- Clinical science
Wounds are a break in the skin and/or a disruption of the skin's normal barrier function. Wound healing is a step-wise cellular response involving fibroblasts, macrophages, endothelial cells, and keratinocytes that restore the structural and functional integrity of the skin. The four general stages of wound healing are exudative, resorptive, proliferative, and maturation. While the three initial stages take place within the first two weeks, the last stage proceeds over months. Many factors affect wound healing, including the size of the wound, tension on wound edges, the presence of foreign bodies or infection, and the baseline health and nutrition of the patient. In addition, chronic health conditions such as and can slow the wound healing process. may lead to the formation of a chronic wound.
- Usually a small, straight, and clean incision
- Primary approximation of the wound edges without irregularities
- Minimal inflammation
- Minimal to no granulation tissue
- Organ-specific tissue forms at the site of healing
- Hairline scar or no scar formation
- Usually larger open wounds with irregular edges (most common type of wound)
- Irregular wound edges that cannot be perfectly approximated
- Pronounced inflammation
- Requires the formation of granulation tissue (increase the length of healing)
- Wound replaced with increased proliferation of fibroblasts
- Scar formation
Tertiary wound closure (also called delayed primary closure)
- Due to an interruption in normal wound healing
- Combination of primary closure and secondary closure: wounds should be cleaned and observed for 2–3 days before surgical closure to ensure there is no infection.
- Results in a larger scar than with primary or secondary closure
- Wounds can result from a variety of trauma (e.g., animal bites, lacerations with foreign bodies)
|Phases of wound healing |
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or chronic wound formation
- Usually occurs in patients with multiple risk factors that cause slowing or failure to progress through one or more stages of wound healing
- The proliferative wound healing phase is delayed in individuals with copper and vitamin C deficiency.
- Zinc deficiency can delay wound healing because the collagenases responsible for collagen remodeling require zinc to function properly.
- Occurs when initial injury cannot be repaired solely by cell regeneration
- Cells that cannot be regenerated (e.g., due to chronic injury or because acute injury is too severe) are replaced by connective tissue.
- After 3 months, 70–80% of tensile strength is regained. 
- Maximum strength of scar tissue is approx. 80% of that of unwounded skin. 
- Dysregulation of the wound healing process during the proliferative stage and maturation stage leads to excess fibroblast replication and collagen deposition.
- Molecular mechanisms 
- Increased production of:
- Decreased production of:
- Cutaneous condition characterized by high fibroblast proliferation and collagen production that leads to a raised scar that does not grow beyond the boundaries of the original lesion.
- See “ .”
- Skin lesions caused by high fibroblast proliferation and collagen production in excessive tissue response to typically small skin injuries
- Lesions grow beyond the original wound margins, leading to a ”claw-like” appearance.
- See “ .”
- Excessive proliferation in myofibroblasts during proliferative and maturation phases leads to contraction of the wound.
- Excessive contraction can reduce the functionality of the injured limbs or organs.
- Wounds that cross a joint (e.g., on the hands and fingers) are at high risk for causing functional deficits from contracture. Periodic exercise of the involved limb can help preserve normal function.