The use of a semiocclusive dressing reduces epidermal inflammatory cytokine expression and mitigates dermal proliferation and inflammation in a rat incisional model.

Occlusive wound dressings are utilized clinically to accelerate wound healing and improve the final appearance of scars. In vivo and in vitro evidence suggests that one mechanism for this effect is maintenance of normal hydration in the epidermis, although the molecular signals remain uncharacterized. We sought to elucidate histological changes and some of the molecular signals involved in this effect in a rat model of wound semiocclusion. We utilized a rat linear incision model with surgical tape occlusion. Histological stains and quantitative real-time PCR analysis were used to characterize the cellular and molecular effects of semiocclusion on the wound healing response. Semioccluded wounds demonstrated decreased epidermal thickness and cellularity and less mitotic epidermal activity when compared with nonoccluded control wounds. Associated dermal cellularity was similarly attenuated by semiocclusion. Finally, levels of proinflammatory cytokines interleukin-1-alpha and tumor necrosis factor-alpha were significantly decreased on postoperative day 3 at the transcriptional level when compared with nonoccluded wounds. Semiocclusive wound treatments significantly decrease epidermal thickness, cellularity, mitotic activity, and dermal cellularity as well as transcriptional levels of important epidermal mediators of inflammation in a rat incisional wound model.