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WOUND HEALING
1
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
2
Wound closure types:
Primary repair
Secondary repair
Tertiary repair
3
 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.
.
4
 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.
5
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
6
7
Wound healing phases:
Inflammation
Proliferation
Maturation
8
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.
9
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 .
10
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
11
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.
12
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.
13
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.
14
Fig-Wound matrix deposition over time, Fibronectin and type III collagen constitute
the early matrix.
15
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.
16
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.
17
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.
18
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)
19
A keloid scar is defined as excessive scar tissue that
extends beyond the boundaries of the original
incision or wound.
Keloid –more collagen III
20
21
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.
22
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
23
References-
 Bailey and Love short practice of surgery.
 Pubmed.nih.gov
 Google images
24
Thankyou
25

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wound healing.pptx

  • 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 2
  • 3. Wound closure types: Primary repair Secondary repair Tertiary repair 3
  • 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. . 4
  • 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. 5
  • 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 6
  • 7. 7
  • 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. 9
  • 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 . 10
  • 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 11
  • 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. 12
  • 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. 13
  • 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. 14
  • 15. Fig-Wound matrix deposition over time, Fibronectin and type III collagen constitute the early matrix. 15
  • 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. 16
  • 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. 17
  • 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. 18
  • 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) 19
  • 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 20
  • 21. 21
  • 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. 22
  • 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 23
  • 24. References-  Bailey and Love short practice of surgery.  Pubmed.nih.gov  Google images 24