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Wound healing

Last updated: February 11, 2021

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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 diabetes and peripheral vascular disease can slow the wound healing process. Delayed wound healing may lead to the formation of a chronic wound.

Phases of wound healing [1]
Phase Timing Cells involved Characteristics Involved tissue mediators

Exudative

  • Day 1

Resorptive

  • Days 1–3

Proliferative

  • Days 3–7
Maturation
  • Weeks to 1 year

Risk factors for delayed wound healing: DID NOT HEAL

Delayed wound healing or chronic wound formation

Scar formation

  • 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. [3]
  • Maximum strength of scar tissue is approx. 80% of that of unwounded skin. [3]

Excessive scar

Hypertrophic scar

Keloid

Contracture

  • 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.
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  2. Zhu Z, Ding J, Tredget EE. The molecular basis of hypertrophic scars.. Burns & trauma. 2016; 4 : p.2. doi: 10.1186/s41038-015-0026-4 . | Open in Read by QxMD
  3. Leivonen SK, Lazaridis K, Decock J, Chantry A, Edwards DR, Kähäri VM. TGF-β-elicited induction of tissue inhibitor of metalloproteinases (TIMP)-3 expression in fibroblasts involves complex interplay between Smad3, p38α, and ERK1/2.. PloS one. 2013; 8 (2): p.e57474. doi: 10.1371/journal.pone.0057474 . | Open in Read by QxMD
  4. Shah M, Foreman DM, Ferguson MW. Neutralisation of TGF-beta 1 and TGF-beta 2 or exogenous addition of TGF-beta 3 to cutaneous rat wounds reduces scarring.. J Cell Sci. 1995; 108 ( Pt 3) : p.985-1002.
  5. Schultz GS, Chin GA, Moldawer L, Diegelmann RF, Fitridge R, Thompson M. Principles of Wound Healing. StatPearls. 2011 .
  6. Köse O, Waseem A. Keloids and hypertrophic scars: are they two different sides of the same coin?. Dermatol Surg. 2008; 34 (3): p.336-46. doi: 10.1111/j.1524-4725.2007.34067.x . | Open in Read by QxMD
  7. Verhaegen PD, van Zuijlen PP, Pennings NM, et al. Differences in collagen architecture between keloid, hypertrophic scar, normotrophic scar, and normal skin: An objective histopathological analysis.. Wound Repair Regen. undefined; 17 (5): p.649-56. doi: 10.1111/j.1524-475X.2009.00533.x . | Open in Read by QxMD
  8. Stadelmann WK, Digenis AG, Tobin GR. Physiology and healing dynamics of chronic cutaneous wounds. Am J Surg. 1998; 176 (2A Suppl): p.26S-38S.
  9. Guo S, DiPietro LA. Factors Affecting Wound Healing. J Dent Res. 2010; 89 (3): p.219-229. doi: 10.1177/0022034509359125 . | Open in Read by QxMD