlation with histology and pathology. Top Magn Reson Imaging.1998, 9:337-347.
9. Carl S, Krishanu BG.Magnetic resonance imaging of focal articular cartilage lesion. Topics in Magnetic Resonance Imaging, 2003; 14(2):131-144.
10. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging .J Bone Joint Surg (Am),1998,80:1276-1284.
11. Disler DG, McCauley TR, Kelman CG, et al. Fat-suppressed three dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: comparison with standard MR imaging and arthroscopy.Am J Roentgenol, 1996,67: 127-132.
12. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
13. Woolf SD, Chesnick S, Frank JA, et al. Magnetization transfer contrasts: MR imaging of the knee. Radiology, 1991, 170:623-628.
14. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivo assessment with delayed GD(DTPA)2- enhanced MR imaging. Radiology, 1997,205:551 .
15. Hayes CW, Conway WF. Evaluation of articular cartilage: radiographic and cross sectional imaging techniques.Radiographyics, 1992, 12:409.
16. Modl JM, Sether LA, Haughton VM, et al. Articular cartilage: correlation of histologic zones with signal in tensity at MR imaging. Radiology, 1991, 181:853.
1. Matsuno H, Yudoh K, Kondo M, etal. Biochemical effect of intra-articular injections of high molecular weight hyaluronate in rheumatoid arthritis patients . Inflamm Res, 1999,48(3): 154.
2.张鸿逵,王韶进,王永惕,等. SH关节腔内注射治疗膝骨关节炎.中国生化药物杂志, 1998,19(5): 231.
3. Dougados M, Nguyen M, Listrat V, et al. High molecular weight sodium hyaluronate (hylectin) in osteoarthritis of the knee: a year placebo controlled trial. J Osteoathritis and cartilage, 1993, 1:97-103.
4. Conrozier T. Death of articular chondrocyte, mechanisms and protection. Pressc Med, 1998,27(36): 1859-1861.
5. Kim HA, Lee YJ, Seong SC, et al. Apoptotic chondrocyte death in human osteoarthritis.J Rheum,2000,27(2):455-462.
6. Kouri JB, Agniera JM, Reyes J, et al. Apoptotic chondrocytes from osteoarthrotic human articular cartilage and abnormal calcification of subchondral . Bone, 2000,27: 1005-1019.
7. Blaw FJ, Guistian R, Vazguez ME, et al. Osteoarthritis chondrocyte did by apoptosis : A possible pathway for osteoarthritis pathology.Arthritis Rheum,1998,41(2): 284-289.
8. Chrisman OD, Ladenbauer-Bellis IM, Panjabi M, et al. The relationship of mechanical trauma and the early biochemical reactions of osteo- arthritic cartilage . Clin Orthop, 1981, 161:275-284.
9. Graf J, Neusel E, Schneider E, et al. Intra-articular treatment with hyaluronic acid in osteoarthritis of the knee joint: a controlled clinical trial versus mucopolysaccharide polysulfuric acid ester. Clin Exp Rheumatol, 1993,11:367-372.
10. Hochberg MC. Role of intra-articular hyaluronic acid preparations inmedical management of osteoarthritis of the knee. Semin Arthritis Rheum, 2000,30(Suppl2): 2-10.
11. Frizziero L, Govoni E, Bacchini P. Intra-articular hyaluronic acid in the treatment of osteoarthritis of the knee: clinical and morpho- logical study. Clin Exp Rheumatol, 1998, 16:441-449.
12. Oshima Y.A study of the effect of intra articular injection of high molecular weight sodium hyaluronate on osteoathritis of the hip .Jpn Pharmacol Ther, 1987,15:1337.
13. Brand KD, Block JA, Michalski JP, et al. Efficacy and safety of intra- articular sodium hyaluronate in knee osteoarthritis. Clin Orthop, 2001, (385): 130-143.
1.吴春营,樊波,李皎,等.MRI在诊断关节软骨炎症上的应用.国外医学临床放射学分册, and 1997,12:91-95.
2. Allum R. Complications of arthroscopy of theknee (Review).J Bone Joint Surg (Br), 2002,84:937-945.
3. Murray JG, Ridley NT, Mitchell N, etal. Juvenile chronic arthritis onthe hip:value of contrast enhanced MR imaging .Clin Radiol,1996, 51:99.
4. Missi MJ, Toyras J, Laasanen MS, et al. Proteoglycan and collagen sensitive MRI evaluation of normal and degenerated articular cartilage. J Orthop Res. 2004,22(3): 557-564.
5. Gylsys-Morin VM, Hajek PC, Sartoris DJ, Resnick D. Articular cartilage defects: Detectability in cadaver knees with MRI. AJR, 1987,148: 1153- 1157.
6. Pilch L, Stewart C, Gordon D, et al: Assessment of cartilage volume in the femorotibial joint with magnetic resonance imaging and 3D computer reconstruction. J Rheumatol, 1994, 21:2307-2321.
7. Cicuttini F, Forbes A, Asbeutah A, et al. Comparison and reproducibility of fast and conventional spoiled gradient-echo magnetic resonance sequences in the determination of knee cartilage volume.J Orthop Res, 2000, 18:580-584.
8. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging. J Bone Joint Surg (Am), 1998,80:1276-1284.
9. Drape JL, Pessis E, Auleley GR, etal. Quantitative MR imaging evaluation of chondropathy in osteoarthritic knees[J]. Radiology, 1998,208(1): 49-55 .
10. Lavid NE, DePaolis DC, Pope TW, etal. Analysis of three dimensional computerized representations of articular cartilage lesions [J].Invest Radiol, 1996,31(9): 577-585.
11.周根泉,沈天真,陈星荣,等。膝关节正常关节软骨及软骨缺损的多序列MR成像比较.中国医学计算机成像杂志,1998,2:123-125.
12. Hardy PA, Recht MP, Piraino D, et al. Optimization of a dual echo in the steady state (DESS) free-precession sequence for imaging carti- lage. J Magn Reson Imaging, 1996, 6:329-335.
13. Hargreaves BA, Pauly JM, Gold GE, et al: 3D-DEFT Echo-planar imaging of knee cartilage. Eighth International Society of Magentic Resonance in Medicine, Denver 2120, 2000 .
14. Peterfy CG, van Dijke CF, Janzen DL, et al. Quantification of articular cartilage in the knee with pulsed saturation transfer subtraction and fat-suppressed MR imaging: optimization and validation. Radiology, 1994, 192:485-491.
15. Rose PM, Demlow TA, Szumowski J, etal. Chondromalacia patellae fat suppressed MR imaging.Radiology, 1994, 193:437-440.
16. Treating S, Huber M, and Breitenseher M, etal. Imaging articular cartilage defects with 3D fat suppressed echo planar imaging: Comparison with conven tional 3D fat suppressed gradient echo sequence and correla- tion with histology. J Comput Assist Tomogr, 1998,22:8.
17. Recht MP, Piraino DW,Paletta GA,et al.Accuracy of fatsuppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the de- tection of patellofemoral articular cartilage abnormalities. Radiology, 1996,198:209-212.
18. Burstein D. Diffusion of small solutes in cartilage as measured by nuclear magnetic resonance (NMR) spectroscopy and imaging. J Orthop Res, 1993, 11:465.
19. Eustace S, Dimasi M, Adams J, etal. In vitro and in vivo spin echo diffusion imaging characteristics of synovial fluid: Potential noninvasive differentiation of inflammatory and degenerative arthritis. Skeletal Radiol, 2000, 29:320.
20. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
21. Bjorkengren AG, Gebore KP, Rydholm U, etal. MR imaging of the knee in acute rheumatoid arthritis: synovial uptake of gadolinium DOTA. AJR, 1990, 155:329.
22.许建荣,杨世埙,王皖,等.关节软骨MR影像表现特点和各种影响因素[J].中华放射学杂志,1999,33:106-109.
23. Gagliardi JA, Chung EM, Chandnani VP, etal. Detection and staging of chondromalacia patellae:relative efficacies of conventional MR imaging,MR arthrography,and CT arthrography.AJR,1994,63:629-636.
24. Rand T, Brossmann J, Pedowitz R, etal. Analysis of patellar cartilage:comparison of conventional MR imaging and MR and CT arthrography incadavers. Acta Radiol, 2000,41:492-497.
25. Kim YJ, Iobst C, Millis MB, et al. Assessment of early osteoarthritis in hip dysplasia and pelvic osteotomy using delayed gadolinium enhanced MRI (dGEMRIC). Presented at the Tenth Scientific Meeting and Exhibition of the International Society of Magnetic Resonance in Medicine, 2002:18–24.
26. Burstein D, Velyvis J, Scott KT et al. Protocol issues for delayed Gd(DTPA)2- enhanced MRI(dGEMRIC) for clinical evaluation of articular cartilage.Magnetic Resonance in Medicine.2001,45(1):36-41.
27. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivoassessment with delayed GD(DTPA)2- enhanced MR imaging.Radiology, 1997,205:551
28. Vladimir M, Siegfried T, Monika H, et al. The role of relaxation times in monitoring proteoglycan depletion in articular cartilage . Journal of Magnetic Resonance Imaging, 1999, 10:497-502.
29. Lesperance LM, Gray ML, Burstein D. Determination of fixed charge density in cartilage using nuclear magnetic resonance. J Orthop Res, 992,10 .
30. Lechner EB, Rechl HP, Gmeinwieser JK, etal. Structure, Function; Degeneration of Bovine Hyaline Cartilage; Assesment With MRI imaging in vitro [J] . Radiology, 1989,170:495-496.
31. Modl JM, Sether LA, Haughton VM, et al. Articular cartilage: correlation of histologic zones with signal in tensity at MR imaging.Radiology, 1991, 181:853.
32. Ruberstein J, Kim JK, Morava I, etal. Effects of collagen orientation on MR imaging characteristics of bovine articular cartilage [J] .Radiology, 1993,188:219-226.
33. Xia Y.Heterogeneity of cartilage lamine in MR imaging [J]. J Magn Reson Imaging, 2000,11:686-693.
34. Trattnig S, Mlynarik V, Huber M, etal. Magnetic resonance imagingof articular cartilage and evaluation of cartilage disease[J].Invest Radiol,2000,35(10):595-601.
35. Holder J, Berthiaume M, Schweeitzer ME, et al.Knee joint hyaline cartilage defects: A comprarative study of MR and anatomic sections [J]. JCAT,1992,16(4):597-603.
36. McCauley TR,Disler DG.MR imaging of articular cartilage.Radiology, 1998, 209:629.
37. Outerbridge RE. The etiology of chondromalacia patellae . J Bone Joint Surg (Br), 1961,43:752-757.
38. Yulish BS, Montanez J, Goodfellow DB, etal. Chondromalacia patellae: assessment with MR imaging.Radiology,1987,164(3):763-766.
39. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
40. Sanders TG, Mentzer KD, Miller MD, etal. Autogenous osteochondral“plug”transfer for the treatment of focal chondral defects: postoperative MR appearance with clinical correlation [J]. Skeletal Radiol, 2001, 30(10):570-578.
41. Brittberg M, Winalski CS. Evaluation of cartilage injuries and repair [J]. J Bone Joint Surg (Am), 2003,85(Suppl2): 58-69.
42.高元贵,蔡幼铨,蔡祖龙.磁共振成像[M].第1版.北京:人民军医出版社, 1993. 677-678.
43. Hayes CW, Conway WF. Evaluation of articular cartilage: radiographic andcross sectional imaging techniques.Radiographyics,1992,12:409.
44.康立丽,卢广文.部分MRI参数对信噪比影响实验研究.实用放射学杂志,2003,19(11):971-973.
45. Link TM, Majumdar S, Peterfy C, et al. High resolution MRI of small joints: impact of spatial resolution on diagnostic performance and SNR. Magn Reson Imaging, 1998, 16:147-155.
46. Edelstein WA, Glover GH, Hardy CJ, et al: The intrinsic signal-to-noise ratio in NMR imaging. Magn Reson Med, 1986, 3:604-618.
2. Moed BR, Wiuson Carr SE, Watson JT.Results of operative treatment of fractures of the posterior wall of the acetabulum .J Bone Joint Surg (Am), 2002,84:752-758.
3. Mears DC, Velyvis JH, Chang CP. Displaced acetabular fractures managed operatively: indicators of outcome. Clin Orthop Relat Res, 2003, (407): 173-186.
4. Giannoudis PV, Grotz MR. Operative treatment of displacedfractures of the acetabulum: a meta-analysis. J Bone Joint Surg(Am),2005,87-B(1): 2-9.
5. Alonso JE.A review of the treatment of hip dislocations associated with acetabular fractures. Clin Orthop Relat Res, 2000, (377): 32-43.
6. Saterbak AM, Marsh JL, Nepola JV, et al. Clinical failure after posterior wall acetabular fractures: the influence of initial fracture patterns. J Orthop Trauma, 2000,14:230-237.
7. Johnson EE, Matta JM, Mast JW, etal. Deloyed reconstruction of acetabular fractures 21～210 days following injury.Clin Orthop, 1994, 305:20-29.
8. Matta JM. Fractures of the acetabulum: accuracy of reduction and clinicalresults in patients managed operatively within three weeks after the injury. J Bone Joint Surg (Am), 1996,78:1632-1645.
9. Letournel E, Judet R. Fractures of the acetabulum. New York: Springer, 1981:21-4, 211-19, 311-15.
10. Wright R, Barrett K, Christie MJ, et al. Acetabular fractures: Long-term follow-up of open reduction and internal fixation. J Orthop Trauma, 1994, 8:397-403.
11. Borrelli J, William M, Ricci MD.Acute effects of cartilage impact. Clin Orthop Relat Res, 2004, (423): 33–39.
12. Repo RU, Finlay J. Survival of articular cartilage after controlledimpact. J Bone Joint Surg (Am), 1977,59:1068–1076.
13. Donohue J, Buss D, Oegema T, et al. The effects of indirect blunt trauma on adult canine articular cartilage . J Bone Joint Surg (Am), 1983, 65: 948-957.
14. Thompson JR, Oegema JT, Lewis JL, et al. Osteoarthrotic changes after acute transarticular load: An animal model. J Bone Joint Surg (Am), 1991,73: 990–1001.
15. Borrelli J, Burns ME, Ricci WM, et al. A method for delivering variable impact stresses to the articular cartilage of rabbit knees. J Orthop Trauma, 2002, 16:182-188.
16. Ewers BJ, Weaver BT, Sevensma ET, et al.Chronic changes in rabbit retropatellar cartilage and subchondral bone after blunt impact loading of the patellofemoral joint. J Orthop Res, 2002, 20:545–550.
17. Borrelli Jr J, Tinsley KW, Ricci WM, et al: Induction of chondrocyte apoptosis following impact load. J Orthop Trauma, 2003, 17:635-641.
18. Costouros JG, Dang AC, Kim HT. Comparison of chonrocyte apoptosis in vivo and in vitro following acute osteochondral injury . J Orthop Res, 2004, 22:678-683.
19. Disler D, Recht M, McCauley TR. MR imaging of articular cartilage. Skeletal Radiol, 2000,29:367-377.
20. Matsuno H, Yudoh K, Kondo M, etal. Biochemical effect of intra-articular injections of high molecular weight hyaluronate in rheumatoid arthritis patients . Inflamm Res, 1999,48(3): 154.
21.张鸿逵,王韶进,王永惕,等. SH关节腔内注射治疗膝骨关节炎.中国生化药物杂志, 1998,19(5): 231.
22. Dougados M, Nguyen M, Listrat V, et al. High molecular weight sodium hyaluronate (hylectin) in osteoarthritis of the knee: a year placebo controlled trial. J Osteoathritis and cartilage, 1993,1:97-103.
23. Letournel E, Judet R. Fractures of the acetabulum. Seconded. Berlin: Springer Verlag, 1998.
24. Asik, M, Eralp L, Cetik O, et al. Mid-to long-term resultsfor the surgical treatment of acetabulum fractures. J Bone Joint Surg (Br), 2001, 83 (Supp-II): 119.
25. Newberry WN, Garcia JJ, Mackenzie CD, et al. Analysis of acute mechanical insult in an animal model of post-traumatic osteoarthrosis. J Biomech Eng, 1998,120:704-709.
26. Vrahas MS, Smith GA, Rosler DM, et al. Method to impact in vivo rabbit femoral cartilage with blows of quantifiable stress. J Orthop Res, 1997,15:314–317.
27. Borrelli JJ, Ricci WM, Steger-May K, et al. Postoperative radiographic assessment of acetabular fractures: a comparison of plain radiographs and CT scans. J Orthop Trauma, 2005,19:299-304.
28. Jeffrey JE, Thomson LA, Aspden RM.Matrix loss and synthesis following a single impact load on articular cartilage in vitro. Biochim Biophys Acta, 1997,1334:223-232.
29. Torzilli PA, Grigiene R, Borrelli JJ, et al. Effect of impact load onarticular cartilage: Cell metabolism and viability, and matrix water content. J Biomech Eng, 1999,121:433–441.
30. Haut RC, Ide TM.Mechanical responses of the rabbit patellofemoral joint to blunt impact. J Biomech Eng, 1995,117:402-408.
31. Jeffrey JE, Gregory DW, Aspden RM.Matrix damage and chondrocyte viability following a single impact load on articular cartilage . Arch Biochem Biophys, 1995,322:87-96.
32. Zhang H, Vrahas MS, Baratta RV, et al. Damage to rabbit femoral articular cartilage following direct impacts of uniform stresses in vitro study.Clin Biomech,1999,14:543-548.
1. Missi MJ, Toyras J, Laasanen MS, et al. Proteoglycan and collagen sensitive MRI evaluation of normal and degenerated articular cartilage. J Orthop Res. 2004, 22(3): 557-564.
2. Graichen H, von ER, Vogl T, et al. Quantitative assessment of cartilage status in osteoarthritis by quantitative magnetic resonance imaging. Technical validation for use in analysis of cartilage volume and further morphological parameters . Arthritis Rheum, 2004,50:811-816.
3. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
4.雷新玮,尹建忠,倪红艳等.膝关节软骨退变的MRI与病理对照研究.中国临床医学影像杂志, 2003,14(6) :424-427.
5. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging. J Bone Joint Surg (Am), 1998,80:1276-1284.
6. Disler DG, McCauley TR, Kelman CG, et al. Fat-suppressed three dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: comparison with standard MR imaging and arthroscopy.Am J Roentgenol, 1996,67:127-132.
7. Woolf SD, Chesnick S, Frank JA, et al. Magnetization transfer contrasts: MR imaging of the knee. Radiology, 1991, 170:623-628.
8. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
9. Kim YJ, Iobst C, Millis MB, et al. Assessment of early osteoarthritis in hip dysplasia and pelvic osteotomy using delayed gadolinium enhanced MRI (dGEMRIC). Presented at the Tenth Scientific Meeting and Exhibition of the International Society of Magnetic Resonance in Medicine, 2002:18–24 .
10. Bacic G, Liu KJ, Goda F, etal. MRI contrast enhanced study of cartilage proteoglycan degradation in the rabbit knee.Magn Reson Imaging,1997,37:764 .
11. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivo assessment with delayed GD(DTPA)2- enhanced MR imaging.Radiology,1997,205:551
12.江浩,何国祥,陈克敏,等.骨与关节MRI [M] .第1版.上海:上海科学技术出版社,2000:249-312.
1. Repo RU, Finlay J. Survival of articular cartilage after controlled impact. J Bone Joint Surg (Am), 1977,59:1068–1076.
2. Jeffrey JE, Thomson LA, Aspden RM.Matrix loss and synthesis following a single impact load on articular cartilage in vitro. Biochim Biophys Acta, 1997, 1334:223-232.
3. Torzilli PA, Grigiene R, Borrelli JJ, et al. Effect of impact load on articular cartilage: Cell metabolism and viability, and matrix water content. J Biomech Eng, 1999,121:433–441.
4. Conrozier T.Death of articular chondrocyte, mechanisms and protection. Pressc Med, 1998,27(36): 1859-1861.
5. Kim HA, Lee YJ, Seong SC, et al. Apoptotic chondrocyte death in human osteoarthritis.J Rheum,2000,27(2):455-462.
6. Kouri JB, Agniera JM, Reyes J, etal. Apoptotic chondrocytes from osteoarthrotic human articular cartilage and abnormal calcification of subchondral . Bone, 2000, 27: 1005-1019.
7. Blaw FJ, Guistian R, Vazguez ME, et al. Osteoarthritis chondrocyte did by apoptosis : A possible pathway for osteoarthritis pathology Arthritis Rheum,1998,41(2): 284-289.
8. Mankin HJ. Current concepts review: The response of articular cartilage to mechanical injury. J Bone Joint Surg (Am), 1982,64:460-466.
9. Mankin HJ, Mow VC, Buckwalter JA, et al . Articular Cartilage Structure, composition and Function . In Buckwalter JA, Einhorn JA, Simon SR (eds). Orthopaedic Basic Science.Biology and Biomechanics of the Musculo- skeletal System . Rosemont, IL, American Academy of Orthopaedic Surgeons, 1999,443–470.
10. Blanco FJ, Ochs RL, Schwarz H, etal. Chondrocyte apoptosis induced by nitric oxide [J] . Am J Pathol, 1995, 146(1): 75-85.
11. Yatsugi N, Tsukazaki T, Osaki M, et al. Apoptosis of articular chondrocytes in reheumatoid arthritis and osteoarthritis: correlation of apoptosis with degree of cartilage destruction and expression of apoptosis-related proteins of p53 and c-myc [J]. J Orthop Sci, 2000, 5(2):150-156.
12. Blanco FJ, Guitian R, Vazquez-Martul E, et al. Osteoarthritis chondrocytes die by apoptosis: a possible pathway for osteoarthritis pathology. Arthritis Rheum 1998, 41:284-289.
13. Hashimoto S, Ochs RL, Komiya S, et al. Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis. Arthritis Rheum 1998,41:1632-1638.
14. Loening AM, James IE, Levenston ME, et al. Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis [J]. Archives of Biochemistry & Biophysics, 2000,381 (2): 205-212.
15. Chen CT, Burton WN, Borden C, et al. Chondrocyte necrosis and apoptosis in impact damaged articular cartilage [J]. Journal of Orthopaedic Res,2001,19(4):703-711.
1. McCauley TR, Disler DG.MR imaging of articular cartilage. Radiology,1998,209:629
2. Hargreaves BA, Gold GE, Beaulieu CF, et al. Comparison of new sequences for high-resolution cartilage imaging. Magn Reson Med, 2003,49:700 -709.
3. Nieminen MT, Rieppo J, Toyras J, et al. T2 relaxation reveals spatial collagen architecture in articular cartilage: a comparative quantitative MRI and polarized light microscopic study. Magn Reson Med, 2001, 46:487 -493.
4. Dahlberg L, Nyquist F, Olsson LE, et al. Biochemical analysis of proteoglycan content in biopsies of repaired human joint cartilage is in line with contrast enhanced MRI results. In: Orthopaedic Research Society.New Orleans, LA, 2003.
5. Konig H, Sauter R, Deimling M, et al. Cartilage disorders: comparison of spin echo,CHESS and FLASH sequence MR images.Radiology,1987,164:753 .
6. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
7.雷新玮,尹建忠,倪红艳等.膝关节软骨退变的MRI与病理对照研究.中国临床医学影像杂志, 2003,14(6) :424-427.
8. Goodwin DW, Dunn JF. High-resolution magnetic resonance imaging of articular cartilage: correlation with histology and pathology. Top Magn Reson Imaging.1998, 9:337-347.
9. Carl S, Krishanu BG.Magnetic resonance imaging of focal articular cartilage lesion. Topics in Magnetic Resonance Imaging, 2003; 14(2):131-144.
10. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging .J Bone Joint Surg (Am),1998,80:1276-1284.
11. Disler DG, McCauley TR, Kelman CG, et al. Fat-suppressed three dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: comparison with standard MR imaging and arthroscopy.Am J Roentgenol, 1996,67: 127-132.
12. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
13. Woolf SD, Chesnick S, Frank JA, et al. Magnetization transfer contrasts: MR imaging of the knee. Radiology, 1991, 170:623-628.
14. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivo assessment with delayed GD(DTPA)2- enhanced MR imaging. Radiology, 1997,205:551 .
15. Hayes CW, Conway WF. Evaluation of articular cartilage: radiographic and cross sectional imaging techniques.Radiographyics, 1992, 12:409.
16. Modl JM, Sether LA, Haughton VM, et al. Articular cartilage: correlation of histologic zones with signal in tensity at MR imaging. Radiology, 1991, 181:853.
1. Matsuno H, Yudoh K, Kondo M, etal. Biochemical effect of intra-articular injections of high molecular weight hyaluronate in rheumatoid arthritis patients . Inflamm Res, 1999,48(3): 154.
2.张鸿逵,王韶进,王永惕,等. SH关节腔内注射治疗膝骨关节炎.中国生化药物杂志, 1998,19(5): 231.
3. Dougados M, Nguyen M, Listrat V, et al. High molecular weight sodium hyaluronate (hylectin) in osteoarthritis of the knee: a year placebo controlled trial. J Osteoathritis and cartilage, 1993, 1:97-103.
4. Conrozier T. Death of articular chondrocyte, mechanisms and protection. Pressc Med, 1998,27(36): 1859-1861.
5. Kim HA, Lee YJ, Seong SC, et al. Apoptotic chondrocyte death in human osteoarthritis.J Rheum,2000,27(2):455-462.
6. Kouri JB, Agniera JM, Reyes J, et al. Apoptotic chondrocytes from osteoarthrotic human articular cartilage and abnormal calcification of subchondral . Bone, 2000,27: 1005-1019.
7. Blaw FJ, Guistian R, Vazguez ME, et al. Osteoarthritis chondrocyte did by apoptosis : A possible pathway for osteoarthritis pathology.Arthritis Rheum,1998,41(2): 284-289.
8. Chrisman OD, Ladenbauer-Bellis IM, Panjabi M, et al. The relationship of mechanical trauma and the early biochemical reactions of osteo- arthritic cartilage . Clin Orthop, 1981, 161:275-284.
9. Graf J, Neusel E, Schneider E, et al. Intra-articular treatment with hyaluronic acid in osteoarthritis of the knee joint: a controlled clinical trial versus mucopolysaccharide polysulfuric acid ester. Clin Exp Rheumatol, 1993,11:367-372.
10. Hochberg MC. Role of intra-articular hyaluronic acid preparations inmedical management of osteoarthritis of the knee. Semin Arthritis Rheum, 2000,30(Suppl2): 2-10.
11. Frizziero L, Govoni E, Bacchini P. Intra-articular hyaluronic acid in the treatment of osteoarthritis of the knee: clinical and morpho- logical study. Clin Exp Rheumatol, 1998, 16:441-449.
12. Oshima Y.A study of the effect of intra articular injection of high molecular weight sodium hyaluronate on osteoathritis of the hip .Jpn Pharmacol Ther, 1987,15:1337.
13. Brand KD, Block JA, Michalski JP, et al. Efficacy and safety of intra- articular sodium hyaluronate in knee osteoarthritis. Clin Orthop, 2001, (385): 130-143.
1.吴春营,樊波,李皎,等.MRI在诊断关节软骨炎症上的应用.国外医学临床放射学分册, and 1997,12:91-95.
2. Allum R. Complications of arthroscopy of theknee (Review).J Bone Joint Surg (Br), 2002,84:937-945.
3. Murray JG, Ridley NT, Mitchell N, etal. Juvenile chronic arthritis onthe hip:value of contrast enhanced MR imaging .Clin Radiol,1996, 51:99.
4. Missi MJ, Toyras J, Laasanen MS, et al. Proteoglycan and collagen sensitive MRI evaluation of normal and degenerated articular cartilage. J Orthop Res. 2004,22(3): 557-564.
5. Gylsys-Morin VM, Hajek PC, Sartoris DJ, Resnick D. Articular cartilage defects: Detectability in cadaver knees with MRI. AJR, 1987,148: 1153- 1157.
6. Pilch L, Stewart C, Gordon D, et al: Assessment of cartilage volume in the femorotibial joint with magnetic resonance imaging and 3D computer reconstruction. J Rheumatol, 1994, 21:2307-2321.
7. Cicuttini F, Forbes A, Asbeutah A, et al. Comparison and reproducibility of fast and conventional spoiled gradient-echo magnetic resonance sequences in the determination of knee cartilage volume.J Orthop Res, 2000, 18:580-584.
8. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast spin echo imaging. J Bone Joint Surg (Am), 1998,80:1276-1284.
9. Drape JL, Pessis E, Auleley GR, etal. Quantitative MR imaging evaluation of chondropathy in osteoarthritic knees[J]. Radiology, 1998,208(1): 49-55 .
10. Lavid NE, DePaolis DC, Pope TW, etal. Analysis of three dimensional computerized representations of articular cartilage lesions [J].Invest Radiol, 1996,31(9): 577-585.
11.周根泉,沈天真,陈星荣,等。膝关节正常关节软骨及软骨缺损的多序列MR成像比较.中国医学计算机成像杂志,1998,2:123-125.
12. Hardy PA, Recht MP, Piraino D, et al. Optimization of a dual echo in the steady state (DESS) free-precession sequence for imaging carti- lage. J Magn Reson Imaging, 1996, 6:329-335.
13. Hargreaves BA, Pauly JM, Gold GE, et al: 3D-DEFT Echo-planar imaging of knee cartilage. Eighth International Society of Magentic Resonance in Medicine, Denver 2120, 2000 .
14. Peterfy CG, van Dijke CF, Janzen DL, et al. Quantification of articular cartilage in the knee with pulsed saturation transfer subtraction and fat-suppressed MR imaging: optimization and validation. Radiology, 1994, 192:485-491.
15. Rose PM, Demlow TA, Szumowski J, etal. Chondromalacia patellae fat suppressed MR imaging.Radiology, 1994, 193:437-440.
16. Treating S, Huber M, and Breitenseher M, etal. Imaging articular cartilage defects with 3D fat suppressed echo planar imaging: Comparison with conven tional 3D fat suppressed gradient echo sequence and correla- tion with histology. J Comput Assist Tomogr, 1998,22:8.
17. Recht MP, Piraino DW,Paletta GA,et al.Accuracy of fatsuppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the de- tection of patellofemoral articular cartilage abnormalities. Radiology, 1996,198:209-212.
18. Burstein D. Diffusion of small solutes in cartilage as measured by nuclear magnetic resonance (NMR) spectroscopy and imaging. J Orthop Res, 1993, 11:465.
19. Eustace S, Dimasi M, Adams J, etal. In vitro and in vivo spin echo diffusion imaging characteristics of synovial fluid: Potential noninvasive differentiation of inflammatory and degenerative arthritis. Skeletal Radiol, 2000, 29:320.
20. Vahlensieck M, Dombrowski F, Leutner C, et al. Magnetization transfer contrast (MTC) and MTC subtraction: Enhancementof cartilage lesions and intracartilaginous degenerationin vitro. Skeletal Radiology, 1994, 23:535–539.
21. Bjorkengren AG, Gebore KP, Rydholm U, etal. MR imaging of the knee in acute rheumatoid arthritis: synovial uptake of gadolinium DOTA. AJR, 1990, 155:329.
22.许建荣,杨世埙,王皖,等.关节软骨MR影像表现特点和各种影响因素[J].中华放射学杂志,1999,33:106-109.
23. Gagliardi JA, Chung EM, Chandnani VP, etal. Detection and staging of chondromalacia patellae:relative efficacies of conventional MR imaging,MR arthrography,and CT arthrography.AJR,1994,63:629-636.
24. Rand T, Brossmann J, Pedowitz R, etal. Analysis of patellar cartilage:comparison of conventional MR imaging and MR and CT arthrography incadavers. Acta Radiol, 2000,41:492-497.
25. Kim YJ, Iobst C, Millis MB, et al. Assessment of early osteoarthritis in hip dysplasia and pelvic osteotomy using delayed gadolinium enhanced MRI (dGEMRIC). Presented at the Tenth Scientific Meeting and Exhibition of the International Society of Magnetic Resonance in Medicine, 2002:18–24.
26. Burstein D, Velyvis J, Scott KT et al. Protocol issues for delayed Gd(DTPA)2- enhanced MRI(dGEMRIC) for clinical evaluation of articular cartilage.Magnetic Resonance in Medicine.2001,45(1):36-41.
27. Bashir A, Gray SM. Glycosaa minoglycan in articular cartilage:In vivoassessment with delayed GD(DTPA)2- enhanced MR imaging.Radiology, 1997,205:551
28. Vladimir M, Siegfried T, Monika H, et al. The role of relaxation times in monitoring proteoglycan depletion in articular cartilage . Journal of Magnetic Resonance Imaging, 1999, 10:497-502.
29. Lesperance LM, Gray ML, Burstein D. Determination of fixed charge density in cartilage using nuclear magnetic resonance. J Orthop Res, 992,10 .
30. Lechner EB, Rechl HP, Gmeinwieser JK, etal. Structure, Function; Degeneration of Bovine Hyaline Cartilage; Assesment With MRI imaging in vitro [J] . Radiology, 1989,170:495-496.
31. Modl JM, Sether LA, Haughton VM, et al. Articular cartilage: correlation of histologic zones with signal in tensity at MR imaging.Radiology, 1991, 181:853.
32. Ruberstein J, Kim JK, Morava I, etal. Effects of collagen orientation on MR imaging characteristics of bovine articular cartilage [J] .Radiology, 1993,188:219-226.
33. Xia Y.Heterogeneity of cartilage lamine in MR imaging [J]. J Magn Reson Imaging, 2000,11:686-693.
34. Trattnig S, Mlynarik V, Huber M, etal. Magnetic resonance imagingof articular cartilage and evaluation of cartilage disease[J].Invest Radiol,2000,35(10):595-601.
35. Holder J, Berthiaume M, Schweeitzer ME, et al.Knee joint hyaline cartilage defects: A comprarative study of MR and anatomic sections [J]. JCAT,1992,16(4):597-603.
36. McCauley TR,Disler DG.MR imaging of articular cartilage.Radiology, 1998, 209:629.
37. Outerbridge RE. The etiology of chondromalacia patellae . J Bone Joint Surg (Br), 1961,43:752-757.
38. Yulish BS, Montanez J, Goodfellow DB, etal. Chondromalacia patellae: assessment with MR imaging.Radiology,1987,164(3):763-766.
39. Recht MP, Piraino DW, Paletta GA, etal. Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities . Radiology, 1996,198(1): 209-212.
40. Sanders TG, Mentzer KD, Miller MD, etal. Autogenous osteochondral“plug”transfer for the treatment of focal chondral defects: postoperative MR appearance with clinical correlation [J]. Skeletal Radiol, 2001, 30(10):570-578.
41. Brittberg M, Winalski CS. Evaluation of cartilage injuries and repair [J]. J Bone Joint Surg (Am), 2003,85(Suppl2): 58-69.
42.高元贵,蔡幼铨,蔡祖龙.磁共振成像[M].第1版.北京:人民军医出版社, 1993. 677-678.
43. Hayes CW, Conway WF. Evaluation of articular cartilage: radiographic andcross sectional imaging techniques.Radiographyics,1992,12:409.
44.康立丽,卢广文.部分MRI参数对信噪比影响实验研究.实用放射学杂志,2003,19(11):971-973.
45. Link TM, Majumdar S, Peterfy C, et al. High resolution MRI of small joints: impact of spatial resolution on diagnostic performance and SNR. Magn Reson Imaging, 1998, 16:147-155.
46. Edelstein WA, Glover GH, Hardy CJ, et al: The intrinsic signal-to-noise ratio in NMR imaging. Magn Reson Med, 1986, 3:604-618.
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