Blockade of Mast Cell Activation Reduces Cutaneous Scar Formation

Damage to the skin initiates a cascade of well-orchestrated events that ultimately leads to repair of the wound. The inflammatory response is key to wound healing both through preventing infection and stimulating proliferation and remodeling of the skin. Mast cells within the tissue are one of the first immune cells to respond to trauma, and upon activation they release pro-inflammatory molecules to initiate recruitment of leukocytes and promote a vascular response in the tissue. Additionally, mast cells stimulate collagen synthesis by dermal fibroblasts, suggesting they may also influence scar formation. To examine the contribution of mast cells in tissue repair, we determined the effects the mast cell inhibitor, disodium cromoglycate (DSCG), on several parameters of dermal repair including, inflammation, re-epithelialization, collagen fiber organization, collagen ultrastructure, scar width and wound breaking strength. Mice treated with DSCG had significantly reduced levels of the inflammatory cytokines IL-1a, IL-1b, and CXCL1. Although DSCG treatment reduced the production of inflammatory mediators, the rate of re-epithelialization was not affected. Compared to control, inhibition of mast cell activity caused a significant decrease in scar width along with accelerated collagen re-organization. Despite the reduced scar width, DSCG treatment did not affect the breaking strength of the healed tissue. Tryptase b1 exclusively produced by mast cells was found to increase significantly in the course of wound healing. However, DSCG treatment did not change its level in the wounds. These results indicate that blockade of mast cell activation reduces scar formation and inflammation without further weakening the healed wound

A Comparative Study of the Burn Wound Healing Properties of Saline-Soaked Dressing and Silver Sulfadiazine in Rats

The purpose of this study was to further investigate that phenomenon and to explore the effect silver sulfadiazine on wound healing. Full-thickness burn wounds were created on the dorsum of Wistar albino rats under anesthesia. The wounds were treated with silver sulfadiazine and saline-soaked dressing for fourteen days, and then observed until healed. Wound surface area was measured each three days. Time to 50% and 90% healing was compared. No clinical infections occurred. Wound half-life and healing times were shortest in the saline-soaked group (P < 0.0001) in full-thickness burns. Wound contraction was delayed by silver sulfadiazine. These data suggest that silver sulfadiazine retard burn wound healing. Infection control without delay of burn wound healing is most appealing and clinical trials are planned