可吸收表皮生长因子复合膜防止肌腱粘连的研究

背景：采用液态分子生物材料作为屏障预防肌腱粘连发生,存在药物降解快、流失量大、屏障作用不理想等问题,因此研究者们越来越多的倾向于膜态屏障材料的研制开发。同时发现肌腱损伤后,腱细胞在多种内源性的生长因子作用下增殖分化,促进了肌腱的内源性愈合,但究竟哪一种因子是肌腱愈合的特异性因子,也是学者们研究的焦点之一。 目的：观察表皮生长因子复合胶原膜在预防鞘管区肌腱粘连、促进肌腱内源性愈合中的作用。 方法：将30只10月龄雄性leghorn公鸡随机分为3组,每组10只。将每只鸡的左足第三趾造成挤压撕脱伤模型,用改良Kessler缝合法缝接。断端分别包裹复合有表皮生长因子的胶原膜、单纯的胶原膜以及断端不加任何处理。术后4周,对标本进行大体观察、生物力学测试、光镜、电镜等观察。 结果与结论：表皮生长因子胶原膜组肌腱粘连程度较轻,腱缝合段内的胶原纤维数量多,以粗大的Ⅰ型胶原为主;成纤维细胞数量少,腱细胞成熟。单纯胶原膜组肌腱粘连较轻,但腱缝合段内的胶原纤维数量少,排列稀疏,以纤细的Ⅲ型胶原为主;空白对照组肌腱与周围组织粘连重,腱缝合段内的胶原纤维数量较多,排列紊乱,Ⅰ、Ⅲ型胶原交错排列。结果表明表皮生长因子来促进肌腱的内源性愈合,可降解胶原膜修复腱鞘可阻止肌腱的外源性愈合,从而达到防止肌腱粘连的目的。

Epidermal growth factor combined with degradable collagen membrance in prevention of tendon adhesion

BACKGROUND: The problems such as fast drug degradation, great drug loss and poor barrier effect exist when using liquid molecular biomaterial as barriers in preventing tendon adhesion. Accordingly, it has aroused increasing attention to seek for membrane biomaterials as barriers. Simultaneously, it found that tendon cells would proliferate and differentiate under controls of multiple endogenous growth factors that promote tendon endogenous healing. However, it is poorly understood which the specificity factor for tendon healing is.  OBJECTIVE:To study effect of epidermal growth factor (EGF) combined with degradable collagen membrane on preventing tendon adhesion and improving tendon endogenous healing. METHODS:Thirty ten-month old leghorn cocks were randomly divided into 3 groups, with 10 animals in each group. The third toe of left foot of each animal was prepared for avulsion model, and sutured with improved Kessler method. The broken ends were encapsulated with EGF combined with degradable collagen membrane (combination group), degradable membrane alone (collagen membrane group) or without treatment (blank control group). Four weeks later, the specimens were evaluated by gross observation, biomechanical test, light microscope and electron microscope. RESULTS AND CONCLUSION:In the combination group, there were a large amount of type Ⅰ collagen inside the sutured tendon, they were closely and lined up in order. The amount of collagen-fibronectin was less and the adhesion obviously was less than the control group. The tendon cells were matured. The adhesion in the collagen membrane group was slightly, there were a large amount of type Ⅲ collagen inside the sutured tendon, which loosely but well organized. In the blank control group, type Ⅰ and Ⅲ collagen arranged crisscrossed, with heavy adhesion. The results suggest that EGF can promote tendon endogenous healing and degradable collagen membrane can prevent tendon exogenous healing, thus, prevent the formation of adhesion.