1 Department of Biomedical Engineering, Rutgers, The State University of New Jersey , Piscataway, New Jersey.
2 Center for Engineering in Medicine, Massachusetts General Hospital and Shriners Burns Hospital , Boston, Massachusetts.
J Neurotrauma. 2018 Mar 15;35(6):815-824. doi: 10.1089/neu.2017.5405. Epub 2018 Jan 11.
Pressure ulcers (PUs) are common debilitating complications of traumatic spinal cord injury (SCI) and tend to occur in soft tissues around bony prominences. There is, however, little known about the impact of SCI on skin wound healing because of the lack of suitable animal models for studies in controlled experimental settings. Herein, we describe a reproducible and clinically relevant mouse model of PUs in the context of complete SCI. Adult male mice (BALB/c) were subjected to thoracic (T9-T10) complete SCI. Immediately after, a skin fold on the back of mice was lifted and sandwiched between two magnetic discs held in place for 12 h, thus creating an ischemic area that developed into a PU over the following days. The wounded areas demonstrated tissue edema and epidermis disappearance by day 3 post-magnet removal. PUs spontaneously healed, although slower in SCI mice compared to control non-SCI mice (5 vs. 3 weeks; p < 0.001). A similar delay in healing was observed for full-thickness excisional wounds. Histology data showed that there was a slower migration of epidermal cells over the granulation tissue in the SCI group compared to the control group. The SCI group also showed the smaller thickness of epidermis and dermis, lower blood vessel density, decreased numbers of proliferating cells, and decreased expression of alpha-smooth muscle actin compared to the control group at the time of wound closure. Taken together, these data suggest that SCI significantly slows down the dynamics of skin wound healing in experimental pressure and excisional wounds in mice.
压力性溃疡（Pressure ulcers，PUs）是创伤性脊髓损伤（traumatic spinal cord injury，SCI）常见的致残性并发症，往往发生在骨突出周围的软组织中。然而，由于缺乏适合的动物模型，用于在受控实验环境中进行研究，SCI 对皮肤伤口愈合的影响知之甚少。在此，我们描述了一种在完全性 SCI 背景下可重复且具有临床相关性的小鼠压力性溃疡模型。成年雄性小鼠（BALB/c）接受胸（T9-T10）部完全性 SCI。SCI 后立即提起小鼠背部的皮肤褶皱，将其夹在两个保持在位 12 小时的磁盘中，从而在接下来的几天内形成一个缺血区域，发展为压力性溃疡。在移除磁体后的第 3 天，受伤区域显示出组织水肿和表皮消失。PU 自发愈合，但 SCI 小鼠比对照非 SCI 小鼠愈合更慢（5 周 vs. 3 周；p < 0.001）。全层切除伤口也观察到愈合延迟相似。组织学数据显示，与对照组相比，SCI 组表皮细胞在肉芽组织上的迁移速度较慢。与对照组相比，SCI 组在伤口闭合时还显示出表皮和真皮较薄、血管密度较低、增殖细胞数量减少以及α-平滑肌肌动蛋白表达减少。综上所述，这些数据表明，SCI 显著减缓了实验性压力性和切除性伤口小鼠皮肤伤口愈合的动力学。
