INTRODUCTION

Acute wounds normally heal in an orderly and efficient manner, and progress smoothly through the four distinct, but overlapping phases of wound healing: haemostasis, inflammation, proliferation and remodelling (Figure 23.1). In contrast, chronic wounds will similarly begin the healing process, but will have prolonged inflammatory, proliferative, or remodelling phases, resulting in tissue fibrosis and in non-healing ulcers. The process of wound healing is complex and involves a variety of specialized cells, such as platelets, macrophages, fibroblasts, epithelial and endothelial cells. These cells interact with each other and with the extracellular matrix. In addition to the various cellular interactions, healing is also influenced by the action of proteins and glycoproteins, such as cytokines, chemokines, growth factors, inhibitors, and their receptors. Each stage of wound healing has certain milestones that must occur in order for normal healing to progress. In order to identify the differences inherent in chronic wounds that prevent healing, it is important to review the process of healing in normal wounds

PHASES OF ACUTE WOUND HEALING

Haemostasis

Haemostasis occurs immediately following an injury. To prevent exsanguination, vasoconstriction occurs and platelets undergo activation, adhesion and aggregation at the site of injury. Platelets become activated when exposed to extravascular collagen (such as type I collagen), which they detect via specific integrin receptors, cell surface receptors that mediate a cell's interactions with the extracellular matrix. Once in contact with collagen, platelets release the soluble mediators (growth factors and cyclic AMP) and adhesive glycoproteins, which signal them to become sticky and aggregate.