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.
Keywords: alpha-smooth muscle actin; excisional wound; pressure ulcer; skin; spinal cord injury.