Tcacencu Ion, Carlsöö Bengt, Stierna Pontus
Department of Otorhinolaryngology, Huddinge University Hospital, Karolinska Institutet, Huddinge, Sweden.
Wound Repair Regen. 2004 May-Jun;12(3):346-50. doi: 10.1111/j.1067-1927.2004.012307.x.
We examined the structural characteristics of repair tissue induced by recombinant human bone morphogenetic protein-2 in a rabbit model of laryngotracheal reconstruction. Twenty-four New Zealand White rabbits were randomly divided into four groups of six rabbits. Two groups were treated with recombinant human bone morphogenetic protein-2 delivered on an absorbable collagen sponge, while two groups were used as controls. Rabbits were euthanized at 1 and 4 weeks after surgery. The larynx was removed, fixed, and sectioned. The sections were stained with hematoxylin-eosin, safranine O/fast green, and immunostained with an antibody for tissue inhibitor of metalloproteinases-1. In rabbits treated with bone morphogenetic protein-2, the defects were filled with new cartilage and bone at 4 weeks after surgery. There were no discontinuities or gaps at the margins of the cartilage defects. Proteoglycans were synthesized in new cartilage in rabbits treated with bone morphogenetic protein-2, and were present 4 weeks after surgery. The general aspects of the vascular pattern and the pattern of tissue inhibitor of metalloproteinases-1 expression were similar in control and treated rabbits, both 1 week and 4 weeks after surgery. The repair tissue induced by recombinant human bone morphogenetic protein-2 consisted of new cartilage and bone perfectly integrated with host tissue at the site of the cricoid cartilage defects. This new cartilage was able to mature and produce proteoglycans.
我们在兔喉气管重建模型中研究了重组人骨形态发生蛋白-2诱导的修复组织的结构特征。将24只新西兰白兔随机分为四组,每组6只。两组用可吸收胶原海绵递送的重组人骨形态发生蛋白-2进行治疗,另外两组作为对照。术后1周和4周对兔子实施安乐死。取出喉部,固定并切片。切片用苏木精-伊红染色、番红O/固绿染色,并用金属蛋白酶组织抑制剂-1抗体进行免疫染色。在用骨形态发生蛋白-2治疗的兔子中,术后4周缺损处被新的软骨和骨填充。软骨缺损边缘没有连续性中断或间隙。在用骨形态发生蛋白-2治疗的兔子中,新软骨中合成了蛋白聚糖,且在术后4周仍然存在。术后1周和4周时,对照兔和治疗兔的血管模式及金属蛋白酶组织抑制剂-1表达模式的总体情况相似。重组人骨形态发生蛋白-2诱导的修复组织由新的软骨和骨组成,在环状软骨缺损部位与宿主组织完美整合。这种新软骨能够成熟并产生蛋白聚糖。