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Jairo Kenupp Bastos. Christopher John Jackson. Leonard, SydneyAustralia. This article belongs to the Section Medical Research. Inflammatory phase: there is the hemostasis of wounded area and acute inflammation through the release of cytokines, growth factors and the migration of leukocytes in the area. Proliferative phase: increase in the migration and proliferation of the keratinocytes, fibroblasts, endothelial cells and leukocytes in the wound.

Increase in the synthesis of extracellular matrix components and improve of angiogenesis and re-epithelialization mechanisms. Remodeling phase: extracellular matrix remodeling, with substitution of collagen III for collagen I. Increase in the activity of MMPs. Apoptosis of provisional endothelial cells, fibroblasts, and myofibroblasts of the injury. Common situations that delay skin wound healing. The skin is the biggest organ of human body which acts as a protective barrier against deleterious agents. When this barrier is damaged, the organism promotes the healing process with several molecular and cellular mechanisms, in order to restore the physiological structure of the skin.

The physiological control of wound healing depends on the correct balance among its different mechanisms. Any disruption in the balance of these mechanisms can lead to problems and delay in wound healing. The impairment of wound healing is linked to underlying factors as well as aging, nutrition, hypoxia, stress, infections, drugs, genetics, and chronic diseases.

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Over the years, numerous studies have been conducted to discover the correct approach and best therapies for wound healing, including surgical procedures and non-surgical treatments such as topical formulations, dressings, or skin substitutes. Thus, this general approach is necessary to facilitate the direction of further studies.

This work provides updated concepts of physiological mechanisms, the factors that can interfere, and updated treatments used in skin wound healing.

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Keywords: skin; wound healing; wound therapies; topical formulation; dressings; skin substitutes skin ; wound healing ; wound therapies ; topical formulation ; dressings ; skin substitutes. Introduction The skin is the largest organ of humans that acts as the first mechanical barrier between the organism and the external environmental, to protect organism against deleterious agents, control thermal regulation, and regulate water and electrolytes homeostasis [ 1 ].

The morphologic structure of skin comprises two layers, the epidermis and dermis [ 2 ]. The epidermis is the most external layer of the skin and is divided into four or five sub-layers, depending on the region of the body [ 2 ]. Among the cells that constitute the epidermis are by far the major cell type, the keratinocytes, as well as melanocytes, Langerhans cells, and Merkel cells.

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The dermis is the layer of connective tissue that supports the epidermis, constituted by extracellular matrix proteins collagens, elastin, proteoglycans, and glycosaminoglycans synthesized by fibroblasts [ 3 ]. If there is a disruption of one or both layers of the skin, the organism starts the wound healing process to regenerate the injured area, involving cellular, molecular and biochemical mechanisms divided in three healing phases: inflammatory, proliferative, and remodeling [ 45 ].

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In this review, we discuss the physiologic mechanism of wound healing, the risk factors that affect healing and provide an update on the main therapies to treat skin wounds. Skin wound healing is a complex process involving interrelated and overlapping mechanisms of cell migration and proliferation, synthesis of extracellular matrix, growth factors and cytokines that coordinate the healing process. Due to this complexity, the wound healing process can be divided in three phases: inflammatory, proliferative, and remodeling phases Figure 1 [ 6 ].

The inflammatory phase of wound healing begins with the activation of platelets, which synthesize the compounds responsible for fibrin clot formation, restoring the local hemostasis and acting as a provisional extracellular matrix for the migration of blood cells [ 5 ]. Initially, neutrophils migrate to the injured area, starting the debridement of necrotic tissue and the phagocytosis of pathogenic antigens. The neutrophils also release VEGF vascular endothelial growth factor and IGF-1 insulin growth factor-1 which activate the local proliferation of fibroblasts, keratinocytes, and endothelial cells [ 78 ].

After a few days, macrophages start to migrate to the wound region to continue the debridement of necrotic tissue and phagocytosis of deleterious antigens, and secrete growth factors and cytokines which coordinate the subsequent mechanisms of the wound healing [ 5 ]. The proliferative phase of wound healing is characterized by the intense migration and proliferation of cells and synthesis of granulation tissue, comprised of provisional extracellular matrix, macrophages, endothelial cells, and fibroblasts [ 10 ].

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Fibroblasts also synthesize compounds of provisional extracellular matrix, including type III collagen, proteoglycans and fibronectin, in order to support cell migration into the area [ 56 ]. The restructuring of vascularization at the wound begins immediately after the injury, but has higher activity in the proliferative phase, providing oxygen and nutrients needed for the migration and proliferation of cells and synthesis of extracellular matrix compounds. Secreted mediators as VEGF and angiopoietins stimulate the proliferation of endothelial cells and restructuring of the vascular system at the wound site [ 11 ].

During the proliferative phase, re-epithelialization occurs to close the epithelial gap and restores the barrier function of the skin [ 512 ]. Firstly, the keratinocytes at the border of wounds are stimulated by growth factors, resulting in the proliferation and differentiation of the keratinocytes.

This stimulus triggers the loss of keratinocyte adhesion molecules, inhibiting the physical contact with desmosomes and hemidesmosomes, and increasing the migration of these cells through the extracellular matrix [ 812 ].

The last stage of skin wound healing is the remodeling phase, which depends on the mechanisms started in early phases. There is a decrease of granulation tissue, substitution of provisional extracellular matrix and apoptosis of provisional cells that migrated to the area [ 5 ]. Additionally, the proteins of provisional extracellular matrix are degraded by MMPs, metal-dependent proteases synthesized by local cells to remodel the wounded extracellular matrix proteins [ 15 ].

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Thus, the fibroblasts in remodeling tissue synthesize type I collagen, elastin, and other compounds of permanent extracellular matrix, resulting in higher resistance and flexibility in the regenerated skin [ 8 ]. Wound healing is a physiological process of vertebrates to maintain organism homeostasis and involves perfect interactions of numerous cell types and molecules [ 5 ].

The imbalance of these interactions can result in the occurrence of errors in the healing mechanisms and lead to the impairment of wound healing [ 16 ]. One of the errors that delays the wound healing is the chronic inflammatory state [ 17 ].

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Due to the imbalance of pro- and anti-inflammatory mediators, there is an exacerbated recruitment of neutrophils and macrophages to the region, with the overexpression of inflammatory cytokines [ 1819 ]. As result, there is the increase in leukocyte recruitment to the region and the release of reactive oxygen species ROS by inflammatory cells [ 1720 ].

Furthermore, the ROS cause the degradation of growth factors involved in healing mechanism, decreasing the quantity and bioavailability of these molecules [ 202122 ]. However, the imbalance between pro- and anti-angiogenic factors promotes the decrease of neovascularization and blood flow in the area, delaying the subsequent mechanisms from proliferative and remodeling phases [ 26 ].

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Delay in the re-epithelialization is another error that can occur in wound healing. Moreover, these keratinocytes differ from normal wound keratinocytes because they are hyperkeratotic and parakeratotic and express low levels of keratins 1, 2 and 10 [ 293031 ]. In addition, the migratory potential of the keratinocytes in abnormal healing is impaired [ 2931 ]. The molecular mechanism of this poor migratory potential of keratinocytes is related to the proteolytic degradation of growth factors and extracellular matrix proteins mandatory for the migration, as well as the reduced expression of laminin 3A32, a precursor of laminin 5 associated with keratinocyte migration [ 1231 ].

Impairment in remodeling is other important failure of wound healing.

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The cells of the injury synthesize excessive amounts of MMPs and other proteases, degrading not only extracellular matrix components, but also cell surface receptors, growth factors, and cytokines [ 3233 ]. In addition, inhibitors of metalloproteinases TIMPs are reduced, contributing to protease deregulation in these injuries [ 3233 ].

As a consequence, there is a degradation of important molecules from extracellular matrix such as collagen, elastin, fibronectin and chondroitin sulfate, impairing proliferation and migration of the cells [ 2023 ]. The human body is susceptible to numerous local and systemic conditions which can negatively affect skin repair through various mechanisms, leading to a delay in the process.

The major conditions that interfere with wound healing are discussed below Figure 2 [ 34 ]. Oxygen is required for ATP synthesis which is essential for cell metabolism and survival. When an injury occurs, there is a decrease in local oxygen supply due to the vascular disruption [ 34 ].

The hypoxic wound microenvironment is important because it provides the release of mediators that coordinate the mechanisms of angiogenesis, re-epithelialization, and synthesis of growth factors and cytokines [ 343536 ]. However, hypoxia le to the synthesis of reactive oxygen species ROS and pro-inflammatory cytokines that can impair the healing process. Furthermore, the correct oxygen concentration is necessary to prevent wound infection, improve the angiogenic response, and increase fibroblast and keratinocyte differentiation, proliferation and migration [ 35 ].

Therefore, the correct balance of oxygenation is necessary to avoid the impairment and consequent delay of wound healing. Wound healing requires numerous vitamins, minerals, fatty acids, carbohydrates, and proteins to perform the correct regenerative process [ 37 ].

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