Cell Biology of Wound Healing

Abstract

Publisher Summary Cutaneous wound repair is a seamless series of events that are initiated whenever tissue integrity is breached. Although extreme diversity exists in the various types of wounds and in their depths of injury, wound repair consists of a predictable set of responses involving migration, proliferation, differentiation, and apoptosis of cell types within the wound environment. This chapter focuses on the roles of these individual cell types throughout the reparative process. Following injury, a series of dynamic interactive processes take place that usually culminates in a mature, healed wound. To study wound repair, wound healing is subdivided into four phases: acute inflammation, epithelialization, granulation tissue formation, and tissue remodeling. These processes follow a specific temporal sequence unless encumbered by various pathologic states such as diabetes, poor arterial perfusion, malnutrition, or sepsis. Following cutaneous injury, the body first acts to stop hemorrhage from blood vessel injury by the action of platelets and by initiation of the clotting cascade. Shortly thereafter, inflammatory cells responding to platelet-released growth and chemotactic factors arrive and predominate in the wound bed. In ideal wounds, monocytes and fixed tissue macrophages reach maximal populations in the next 48 hr. The later phases of inflammation overlap with a period of proliferation that is characterized by migration of fibroblasts and endothelial cells. Epithelialization is the major mechanism of repair in partial loss of skin thickness, whether from accidental abrasions, thermal or chemical injuries, or surgically planned skin graft harvest. The process of resurfacing is of minor consequence in wounds coapted with sutures and is short lived.