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Figure 1: Distinct and overlapping phases of wound healing

resulting in excessive healing and the formation of released by platelets after injury. Thrombin, released by
[4]
fibroproliferative scar‑like keloids and hypertrophic scars. platelets at the wound site, is an early mediator of clot
This review provides a general overview of the physiology development. Thrombin also induces the release of
[8]
of adult wound healing, focusing specifically on how pro‑inflammatory cytokines like CCL2, interleukin‑6 (IL‑6)
recent advances could translate into improved clinical and IL‑8 by endothelial cells. These cytokines induce
outcomes. monocyte chemotaxis. Of the injury response chemokines,
[9]
chemokine (C‑X‑C motif) ligand 4 (CXCL4) participates
HEMOSTASIS in the coagulation process and prevents the premature
development of blood vessels. The degradation of fibrin
[10]
Acute wounds cause vascular injury and bleeding from and subsequent activation of the complement system play
the wound, and the immediate priority is to prevent a crucial role in mounting the inflammatory process, as
blood loss by vasoconstriction and formation of a blood well as in facilitating wound angiogenesis and stromal
clot to seal the vessel. Hemostasis is initiated by the cell proliferation. Fibrin binds to integrin CD11b/CD18
exposure of blood components to the subendothelial on infiltrating monocytes and neutrophils. It also binds
layers of the vessel wall. Platelets adhere, aggregate to fibroblast growth factor‑2 (FGF‑2) and VEGF that help
and form the initial hemostatic plug. The coagulation the wound tissue vascularize. In addition, fibrin binds to
and complement cascades are then initiated. Within the insulin‑like growth factor‑1 (IGF‑1) and promotes stromal
tissue, prothrombin is activated to form thrombin, which cell proliferation. [5,11,12] Under thrombocytopenic conditions,
then cleaves fibrinogen to generate fibrin. Along with macrophages and T cells at the wound site compensate
platelets and the plasma fibronectin, fibrin forms the clot. for the lack of PDGFs and initiation of the inflammatory
The blood clot is made up primarily of cross‑linked phase. [13]
fibrin, cells such as erythrocytes and platelets, as well
as other ECM proteins such as fibronectin, vitronectin INFLAMMATION
and thrombospondin. In addition to containment
[5]
of blood loss, the blood clot serves as a first defense The inflammatory process involves the recruitment
against microbial invasion and a provisional matrix for of neutrophils, macrophages, and lymphocytes. After
the homing of inflammatory cells. The adhesiveness hemostasis, local vessels dilate secondarily to the effects
[5]
of platelets is mediated by activated integrin receptors of the coagulation and complement cascades. Bradykinin
on their surface. [6,7] The platelets in the clot undergo (generated by the coagulation cascade) and C3a and C5a
degranulation, releasing potent chemoattractants for anaphylatoxins (generated by the complement cascade)
inflammatory cells, activation factors for local fibroblasts and increase blood vessel permeability and attract neutrophils
endothelial cells and vasoconstrictors, such as chemokine and monocytes to the wound. The C3a and C5a
[14]
(C‑C motif) ligand 5 (CCL5), thrombin, transforming growth anaphylatoxins also stimulate the release of histamine and
factor‑b (TGF‑b), platelet‑derived growth factor (PDGF) leukotrienes from mast cells. The local endothelial cells
and vascular endothelial growth factor (VEGF). CCL5 then break cell‑to‑cell contact and increase permeability,
[5]
is one of the most potent monocyte chemoattractants enhancing the margination of inflammatory cells at the
Plast Aesthet Res || Vol 2 || Issue 5 || Sep 15, 2015 251