Reducing Dermal Scarring

Scars are areas of dermal fibrosis that replaces 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. Hypertophic 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.

Dermal ScarringWound 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 affects the degree of scarring.

TITRATED EXTRACT OF CENTELLA ASIATICAMany of the extraordinary 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, Viniferamine® skin and wound care products con­tain other ingredients that are an­ti-inflammatory including asiatico­ side, a component of titrated extract of Centella asiatica (TECA) and the important antioxidant, melatonin.

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.

Oleuropein has been used in a scar management program due to the fact that exuberant inflammation can be downregulated or modulated by oleuropein.  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 glycyrrhizinate 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 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 Viniferamine® skin and wound care products help protect against excessive inflammation, pro­mote normal wound healing and im­prove skin hydration to reduce der­mal scarring.

References

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  5. Clin Cosm Invest Dermatol 2014; 7: 301-311.
  6. Adv Wound Care 2013; 3: 356-365.
  7. Dermatol Res Pract 2009; ID 625376, 1-7.
  8. BMJ 2003; 326: 88-92.
  9. Wound Rep Reg 2013; 21: 616-623.
  10. Biosci Biotechnol Biochem 2013; 77: 2389-2396.
  11. Wound Rep Reg 2010; 18: 80-88.
  12. Aesth Plast Surg 2009; 33: 533-543.
  13. J Cutan Path 2009; 36: 234-239.
  14. Arch Dermatol Res 2011; 303: 562-572.
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  17. Pathol Biol 2015; 63: 32-34.

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.

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