The effect of Wound healing

Wound healing is a complex cascade of events on a cellular level which comprises four stages: hemostasis, inflammation, proliferation, and remodeling. Hemostasis is dominated by platelets, which release two main factors: platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-β). Inflammatory cells such as neutrophils, mast cells, macrophages, and T lymphocytes clean the wound from injured and contaminated tissue in the inflammatory phase. Characteristic features of the proliferation phase epithelialization, fibroplasia, and angiogenesis. Epithelialization is stimulated by epidermal growth factor (EGF) and TGF-α, which are produced by macrophages. Angiogenesis is initiated by vascular endothelial cell growth factor (VEGF), basic fibroblast growth factor (bFGF), and TGF-β. During remodeling, matrix proteins such as collagen, proteoglycans, and fibronectin are produced and form tight connections to increase the strength of the scar.

Mechanism of wound healing. Wound healing is a complex cascade characterized by four overlapping phases: bleeding and hemostasis, inflammation, proliferation, and remodeling. At the time of injury, the tissue is disrupted, and the platelets stick together to seal damage to the blood vessel. After this, fibrin strands begin to adhere. Following hemostasis, the neutrophils enter the wound site and begin removing foreign materials, bacteria, and damaged tissue. The inflammatory phase continues with highly phagocytic macrophages that are responsible for removing nonfunctional host cells, bacterium-filled neutrophils, damaged matrix, foreign debris, and any remaining bacteria. Once the wound site is cleaned out, the migrated fibroblasts begin the proliferation phase. The objective of the proliferation phase is for the wound to be “rebuilt” with new granulation tissue, which is comprised of collagen and extracellular matrix and into which a new network of blood vessels develops, a process known as angiogenesis. Epithelial cells finally resurface the wound, a process known as epithelization. During the final remodeling phase, the collagen forms well-organized stable cross-links.

Dysregulation of this complex mechanism will result in fibrosis and chronic ulceration and is associated with increased morbidity and mortality. According to the literature, the function of many factors involved in wound healing is dependent on and modulated by copper ions, and thus, copper is involved in all four stages of wound healing. It is hypothesized that delayed wound healing could partially be explained by depleted copper levels, which in turn reinforces a role for this element as an essential micro-trace nutrient required from diet.

（To be continued）

Copy from cmr.asm.org

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