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Hemostasis in Wound Healing ClotFoam formulations: From the prevention of hemorrhage to faster and better wound healing and collagen formation |
The first process that takes place as a reaction to a wound is the prevention of local hemorrhage. Endothelial injury activates blood platelets and thus initiates the formation of a platelet plug that will stop bleeding. Simultaneously, the coagulation cascade is initiated and results in the conversion of soluble fibrinogen to a network of insoluble fibrin fibers. The resulting blood clot contributes to arrest the bleeding and then functions as a provisional matrix for the wound healing that begins hours after injury. The fibrin matrix not only reduces blood loss, but also is the most important temporary ECM in the wound area and, as such, plays an important role in tissue repair, leukocyte cell adhesion, and EC migration during angiogenesis. When platelets are activated, they secrete a number of growth factors, that stimulate the process of wound healing by the activation of fibroblasts to produce collagen, glycosaminoglycans, and proteoglycans. Leukocytes, fibroblasts, and blood vessels move into the wound space and each contributes to the wound healing process. New capillaries endow the neostroma with its granular appearance. The macrophages provide a continuing source of cytokines, which are necessary to stimulate fibroplasia and angiogenesis, a process in which new blood vessels are formed from pre-existing ones. Fibrinogen is assembled into the ECM at the sites of tissue damage, where it may contribute to cell type-specific mechanisms of wound repair. The newly formed temporary fibrin matrix also promotes granulation and tissue formation. Once fibroblasts and ECs express the proper integrin receptors, they invade the fibrin/fibronectin rich clot in the wound space, and start synthesizing a permanent ECM. ClotFoam wound healing techniques are at the forefront of current science.
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