Proliferation and Fibroplasia

This proliferative phase of wound healing starts 48-72 hours after the injury and as is characterized by fibroblast activation and infiltration, and subsequent synthesis of the extracellular matrix (ECM) and collagen. Fibroblast function is driven by platelet and macrophage-produced growth factors (most importantly TGF-p). The ECM is composed of a group of complex proteins called glycosaminoglycan (GAG) and hyaluronic acid, which with the addition of fibronectin, the primary adhesive protein of the ECM, serve as a scaffold for migrating cells and nutrient diffusion into the wound. Fibronectin also serves as a chemoattractant for macrophages as well as to assist in activating them locally.

Macrophages are also actively involved in this phase by secreting growth factors that promote angiogenesis by inducing proliferation of endothelial cells from adjacent vessels. These endothelial cells establish a new capillary network in the wound until a rising oxygen tension serves as a negative feedback to the process. Angiogen-esis begins at the periphery of the wound from capillary buds that branch off of neighboring venules and proceeds to arborize into a fine vascular network across the wound.

In a normally healing wound, by the end of the first week, few remaining PMNs and macrophages should be present in the wound. The inflammatory phase may become persistent however, due to the presence of necrotic material, foreign bodies, or bacterial colonization and delay the normal progression of healing for some time until they are removed by the host defenses or by medical/surgical care of the wound.

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