Wound healing, or wound repair, is a complex process by which the skin (or any other organ) repairs itself after injury.

In normal skin, the epithelial (outermost layer) and endoderm (inner layer) remain in a steady-state equilibrium and maintain a protective barrier against the external environment. The normal (physiological) process of wound healing begins immediately after the protective barrier is broken.

The ideal pattern of wound repair is divided into three or four successive, but overlapping, stages: (1) hemorrhage (stop bleeding) (this is not considered a stage by some authors), (2) inflammation, (3) ) production and (4) reconstruction. skin injury,

A complex biochemical event takes place in the form of a finely tuned cascade for wound repair. Within minutes after injury, clotting cells (thrombocyte) accumulate at the site of injury to form a fibrin clot.

This clot acts to stop active bleeding (hemorrhage). In the inflammatory stage, the bacteria and residues are consumed by the predator cells, and factors are released that cause the cells in the proliferative stage to migrate and divide.

In the proliferative stage, there is blood vessel formation, collagen storage, granulation tissue formation, epithelialization and wound contraction. In blood vessel formation, new blood vessels are formed by vascular endothelial cells.

In fibrogenesis and granulation tissue formation, fibroblasts proliferate and secrete collagen and fibronectin to form new, functioning extracellular matrix (ECM). Additionally, epidermal re-epithelialization occurs, in which epithelial cells proliferate and “crawl” over the wound to provide cover for new tissue.

In contraction, the wound is further reduced in size by the action of myofibroblasts, which form a grip on the ends of the wound and compress themselves using a process similar to that of smooth muscle cells. When the role of these cells is fulfilled, then spontaneous cell death of unnecessary cells occurs. In the maturation and remodeling stage, collagen regenerates and rearranges along stress lines and cells that are no longer needed are automatically removed by cell death.

However, this process is not only complicated but also brittle, and it is likely to fail or fail leading to long-term canker sores. Factors that contribute to this include diabetes, vein or artery disease, old age, and infection.