Scar Free Healing
Summary: Scars seem to be an primitive method to isolate the body from external hazards. Unlike adult individuals, embryos are capable to reach a totally scarless healing of their wounds.
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Two important differences between embryo and adult are critical in understanding the molecular and cellular environments of scar-free versus scarring mechanisms of wound healing process.
First, the immune system of an embryo is not fully developed. Consequently, the repertoire of inflammatory cells, the extent of inflammatory cell differentiation and the duration of the inflammatory response in embryonic skin are all remarkably diminished compared to adult skin.
Second, the embryo is undergoing quick growth and differentiation, stimulated by exposure to growth factors and cytokines at levels and combinations unseen in adults.
Embryonic and adult wounds differ greatly in the levels and isoforms of cytokines and growth factors detected in the wound environment, such as transforming growth factor beta (TGF-Beta), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF).
In embryos, the cytokine and growth factor stock in the wound environment comes from fibroblasts and keratinocytes, and thus from the natural immune response, while in adults it is derived from platelets and inflammatory cells which are part of the adaptive immune system.
Embryonic cells contain high levels of the TGF-Beta3 isoform, derived from keratinocytes and fibroblasts, and low levels of the TGF-Beta1 and TGF-Beta2 isoforms, derived from degranulating platelets and inflammatory cells in adult wounds. FGF is expressed at high quantities in embryos, but PDGF expression is not detected. By contrast, TGF-Beta1, TGF-Beta2 and PDGF expression is high in adult wounds, with low if any expression of TGF-Beta3 or FGF.
Studies of wound healing in animal models suggest an hypothetical treatment role for TGF-Beta isoforms. Wound healing investigations in rodents have demonstrated that neutralization of TGF-Beta1 and TGF-Beta2 by antibodies greatly improves scarring. Also, wounds heal with less scarring following topical application of mannose-6-phosphate, which inhibits activation of TGF-Beta1 and of TGF-Beta2. By contrast, addition of exogenous TGF-Beta3 improves scarring in rodent models, and TGF-Beta3 deficiency in heterozygous null knockout mice results in impaired healing with scar formation.
Scar formation is the last stage in the wound healing process, and scars are not considered stable and mature until several weeks after the wounding. Nevertheless, the first 48 hours appears to be very important for determining the scar outcome. Best results were achieved in animal models when interventions were made within this window.
A tentative explanation is that the small number of master signaling molecules in the initial cytokine cascade triggered by the wound healing process can greatly affect the levels and ratios of inflammatory cells and growth factors recruited to the wound site. In addition, the recruited cells modify the receptor profiles on the target cells, further modifying the wound healing response and subsequent scar appearance.
Evolutionary relics
During our evolutionary drift injuries and wounds meant a serious hazard to our body, not only due to blood loss, but also due to tissue damage or infection from the invasion of foreign bodies such as dirt, splinters and bacteria. The adult wound healing mechanism that evolved to act against this threat has two basic characteristics:
First, there is a quick and robust inflammatory response, with recruitment of activated macrophages, neutrophils and lymphocytes to the damaged site; and
Second, there is a fibrotic "walling-off" response to isolate the foreign body, with liquefaction of adjacent tissue leading to abscess formation and scarring.
Is this response still appropriate?
"A scar is not an evolutionarily optimized end point for today's wounds," Dr. Ferguson says. "The scarring response, with its massive inflammatory overdrive, is optimized for a very different type of wound than the common sharp, clean wounds seen today. The scar is induced by this inappropriate inflammatory response."
The scars in most adults have arisen from surgical interventions. The "wounds" were inflicted with a sharp instrument under sterile conditions, with no contamination by foreign bodies. These wounds should therefore be ideal candidates for healing, without complications, by a regenerative wound healing mechanism rather than a scarring mechanism.
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Scars are traces of ancient, hard times. Several studies keep searching for the definitive scars solution.
Recent Research about Scar Free Healing
Fetal scarless wound healing
Colwell AS, Krummel TM, Longaker MT, Lorenz HP.
Department of Surgery, Division of Plastic Surgery, Children's Surgical Research Program, Tissue Regeneration Laboratory, Stanford, Calif. 94305-5148, USA.
BACKGROUND: Lysyl oxidase cross-links collagen and elastin. Because cross-linking likely influences collagen architecture, a study was performed comparing lysyl oxidase expression during scarless and scarring fetal dermal wound repair.
METHODS: Excisional dermal wounds were made on E17 (gestational day 16.5) and E19 (gestational day 18.5) mouse fetuses. Skin and wound RNA was collected at 8, 12, and 24 hours. Quantitative real-time polymerase chain reaction was performed for lysyl oxidase. The effect of transforming growth factor (TGF)-beta1 on lysyl oxidase expression in fetal fibroblasts was tested. Confluent primary fetal and postnatal fibroblast cultures were stimulated with TGF-beta1 for 24 hours, and lysyl oxidase expression was quantitated by performing real-time polymerase chain reaction. Lysyl oxidase expression was also quantitated in unwounded fetal skin to determine its expression profile during development.
RESULTS: E17 and E19 fetal skin had approximately 2-fold greater lysyl oxidase expression than postnatal skin (p < 0.01), and fetal fibroblasts had greater baseline lysyl oxidase expression than postnatal fibroblasts. After TGF-beta1 stimulation, fetal and postnatal fibroblasts responded with increases in lysyl oxidase expression. In E17 early-gestation scarless fetal wounds, lysyl oxidase had small increases (<1.5-fold) in expression from 1 to 12 hours. In late-gestation E19 scarring fetal wounds, lysyl oxidase increased 1.8-fold at 8 hours and 2-fold at 12 hours, which was significantly greater than the changes observed in E17 scarless wounds (p < 0.01 for each).
CONCLUSIONS: Lysyl oxidase has greater expression in E19 late-gestation wounds that heal with scar compared with E17 early-gestation scarless wounds. This suggests a role for lysyl oxidase in scar formation.
Usefulness of Scarring, Perfect Wound Healing, Embryonic and Adult Scarring, Scarring Process Evolution, Scarring Response.
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