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Wound Healing

Ferry Senjaya
Wound healing is the response to acute or chronic injury, a
process by which a damaged tissue is restored, as closely
as possible, to its normal state

1. Inflammatory
2. Proliferative
3. Remodelling

 Begin at the time of injury ; lasts 2-3 days
 Begin with vasoconstriction
 Platelet plug forms & clotting cascade activated →
fibrin deposition
 Platelets release PDGF & TGF-β, attracting
inflammatory cells
 After hemostasis achieved, vasodilation occurs &
vascular permeability increases, aiding infiltration of
inflammatory cells into the wound
 Neutrophils peak at 24 hours → debridement
 Monocytes → macrophages (peak within 2-3 days)
 Macrophages produce PDGF & TGF-β, attracting
fibroblast → collagen production
 Begin around day 3, as fibroblast arrive ; lasts through
week 3
 Fibroblast : attracted & activated by PDGF & TGF-β
 Collagen synthesis (mainly type III), angiogenesis, &
epithelialization occur
 Total collagen content increases for 3 weeks, until
collagen production & breaksown become equal →
remodelling phase begins
 Increased collagen production & breakdown continue for
6 months to 1 year
 Type I collagen replaces type III until it reaches 4:1 ratio
of type I to type III
 Wound strength increases as collagen reorganizes along
lines of tension & is cross-linked
 Vascularity decreases
 Fibroblast & myofibroblasts cause wound contraction
 Wounds have little strength during the first 2-3 weeks
(inflammatory & proliferative phase)
 By the third week, the wound begin to gain strength
rapidly as remodelling occurs
 Wound have 50% of their final strength at 6 weeks, &
most of their final strength a few weeks later
 Strength may continue to slowly increase until 6 to 12
months fron the time of injury
 Max strength is about 75% of normal tissue
 In addition to production of connective tissue & wound
contraction, epithelialization occurs
 A single layer of cells advances from the wound edges (&
adnexal structures in partial thickness wounds), then
 If epithelialization is prolonged as in healing by
secondary intention or in the deep partial-thickness
wound or burn, the inflammatory phase lasts longer,
resulting in increased collagen production & contraction
 The fracture site undergoes inflammatory phase
 Osteoinduction : precursor cells in the endosteum,
periosteum, & surrounding tissue become osteoblasts
 Osteoconduction : osteoblasts enter the fracture site
 A callus then forms, containing fibroblasts, osteoblasts,
& other cells
 Chondroblasts produce ground substance, fibroblasts
produce collagen, osteoblasts produce hydroxyapatite
 Both apposition of bone & endochondral ossification
 At first the callus consists of poorly organized woven
bone, which is remodeled by osteoclasts & osteoblasts into
lamellar bone
 The more rigidly fixed & well reduced the fracture is, the
less prominent the callus formation & endochondral
ossification are ; healing mainly occur by apposition
 Once remodeling is finished, the healed bone structure is
the same as normal bone, with no remaining scar
 Tendon heals by combination of 2 mechanisms : intrinsic
& extrinsic healing
 Intrinsic healing :
 The inflammatory phase is minimal
 Epitenon cells move to the site of injury, producing
collagen, acting like fibroblasts
 Intrinsic healing is increased by tendon motion
 Extrinsic healing :
 Inflammatory, proliferative, & remodelling phases occur
 After hemostasis, inflammatory cells infiltrate the wound
 Fibroblasts are attracted & produce collage, which is
eventually remodelled
 Adhesions forms between the site of injury & surrounding
tissues, & acts as pathway for cell migration &
 Adhesions, & therefore extrinsic healing, are increased by

 Axons distal to the injury are phagocytized by
macrophages & Schwann cells (Wallerian degeneration)
 The proximal axons each produce one or more myelinated
regenerating fibers with growth cones at the distal end of
each fiber (regenerating units)
 The regenerating units grows distally, directed by
chemical factors
 The liver is the only adult organ that undergoes
 All hepatic cells, are involved in recreating normal
heopatic histology without scar formation
 Scarring (cirrhosis) occurs with chronic or severe damage
 Primary union / healing by first intention
 Secondary union / healing by second intention

1. Primary closure
2. Delayed primary closure
3. Secondary closure
 Wound closed surgically soon after creation
 Wound remains open for afew day before surgical closure
 Decrease the risk of infection in contaminated wounds
 Wound closes over time by contraction
 Appropriate for infected or contaminated wounds
 Allows drainage of fluid
 Allows debridement with dressing changes
 Prolonged inflamatory phase, leading to increased
scarring & wound contracture