Wound healing refers to a living organism's replacement of destroyed or damaged tissue by newly produced tissue. In undamaged skin, the epidermis and dermis form a protective barrier against the external environment

1. WOUND HEALING

2. Today’s talk
• Types, etiopathogenesis
• Mechanism of healing – Primary and
secondary intention
• Factors affecting Healings – Promoting &
Delaying

5. Definitions:
• Regeneration: refers to growth of cells and
tissues to replace lost structures
• Healing is usually a tissue response
– to a wound (commonly in the skin),
– to inflammatory processes in internal organs,
or
– to cell necrosis in organs incapable of
regeneration.

6. Healing
Regeneration scar formation

7. • When healing can not be
accomplished by regeneration,
the main healing process is
repair by deposition of collagen
and other ECM components,
causing the formation of a scar.

8. wound healing
• inflammation
• angiogenesis
• migration and proliferation of fibroblasts
• scar formation
• connective tissue remodeling

9. Wound healing
complex but orderly phenomenon involving a number of
processes:
1) Induction of an inflammatory process in response to
the initial injury
2) Proliferation and migration of parenchymal and
connective tissue cells
3) Formation of new blood vessels (angiogenesis) and
granulation tissue
4) Synthesis of ECM proteins and collagen deposition
5) Tissue remodelling
6) Wound contraction
7) Acquisition of wound strength

10. Cutaneous wound healing is generally divided
into three phases:
(1)inflammation (early and late);
(2)granulation tissue formation and re-
epithelialization; and
(3)wound contraction, ECM deposition, and
remodelling

11. Phases of cutaneous wound healing

12. Types of wound healing
1. Primary intention
2. Secondary intention

13. WOUND HEALING BY PRIMARY
INTENTION
• The healing of a clean, uninfected surgical
incision approximated by surgical sutures
• Such healing is referred to as primary
union or healing by first intention

14. Healing process follows a series of
sequential steps:
Within 24 hours:
– neutrophils appear at the margins of the
incision, moving towards the fibrin clot.

15. In 24 to 48 hours:
• epithelial cells move from the wound edges
(with little cell proliferation) along the cut
margins of the dermis
• Deposition of basement membrane components
as they move

16. By day 3:
• neutrophils replaced by macrophages
• Granulation tissue progressively invades the
incision space.
• Collagen fibers are now present in the margins of
the incision, but at first these are vertically
oriented and do not bridge the incision.
• Epithelial cell proliferation thickens the epidermal
layer

17. By day 5:
• the incisional space is filled with granulation
tissue.
• Neovascularization is maximal.
• Collagen fibrils  more abundant and begin to
bridge the incision.
• differentiation of surface cells yields a mature
epidermal architecture with surface
keratinization.

18. During the second week:
collagen +++
proliferation of fibroblasts ++
leukocytic infiltrate, edema, and vascularity
largely disappear
the long process of blanching begins,
accomplished by the increased accumulation of
collagen within the incisional scar

19. By the end of the first month:
• Scar is made up of a cellular connective tissue
devoid of inflammatory infiltrate, covered now
by intact epidermis.
• The dermal appendages  permanently lost.
• Tensile strength of the wound increases

21. WOUND HEALING BY SECONDARY
INTENTION
• referred to as secondary union or healing by
second intention
• Occurs when there is
– more extensive loss of cells and tissue
– large defects in surface wounds
• The reparative process is more complicated
• Abundant granulation tissue grows in from the
margin to complete the repair.

22. Healing by 20 intention differs from
10intention by the following points:
1. Large tissue defects  a larger fibrin clot that
fills the defect more necrotic debris and
exudates that must be removed. Inflammatory
reaction is more intense.
2. Much larger amounts of granulation tissue are
formed.

23. 3. wound contraction
– size of the wound markedly reduced from its
original size
– Done by MYOFIBROBLAST – are altered
fibroblast having ultrastructural features of
smooth muscle cells , so they can contract
4. Scar formation and thinning of the epidermis.

25. HEALING OF SKIN ULCER

26. Granulation tissue showing numerous blood vessels, edema,
and a loose ECM containing occasional inflammatory cells

27. WOUND STRENGTH
After removal of sutures:
–At the end of first wk  wound
strength is ~ 10% that of the
unwounded skin
–After 3rd mth  ~70% to 80% of
normal skin

28. FACTORS THAT INFLUENCE WOUND
HEALING:
SYSTEMIC:
1. Nutrition
– Protein deficiency  retard healing
– vitamin C deficiency  inhibit collagen synthesis
 retard healing
2. Metabolic status
– Diabetes mellitus  retard healing

29. 3. Circulatory status
– Inadequate blood supply, arteriosclerosis or
venous abnormalities (e.g., varicose veins) 
retard venous drainage, also impairs healing
4. Hormones
– glucocorticoids  inhibit collagen synthesis 
impairs healing

30. LOCAL:
1. Infection
– persistent tissue injury and inflammation  delay
2. Mechanical factors
– early motion of wounds compressing blood
vessels and separating the edges of the wound 
delay
3. Foreign bodies
– unnecessary sutures or fragments of steel, glass, or
even bone – delays wound healing
4. Size, location & type of injury
– Small wound – heals faster than larger wound
– Wounds in richly vascularized area – heals faster

31. COMPLICATIONS OF WOUND
HEALING
(1)Wound dehiscence and ulceration
– Wound rupture – d/t inc in mechanical stress
– Ulceration of wound
• Inadequate formation of granulation tissue or
assembly of a scar
• d/t inadequate vascularization (atherosclerotic
peripheral vascular disease)
• Non-healing ulcers (neuropathic ulcers) – as no
sensation in diabetic peripheral neuropathy

32. (2) Formation of contractures:
•An exaggeration of
contraction gives rise to
contracture and results in
deformities of the wound and
the surrounding tissues.
•common sites: palms, the soles,
and the anterior aspect of the
thorax

33. (3) excessive formation of the repair
components
– hypertrophic scar
– keloid
– exuberant granulation
– desmoids, or aggressive fibromatoses

34. Development of fibrosis in chronic inflammation

35. Repair, regeneration, and fibrosis after injury and inflammation