title: Homeostasis of the epidermal barrier layer: a theory of how occlusion reduces hypertrophic scarring.
abstract: 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.
authors.affiliation: 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.
authors.forename: Kristina D
authors.initials: KD
authors.lastname: O'Shaughnessy
authors.forename: Mauricio
authors.initials: M
authors.lastname: De La Garza
authors.forename: Nakshatra K
authors.initials: NK
authors.lastname: Roy
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Mustoe
mesh_terms: D000818:Animals; D001672:Biocompatible Materials / Q000008:administration & dosage*; D017439:Cicatrix, Hypertrophic / Q000503:physiopathology* / Q000628:therapy*; D004195:Disease Models, Animal; D004817:Epidermis; D005260:Female; D006706:Homeostasis; D009779:Occlusive Dressings; D011817:Rabbits; D020034:Silicone Gels / Q000008:administration & dosage*; D014945:Wound Healing / Q000502:physiology*
chemical_list: D001672:Biocompatible Materials; D020034:Silicone Gels