St.Johns University Physician Assistant Program: Wound Healing
Summary
-wounds: break in skin/disruption of skin’s normal barrier function
-wound healing: step-wise cellular response involving fibroblasts, macrophages,
endothelial cells, keratinocytes
4 stages: exudative, resorptive, proliferative, maturation
-3 initial stages occur within first two weeks
-last stage proceeds over months
-factors involving healing
1 size of wound
2 tension wound edges
3 +/- foreign bodies or infection
4 baseline health/nutrition
5 chronic health conditions: DM, PVD
Phases of wound healing [1]
Phase Timing Cells involved Characteristics Involved tissue mediators
Exudati Day 1 Platelets ● Hemostasis: platelet ● PDGF
ve Neutrophils aggregation → clot formation ● FGF
Hemos
Macrophages (exposed ● EGF
tasis
subendolitheum→collagen and ● Prostaglandins
tissue factor→plt aggregation) ● TXA2
● Scab formation
● Immediate local
vasoconstriction (lasts 5–10
minutes) due to the release of
prostaglandins, kinins,
leukotrienes, and thromboxane
A2 (TXA2) from ruptured cell
membranes and platelets
● Followed by vasodilation and
increased vessel permeability
● Wound pain may occur. (from
tissue swelling, hypoxia,
, St.Johns University Physician Assistant Program: Wound Healing
alteration in pH from tissue
destruction or infection)
Resorp Days ● Chemotaxis (via PAF, PDGF, and ● PAF
tive 1–3 TGF-β) of inflammatory cells (i.e., ● PDGF
Inflam
neutrophils, macrophages, ● TGF-β
mation
lymphocytes) to the site of
injury
○ Macrophages
release growth
factors and
cytokines that
recruit other
immune cells,
stimulate fibroblast
proliferation
(fibrosis) and resorb
debris.
○ Lymphocytes
migrate to injury
approx. 72 hours
after the injury to
promote cellular
immunity.
● Continued vasodilation
● EGF induces tyrosine kinases
such as EGFR → epithelium at
wound margins begins to
proliferate
Summary
-wounds: break in skin/disruption of skin’s normal barrier function
-wound healing: step-wise cellular response involving fibroblasts, macrophages,
endothelial cells, keratinocytes
4 stages: exudative, resorptive, proliferative, maturation
-3 initial stages occur within first two weeks
-last stage proceeds over months
-factors involving healing
1 size of wound
2 tension wound edges
3 +/- foreign bodies or infection
4 baseline health/nutrition
5 chronic health conditions: DM, PVD
Phases of wound healing [1]
Phase Timing Cells involved Characteristics Involved tissue mediators
Exudati Day 1 Platelets ● Hemostasis: platelet ● PDGF
ve Neutrophils aggregation → clot formation ● FGF
Hemos
Macrophages (exposed ● EGF
tasis
subendolitheum→collagen and ● Prostaglandins
tissue factor→plt aggregation) ● TXA2
● Scab formation
● Immediate local
vasoconstriction (lasts 5–10
minutes) due to the release of
prostaglandins, kinins,
leukotrienes, and thromboxane
A2 (TXA2) from ruptured cell
membranes and platelets
● Followed by vasodilation and
increased vessel permeability
● Wound pain may occur. (from
tissue swelling, hypoxia,
, St.Johns University Physician Assistant Program: Wound Healing
alteration in pH from tissue
destruction or infection)
Resorp Days ● Chemotaxis (via PAF, PDGF, and ● PAF
tive 1–3 TGF-β) of inflammatory cells (i.e., ● PDGF
Inflam
neutrophils, macrophages, ● TGF-β
mation
lymphocytes) to the site of
injury
○ Macrophages
release growth
factors and
cytokines that
recruit other
immune cells,
stimulate fibroblast
proliferation
(fibrosis) and resorb
debris.
○ Lymphocytes
migrate to injury
approx. 72 hours
after the injury to
promote cellular
immunity.
● Continued vasodilation
● EGF induces tyrosine kinases
such as EGFR → epithelium at
wound margins begins to
proliferate
