腰椎小关节骨性关节炎的病理学、影像学及炎性因子表达变化的相关研究
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摘要
本研究包括以下三个实验:
实验一腰椎小关节骨性关节炎的病理学及影像学对比研究
【目的】:对比腰椎小关节骨性关节炎的病理学及影像学检查之间的关系。
【方法】:选取我科接受后路腰椎手术的患者共20例,其中男性8例,女性12例。采用Weishaup的分级标准评估小关节退变程度;甲苯胺蓝染色法后镜下观察关节软骨组织学改变,采用Nicola提出的分级法对软骨的退变程度进行分级。【结果】:对比影像学分级与软骨分级,其中影像学0级时软骨退变1级1例,2级1例,3级1例;影像学1级时组织学软骨退变1级1例,3级1例,4级1例;影像学退变2、3级时组织学软骨退变均为3、4级。【结论】:镜下观察到的病理改变与退变的软骨病变、坏死现象完全一致;在影像学检测小关节退变0级与1级时,软骨病理学分级较为严重,与影像学分级明显不符。而影像学退变2、3级时组织学软骨退变均为3、4级,影像学检查与病理学分级相符程度很高,提示在临床上,CT与MRI在诊断早期小关节骨性关节炎时还有一定的局限性,但其在诊断中晚期小关节骨性关节炎时参考意义较大。
实验二炎性因子在腰椎小关节骨性关节炎中的表达及其与疼痛关联的初步探讨
【目的】:初步探讨小关节源性炎性因子在退变性腰椎小关节中的表达及其与下腰痛间的联系。【方法】:选取我科接受后路手术的退变性腰椎管狭窄(41例)及腰椎间盘突出患者(34例)共75例,采用Weishaup的分级标准评估小关节退变程度,记录术前腰腿痛,下肢痛及功能障碍评分。收集术中切除的一侧腰椎小关节标本;酶联免疫吸附剂测定法测定腰椎小关节退变关节软骨中白细胞介素1β及肿瘤坏死因子α含量。【结果】: TNF-α各组测量均为阴性结果。退变性腰椎管狭窄组IL-1β阳性率高于腰椎间盘突出组。IL-1β含量与腰椎小关节退变程度成正比,随退变程度增加而升高。退变性腰椎管狭窄组中IL-1β阳性患者腰背痛、下肢痛及功能障碍评分均高于IL-1β阴性患者,而腰椎间盘突出组内则无明显差异。【结论】:退变性腰椎小关节软骨产生IL-1β增加;小关节源性炎性因子可能是导致退变性腰椎管狭窄患者腰背痛、下肢痛及功能障碍的原因之一。
实验三SD大鼠腰椎小关节胶原酶诱导骨性关节炎模型中TNF–α,IL- 1β及NO的表达变化
【目的】:初步探讨白细胞介素1β及肿瘤坏死因子α及一氧化氮在小关节骨性关节炎病程中表达的变化。【方法】:选取SD大鼠(48例)随机分为胶原酶注射组(24例)和对照组(24例),采用关节腔内注射胶原酶诱导骨性关节炎,术后于1周、2周、4周、8周取各组实验动物各6只处死后立即取出腰5/6小关节突,倒置显微镜下观察软骨组织学连续动态改变,酶联免疫吸附剂测定法测定关节软骨中白细胞介素1β及肿瘤坏死因子α含量,免疫组织化学染色法检测软骨中一氧化氮合成酶的表达并利用细胞图像分析仪,对各实验期免疫组化染色后的切片做一氧化氮合成酶定量分析。【结果】:倒置显微镜下观察结果显示胶原酶诱导骨性关节炎模型关节软骨损伤随时间延长而加重;免疫组化显示,实验组动物软骨中iNOS含量在术后1周时在软骨浅层有少量染色,术后2周时阳性染色结果明显增多,而在术后4周时阳性染色大量增多并且在软骨中下层有所表达,在术后8周时软骨全层可见大量阳性染色;iNOS的染色强度与对照组相比在术后1周时即明显增高,术后2周、4周、8周时,iNOS染色强度一直维持在较高的水平;软骨中炎性因子IL - 1β和TNF -α表达与对照组明显升高,IL - 1β在术后2周时达峰值,此后逐渐下降,到8周仍处于较高水平,TNF -α在1周时明显升高,2周时有所下降,4周时明显下降,8周时表达与对照组无明显差异。【结论】:关节腔注射胶原酶诱导骨性关节炎模型实验组小关节退变软骨的病理改变与临床小关节退变患者关节软骨病理改变基本相同,并随着病程的进行,软骨的退变逐步加重;小关节源性IL- 1β与软骨的退变程度成正相关,但不随软骨退变的加重而进一步升高。TNF–α与IL- 1β可能在炎症的不同时期发挥作用,其中TNF–α主要作用于炎症早期。退变关节软骨中iNOS含量持续增高,提示NO在骨性关节炎的病程发展中也可能起到了重要的作用。
The research consist the following three experiments:
1 To compare the pathologic changes and iconographic changes of lumbar facet joint osteoarthritis
Objective:To compare the pathologic and imaging changes seen in lumbar facet joint osteoarthritis. Methods:A totally of 20 patients (male 8, female 12) undergoing posterior lumbar spinal surgery in our department were evaluated regarding the extent of degenerative arthrosis according to the Weishaup grading criteria. We used toluidine blue staining to observe histological changes in articular cartilage and graded the extent of degenerative cartilage using the classification method proposed by Nicloa. Results:When comparing the imaging changes with thoes seen in histological studits,we obsorved grade 3 in one when imging grade was grade 0; grade 1 degeneration in one case,grade 3 in one and grade 4 in one when imaging grade was grade 1; finally, grades 3 and 4 degeneration corresponded to imaging changes of grades 2 and 3. Conclusion: The pathological changes was consistent with the lesion and necrosis of degenerative cartilage. When iconographic classification was grade 0 and 1, cartilage classification was more severe and was obviously imaging with the imaging greading. But, when imaging grades was grade 2 and 3, the cartilage classification was all grade 3 and 4. They were highly consistent with each other. This phenomenon suggested that CT and MRI have some limitations in the early diagnosis of facet joint osteoarthritis, but they may provide a good reference in the diagnosis of late facet osteoarthritis.
2 To initially identify the expression of inflammatory factors in lumbar facet joint osteoarthritis and determine that whether these factors associate with pain.
Objective: To initially approach the role of lumbar facet joint derived inflammatory factors in degenerative lumbar spinal canal stenosis; Method: Totally 75 cases of degenerative lumbar spinal canal stenosis(41 cases) and lumbar intervertebral disc herniation(34 cases)undergoing posterior lumbar spinal surgery in our department were evaluated extent of degenerative arthrosis according to the Weishaup grading criteria. The grading of backleg pain, melosalgia and functional impairment were recorded. The excisional lumbar facet joints were collected as species. The content of interleukin-1βand tumor necrosis factor-αin the species were determined by ELISA. Results: there was no TNF-αdetected in both of the two groups. More IL-1βwas detected in degenerative lumbar spinal canal stenosis group than that in lumbar intervertebral disc herniation group. It was demonstrated that the content of IL-1βin the species increased as the degeneration of lumbar facet joint sharpened. In degenerative lumbar spinal canal stenosis group, the grading of backleg pain, melosalgia and functional impairment was apparently higher than when IL-1βwas detected while there was no statistical difference in all the species in lumbar intervertebral disc herniation group. Conclusion: the cartilage of degenerative lumbar spinal canal produced more IL-1β. Lumbar facet joint derived inflammatory factors might be one of the reasons that cause backleg pain and melosalgia and functional impairment in degenerative lumbar spinal canal stenosis patients.
3 To evaluate the expression of TNF–α,IL- 1βand NO in rat lumbar facet joint osteoarthritis induced by collagenase.
Objective: to initially explore the changes in the expression of TNF–α,IL- 1βand NO in the development of facet joint osteoarthritis. Method: Adult SD rats (48 cases) were randomly divided into two groups: collagenase injection group (24 cases),normal control group (24 cases). Osteoarthritis were induced by intra-articular injection of collagenase. After 1 week, 2 weeks,4 weeks,8weeks 6 rats of each group were killed and L5/6 facet joint were taken out immediately. Dynamic changes in cartilage tissue were continuously observed under inverted microscope.IL-1βand TNF-αin the arthrodial cartilage were detected by ELISA. Nitric oxide synthase were detected by immunohistochemical staining and were quantitatively analyzed by cell image analysis. Results: In the osteoarthritis model induced by collagenase, articular cartilage damage increased with time. Immunohistochemistry of iNOS showed that, in superfacial cartilage there are small amount of straining after 1 week. After 2 weeks, positive staining increased obviously. After 4 weeks, positive staining increased significantly and was observed in the middle and subnatant cartilage. After 8 weeks, more positive strain was observed in the full-thickness cartilage; After 1 week, the staining intensity of iNOS compared with the control group increased significantly. After 2 weeks, 4 weeks and 8 weeks, iNOS staining intensity has remained at a high level; IL-1βand TNF-αin the collagenase injection group were significantly higher than the control group. After 2 weeks, IL-1βreached the peak, then decreased gradually. After 8 weeks, IL-1βwas still at a high level. TNF-αincreased significantly after 1 week and decreased after 2 weeks. After 4 weeks, it decreased significantly. After 8 weeks, there was no significant difference between the two groups. Conclusion: The pathological changes in the osteoarthritis model induced by collagenase injection was similar with that of patients with facet joint degeneration. And degeneration of cartilage gradually increased with the course of disease; Facet joint-derived IL-1βwas positively correlated with the extent of degeneration in the cartilage, but it didn’t increase with the aggravation of cartilage degeneration. TNF–αand IL - 1βmaybe act at different stages of inflammation and TNF–αact in early stage. The content of iNOS in degenerative aritcular cartilage increased with time suggesting that NO may play an important role in the course of osteoarthritis.
实验一腰椎小关节骨性关节炎的病理学及影像学对比研究
【目的】:对比腰椎小关节骨性关节炎的病理学及影像学检查之间的关系。
【方法】:选取我科接受后路腰椎手术的患者共20例,其中男性8例,女性12例。采用Weishaup的分级标准评估小关节退变程度;甲苯胺蓝染色法后镜下观察关节软骨组织学改变,采用Nicola提出的分级法对软骨的退变程度进行分级。【结果】:对比影像学分级与软骨分级,其中影像学0级时软骨退变1级1例,2级1例,3级1例;影像学1级时组织学软骨退变1级1例,3级1例,4级1例;影像学退变2、3级时组织学软骨退变均为3、4级。【结论】:镜下观察到的病理改变与退变的软骨病变、坏死现象完全一致;在影像学检测小关节退变0级与1级时,软骨病理学分级较为严重,与影像学分级明显不符。而影像学退变2、3级时组织学软骨退变均为3、4级,影像学检查与病理学分级相符程度很高,提示在临床上,CT与MRI在诊断早期小关节骨性关节炎时还有一定的局限性,但其在诊断中晚期小关节骨性关节炎时参考意义较大。
实验二炎性因子在腰椎小关节骨性关节炎中的表达及其与疼痛关联的初步探讨
【目的】:初步探讨小关节源性炎性因子在退变性腰椎小关节中的表达及其与下腰痛间的联系。【方法】:选取我科接受后路手术的退变性腰椎管狭窄(41例)及腰椎间盘突出患者(34例)共75例,采用Weishaup的分级标准评估小关节退变程度,记录术前腰腿痛,下肢痛及功能障碍评分。收集术中切除的一侧腰椎小关节标本;酶联免疫吸附剂测定法测定腰椎小关节退变关节软骨中白细胞介素1β及肿瘤坏死因子α含量。【结果】: TNF-α各组测量均为阴性结果。退变性腰椎管狭窄组IL-1β阳性率高于腰椎间盘突出组。IL-1β含量与腰椎小关节退变程度成正比,随退变程度增加而升高。退变性腰椎管狭窄组中IL-1β阳性患者腰背痛、下肢痛及功能障碍评分均高于IL-1β阴性患者,而腰椎间盘突出组内则无明显差异。【结论】:退变性腰椎小关节软骨产生IL-1β增加;小关节源性炎性因子可能是导致退变性腰椎管狭窄患者腰背痛、下肢痛及功能障碍的原因之一。
实验三SD大鼠腰椎小关节胶原酶诱导骨性关节炎模型中TNF–α,IL- 1β及NO的表达变化
【目的】:初步探讨白细胞介素1β及肿瘤坏死因子α及一氧化氮在小关节骨性关节炎病程中表达的变化。【方法】:选取SD大鼠(48例)随机分为胶原酶注射组(24例)和对照组(24例),采用关节腔内注射胶原酶诱导骨性关节炎,术后于1周、2周、4周、8周取各组实验动物各6只处死后立即取出腰5/6小关节突,倒置显微镜下观察软骨组织学连续动态改变,酶联免疫吸附剂测定法测定关节软骨中白细胞介素1β及肿瘤坏死因子α含量,免疫组织化学染色法检测软骨中一氧化氮合成酶的表达并利用细胞图像分析仪,对各实验期免疫组化染色后的切片做一氧化氮合成酶定量分析。【结果】:倒置显微镜下观察结果显示胶原酶诱导骨性关节炎模型关节软骨损伤随时间延长而加重;免疫组化显示,实验组动物软骨中iNOS含量在术后1周时在软骨浅层有少量染色,术后2周时阳性染色结果明显增多,而在术后4周时阳性染色大量增多并且在软骨中下层有所表达,在术后8周时软骨全层可见大量阳性染色;iNOS的染色强度与对照组相比在术后1周时即明显增高,术后2周、4周、8周时,iNOS染色强度一直维持在较高的水平;软骨中炎性因子IL - 1β和TNF -α表达与对照组明显升高,IL - 1β在术后2周时达峰值,此后逐渐下降,到8周仍处于较高水平,TNF -α在1周时明显升高,2周时有所下降,4周时明显下降,8周时表达与对照组无明显差异。【结论】:关节腔注射胶原酶诱导骨性关节炎模型实验组小关节退变软骨的病理改变与临床小关节退变患者关节软骨病理改变基本相同,并随着病程的进行,软骨的退变逐步加重;小关节源性IL- 1β与软骨的退变程度成正相关,但不随软骨退变的加重而进一步升高。TNF–α与IL- 1β可能在炎症的不同时期发挥作用,其中TNF–α主要作用于炎症早期。退变关节软骨中iNOS含量持续增高,提示NO在骨性关节炎的病程发展中也可能起到了重要的作用。
The research consist the following three experiments:
1 To compare the pathologic changes and iconographic changes of lumbar facet joint osteoarthritis
Objective:To compare the pathologic and imaging changes seen in lumbar facet joint osteoarthritis. Methods:A totally of 20 patients (male 8, female 12) undergoing posterior lumbar spinal surgery in our department were evaluated regarding the extent of degenerative arthrosis according to the Weishaup grading criteria. We used toluidine blue staining to observe histological changes in articular cartilage and graded the extent of degenerative cartilage using the classification method proposed by Nicloa. Results:When comparing the imaging changes with thoes seen in histological studits,we obsorved grade 3 in one when imging grade was grade 0; grade 1 degeneration in one case,grade 3 in one and grade 4 in one when imaging grade was grade 1; finally, grades 3 and 4 degeneration corresponded to imaging changes of grades 2 and 3. Conclusion: The pathological changes was consistent with the lesion and necrosis of degenerative cartilage. When iconographic classification was grade 0 and 1, cartilage classification was more severe and was obviously imaging with the imaging greading. But, when imaging grades was grade 2 and 3, the cartilage classification was all grade 3 and 4. They were highly consistent with each other. This phenomenon suggested that CT and MRI have some limitations in the early diagnosis of facet joint osteoarthritis, but they may provide a good reference in the diagnosis of late facet osteoarthritis.
2 To initially identify the expression of inflammatory factors in lumbar facet joint osteoarthritis and determine that whether these factors associate with pain.
Objective: To initially approach the role of lumbar facet joint derived inflammatory factors in degenerative lumbar spinal canal stenosis; Method: Totally 75 cases of degenerative lumbar spinal canal stenosis(41 cases) and lumbar intervertebral disc herniation(34 cases)undergoing posterior lumbar spinal surgery in our department were evaluated extent of degenerative arthrosis according to the Weishaup grading criteria. The grading of backleg pain, melosalgia and functional impairment were recorded. The excisional lumbar facet joints were collected as species. The content of interleukin-1βand tumor necrosis factor-αin the species were determined by ELISA. Results: there was no TNF-αdetected in both of the two groups. More IL-1βwas detected in degenerative lumbar spinal canal stenosis group than that in lumbar intervertebral disc herniation group. It was demonstrated that the content of IL-1βin the species increased as the degeneration of lumbar facet joint sharpened. In degenerative lumbar spinal canal stenosis group, the grading of backleg pain, melosalgia and functional impairment was apparently higher than when IL-1βwas detected while there was no statistical difference in all the species in lumbar intervertebral disc herniation group. Conclusion: the cartilage of degenerative lumbar spinal canal produced more IL-1β. Lumbar facet joint derived inflammatory factors might be one of the reasons that cause backleg pain and melosalgia and functional impairment in degenerative lumbar spinal canal stenosis patients.
3 To evaluate the expression of TNF–α,IL- 1βand NO in rat lumbar facet joint osteoarthritis induced by collagenase.
Objective: to initially explore the changes in the expression of TNF–α,IL- 1βand NO in the development of facet joint osteoarthritis. Method: Adult SD rats (48 cases) were randomly divided into two groups: collagenase injection group (24 cases),normal control group (24 cases). Osteoarthritis were induced by intra-articular injection of collagenase. After 1 week, 2 weeks,4 weeks,8weeks 6 rats of each group were killed and L5/6 facet joint were taken out immediately. Dynamic changes in cartilage tissue were continuously observed under inverted microscope.IL-1βand TNF-αin the arthrodial cartilage were detected by ELISA. Nitric oxide synthase were detected by immunohistochemical staining and were quantitatively analyzed by cell image analysis. Results: In the osteoarthritis model induced by collagenase, articular cartilage damage increased with time. Immunohistochemistry of iNOS showed that, in superfacial cartilage there are small amount of straining after 1 week. After 2 weeks, positive staining increased obviously. After 4 weeks, positive staining increased significantly and was observed in the middle and subnatant cartilage. After 8 weeks, more positive strain was observed in the full-thickness cartilage; After 1 week, the staining intensity of iNOS compared with the control group increased significantly. After 2 weeks, 4 weeks and 8 weeks, iNOS staining intensity has remained at a high level; IL-1βand TNF-αin the collagenase injection group were significantly higher than the control group. After 2 weeks, IL-1βreached the peak, then decreased gradually. After 8 weeks, IL-1βwas still at a high level. TNF-αincreased significantly after 1 week and decreased after 2 weeks. After 4 weeks, it decreased significantly. After 8 weeks, there was no significant difference between the two groups. Conclusion: The pathological changes in the osteoarthritis model induced by collagenase injection was similar with that of patients with facet joint degeneration. And degeneration of cartilage gradually increased with the course of disease; Facet joint-derived IL-1βwas positively correlated with the extent of degeneration in the cartilage, but it didn’t increase with the aggravation of cartilage degeneration. TNF–αand IL - 1βmaybe act at different stages of inflammation and TNF–αact in early stage. The content of iNOS in degenerative aritcular cartilage increased with time suggesting that NO may play an important role in the course of osteoarthritis.
引文
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