Scarless Healing of Acne Scars with Natural Serum

Two major differences between embryo and adult are critical in understanding the molecular and cellular environments of scar-free versus scarring mechanisms of wound healing. 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 considerably diminished compared to adult skin.

Second, the embryo is undergoing rapid growth and differentiation, stimulated by exposure to 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 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 repertoire in the wound environment is derived from fibroblasts and keratinocytes, and thus from the innate immune response, whereas in adults it is derived from platelets and inflammatory cells which are part of the adaptive immune system.

Embryonic cells express 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 not detected. By contrast, TGF-Beta1, TGF-Beta2 and PDGF expression is high in adult wounds, with little if any expression of TGF-Beta3 or FGF.

Studies of wound healing in animal models suggest a possible therapeutic role for TGF-Beta isoforms. Wound healing studies in rodents have shown that neutralization of TGF-Beta1 and TGF-Beta2 by antibodies markedly improves scarring. Similarly, 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 final event 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 obtained in animal models when interventions were made within this window.

A possible explanation is that the small number of master signaling molecules in the initial cytokine cascade triggered by the wound healing process can profoundly affect the levels and ratios of inflammatory cells and growth factors recruited to the wound site. In addition, the recruited cells influence the receptor profiles on the target cells, further affecting the wound healing response and subsequent scar formation.

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 mechanism that evolved to respond to this threat has two fundamental characteristics:

First, there is a rapid and robust 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 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."

Lesions that affect the cells lining the sebum canals, arising from a sudden overflow of sebum or pinched-off sebum glands, occur in an otherwise clean skin without dirt or contamination by foreign bodies. These lesions should therefore be ideal candidates for healing, without complications, by a regenerative wound healing mechanism rather than a scarring mechanism. And the outcome should be characterized by scar less healing.

The healing process inside the hair follicles should be very much like what our system accomplishes for fetal wounds which heal quickly by regenerating cells and leaving absolutely no trace behind.

Something is missing in all the products out there. Something that would signal your body it is being taken care of properly and does not need to overly react with its inflammatory army. Not just the natural or chemical ingredients that fight the symptoms, when it is already too late: acne bacteria gone wild, occlusion of the ducts (microcomedones) and then enlarged comedones that become inflammatory lesions.

This is a vicious cycle causing continued and/or increased obstruction of the outflow of the sebum, which in turn leads to more pressure, more inflammation and continued or progressive infection.

Such continued obstruction, with or without infection, leads to the formation of cysts. Infection of a cyst results in the formation of an abscess which leads to local tissue destruction. If this destruction of tissue has involved the connective tissue elements of the skin or subcutaneous tissues to a sufficient degree, healing is frequently accompanied and/or followed by scar formation.

Acne scars can vary from minimal to extensive and severely disfiguring problems which are permanent sequallae of acne. While the process by which acne arises and lasts for an indefinite time may and frequently does come to a halt as a result of treatment or spontaneously but the scars persist for life unless they are removed.

A Surprising Solution from Life's Genius

Fortunately we have found, by chance and keen observation, a better model. One geared as a different evolutionary immune response and cell regeneration system, by a family of invertebrates (spineless animals). It is known as the innate immune system, also present as a first line of defense and immediate maximal response against infections and foreign matters in our human body, and different than the laged layered response of our adaptive or acquired immune system.

The innate immune system is comprised of the cells and mechanisms that defend the host from infection by other organisms, in a non-specific manner. This means that the cells of the innate system recognize, and respond to, pathogens in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host.

Although apparently less sophisticated than the immune systems of vertebrates, invertebrate immunity is much older in terms of its evolution, and likely served as the progenitor to sophisticated vertebrate systems, and also has apparently served these animals well enough to keep their lineage alive for the past several hundred million years.

Invertebrates also respond to injury and insult from the environment by regenerating damaged cells, and even full organs and their skin, without an immoderate inflammatory reaction and yield quick results and an orderly, fully orchestrated, skin repair and remodeling without aberrant scar healing! Yes, this is accomplished by little creatures that we, arrogant humans, many times consider an inferior form of life, in a less evolved stage.

Unlike clever herbal, botanical, chemical or cosmeceutical concoctions designed in a pharmacy, or by the cosmetic industry, a complex natural serum secreted by spineless creatures of a specific family of land invertebrates is already a complete and balanced solution for scar less healing of skin lesions —and its effects on acne & rosacea skin disorders may far exceed attempts to mimic life's genius in the laboratory.