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Received Dec 4, 2017; Accepted Mar 8, 2018
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1. Wound Healing: A Vital Process
Wound healing occurs after a chemical, physical, or biological insult results in epithelial barrier disruption. This process involves activation of platelets, neutrophils, macrophages, endothelial cells, keratinocytes, and fibroblasts; moreover, the production and release of protein mediators (growth factors and cytokines) released by these cell types and lipid mediators (prostaglandins, leukotrienes, thromboxanes, and lipoxins) are needed to coordinate the tissue repair and to reestablish tissue homeostasis [1, 2].
The process is divided into 3 concomitant and overlapping phases: inflammation, proliferation, and remodelling (Figure 1).
[figure omitted; refer to PDF]After a tissue lesion, the disruption in vasculature blocks the oxygen and nutrient supply to the injured area, leading to a hypoxic condition that induces the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) [3–5], initiating a coagulation cascade. Blood elements such as platelets, erythrocytes, and fibrin form a framework for the recruitment of immune cells [6, 7]. Platelets produce platelet-derived growth factor (PDGF), transforming growth factor-β (TGF-β), and epidermal growth factor (EGF) that induce migration and activation of immune cells [8].
The extracellular matrix (ECM), which is composed of fibronectin, fibrinogen, fibrin, thrombospondin, and vitronectin, fills the tissue defect and enables migration of different cell types required for the healing process [9].
Inflammation is the body’s natural and essential defence mechanism responsible for combating antigens, restoring homeostasis, and repairing tissue damage [10, 11]. The inflammatory response consists of a variety of events triggered by immune cells, which involves influx of leukocytes to the injured area and production of pro- and anti-inflammatory mediators [12].
Neutrophils are the predominant cells in the first hours after the tissue injury, and they respond to proinflammatory cytokines, such as interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) at the lesion site, phagocytizing microorganisms and cellular debris [10, 13]. For microorganism destruction, the degranulation process occurs, releasing granule enzymes such as defensins, cathelicidins, elastase, myeloperoxidase (MPO), lactoferrins, and cathepsins inside the phagosome....