老年性上睑下垂提上睑肌腱膜的病理学观察

Pathological changes of levator aponeurosis with senile ptosis

目的通过研究老年性上睑下垂提上睑肌腱膜的病理结构的改变,探讨老年性上睑下垂的发病机制。方法选自我科2011年6月至2013年6月就诊的老年性上睑下垂患者30例,根据下垂量分为轻度、中度、重度,将提上睑肌缩短手术中取得的提上睑肌腱膜组织,进行HE染色、弹性蛋白(Elastin)及基质金属蛋白酶(matrix metalloproteinase,MMP)-9免疫组织化学染色检查,并行透射电镜超微结构观察。结果术中可见患眼提上睑肌腱膜变长、变薄,有的出现裂孔,部分或全部从睑板表面断裂,有的出现脂肪样变性;HE染色可见患眼提上睑肌肌浆内出现大量脂肪样变性;免疫组织化学染色结果示Elastin含量下降,与下垂程度呈负相关(r=-2.782,P=0.002),MMP-9的含量增加,与下垂程度呈正相关(r=4.376,P=0.030);透射电镜显示成纤维细胞的细胞膜局部有缺损、外形不规则,胞质肿胀,内质网扩张、脱颗粒,胶原纤维周围可见脂滴。结论老年性上睑下垂的提上睑肌腱膜变薄或破裂,脂肪样变和肌纤维萎缩,Elastin含量下降,胶原纤维分裂,呈现退化改变。

Objective Through studying the pathological changes of levator aponeurosis in patients with senile ptosis, to investigate the pathogenesis of senile ptosis. Methods Thirty patients with senile ptosis were randomly selected in our department from June 2011 to June 2013. The patients were divided into fight,medium and heavy degrees. Samples of the levator aponeurosis were obtained during the levator palpebrae superioris muscle shortening surgery. The anatomy structure of levator aponeurosis, parallel Elastic protein and matrix metalloproteinase-9 （MMP-9） were detected by immunohistochemlstry, and ultrastructural changes were observed by transmission electron microscope. Results Anatomy structures showed the irregular thin, irregular laceration or rupture hole of levator aponeurosis. The fatty degeneration, muscle fiber thinner, and a small amount of vascular tissue were seen in HE staining. The decrease of elastic protein and the increase of matrix metalloproteinase were found by immunohistochemistry staining. The contents of Elastin protein decreased gradually with the degrees of senile ptosis, which showed negative correlation （ r = - 2. 782, P = 0. 002 ）. The content of MMP-9 increased gradually with the degrees of senile ptosis, and showed positively correlation （r = 4. 376, P = 0.030）. The local defect, and irregular shape of fibroblast cell membrane, cytoplasmic swelling, endoplasmic reticulum expansion and degranulation, collagen fibers split were seen by transmission electron microscope. Conclusion The retrogressive changes of levator aponeurosis are found in patients with senile ptosis,inchiding thinner or rupture holeof anatomy structure, the decrease of elastic protein and the increase of matrix metalloproteinase, the fatty degeneration, muscle fiber thinner and collagen fiber splitting.