Examining the contribution of surrounding intact skin during cutaneous healing

Abstract

Severe cutaneous wounds expose the body to the external environment, which may lead to impairments in bodily functions and increased risk of infection. There is a need to develop skin substitutes which could effectively promote complete skin regeneration following an injury. Murine models are used to test such skin substitutes, but their healing involves contraction of the dermis not found in human wounds. We have previously described a device called a dome, which comes in two models, that is used to prevent skin contraction in mice. One model provides a physical barrier to minimize contraction, and the other model has additional perforations in the barrier to allow cellular contribution from the surrounding intact skin. Taking advantage of an enhanced version of these two models, we compared granulation tissue formation, the extent of vascularization, and the transition to myofibroblastic phenotype between the models. We enhanced the dome by developing a twist open cap dome and applied the two models of the dome into the excisional wound biopsy in mice. We demonstrate that the dome can be used to prevent skin contraction in mice. The control model prevented skin contraction while barricading the contribution of surrounding intact skin. When not barricaded, the intact skin enhances wound healing by increasing the number of myofibroblasts and neovascularization. Using a novel model of inhibition of skin contraction in rodents, we examined the contribution from the surrounding intact skin to granulation tissue formation, myofibroblastic differentiation, and neovascularization during the course of skin healing in mice.

Promotion of dermal regeneration using pullulan/gelatin porous skin substitute

“…The dome on the mouse was to allow the skin to stretch and secure the applied skin substitutes. An 8‐mm skin substitute (either PG2 or Control) was placed inside the dome (Aljghami, Jeschke, & Amini‐Nik, ; M. G. Jeschke, A. R. Sadri, C. Belo, & S. Amini‐Nik, 2017). The wounds were monitored daily until 20 days post the surgery to determine the general conditions of the wounds and the treatments.…”

Efficacy of perioperative antibiotic prophylaxis in elective soft-tissue-only wrist arthroscopy

“…Through the break in the skin barrier bacteria can colonize the wound hereby increase the risk of wound infection. 10,11 To reduce the risk of surgical site infections (SSIs), perioperative antibiotic prophylaxis (PAP) may be administered, considering patient-and surgery-related risk factors. [12][13][14][15] For most interventions, a cephalosporine antibiotic is the recommended PAP.…”

OMICS Approaches Evaluating Keloid and Hypertrophic Scars

“…Behind these migrating cells, epidermal cells start proliferating. Fibroblasts, which are mainly attracted to the wound edge are stimulated by macrophages to differentiate into myofibroblasts [10][11][12]. Myofibroblasts in turn help pull the wound edges together, leading to faster contraction, which then leads to wound healing [11][12][13].…”

“…Fibroblasts, which are mainly attracted to the wound edge are stimulated by macrophages to differentiate into myofibroblasts [10][11][12]. Myofibroblasts in turn help pull the wound edges together, leading to faster contraction, which then leads to wound healing [11][12][13]. Fibroblasts and myofibroblasts produce ECM, primarily collagen, which forms the structural framework of granulation tissue [4,14].…”

“…Alogether, this results in wound contraction and the reconstitution of damaged skin, which is associated with scar formation in humans. At the completion of wound healing, myofibroblasts undergo apoptosis, and the failure of these cells to undergo apoptosis often leads to pathological scarring [ 12 , 15 ]. The proteins participating in re-epithelialization include multiple extracellular-matrix proteins and their receptors, proteases, cytoskeletal proteins, and enzymes that modulate the cellular redox balance [ 4 ].…”