Tandara Andrea A, Mustoe Thomas A
Division of Plastic and Reconstructive Surgery, Wound Healing Research Laboratory, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
J Plast Reconstr Aesthet Surg. 2008 Oct;61(10):1219-25. doi: 10.1016/j.bjps.2008.03.022. Epub 2008 Jul 23.
Hypertrophic scars can be reduced by the application of silicone dressing; however, the detailed mechanism of silicone action is still unknown. It is known that silicone gel sheets cause a hydration of the epidermal layer of the skin. An in vitro co-culture experiment has shown that hydration of keratinocytes has a suppressive effect on the metabolism of the underlying fibroblasts resulting in reduced collagen deposition. We tested the hypothesis that silicone sheeting in vivo has a beneficial effect on scarring by reducing keratinocyte stimulation, with a resulting decrease in dermal thickness, hence scar hypertrophy. Silicone adhesive gel sheets were applied to scars in our rabbit ear model of hypertrophic scarring 14 days postwounding for a total of 16 days. Scarring was measured in this model by the scar elevation index (SEI), a ratio of the area of newly formed dermis to the area of the dermis of unwounded skin, and the epidermal thickness index (ETI), a ratio of the averaged epidermal height of the scar to the epidermal thickness of normal epidermis. Specific staining [anti-PCNA (proliferating cell nuclear antigen) and Masson trichrome] was performed to reveal differences in scar morphology. SEIs were significantly reduced after silicone gel sheet application versus untreated scars corresponding to a 70% reduction in scar hypertrophy. Total occlusion reduced scar hypertrophy by 80% compared to semi-occlusion. ETIs of untreated scars were increased by more than 100% compared to uninjured skin. Silicone gel treatment significantly reduced epidermal thickness by more than 30%. Our findings demonstrate that 2 weeks of silicone gel application at a very early onset of scarring reduces dermal and epidermal thickness which appears to be due to a reduction in keratinocyte stimulation. Oxygen can be ruled out as a mechanism of action of silicone occlusive treatment. Hydration of the keratinocytes seems to be the key stimulus.
应用硅胶敷料可减轻增生性瘢痕；然而，硅胶作用的详细机制仍不清楚。已知硅胶凝胶片可使皮肤表皮层水化。一项体外共培养实验表明，角质形成细胞的水化对其下方成纤维细胞的代谢具有抑制作用，从而导致胶原蛋白沉积减少。我们验证了这样一个假设：体内硅胶片通过减少角质形成细胞刺激对瘢痕形成具有有益作用，进而使真皮厚度减小，从而减轻瘢痕增生。在我们的兔耳增生性瘢痕模型中，于创伤后14天开始应用硅胶黏附凝胶片，共使用16天。通过瘢痕隆起指数（SEI，即新形成真皮面积与未受伤皮肤真皮面积之比）和表皮厚度指数（ETI，即瘢痕平均表皮高度与正常表皮厚度之比）来测量该模型中的瘢痕形成情况。进行特异性染色（抗增殖细胞核抗原和马松三色染色）以揭示瘢痕形态的差异。与未处理的瘢痕相比，应用硅胶凝胶片后SEI显著降低，相当于瘢痕增生减少70%。与半封闭相比，完全封闭使瘢痕增生减少80%。与未受伤皮肤相比，未处理瘢痕的ETI增加了100%以上。硅胶凝胶治疗使表皮厚度显著降低了30%以上。我们的研究结果表明，在瘢痕形成的早期应用2周硅胶凝胶可减小真皮和表皮厚度，这似乎是由于角质形成细胞刺激减少所致。可以排除氧气作为硅胶封闭治疗的作用机制。角质形成细胞的水化似乎是关键刺激因素。
