The role of the epidermis in the control of scarring: evidence for mechanism of action for silicone gel.
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.
Tandara
Andrea A
AA
Division of Plastic and Reconstructive Surgery, Wound Healing Research Laboratory, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Mustoe
Thomas A
TA
D000818:Animals; D017439:Cicatrix, Hypertrophic / Q000473:pathology / Q000517:prevention & control*; D020405:Dermis / Q000187:drug effects* / Q000473:pathology; D004195:Disease Models, Animal; D004817:Epidermis / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D005260:Female; D015603:Keratinocytes / Q000378:metabolism; D009779:Occlusive Dressings; D011817:Rabbits; D020034:Silicone Gels / Q000008:administration & dosage*
D020034:Silicone Gels