2. Wound healing
Mechanism whereby the body attempts to
restore the integrity of injured part.
Regeneration: restoration of the
preexisting tissue architecture in the absence
of scar formation
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4. Primary, or first-intention, closure:
Wounds are sealed immediately
Done by simple suturing, skin graft placement, or
flap closure.
E.g- closure of surgical incision.
.
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5. Closure by secondary intention:
No active intent to seal the wound.
Eg: a highly contaminated wound and will close
by re-epithelialization, results in contraction of
the wound.
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6. Wound closure by tertiary intention/Delayed
primary closure
A contaminated wound is initially treated by repeated
débridement, systemic or topical antibiotics.
For several days to control infection.
Once the wound is assessed as being ready for closure, then
wound is closed
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9. Inflammatory phase
Occurs immediately and lasts for 2-3days.
Following events occurs-
Bleeding
Vasoconstriction and thrombus formation.
Sticking of platelets to the damaged endothelial
lining vessel, and release of ADP
Release of PDGF, Platelet factor iv and TGF.
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10. Contd..
Attract - polymorphonuclear (PMN) and macrophages.
Releases - histamine, serotonin & PG, they in turn increase
the vascular permeability.
Macrophages remove devitalized tissue and microorganisms.
Fibrin produced by fibrinogen provides framework for
structural support of cells .
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11. Proliferative phase
From the third day to the third week.
Characterized by the formation of granulation tissue.
Consists of a capillary bed, fibroblasts, macrophages,
and a loose arrangement of collagen, fibronectin, and
hyaluronic acid.
Angiogenesis ,Fibroplasia ,Epithelialization
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12. Angiogenesis-
Process of new blood vessel formation, necessary to
support a healing wound environment.
FGF-2 :initial angiogenic stimulus within first 3 days of
wound repair
VEGF : subsequent prolonged stimulus, day 4-7.
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13. Fibroplasia:
• Fibroblasts are specialized cells that differentiate from resting
mesenchymal cells in connective tissue.
• TGF B, PDGF, FGF-2, EGF, IGF-1
• Fibroblasts require vitamin C to produce
collagen.
• Formation of collagen type III.
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14. Epithelialization:
The epidermis serves as a physical barrier to prevent fluid
loss and bacterial invasion.
Tight cell junctions within the epithelium contribute to
its impermeability.
Basement membrane zone gives structural support and
provides attachment between the epidermis and the
dermis.
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16. Maturational phase
The remodelling phase is characterised by maturation
of collagen .
Type I replacing type III until a ratio of 4:1 is achieved.
There is a realignment of collagen , decreased wound
vascularity, and wound contraction due to fibroblast
and myofibroblast activity.
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17. Remodeling:
The fibroblast population decreases and the dense capillary
network regresses.
Wound strength increases rapidly within 1 to 6 weeks and
then appears to plateau up to 1 year after the injury.
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18. Scars
It is remains after maturation phase of wound healing.
Can be-
1. Atrophic
2. Hypertrophic
3. Keloid
An atrophic scar is pale, flat and stretched in appearance,
often appearing on the back and in areas of tension.
It is easily traumatized as the epidermis and dermis are
thinned.
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19. A hypertrophic scar is defined as excessive scar tissue
that does not extend beyond the boundary of the
original incision or wound.
Due to prolonged inflammatory phase of wound
healing and from unfavourable scar site (i.e. across the
lines of skin tension)
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20. A keloid scar is defined as excessive scar tissue that
extends beyond the boundaries of the original
incision or wound.
Keloid –more collagen III
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22. Treatment of hypertrophic and keloid scars
Pressure – local moulds or elasticated garments
Silicone gel sheeting (mechanism unknown)
Intralesional steroid injection (triamcinolone)
Excision and steroid injections.
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23. Excision and postoperative radiation (external beam or
brachytherapy)
Intralesional excision (keloids only)
Laser – to reduce redness (which may resolve in any
event)
Vitamin E or palm oil massage (unproven
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