Scarless Healing

Summary: Scarring seem to be an arcaic way to protect the body against external contamination. Unlike adult individuals, embryos are able to perform a totally scarless healing of their injuries.

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Two distinctive differences between embryo and adult are critical in understanding the molecular and cellular behaviour of scar-free versus scarring mechanisms of wound repair.

First, the immune system of an embryo is not fully developed. Therefore, the number of inflammatory cells, the extent of inflammatory cell differentiation and the duration of the inflammatory response in embryonic skin are all considerably diminished compared to adult skin.

Second, the embryo is going through quick growth and differentiation, stimulated by growth factors and cytokines at levels and combinations not seen in adults.

Embryonic and adult wounds differ significantly in the levels and isoforms of cytokines and growth factors present in the injury 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 repertoire in the injury environment comes from fibroblasts and keratinocytes, and thus from the innate immune reaction, 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 levels in embryos, but PDGF expression is undetected. 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 a possible therapeutic role for TGF-Beta isoforms. Injuries healing investigations in rodents have demonstrated that neutralization of TGF-Beta1 and TGF-Beta2 by antibodies markedly helps with scarring. Also, wounds heal with less scarring following topical use of mannose-6-phosphate, which inhibits activation of TGF-Beta1 and of TGF-Beta2. By contrast, addition of exogenous TGF-Beta3 helps with scarring in rodent models, and TGF-Beta3 deficiency in heterozygous null knockout mice results in impaired healing with scar formation.

Scar formation is the final stage in the wound healing process, and scars are not considered stable and mature until several weeks post-wounding. Nevertheless, the first 48 hours appears to be critical in determining the scar outcome. Best results were achieved in animal models when interventions were made within this time.

A tentative explanation is that the small number of master signaling molecules in the initial cytokine cascade triggered by the injury 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 affecting the wound healing response and subsequent scar appearance.

Evolutionary relics

During our evolutionary drift injuries and wounds represented a serious threat to our organism, 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 process that evolved to act against this threat has two basic characteristics:

First, there is a quick and strong inflammatory response, with recruitment of activated macrophages, neutrophils and lymphocytes to the injured site; and

Second, there is a fibrotic "walling-off" response to isolate the foreign body, with liquefaction of adjacent tissues 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 appeared after surgical interventions. The "wounds" were done with a sharp instrument under aseptic conditions, without contamination by foreign bodies. These wounds should therefore be ideal candidates for healing, without complications, by a regenerative wound healing process rather than a scarring process.

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There's still no such thing like a scarless healing solution, but an adequate Scar Treatment can achieve more than satisfactory results.

Recent Research about Scarless Healing

Psoriatic plaques and tissue repair

Nickoloff BJ, Bonish BK, Marble DJ, Schriedel KA, DiPietro LA, Gordon KB, Lingen MW.
Department of Pathology, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, Illinois 60153, USA.

After being damaged, skin must keep a balance between too little inflammation increasing risk of infection, and excessive inflammation contributing to delayed wound healing and scarring.

Mounting evidence indicates both initiation and termination of inflammation involve active mechanisms. Not only does inflammation itself seem to be a paradox because inflammatory responses are both essential and potentially detrimental, but one chronic inflammatory skin disease (e.g. psoriasis) presents additional paradoxes. While plaques share several factors with wound healing, two understudied and puzzling aspects include why do not inflamed plaques more frequently transform?; and why do not plaques result in scarring? To get at these questions, we review responses involved in wound repair. Oral mucosa was probed because, like fetal skin, wound repair is characterized by its rapidity, low inflammation, and scarless resolution. Active roles for macrophages as both initiators and terminators of inflammation are highlighted.

Therapeutic implications are discussed regarding psoriasis and pyoderma gangrenosum. Based on biochemical and immunohistochemical considerations linking psoriatic plaques to hard palate, a novel metaplastic model is presented. We hypothesize saliva and chronic trauma contribute to a constitutive epithelial program where keratinocyte proliferation is more intense prior to differentiation, accompanied by keratin 16 expression in hard palate, thereby resembling plaques.

Rather than viewing psoriasis as a nonspecific response to inflammation, we postulate a metaplastic switch by which prepsoriatic skin is converted to a distinct adult tissue type resembling hard palate. In summary, many lessons can be learned by focusing on complex processes involved in regulation of inflammation, tissue repair, and remodeling.