在分子生物学水平对脊柱侧凸患者椎旁肌结构特点进行相关的病因学研究

Etiological Research on Structural Features of Paraspinal Muscles in Patients with Scoliosisi:in Molecular Biology Level

目的探讨脊柱侧凸患者椎旁肌结构改变与病因的相互关系。方法 KingII,III型脊柱侧凸患者97例,男24例,女73例;年龄13岁～15岁(平均年龄14.64岁)。获得胸椎,胸腰椎,腰椎的代偿弯和主弯的楔形变和旋转畸形变节段的877块椎旁肌标本,并进行超薄组织切片。对肌蛋白(肌动蛋白、肌球蛋白)进行染色后的光学显微镜和电子显微镜下的组织形态学和组织化学观察,并对侧弯脊柱椎旁肌畸形变的程度和形变机制进行研究分析。结果大部分肌纤维的结构完全丧失:在一部分肌纤维中,肌质呈均质样改变,另一些肌纤维中,肌质被分解成小颗粒或片断。肌纤维中只剩余1个携带畸形变的细胞核,胞浆呈脆性变,以及含有剩余肌纤维部分肌纤维链的肌细胞。被破坏的肌纤维分解为间质性结缔组织和脂肪组织,肌糖原呈弱势。脂肪组织呈营养障碍性退行性改变。电镜下,疾病的早期是肌纤维中线粒体的改变,肌原纤维结构的改变,膜结构的变化,与膜增宽的现象同时存在的还有明显的突触的存在。重度脊柱侧弯患者被严重挫伤的椎旁肌纤维中保留的糖原特征。结论脊柱侧凸疾病导致患者椎旁肌中存在深度的营养不良性变的过程,并伴随蛋白质的化学活性的破坏过程,提示椎旁肌受损(破坏)为继发性。

Objective To investigate the mutual relations between structural changes ofparaspinal muscles in patients with scoliosis and the etiology. Methods 97 cases of patients with scoliosis of King II, III, male 24 cases, female 73 cases; aged 13 to 15 （mean age 14.64）. 877 specimens of paraspinal muscles were obtained from wedge-shaped variablity segments and rotational deformity variablity segments of compensatory bending and main bending of thoracic, thoracolumbar, lumbar, for ultra-thin tissue sections. Pairs of muscle proteins （actin, myosin） were dyed for morphology and histochemical observations under optical microscopy and electron microscopy, and for research and analysis of the deformity extent and mechanism ofparaspinal muscles in scoliosis spine. Results Most of complete loss of muscle fiber structure： in one part of the muscle fibers, muscle mass showed homogeneous-like change, and in other muscle fibers, muscle mass was broken down into small particles or fragments. Muscle fibers carried only a remaining nucleus of deformity, with brittle cytoplasm, and with muscle cells of muscle fiber chain in the remaining part of muscle fiber. The damaged muscle fibers tended to break down into the interstitial connective tissue and adipose tissue, with weak muscle glycogen. Adipose tissue showed degenerative changes of nutritional disorder. Under electron microscope, the early disease was the mitochondrial changes in muscle fiber, myofibril structural changes, membrane structural changes, and evident synapses simultaneously with widened membrane phenomenon. Pathological specimens showed the seriously damaged paravertebral muscle fibers in severe scoliosis patients retained the characteristics of glycogen. Conclusion The process of scoliosis diseases leading to malnutrition variablity in deep paraspinal muscles, accompanied with the process of chemical activity destruction of protein, suggests paraspinal muscle damage （destruction） as secondary.