Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
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Hypertrophic scars resulting from severe burns are usually treated by continuous elastic compression. Although pressure therapy reaches success rates of 60-85% its mechanisms of action are still poorly understood. In this study, apoptosis induction and release of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were evaluated in normal (n = 3) and hypertrophic (=7) scars from burns after in vitro mechanical compression. ⋯ TNF-alpha basal release was significantly higher in hypertrophic scar (14.74 +/- 1.42 ng/g) compared to normal scar samples and TNF-alpha secretion was diminished (3.52 +/- 0.97 ng/g) after compression. In conclusion, in our in vitro model, mechanical compression resembling the clinical use of elastocompression was able to strongly increase apoptosis in the hypertrophic scar derma as observed during granulation tissue regression in normal wound healing. Moreover, the observed modulation of IL-1beta and TNF-alpha release by mechanical loading could play a key role in hypertrophy regression induced by elastocompression.
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The aim of the current study was to evaluate the influence of platelet-derived growth factor (PDGF) on skin microcirculation during normal and impaired wound healing. Secondary healing wounds were created on the ears of hairless mice and treated once with 3 microg of PDGF-BB immediately after wound creation. Intravital fluorescence microscopy was used to quantify reepithelialization, revascularization, vessel diameters, vascular permeability, and leukocyte-endothelium interactions up to 24 days after wound creation. ⋯ This study confirms the positive influence of PDGF on wound healing under pathophysiological conditions. The effects in this model seem to be primarily due to the mitogenic potency of PDGF on keratinocytes and endothelial cells. A significant effect on leukocyte activation during the inflammatory process was not observed.