Components:

• Angiogenesis

• Fibroblast proliferation
• Epithelial cell proliferation

Angiogenesis: The wound surface or edge is relatively ischemic and healing cannot effectively proceed until sufficient blood flow is restored to allow delivery of nutrients.  Macrophages secrete a substance known as angiogenesis factor, which is felt to be a chemo-attractant for mesothelial and vascular endothelial cells.  The remarkable process of neo-vascularization or angiogenesis begins in the first several days although the process is delayed if a thick layer of surface necrosis is present.  Endothelial cells proliferate and form capillary buds at the wound surface.  The buds form a network of loops which fuse with other buds forming a new capillary bed.  If the wound edges are approximated, the capillaries can bridge the wound.

Impairment: Excess Inflammation

• Surface dead tissue
• Wound exudates
• Decreased perfusion
• Corticosteriods

Fibroblast Proliferation: The fibroblast begins to appear in the wound about 2 days after injury.  The initial cells on the scene appear to migrate from nearby connective tissue.  The stimulus for subsequent fibroblast proliferation as well as subsequent collagen synthesis appears to be growth factors from platelets and macrophages.  The fibroblasts migrate into the wound along local fibrin strands from the initial wound coagulation as well as any remaining collagen strands.  The fibroblasts, being metabolically active, depend on the adequacy of local O₂ supply and the adequacy of neo-vascularization for continued proliferation.

Impairment:

• Decreased perfusion
• Inadequate nutrients
• Decreased anabolic activity
• Corticosteriods

Epithelialization: The epidermal lining of skin is in a continual state of proliferation and desquamation as opposed to the more dormant mesenchymal tissues.  With loss of the epidermis, adjacent cells become reprogrammed.  They appear detached from their basement membrane, divide, and migrate toward and across the wound, first forming a single cell layer.  Various epidermal growth factors released from the macrophage and platelet, initiate the response.  This process, however, is quite limited and any dead tissue on the surface will retard epithelialization.  Also the cell distance traveled is limited to about 3 cm from the wound edge.  The re-epithelialization process can be rapid, i.e., 3 to 5 days in a superficial injury or several months, depending on the size of the defect, the nutrient supply, the number of remaining basal cells, and the wound environment   Once a single layer develops, additional layers form from mitotic division.

Impairment:

• Desiccation
• Destruction by excessive proteases
• Excess inflammation
• Impaired perfusion
• Lack of adequate nutrients
• Corticosteriods

Epithelial cells are proliferating and migrating towards each other close to the partial thickness wound.