Inflammation, proliferation, and remodelling have historically been considered the three different stages of wound healing. Numerous well planned interactions and reactions between cells and substances are put into play during each phase. For each phase, there is substantial overlap, and the boundaries between them are hazy. The reader will first receive a general overview of the wound healing process in this article, which will be followed by a more in-depth examination of the cells and inflammatory mediators involved in wound healing. The start of the healing process and its base are provided by haemostasis. Vasodilation and higher vascular permeability are brought on by inflammation. But controlling bleeding is the first thing the body does after being wounded. Vasoconstriction occurs in the damaged blood artery, and the endothelium and surrounding platelets activate the intrinsic component. Cellular cues that cause a neutrophil response are produced as soon as the clot forms. Neutrophils are attracted to the injured area by interleukin, tumour necrosis factor, transforming growth factor, PF4, and bacterial "products" as the inflammatory mediators build up, prostaglandins are elaborated, and the nearby blood vessels vasodilate to facilitate the increased cellular traffic. Around 48 to 96 hours after damage, monocytes in the adjacent tissue and blood are drawn to the region and undergo a transformation into macrophages. It's crucial to get the inflammatory cells going, especially the macrophage. In order to enter the proliferative phase, a macrophage must be stimulated. Vascular endothelial growth factor, fibroblast growth factor, and other factors will be synthesised by an activated macrophage to drive a giogenesis.