Scarless Healing

What Helps Counteract The Scarring Triggers?

Got the point? Two processes must be in place for success:

•  Stimulation cytokine and growth factor production by fibroblasts and keratinocytes

•  Modulation of an overzealous inflammatory response

Stimulating the production of cytokine and growth factor by fibroblasts and keratinocytes

While the physical barrier function of the epidermis was formerly believed to play the major role in the protection against infections, the recent description of Toll-like receptors (TLRs) and antimicrobial peptides in the epidermis indicates that keratinocytes play an active role in innate immunity.

The innate immune system is our first line of defense that provides immediate maximal response against destruction of tissues, infections and foreign matters in our body, and it is different than the lagged layered response of our adaptive or acquired immune system.

Whenever the skin is breached by an injury, invading pathogens are eliminated first by the innate, followed by adaptive immune reactions. The innate immune network of the skin consists of a range of preexisting, rapidly mobilized host defense components including keratinocytes, neutrophils, mast cells, eosinophils and macrophages. Essential to innate immunity are receptors that initiate a host defense reaction.

Circulating neutrophils with abundant amounts of antimicrobial peptides are rapidly recruited to epithelial sites even in sterile wounding and may provide early antimicrobial protection. Certain high-risk situations for infections alert the innate immune system in the skin even in the absence of microbes and induce alterations in the epidermis that prevent harm from microbial colonization and infection.

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.

Cells of the innate immunity express a wide variety of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and mannose receptors that are activated by components of microbial pathogens. These PRRs are specific for pathogen associated molecular patterns (PAMPs) that are relatively invariant within a given class of microorganisms. Such PAMPs are the lipopolysaccharide (LPS) of Gram-negative bacteria, mannan and zymosan in the yeast cell wall, the mycobacterial cell-wall component lipoarabinomannan (LAM), and the peptidoglycan (PGN) or lipoteicoic acid (LTA) of Gram-positive bacteria and lipo-peptides of various microorganisms. Recognition of PAMPs by the PRRs initiates various quick innate immune responses such as phagocytosis, production of antimicrobial peptides and inflammatory mediators, which in turn leads to killing of microorganisms and after a longer presence of the infectious agents, the initiation of the more efficient acquired immune response.

Furthermore, the ability of keratinocytes to distinguish between pathogenic and commensal microorganisms suggest that keratinocytes possess a highly sophisticated innate pattern recognition system in which the simultaneous recognition of a pathogen by different classes of PRRs could provide a specific immune response or (in the case of commensals) unresponsiveness to microorganisms.

It is also known that several peptides exercise an anti-infective therapy through the boosting of innate immunity with the co-incident suppression of potentially harmful inflammatory responses.

Modulating the inflammaging process.

When we're hurt or seriously ill, our first response is to call a doctor or head for the nearest emergency room. But faster than you can dial 9-1-1 , the body's internal emergency response team is already on the scene. Responding instantly to biochemical distress signals from damaged tissue, specialized cells and proteins have already started to seal off the injured area by contraction and scar formation, destroying damaged tissue and killing invading bacteria.

It's the inflammaging processs or inflammatory response, and the pain, heat, swelling, redness and loss of function we associate with injury are signs that it's working.

Yes, our body reacts in very much the same way it learned to react during the thousands of years of our evolutionary drift. By sending to the site of injury and insult all its army of immune system soldiers (lymphocytes, macrophages, neutrophils...) overcharged with chemical death weapons to get rid of the offenders, with no consideration even for its own cells that might happen to be in their way and also do get killed. After all... it used to be a matter of life or death!

This is what is meant by "inflammatory reaction". And, Oh Boy! You might as well bet those soldiers are inflamed!

Like everything else in the human immune system, the inflammatory response is controlled by an incredibly complicated communications network made up of multiple cells, cascading signal pathways and feedback loops. It starts when scavenger cells called neutrophils arrive at the site of injury or infection. They surround and engulf toxins, microbes or damaged tissue and broadcast biochemical "SOS" signals calling for reinforcements. Complement proteins join the fray triggering the production of powerful, pro-inflammatory molecules and tissue-destroying enzymes. This intensifies the response and causes inflammation to spread to surrounding tissue. Once activated, the feeding frenzy will continue until the immune system sends an all-clear signal to indicate that the crisis is over.

Inflammation only exacerbates when bacteria (e.g. acne bacteria Propionibacterium acnes and other deliriously happy bacteria) always present on the surface of the skin ( Staphylococcus aureus , Staph. epidermidis , diphtheroids , streptococci , Candida , etc) start to proliferate uncontrolled in skin punctured or broken. The problem is magnified if right there the deliciously rich feeding fatty sebum characteristic of acne prone skin is plenty.

Aberrant Scars

These views also explain aberrant scar formation, for although inflammation is the body's first line of defense against injury and infection, it's also a double-edged sword.

Fact is our body is ingrained with the memories of past battles, fought to protect our system whenever damaged or injured and does not listen to just any argument made up by the pharmaceutical companies or those selling silicon products aiming to control the outgrowth of scar tissues.

An out-of-control inflammaging response can destroy healthy tissue and cause more damage than the original problem. Keeping it under control means the immune system must maintain a balance between fanning the flames of inflammaging and cooling it down.

Something is missing 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. Plus not just the natural or chemical ingredients that fight the symptoms, when it is already too late: bacteria gone wild, the chemical cascade launched for good and bad. but something that would effectively signal your body that it is being taken care of and needs NOT respond to disturbing agents with uncontrolled inflammatory reactions, for it is being supplied with the proper proteins, enzymes and nutrients necessary to quickly control bacteria and to trigger scar less healing.

Two new approaches that can solve the riddle:

1) A promising pharmaceutical approach to scar treatment

2) A natural immune modulator and skin regenerating substance that supports our innate immune system at the site of injury.

A natural skin care product for keloid & hypertrophic scarring