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Purpose:
Hypertrophic scar formation is unpredictable and poorly understood, afflicting both the pediatric and adult populations. Treatment methods with conservative and invasive approaches have low rates of compliance and high rates of morbidity[1]-4. The purpose of this study is to develop a reproducible scar model and investigate an early technique of scar modification through the use of adipose-derived stromal progenitor cells (ASCs).
Methods:
20 thermal deep-partial thickness contact burns were created on the dorsum of three 8-week old domestic swine and allowed to mature for 6 weeks. Scars were then injected with 2 cc saline, expanded autologous ASCs, or 2 cc fresh lipoaspirate and sampled at 2 week intervals up to 8 weeks post injection. Volumetric analysis with a 3-D scanner, mechanical elasticity testing through negative pressure transduction, and standardized photography evaluation with the Vancouver Scar Scale was performed. Biopsies were taken at 2 week intervals and histologically analyzed for collagen deposition and vascularity. Flow cytometry was performed to confirm ASC surface antigens. Expression of collagen proteins, angiogenic and adipogenic growth factors were targeted with quantitative real-time polymerase chain reactions.
Results:
Volumetric analysis demonstrates a reduction in average scar thickness at 6 weeks when injected with ASCs (-1.601 cc³) and autologous fat (-1.965 cc³) relative to controls (-0.121 cc³, p < 0.05). Scars injected with autologous fat or ASCs resulted in an initial decrease in overall compliance compared to unburned skin (35.99/ 37.94 vs 49.36 mmHg*mm), but improvement in elasticity at 6 weeks (p <0.05). Qualitative photo analysis with the Vancouver Scar Scale showed improvement in erythema and height to the scars 14 weeks post injury of both ASC and immediate fat injection versus controls. Rt-PCR expression levels of COL1a1, COL3a1, VEGF, PPAR-ɤ, FABP-4 over time will be presented.
Conclusions:
Early results suggest that autologous fat and/or ASCs may improve healing of hypertrophic scarring by altering the cellular and structural components during wound remodeling up to 14 weeks after injury. This may have beneficial applications in early treatment of large or cosmetically sensitive immature burn scars.
