Vascularization Pattern in Hypertrophic Scars and Keloids: A Stereological Analysis

Effect of eccentric exercise on the healing process of injured patellar tendon in rats

“…Abnormal vascularization can be involved in the development of hypertrophic scars and keloids. 15 The presence of scar tissue in the healing tendon and muscle is recognized clinically to be a risk factor for injury recurrence and alteration of normal musculoskeletal structure. Scar tissue production in the healing tendon inhibits complete tendon tissue regeneration and may lead to decreased tendon strength.…”

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

“…Interestingly, abnormal vascularization has been associated not only with pronounced proliferation of endothelial cells [60] and hypoxia [11,61], but also with an elevated Gal-1 expression [62,63]. In fact, studies have shown that Gal-1 can induce endothelial cell proliferation [64,65] and that Gal-1 expression can be regulated by hypoxia [66,67].…”

“…In fact, studies have shown that Gal-1 can induce endothelial cell proliferation [64,65] and that Gal-1 expression can be regulated by hypoxia [66,67]. Also of significance, some studies have provided evidence that local hypoxia not only promotes keratinocyte motility and migration during wound healing [68] but also stimulates the deposition of collagen by fibroblasts in wounds and keloids [69][70][71] and abnormal vascularization in keloids [11]. Thus, we believe that the increased immunopositivity for Gal-1 observed in dermal thickening would be associated with the fibroblasts proliferation, excessive deposition of collagen and abnormal vascularization; moreover, considering that hypoxia seems to be an important element in the pathogenesis of keloids [4,70].…”

“…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].…”

Avaliação da cicatrização cutânea: fluorescência e estereologia

“…Na cicatrização, estudos comparativos são empregados para quantificar diversas estruturas teciduais, como: fibroblastos e colágeno (McGaw e Ten Cate, 1983;Ricketts et al, 1999;Brahmatewari et al, 2000;Garcia et al, 2008), vascularização tecidual e vasos neoformados (Khozani et al, 2004;Amadeu et al, 2003;Garcia et al, 2008), matriz extracelular (Burugapalli e Pandit, 2007), infiltrado celular inflamatório e epitelização (Garcia et al, 2008).…”