Phases of Wound Healing

Hemostasis occurs right after initial injury. At the time of injury, epinephrine, a chemical that constricts peripheral blood vessels, is released in an attempt to minimize bleeding into the soft tissues. The key cell responsible for this function is the platelet, which causes the body to form a clot to prevent further bleeding. There is an increased aggregation of platelets to enable the wounded vessel to complete the clotting process. Platelets also release key cytokines, such as platelet-derived growth factor, that call in cells to participate in later phases of healing.

The objective of the hemostasis phase of wound healing is to control bleeding. In hemostasis, the inflammatory phase begins. The local signs and symptoms that occur during the inflammatory phase are swelling, fission of blood, red histamine, heat, histamine response, and pain. The inflammatory phase is characterized by a host of cells, leukocytes and macrophages, infiltrating the wound sites. Bleeding is controlled by hemostasis. Any bacteria that is present is destroyed by leukocyte-destroyed bacteria, cleansing the wound of cellular debris. Macrophages replace the leukocytes and produce a host of cytokines and growth factors

and tractants to other cells needed for tissue repair. Macrophages also convert macromolecules into the amino acids and sugars necessary for wound healing. It is thought that the macrophage also attracts contractual cells to the wound to encourage wound contraction. Vasodilation, with resultant edema, warmth, and ruber, are the result of factors secreted from the macrophage and other in response to the inflammatory process. The objectives of the inflammatory phase of wound healing are to clean debris and bacteria, and prevent infection. Scar tissue formation is characterized by three distinct phases.

Granulation, contraction, epithelialization. Click on one of the phases to learn more. She was generated, producing red fibroblasts. It gives tissue its tensile granulation tissue, its margins contract or pull together, decreasing the size of the wound, tissue, realization, divide, and tissue. Epithelial cells will not migrate across a dry surface or necrotic tissue. Curation phase, the collagen fibers reorganize, remodel, and mature, gaining tensile strength. Collagen fibers, proteoblacens, and fibromectin, distributed. The scar becomes less cellular and gains tensile strength. This tissue will always be at risk for breakdown, because its tensile strength is less than that of fibroblasts,

with collagen fibers is a complicated process, key growth factors in the development of procollagen. Procollagen fibers mature into collagen fiber, connected within a single collagen fiber. Research is currently underway to determine the chemical details associated with collagen synthesis.