Wound healing is a dynamic, multifaceted, well-orchestrated, and highly efficient process that should proceed linearly to restore tissue homeostasis in response to injury. Wound repair proceeds through the coordinated integration of biological and molecular events in the extracellular wound micro-environment during four overlapping phases of hemostasis, inflammation, proliferation and tissue remodeling. It includes the migration, adhesion, proliferation, and differentiation of various cell types, i.e., keratinocytes, fibroblasts, macrophages, mesenchymal stem cells, and endothelial cells, and their interaction with different cytokines, growth factors, and extracellular matrix (ECM) molecules. A cascade of healing events begins with the formation of a fibrin clot, which provides protection to the underlying tissues and serves as a provisional matrix through which cells can migrate and acts as a reservoir for growth factors. During inflammation, aggregated platelets release pro-inflammatory cytokines to recruit neutrophils and macrophages at the wound site. These inflammatory cells phagocytose debris and invading micro-organisms, and they also secrete mediators to stimulate the chemotaxis of cell types necessary for the proliferative phase. In the proliferative phase, fibroblasts, keratinocytes, and endothelial and smooth muscle cells migrate through the wound bed and proliferate, leading to re-epithelialization of the denuded surface. They also synthesize and deposit a provisional ECM, form new blood vessels (angiogenesis), and lead to contraction of the wound size. During the final stage, the newly formed granulation tissue is remodeled by the activity of matrix metalloproteinases (MMPs), which are balanced by the action of “tissue inhibitors of metalloproteinases” (TIMPs).