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肝肾亏虚老年下腰痛患者腰椎小关节软骨超微结构观察 被引量:3

Ultrastructural Observation of Lumbar Facet Joint Cartilage in Elderly Patients with Deficiency of Liver and Kidney
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摘要 目的基于“肾主骨、肝主筋”理论,观察肝肾亏虚老年患者腰椎小关节软骨超微结构的变化,旨在从微观组织形态学角度探讨肝肾亏虚患者腰椎小关节退变的可能机制。方法选取2018年1月—2019年7月于广西中医药大学附属瑞康医院脊柱外科住院且行腰椎开放手术的下腰痛患者,分为肝肾亏虚组和非肝肾亏虚组,术中收取两组患者腰椎小关节,HE染色后观察其组织形态学结构差异,并通过透射电镜观察两组小关节软骨超微结构,初步探讨肝肾亏虚患者腰椎小关节退变的可能机制。结果本实验从病理组织形态学角度对比肝肾亏虚组与非肝肾亏虚组的腰椎小关节,发现非肝肾亏虚组腰椎小关节关节软骨表面平滑连续,软骨层较厚,细胞数目较多,形态规则,排列整齐,层次分明,“潮线”清晰;肝肾亏虚组关节软骨表面损伤,细胞层次不清,“潮线”扭曲不规则甚至消失,在钙化层中可见骨小梁,软骨下骨重建,属于明显退变表现。从超微组织学角度观察发现非肝肾亏虚组软骨细胞超微结构基本正常,细胞及细胞外基质形态完好;肝肾亏虚组软骨细胞衰老,并出现软骨细胞皱缩、线粒体肿胀空泡、内质网扩张、高尔基体紊乱,以及染色质固缩边集等细胞凋亡现象,部分软骨基质溶解。结论长期肝肾亏虚的下腰痛患者腰椎小关节退变明显,其机制为长期肝肾亏虚可能会通过改变机体的内环境,使软骨细胞衰老死亡,软骨基质降解变性,从而出现小关节软骨退变。 Objective To observe the ultrastructural changes of human lumbar facet joint cartilage degeneration based on the theory that“the liver governs the sinews and the kidney governs the bones”,aiming to explore the possible mechanism of lumbar facet joint degeneration in patients with deficiency of liver and kidney from the perspective of microscopic histomorphology.Methods From January 2018 to July 2019,at Ruikang Hospital Affiliated to Guangxi University of Traditional Chinese Medicine,patients with lower back pain who were hospitalized for spinal surgery and lumbar spine surgery were divided into deficiency of liver and kidney group and non-liver-kidney deficiency group.The lumbar facet joints of the two groups were collected during operation,and the histomorphological differences were observed.The ultrastructural changes of the facet joint cartilage were observed by transmission electron microscopy.The possible mechanism of lumbar facet joint degeneration in patients with liver and kidney deficiency was discussed.Results In this study,the lumbar facet joints of the deficiency of liver and kidney group and the non-liver-kidney deficiency group were compared from the pathological histomorphology.It was found that the non-liver-kidney deficiency group had smooth and continuous surface of the articular cartilage of the facet joint,and the cartilage layer was thicker and the number of cells was larger.The cells were regularly and neatly arranged,with clear“tidal line”.The deficiency of liver and kidney group's articular cartilage surface was damaged and the cell layer was unclear,with irregular or even disappeared“tidal line”.There were trabecular bone in the calcified layer and subchondral bone reconstruction.From the perspective of ultramicroscopic histology,the ultrastructure of chondrocytes in the non-liver-kidney deficiency group was basically normal,and the morphology of cells and extracellular matrix was intact.The chondrocytes in the deficiency of liver and kidney group were senescent,and chondrocyte shrinkage and mitochondrial swelling vacuoles appeared.There was apoptosis of the endoplasmic reticulum,chromatin condensation and so on.Conclusion Long-term deficiency of liver and kidney in patients with low back pain,lumbar facet joint degeneration is obvious.The possible mechanism is that long-term deficiency of liver and kidney will change the internal environment of the body to affect bone metabolism,and so chondrocyte aging and death and cartilage matrix degradation result in small articular cartilage degeneration.On the other hand,deficiency of liver and kidney affects bone metabolism,rebuilds subchondral bone,and interacts with cartilage degeneration to participate in facet joint degeneration.
作者 陆佳辰 陈锋 闫乾 黄知见 吴晓飞 戈超 李枝发 刘宁 LU Jiachen;CHEN Feng;YAN Qian;HUANG Zhijian;WU Xiaofei;GE Chao;LI Zhifa;LIU Ning(Guangxi University of Traditional Chinese Medicine,Nanning 530001,Guangxi,China;Ruikang Hospital Affiliated to Guangxi University of Traditional Chinese Medicine,Nanning 530011,Guangxi,China;Guangxi Orhopaedic Traumatology Hospital,Nanning 530012,Guangxi,China)
出处 《辽宁中医杂志》 CAS 2021年第4期105-111,I0003,共8页 Liaoning Journal of Traditional Chinese Medicine
基金 国家自然科学基金(81560778) 广西中药管理局中医壮瑶医优势病种推广项应用项目(GZZX15-20) 广西壮族自治区科学技术厅重点研发项目(桂科AB18221012)。
关键词 肝肾亏虚 腰椎小关节 软骨细胞 细胞凋亡 deficiency of liver and kidney lumbar facet joint subchondral bone chondrocytes apoptosis
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