Up-to-date approach to manage keloids and hypertrophic scars: A useful guide

Abstract

Keloids and hypertrophic scars occur anywhere from 30 to 90% of patients, and are characterized by pathologically excessive dermal fibrosis and aberrant wound healing. Both entities have different clinical and histochemical characteristics, and unfortunately still represent a great challenge for clinicians due to lack of efficacious treatments. Current advances in molecular biology and genetics reveal new preventive and therapeutical options which represent a hope to manage this highly prevalent, chronic and disabling problem, with long-term beneficial outcomes and improvement of quality of life. While we wait for these translational clinical products to be marketed, however, it is imperative to know the basics of the currently existing wide array of strategies to deal with excessive scars: from the classical corticotherapy, to the most recent botulinum toxin and lasers. The main aim of this review paper is to offer a useful up-to-date guideline to prevent and treat keloids and hypertrophic scars.

Novel Insights on Understanding of Keloid Scar: Article Review

“…Simman et al, also found that there was a proliferation of keloid fibroblasts in vitro after three weeks period and suggest that this agent might be in clinical trial post-keloid surgical excision. 36 Based on this in vitro study, a clinical trial was conducted by Bailey et al, on a group of 10 patients who received 1 mg ML of MMC topically for 3 min post-shaving removal of keloid scar with a repeated dose after three weeks. The patients follow up was every 2 months for 6 months and the keloid scar was photographed; pre-and post-treatment photos were assessed by two dermatologists who were not involved in the study.…”

Association of Surgery and Pulsed Dye Laser for the Treatment of an Ear Keloid: A Case Report

“…The association between different techniques seems to be the only chance to treat keloids and reduce recurrence rate [15] , furthermore surgery is frequently the only opportunity to restore the correct anatomy distorted by the scar. …”

Presence of galectin-1 in the epidermal and dermal thickening of keloid tissues

“…There is controversy not only regarding the presence of myofibroblasts in keloid tissues [2,4,8,44] but also regarding the conversion of fibroblasts into myofibroblasts by Gal-1 [24,26,45]; therefore, we sought to determine by double-immunofluorescence staining whether α-SM actin, the most common marker for myofibroblasts identification [46], was present in the fibroblasts of keloid tissues examined. Immunolocalization demonstrated that α-SM actin was completely absent in the fibroblasts expressing Gal-1 as well as in those that did not it (Fig.…”

“…frequently occur on the anterior portion of the chest, shoulders, upper back, arms, cheeks and earlobes [1,2,[5][6][7][8][9][10]. Histopathologically, keloids are defined as inflammatory disorders characterized by exhibiting a thickened dermis containing numerous fibroblasts, abnormal vascularization, increased inflammatory immune cells, abundant hyalinised collagen bundles (keloidal collagen) and extracellular matrix (ECM) components including collagen, elastin, fibronectin and proteoglycans such as syndecan and versican, mainly produced by activated fibroblasts [1][2][3][4][5][6][7][8][9][10][11][12][13][14].…”

“…Histopathologically, keloids are defined as inflammatory disorders characterized by exhibiting a thickened dermis containing numerous fibroblasts, abnormal vascularization, increased inflammatory immune cells, abundant hyalinised collagen bundles (keloidal collagen) and extracellular matrix (ECM) components including collagen, elastin, fibronectin and proteoglycans such as syndecan and versican, mainly produced by activated fibroblasts [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. These histological alterations proper of the keloid tissue have been associated with the elevated production of growth factors such as TGF-β, FGF-2, PDGF, EGF, IGF and VEGF which regulate fibroblast proliferation, ECM synthesis and angiogenesis, and pro-inflammatory cytokines including IL-1α, IL-1β, IL-6 and TNFα which promote fibroblast activation and consequently an excessive deposition of ECM components [1,2,[5][6][7]9,10,15,16].…”