Basic science of wound healing

Abstract

Acute wound healing involves a complex series of events including chemotaxis, cell division, neovascularization, synthesis of new extracellular matrix, and the formation and remodelling of the scar tissue. These events are regulated by several mediators including platelets, inflammatory cells, cytokines and growth factors, and matrix metalloproteinases and their inhibitors. In acute wounds, these processes (which are triggered by tissue injury) involve the four overlapping (but well-defined) phases of haemostasis, inflammation, proliferation, and remodelling; an avascular scar is the final stage of the wound healing process. In contrast to this, some wounds fail to heal in a timely and orderly manner, resulting in chronic non-healing wounds. Alterations in one or more of these components could account for the impaired healing observed in chronic wounds because cytokines, growth factors, proteases, and cellular and extracellular elements all play important roles in different stages of the healing process. Also, dysregulation in certain stages of the healing process could result in excessive deposition of collagen and formation of abnormal scar, as seen in hypertrophic scars and keloids. In this review, the cellular and molecular events involved in acute wound healing and the mechanisms resulting in abnormal healing are discussed; the various types of wound healing are also discussed.