HLA Antigens in Keloids and Hypertrophic Scars

Keloid formation after syndactyly release in patients with associated macrodactyly: management with methotrexate therapy

“…Current opinion suggests that keloid formation is the result of a multifaceted process with aberration at all stages of normal wound healing, including haemostasis, inflammation, granulation, and early remodelling. Abnormal epithelial-mesenchymal interactions (Al-Attar et al, 2006; Butler et al, 2008), altered fibroblastic activity (Appleton et al, 1996; Kose and Waseem, 2008; Louw, 2007; Tuan and Nichter, 1998; Yang et al, 2003), collagen dysregulation (Abergel et al, 1985; Diegelmann et al, 1977; Rockwell et al, 1989; Tuan et al, 1996), altered immune function (Kazeem, 1988; Kischer et al, 1982; Laurentaci and Dioguardi, 1977), failure of apoptosis (Kischer et al, 1990; Ladin et al, 1998; Messadi et al, 1999) and tissue hypoxia (Le et al, 2004; Steinbrech et al, 1999) have all been proposed as mechanisms of keloid growth. However, no single unifying hypothesis has been established.…”

From scarless fetal wounds to keloids: Molecular studies in wound healing

“…The frequently raised question of inherited susceptibility to keloids has also been studied to some extent. To date, however, such genetic predisposition remains inconclusive with no consistent pattern 66–68 …”

“…To date, however, such genetic predisposition remains inconclusive with no consistent pattern. [66][67][68] At the cellular level, the keloid fibroblast has been well characterized because of its role in producing the collagen and ECM components that make up the fibrous keloid lesion. The histological and electron microscopic appearance, 69 pattern of collagen production, 70,71 propensity for increased proliferation in the active growing phase, 72,73 and more recently, the complex molecular biological interactions that might be involved its pathogenesis have been extensively investigated.…”

Upregulation of the NNP-1 (novel nuclear protein-1, D21S2056E) gene in keloid tissue determined by cDNA microarray and in situ hybridization

“…10,11 No specific gene or set of genes has been identified as affecting keloid development; however, the increased incidence of keloids paralleling increased cutaneous pigmentation suggests a genetic basis or, at least, a genetic linkage. Keloids and hypertrophic scars have been reported to have an association with human leucocyte antigens 12,13 and blood group A. 14 Some cases of keloid suggest familial predisposition and typically occur in certain races.…”