应用人工真皮修复骨外露创面的机制

Repair mechanisms of the wounds with exposed bone structures using an artificial dermis

目的探讨应用人工真皮修复骨外露创面的机制。方法新西兰大耳兔72只，于头颅顶部制作创面模型，根据创面基底情况按随机数字表法随机分成3组各24只：（1）皮肤缺损组：切除皮肤保留颅骨骨膜；（2）骨膜缺损组：切除皮肤及颅骨骨膜，暴露颅骨；（3）骨烧伤组：在骨膜缺损组的基础上，将裸露颅骨用电烙铁烫伤致颅骨表层坏死，然后在各个创面上移植人工真皮。于移植后1、2、3、4周每组各取2只切取移植的人工真皮制作标本，HE染色观察人工真皮血管化情况；每组各4只进行伊文蓝灌注实验，定量检测组织中伊文蓝含量，间接测定人工真皮血管化程度。结果移植后1周，皮肤缺损组人工真皮内细胞充填较多，并有少量新生血管生长，其余2组仅见少量炎性细胞，新生血管很少；移植后2周，皮肤缺损组人工真皮内大量新生血管和成纤维细胞充填，骨膜缺损组和骨膜烧伤组人工真皮血管化迟滞；移植后3～4周骨膜缺损组和骨膜烧伤组人工真皮血管化程度接近皮肤缺损组，血管化较满意，形成有血运的薄层组织膜。伊文蓝灌注实验结果：移植后2周后人工真皮内染料灌注量皮肤缺损组即接近峰值，均显著高于骨膜缺损组和骨烧伤组[（2741±976）比（1039±590）和（403±209）μg/g，均P〈0．01]。移植后3周皮肤缺损组和骨膜缺损组均达峰值，两组间差异无统计学意义；但均显著高于骨烧伤组[（2943±793）和（2255±316）比（1125±404）μg/g，均P〈0．01]；移植后4周骨烧伤组达峰值，仍均低于皮肤缺损组和骨膜烧伤组，但差异无统计学意义[（1609±787）比（2298±778）和（2141±385）μg/g，均P〉0．05]。结论由于骨膜的缺乏和损伤，骨外露创面移植人工真皮后血管化过程延迟，其血管化过程主要起源自骨外露创面周边正常组织。

Objective To investigate the repair mechanisms of the wounds with bone exposed by artificial dermis transplantation. Methods Seventy two rabbits were randomly divided into 3 groups of 24 rabbits, the wound model was made on the top of head. In the skin defect group （SD group）, skin was removed and skull periosteum was retained. In the periosteal defect group （PD group）, the skin and skull periosteum were both removed, and the skull was exposed. In the skull burn group （SB group）, after the periosteum was removed, the exposed skull bone was burned out with electric iron to cause skull surface necrosis, then the artificial dermis transplantation were performed in each group. In l, 2, 3 and 4 weeks after transplantation, 2 specimens including artificial dermis and the underlying tissue in each group were cut for biopsy with HE staining to observe the angiogenesis in artificial dermis. Evans Blue perfusion was performed in four animals from each group to quantify angiogenesis in artificial dermis. Results One week after transplantation, in SD group, a few microvessels can be observed in artificial dermis, but in the rest of the two groups, only a small amount of inflammatory cells can be seen. Two weeks after transplantation, in SD group, a large number of new blood vessels and fibroblasts can be seen filling in the artificial dermis, hut angiogenesis delayed obviously in the PD and SB group. Three weeks after transplantation, the angiogenesis of artificial dermis in the PD and SB group accelerated obviously, and a thin layer of blood rich tissue membrane can be seen over the burned skull. The Evans Blue perfusion showed that the content of dye perfusion in the artificial dermis was closed to the peek value at 2 weeks after transplantation in the SD group, which was significantly higher than that in PD and SB group [ （2 741 ±976） vs （ 1 039±590） and （403 ±209）μg/g, P 〈 0. 01 ]. Three weeks after transplantation, the content of Evans Blue in artificial dermis reached the peek value in SD and PD group, no significant difference was found between this two groups, but both significantly higher than that in SB group [ （2 943±793） and （2 255±316） vs （1 125 ± 404） μg/, P 〈 0. 01 ]. Four weeks after transplantation, the content of Evans Blue in artificial dermis reached the peek value in SB group, although the value was still lower than that in SD and PD group, the difference was not significant [ （ 1 609 ± 787） vs （2 298± 778） and （2 141 ± 385 ） μg/, P 〉 0.05 ]. Coneluslons Lack or injury of periosteum can cause vascularization delay after artificial dermis transplantation. The vascularization of artificial dermis mainly originates from the normal tissues surrounding the wound when artificial dermis is transplanted on the wound with periosteum defect or bone exposed.