Wound healing is a dynamic, multi phase biological process that restores tissue integrity after injury. It begins with hemostasis, where blood vessels constrict and platelets form a clot that stops bleeding and provides a provisional matrix. This is followed by inflammation, during which neutrophils and macrophages clear debris and pathogens while releasing cytokines and growth factors that orchestrate later repair.

The proliferative phase features the central processes of tissue rebuilding. Fibroblasts migrate into the wound and produce collagen and extracellular matrix, while endothelial cells form new blood vessels through angiogenesis. Keratinocytes at the wound edge proliferate and migrate to re establish the epidermal barrier. Granulation tissue, rich in cells, matrix and capillaries, fills the wound space.

Remodeling, the final phase, can persist for months. Collagen III laid down early is gradually replaced by stronger collagen I, fibers are realigned along tension lines and overall cellularity decreases. The resulting scar has less elasticity and different structure than uninjured skin.

Many factors modulate healing efficiency. Age, diabetes, vascular disease and malnutrition impair repair, as do infection, persistent inflammation and mechanical stress. At the molecular level, signaling pathways involving growth factors such as TGF beta, VEGF and PDGF, and immune mediators such as interleukins, tightly regulate cellular behavior.

Current research focuses on therapies that can improve or accelerate healing, especially in chronic wounds. These include advanced dressings that control moisture and infection, bioengineered skin substitutes, growth factor and stem cell based treatments and strategies to modulate immune responses and fibrosis, aiming to reduce scarring and restore more normal tissue function.