Abstract

Partial thickness burns can advance to full thickness after initial injury due to inadequate tissue perfusion and increased production of inflammatory cytokines, which has been referred to as burn wound progression. In previous work, we demonstrated that a keratin biomaterial hydrogel appeared to reduce burn wound progression. In the present study, we tested the hypothesis that a modified keratin hydrogel could reduce burn wound progression and speed healing. Standardized burn wounds were created in Yorkshire swine and treated within 30 minutes with keratin hydrogel (modified and unmodified), collagen hydrogel, or silver sulfadiazine (SSD). Digital images of each wound were taken for area measurements immediately prior to cleaning and dressing changes. Wound tissue was collected and assessed histologically at several time points. Wound area showed a significant difference between hydrogels and SSD groups, and rates of reepithelialization at early time points showed an increase when keratin treatment was used compared to both collagen and SSD. A linear regression model predicted a time to wound closure of approximately 25 days for keratin hydrogel while SSD treatment required 35 days. There appeared to be no measurable differences between the modified and unmodified formulations of keratin hydrogels.

Highlights

  • Burns are one of the most catastrophic injuries to treat

  • In 1953, Jackson described a model of burn injury in terms of three zones of tissue damage: (1) the inner zone of coagulation, which is characterized by necrotic tissue, (2) an intermediate zone of stasis, which is characterized by damaged cells that may live or die depending on treatment and other factors, and (3) an outer zone of hyperemia where cells are stressed but will likely survive if the wound does not get infected and standard treatment is given [2]

  • We aimed to understand if a particular formulation of keratin hydrogel containing a reduced concentration of gamma keratose, modified keratose hydrogel (MKH), could have a beneficial effect on burn wound healing

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Summary

Introduction

Burns are one of the most catastrophic injuries to treat. Often, partial thickness burns convert to full thickness due to inadequate tissue perfusion and increased production of inflammatory cytokines leading to protein denaturation and necrosis [1]. In vivo studies have shown that treatments like cerium nitrate, curcumin, activated protein C (APC), recombinant tissue type plasminogen (r-TPA), TAK-044 (nonselective endothelin receptor antagonist), simvastatin, and beraprost sodium (prostaglandin I2 analogue) were able to control burn injury progression in rats by preventing tissue necrosis in the zone of stasis [4,5,6,7,8,9,10,11].

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