The Wound Healing Process

1. Wound healing process

Wound healing, a physiological response to the disruption in tissue integrity, is a dynamic and complex process imperative for maintaining homeostasis. It consists of four partially overlapping phases, which are the inflammatory, migratory, proliferative and maturation phase. Notably, this process is non-linear wherein it can advance and retract through the phases depending on various factors within the patients.

1.1 Inflammatory phase

Inflammatory phase can be further divided into hemostasis and inflammation, which is triggered immediately and continue for about two to five days succeeding injury.

1.1.1 Hemostasis

Hemostasis, the process of stopping bleeding after an injury, involves three key processes, namely

Specifically, inflammation begins when the inflammatory cells reach the wound and generally persists for several days. Upon injury, the resident mast cells undergo degranulation and secrete chemotactic agents that induce neutrophils recruitment. Furthermore, activated platelets also release proteins that stimulate the migration and adhesion of neutrophils and monocytes. Thus, the first inflammatory cells that infiltrate the wound are the neutrophils. These neutrophils, upon infiltration, first attach to the endothelium followed by undergoing diapedesis and migrate towards the area of inflammation. Subsequently, neutrophils release cytokines, growth factors and proteases to amplify inflammation reactions, promote cell proliferation and degrade extracellular matrix as well as debris respectively. Second inflammatory cells that enter the injured tissues are the mature macrophages differentiated from the circulating monocytes. Among other functions, activated macrophages phagocytosed microbes, foreign materials, apoptotic neutrophils and dying tissues from the wound in preparation for repair. They also synthesize a multitude of pro-inflammatory mediators and cytokines to trigger and sustain inflammatory responses. Eventually, during the late-inflammatory phase, T-lymphocytes

Within the first three days of wound repair, basic FGF from macrophages initiate angiogenesis and the subsequent injury–induced hypoxia stimulates the production of VEGF by epidermal cells. VEGF sustains the angiogenesis stimulus for the next four days. Next, both plasmin and collagenase works synergistically to digest basement membranes so as to allow the endothelial cells to migrate and form new blood vessels at the injured site. Once the wound is filled with new granulation tissues, angiogenesis ceases and many of the new blood vessels undergo apoptosis. On a similar note, there is continued growth of damage blood