Novel Insights on Understanding of Keloid Scar: Article Review

Abstract

Keloid scar, dermal benign fibro-proliferative growth that extends outside the original wound and invades adjacent dermal tissue due to extensive production of extracellular matrix, especially collagen, which caused by over expression of cytokines and growth factors. Although many attempts were made to understand the exact pathophysiology and the molecular abnormalities, the pathogenesis of keloid scar is yet to be determined. Even though there are several treatment options for keloid scars include combination of medical and surgical therapies like combination of surgical removal followed by cryotherapy or intralesional steroid therapy, the reoccurrence rate is still high despite the present treatment. In this review, PubMed, clinical key and Wright State Library web site have been used to investigate any update regarding Keloid disease. We used Keloid, scar formation, hypertrophic scar and collagen as key words. More than 40 articles have been reviewed. This paper reviews literature about keloid scar formation mechanism, the most recent therapeutic options including the ones under research.

Giant relapsing earlobe keloid – Successful combined treatment by surgery and pressure earring

“…Insulin-like growth factor-I-inhibition results in decreased and normalized keloid-fibroblast activity in vitro. [1] In a recent microarray study on long non-coding RNAs, an increased expression of the following genes was found in keloid-fibroblasts: FNDC1, CILP2, THBS4, NPTX2, COL5A1, GRIN2D, and CTHRC1. Other genes were downregulated.…”

“…Earlobes are one of the most common anatomical sites for acquired keloids. [1] Pathologically, fibroblasts from keloids show peculiarities. They are metabolically hyperactive and show an increased migratory activity in cell culture.…”

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

“…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]. This is why most studies on keloids focus on dermis and few on epidermis [4,17].…”

“…Moreover, there is evidence suggesting that epigenetic modifications would be involved in the pathogenesis of keloids by regulation of fibroblasts activation, proliferation and apoptosis, as well as collagen and elastin synthesis [3,[20][21][22]. Nevertheless, the etiology and pathophysiology of keloids is not fully elucidated yet [3][4][5][6][7]18].…”