Skin Wound Healing Process and New Emerging Technologies for Skin Wound Care and Regeneration



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pharmaceutics-12-00735
Figure 1. Schematic representation of wound healing process with cells involved in each phase. 
The regeneration process involves sequential phases regulated by gene expression, via 
autocrine or paracrine mechanisms. The ending of active processes is achieved by gene silencing 
during the progression of the regeneration process [11]. Wound healing is one of most complex 
process in the human body, since it involves the spatial and temporal synchronization of the 
inflammatory phase with tissue regeneration and remodeling. The inflammatory phase follows the 
injurious event and it includes the coagulation cascade, inflammatory pathway and immune system 
involvement [12]. All these events take place to prevent an excessive loss of blood, fluids and the 
development of infections, and to facilitate the removal of dead or devitalized tissue. Hemostasis is 
achieved by platelet clot generation, followed by fibrin matrix formation, which acts as a scaffold for 
cell infiltration. As a result of platelet degranulation, the release of chemotactic signals by necrotic 
tissues, and of bacterial degradation products, the complementary system is activated and 
neutrophils arrive at the lesion [13]. Finally, macrophages coordinate all events evolved in response 
to damage. These cells are responsible for fibrin phagocytosis activity and cellular debris, and they 
secrete macrophage-derived growth factor (MDGF) for fibroblasts and endothelial cells [14]. New 
tissue formation begins within two to ten days after the lesion and consists of cell proliferation and 
the migration of different cytotypes. When the lesion involves the dermis, a poorly differentiated 
and highly vascularized connective tissue called granulation tissue is formed, which consists of 
cellular and fibrillar components integrated in an apparently amorphous matrix. The cells of 
granulation tissue are (i) fibroblasts, responsible for the synthesis of the fibrillar component; (ii) 
myofibroblasts, involved in the wound contraction mechanism and (iii) endothelial cells, responsible 
for the neo-angiogenesis process [15]. 
The re-epithelization process, characterized by the proliferation and migration of keratinocytes 
towards the core part of the lesion, originates in this phase as the area between the bottom and the 
edges of the wound is filled with granulation tissue. This represents the matrix in which 
keratinocytes, residing on lesion edges, migrate and proliferate [14]. Skin re-epithelization structural 
organization can be explained by two models: sliding and rolling models. According to the sliding 
model, keratinocytes of the basal layer suffer a modification of their anchoring joints (desmosomes 

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