Shopping Bag

Reducing Dermal Scarring

Posted by Nancy Ray on

Scars are areas of dermal fibrosis that replace normal tissue after injury and during wound healing.

There are several types of dermal scars including:

1. Atrophic scars that appear as sunken or pitted areas of skin

2. Hypertrophic scars that are characterized by raised areas of skin

3. Keloid scars characterized by growth outside the original wound area

4. Striae distensae (stretch marks) characterized by linear bands of atrophic-appearing skin.

Wound healing involves 4 critical phases that overlap: the coagulation phase, the inflammatory phase, the migration-proliferation phase (development of granulation tissue), and the remodeling-regeneration phase that includes maturation, scar formation and re-epithelialization.  The magnitude of the second phase, inflammation, affects the amount of scar tissue that is produced at the conclusion of the healing process.  Regeneration is thought of as replacement of tissue, however, scar formation actually involves a progressive remodeling of granulation tissue.  In fact, scars are defined as dermal fibrous replacement tissue that results from a wound that has healed by resolution (rather than regeneration).

Scarring typically occurs following damage to more than 33% of the skin thickness from trauma or surgery.  Can skin damaged in this way ever heal without scarring? Actually, complete regeneration occurs exclusively in lower vertebrates.  Scarless healing in humans only occurs in early embryo development.  So, why do we form scars after early development?  One theory suggests that wound healing in mammals is optimized for fast healing in a fast-moving, microbial-rich environment.  Rapid inflammatory responses may allow quick healing to prevent infections.

Scar tissue is composed mostly of disorganized collagen-rich extracellular matrix produced by skin cells called myofibroblasts, which are stimulated by the signaling molecule (cytokine), transforming growth factor beta (TGF-beta).  Typically, myofibroblasts are programmed to die in a process called apoptosis that leaves a normal scar, however, in some pathological conditions these cells fail to undergo cell death and persist, as in the case of excessive scarring.

Scars may seem trivial, however, scar tissue is weaker than normal tissue, and scars can cause many problems including limited joint mobility, growth impairment and loss of normal skin function.  In addition, scars can be disfiguring and may cause severe itching, tenderness, pain, sleep disturbance, and anxiety, particularly in the case of excessive scars that can develop after trauma to the deep dermis such as from burns or lacerations.  Excessive or pathological scars including hypertrophic scars and keloids may be caused by the dysregulation of collagen synthesis.

As mentioned, excessive inflammation during wound healing may affect the degree of scarring.  Many of the ingredients in Viniferamine® skin and wound care products are anti-inflammatory including the polyphenol resveratrol from grapevines, the polyphenol epigallocatechin-3-gallate (EGCG) from green tea, and the polyphenol oleuropein from olive leaves.  In addition, other ingredients are anti-inflammatory including asiaticoside, a component of titrated extract of Centella asiatica (TECA) and the important antioxidant, melatonin, as well as aloe vera and dipotassium glycyrrhizate (from licorice).

Resveratrol has also been shown to inhibit growth and induce apoptosis in keloid fibroblasts.  In addition, resveratrol decreases the production of TGF-beta by human keloid fibroblasts, suggesting that resveratrol may help in the treatment of keloids.  Furthermore, resveratrol has been shown to reduce collagen production in human hypertrophic scar fibroblasts by inhibiting proliferation and inducing apoptosis.

EGCG has been shown to decrease collagen expression in normal human and keloid (human) fibroblasts, and attenuate the TGF-beta-induced differentiation of myofibroblasts, suggesting that EGCG may have a role in improving wound healing and scarring.

Asiaticoside has been shown to reduce scarring and decrease TGF-beta expression in a rabbit ear model of hypertrophic scarring.  In addition, asiaticoside was shown to suppress collagen expression and TGF signaling in normal human fibroblasts, human keloid fibroblasts, and human hypertrophic scar fibroblasts.

It has been shown that scars have increased transepidermal loss (TEWL).  Changes in skin barrier function are clearly evident with scarring.  Hydration is important for reducing scarring since it reduces water loss and restores homeostasis to the scar reducing collagen deposition and excessive scar formation.  Dipotassium glycyrrhizate promotes skin hydration by maintaining levels of hyaluronic acid, which has a high capacity for retaining water.  Hyaluronic acid has also been shown to reduce dermal scarring.  In addition, one of the most consistently successful hydrating agents used in scar management has been silicone (included in Silicone Barrier and Renewal Moisturizer) in dimethicone topical applications.  Viniferamine® skin care products contain beneficial ingredients including dipotassium glycyrrhizinate and dimethicone to improve and maintain skin hydration.

It’s good to know that beneficial ingredients in the Viniferamine® skin and wound care products including Silicone Barrier and Renewal Moisturizer help promote normal wound healing and protect against excessive inflammation.

About the author: Nancy Ray, PhD is the Science Officer at McCord Research. Dr. Ray received her PhD in Biochemistry and Biophysics and was a postdoctoral fellow at NIH, Harvard University and Dana-Farber Cancer Institute, and the University of Iowa. She also earned bachelor of science degrees in Chemistry and Microbiology.

 References

  1. Clin Cosm Invest Dermatol 2014; 7: 301-311.
  2. Adv Wound Care 2013; 3: 356-365.
  3. Dermatol Res Pract 2009; ID 625376, 1-7.
  4. BMJ 2003; 326: 88-92.
  5. Mol Med 2011; 17: 113-125.
  6. Wound Rep Reg 2013; 21: 616-623.
  7. Biosci Biotechnol Biochem 2013; 77: 2389-2396.
  8. Wound Rep Reg 2010; 18: 80-88.
  9. J Cutan Path 2009; 36: 234-239.
  10. Arch Dermatol Res 2011; 303: 562-572.
  11. Clin Exp Derm 2007; 33: 171-175.

Disclaimer: These statements have not been reviewed by the FDA. The decision to use these products should be discussed with a trusted healthcare provider. The authors and the publisher of this work have made every effort to use sources believed to be reliable to provide information that is accurate and compatible with the standards generally accepted at the time of publication. The authors and the publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance on, the information contained in this article. The publisher has no responsibility for the persistence or accuracy of URLs for external or third party Internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate.


Older Post Newer Post