O'Shaughnessy Kristina D, De La Garza Mauricio, Roy Nakshatra K, Mustoe Thomas A
Wound Healing Research Laboratory, Department of Surgery, Division of Plastic Surgery, Feinberg School of Medicine, Northwestern University, 675 N. St. Clair St., Chicago, IL 60611, USA.
Wound Repair Regen. 2009 Sep-Oct;17(5):700-8. doi: 10.1111/j.1524-475X.2009.00534.x.
The mechanism of hypertrophic scar reduction using silicone gel sheeting remains elusive. We hypothesize that the decrease in scar formation is due to occlusion and homeostasis of the barrier layer. Using an established model of hypertrophic scarring, rabbits were divided into four groups and scars were tape-stripped or occluded with Kelocote, Cavilon, or Indermil, with each rabbit serving as its own internal control. All wounds were harvested on day 28 and examined histologically to measure the scar elevation index (SEI), epithelial thickness, and cellularity. Immunohistochemistry fluorescence was used to quantify inflammation in the dermis. Transepidermal water loss (TEWL) was measured for each occlusive agent and tape stripping. Ultrastructural analysis was performed by electron microscopy. Kelocote, Cavilon, and Indermil all significantly decreased SEI when compared with controls. Each of the occlusive treatments was shown to decrease TEWL while tape stripping increased TEWL. Tape stripping significantly increased the SEI, epithelial thickness, and cellularity. Immunostaining for macrophages showed increased density of inflammatory cells in the tape-stripped scars. Under electron microscopy, the tape-stripped wounds displayed extensive inflammation and keratinocyte damage. Both unwounded skin and occlusion-treated scars did not display these characteristics. In conclusion, hypertrophic scarring was reduced regardless of occlusive method used. Furthermore, repeated disruption of the permeability barrier by tape stripping led to an increase in scarring. Ultrastructural analysis suggests that occluded wounds may be in an advanced state of wound repair. Occlusion may mediate its effects through establishing homeostasis of the epidermal barrier layer.
使用硅胶片减少增生性瘢痕的机制仍不清楚。我们推测瘢痕形成的减少是由于屏障层的封闭作用和内环境稳定。利用已建立的增生性瘢痕模型，将兔子分为四组，瘢痕用胶带剥离或用凯洛可、卡维隆或因德米尔封闭，每只兔子作为自身的内部对照。所有伤口在第28天取材，进行组织学检查以测量瘢痕隆起指数（SEI）、上皮厚度和细胞密度。采用免疫组织化学荧光法对真皮内的炎症进行定量分析。测量每种封闭剂和胶带剥离后的经表皮水分流失（TEWL）。通过电子显微镜进行超微结构分析。与对照组相比，凯洛可、卡维隆和因德米尔均显著降低了SEI。每种封闭处理均显示可降低TEWL，而胶带剥离则增加TEWL。胶带剥离显著增加了SEI、上皮厚度和细胞密度。巨噬细胞免疫染色显示胶带剥离的瘢痕中炎症细胞密度增加。在电子显微镜下，胶带剥离的伤口显示出广泛的炎症和角质形成细胞损伤。未受伤的皮肤和封闭处理的瘢痕均未表现出这些特征。总之，无论采用何种封闭方法，增生性瘢痕均有所减轻。此外，胶带剥离反复破坏渗透屏障会导致瘢痕增加。超微结构分析表明，封闭的伤口可能处于伤口修复的晚期状态。封闭可能通过建立表皮屏障层的内环境稳定来介导其作用。
