This document discusses wound healing and its stages. It begins by defining wounds and ulcers, and classifying wounds. The main stages of wound healing discussed are inflammation, proliferation, and remodeling. Inflammation begins immediately after injury and involves vasodilation, increased permeability, and immune cell infiltration. Proliferation involves cell migration, angiogenesis, and re-epithelialization. Remodeling occurs over months as collagen is reorganized and strengthened. Disturbances like infection, radiation, and malnutrition can impair healing. Hypertrophic scarring and keloids represent excessive healing with increased collagen deposition.

1. Wound Healing
Dr. Alok Kumar
Ph.D. Shalya tantra
NEIAH, Shillong

2. Wound
 Break in
continuity of skin
or covering
epithelium is
called wound.
 Usually When
wound become
chronic then
called ulcer

3. Introduction
 Over the ages, many agents have been
placed on wounds to improve healing.
 To date nothing has been identified that can
accelerate healing in a normal individual.
 Many hinder the healing process.
 A surgeon’s goal in wound management is
to create an environment where the healing
process can proceed optimally

4. Classification of wound
 Open
 Incisions
 Lacerations
 Abrasions (grazes)
 Avulsions ( De-glovening)
 Puncture wounds
 Penetration wounds
 Gunshot wounds
 Close
 Hematoma
 Crush injury

5. On the basis of level of contamination
 Clean
 Clean contaminated
 Contaminated
 Infected
 Colonized

6. Clean Avulsion
ContaminatedColonised

7. Classification of wound/ulcer
Pathological-
1. Non-specific
1. Traumatic
2. Venous
3. Arterial
4. Neurogenic
5. Tropic
6. Diabetic
7. Blood dyscrasia
2. Specific
3. Malignant
Clinical
1. Spreading
2. Healing
3. Callous

8. Component of wound /ulcer
 Base
 Floor
 Edge
 Margin

9. Clinical examination of chronic
wound
Inspection
 Location
 Arterial ulcer ( distal part i.e. tip of toe, dorsum of foot)
 Venous ulcer (medial side just proximal to medial malleolus
 Floor of ulcer
 Red with granulation tissue
 Necrotic tissue, slough
 Pale, scanty granulation
 Wash leather slough
 Black tissue

10. Discharge
 Serous
 Purulent
 Blood
 Greenish
 Discharge with bony spicules

11. Edges
 This is the junction between normal
epithelial and ulcer bed.
 Sloping edges (healing)
 Punched out edges ( trophic, bed sore)
 Undermined ( tubercular)
 Raised ( basal cell Ca)
 Everted or rolled out (marzillin’s ulcer in squamous
cell Ca)

12. Palpation
 Edges
 Base
 Mobility
 Bleeding
 Surrounding area

13. Types of wound healing
Primary intension
Tertiary intension
Secondary intension

14. Stages of wound healing
Inflammation
Maturation
Proliferation
BleedingEarly
Late
Intermediate

15. Early Wound Healing Events
Early Inflammation
Coagulation
Late inflammation

16. Stages of Wound Healing

17. Wounding
 Blood vessels are disrupted,
resulting in bleeding.
Hemostasis is the first goal
achieved in the healing
process.
 Cellular damage occurs, this
initiates an inflammatory
response.
 The inflammatory response
triggers events that have
implications for the entire
healing process.
 Step one then is hemostasis,
resulting in Fibrin.

18. Stages of

19. Early Events
 Homeostasis

20. Inflammation
 Erythema
 Edema
 Pain
 Heat

21. Signs of Inflammation
 Immediately after injury, intense
vasoconstriction leads to
blanching, a process mediated by
epinephrine, NE, and
prostaglandins released by injured
cells.
 Vasoconstriction reversed after
10min, by vasodilatation.
 Now redness and warmth.
 Vasodilatation mediated by
histamine, linins, prostaglandins.

22. Inflammation
 As microvenules dilate, gaps
form between the endothelial
cells,resulting in vascular
permeability. Plasma leaks out
into extravascular space.
 Leukocytes now migrate into
the wound by diapedesis,
adhere to endothelial cells, to
wounded tissues.
 Alteration in pH from
breakdown products of tissue
and bacteria, along with
swelling causes the pain.

23. Inflammation
 Neutrophils, macrophages and lymphocytes come
into wound.
 Neutrophils first on scene, engulf and clean up.
Macrophages then eat them or they die releasing
O2 radicals and destructive enzymes into wound.
 Monocytes migrate into extravascular space and
turn into macrophages.
 Macrophages very important in normal wound
healing.

24. Inflammation
 Macrophages eat bacteria, dead tissue, secrete
matrix metalloproteinases that break down
damaged matrix.
 Macrophages source of cytokines that stimulate
fibroblast proliferation, collagen production.
 Lymphocytes produce factors like FGF, EGF,
IL-2.
 At 48-72 hrs, macrophages outnumber neuts.
 By days 5-7 few remain.
 PDGF= platelet derived growth factor, FGF= fibroblast growth factor , EGE=Epidermal growth factor,
TGF=transforming growth factor

25. Intermediate Events

26. Proliferation
 Mesenchymal cell chemotaxis
 Mesenchymal cell proliferation
 Angiogenesis
 Epithelialization

27. Proliferation
 Fibroblasts are the major mesenchymal cells
involved in wound healing, although smooth
muscle cells are also involved.
 Normally reside in dermis, damaged by
wounding.
 Macrophage products are chemotactic for
fibroblasts. PDGF, EGF, TGF, IL-1, lymphocytes
are as well.
 PDGF= platelet derived growth factor, FGF= fibroblast growth factor , EGE=Epidermal growth factor,
TGF=transforming growth factor, VEGF= Vascular endothelial growth factor

28. Proliferation
 Angiogenesis reconstructs vasculature in areas
damaged by wounding, stimulated by high lactate
levels, acidic pH, decreased O2 tension in tissues.
 Cytokines directly stimulate the endothelial cell
migration and proliferation required for
angiogenesis.
 FGF-1 is most potent angiogenic stimulant
identified. Heparin important as cofactor, TGF-
alpha, beta, prostaglandins also stimulate.

29. Epithelialization
 The process of epithelial renewal after injury.
 Particularly important in partial thickness
injuries, but plays a role in all healing.
 Partial thickness wounds have epidermis and
dermis damaged, with some dermis preserved.
Epithelial cells involved in healing come from
wound edges and sweat glands, sebaceous glands
in the more central portion of wound.

30. Epithelialization
 In contrast in an incisional wound, cellular
migration occurs over a short distance.
 Incisional wounds are re-epithelialized in
24-48h.
 The sequence of events here are cellular
detachment, migration, proliferation,
differentiation.

31. Epithelialization
 First 24h, basal cell layer thickens, then elongate,
detach from basement membrane and migrate to
wound as a monolayer across denuded area.
 Generation of a provisional BM which includes
fibronectin, collagens type 1 and 5.
 Basal cells at edge of wound divide 48-72 h after
injury.
 Epithelial cells proliferation contributes new cells
to the monolayer. Contact inhibition when edges
come together.

32. Late Wound Healing Events

33. Collagen
 Synthesized by fibroblasts beginning 3-5 days
after injury.
 Rate increases rapidly, and continues at a rapid
rate for 2-4 weeks in most wounds.
 As more collagen is synthesized, it gradually
replaces fibrin as the primary matrix in the
wound.
 After 4 weeks, synthesis declines, balancing
destruction by collagenase.

35. Collagen
 Age, tension, pressure and stress affect rate of
collagen synthesis.
 TGF-b stimulates it, glucocorticoids inhibit it.
 19 types identified. Type 1(80-90%) most
common, found in all tissue. The primary
collagen in a healed wound.
 Type 3(10-20%) seen in early phases of wound
healing. Type V smooth muscle, Types 2,11
cartilage, Type 4 in BM.

36. Collagen
 Three polypeptide chains, right handed
helix.
 Most polypeptide chains used in collagen
assembly are alpha chains.

38. Collagen
 Every third AA residue is Glycine.
 Another critical component is hydroxylation of
lysine and proline within the chains.
Hydroxyproline is necessary for this. Requires
Vit C, ferrous iron, and alpha ketoglutarate as co-
enzymes. Steroids suppress much of this,
resulting in underhydroxylated collagen, which is
incapable of making strong cross-links leading to
easy breakdown.

39. Wound Contraction
 Begins approximately 4-5 days after
wounding.
 Represents centripetal movement of the
wound edge towards the center of the
wound.
 Maximal contraction occurs for 12-15
days, although it will continue longer if
wound remains open.

40. Wound Contraction
 The wound edges move toward each other
at an average rate of 0.6 to .75 mm/day.
 Wound contraction depends on laxity of
tissues, so a buttocks wound will contract
faster than a wound on the scalp or
pretibial area.
 Wound shape also a factor, square is faster
than circular.

41. Wound Contraction
 Contraction of a wound across a joint can
cause contracture.
 Can be limited by skin grafts, full better
than split thickness.
 The earlier the graft the less contraction.
 Splints temporarily slow contraction.

42. Terminal Wound Healing Event

43. Remodeling
 After 21 days, net accumulation of collagen
becomes stable. Bursting strength is only
15% of normal at this point. Remodeling
dramatically increases this.
 3-6 weeks after wounding greatest rate of
increase, so at 6 weeks you are at 80% to
90% of eventual strength and at 6mos 90%
of skin breaking strength.

44. Remodeling
 The number of intra and intermolecular cross-
links between collagen fibers increases
dramatically.
 A major contributor to the increase in wound
breaking strength.
 Quantity of Type 3 collagen decreases replaced
by Type 1 collagen
 Remodeling continues for 12 mos, so scar
revision should not be done prematurely.

45. Disturbances in Wound Healing

46. Local Factors
 Infection versus contamination
 Infection is when number or virulence of
bacteria exceed the ability of local defenses
to control them.
 100000 organisms per gram of tissue.
 Foreign bodies, hematomas promote
infection, impaired circulation, radiation.
 Systemic: AIDS, diabetes, uremia, cancer.

47. Local Factors
 Smoking stimulates vasoconstriction.
 Increases platelet adhesiveness
 Limits O2 carrying capacity
 Endothelial changes
 Diminished amount of collagen deposition.

48. Local Factors
 Radiation damages the DNA of cells in exposed
areas.
 Fibroblasts that migrate into radiated tissues are
abnormal.
 Collagen is synthesized to an abnormal degree in
irradiated tissue causing fibrosis.
 Blood vessels become occluded.
 Damage to hair and sweat glands
 Vitamin A has been used to counteract this.

49. Systemic Factors
 Malnutrition
 Cancer
 Old Age
 Diabetes- impaired neutrophil chemotaxis,
phagocytosis.
 Steroids and immunosuppression suppresses
macrophage migration, fibroblast proliferation,
collagen accumulation, and angiogenesis.
Reversed by Vitamin A 25,000u per day.

50. IMPROPER HEALING
Hypertrophic Scars and Keloids
 Excessive healing results in a raised, thickened scar,
with both functional and cosmetic complications.
 If it stays within margins of wound it is hypertrophic.
Keloids extend beyond the confines of the original
injury.
 Dark skinned, ages of 2-40. Wound in the presternal
or deltoid area, wounds that cross langerhans lines.

51. Keloids and Hypertrophic Scars
 Keloids more familial
 Hypertrophic scars develop soon after
injury, keloids up to a year later.
 Hypertrophic scars may subside in
time, keloids rarely do.
 Hypertrophic scars more likely to cause
contracture over joint surface.

52. Keloids and Hypertrophic Scars
 Both from an overall increase in the
quantity of collagen synthesized.
 Recent evidence suggests that the
fibroblasts within keloids are different from
those within normal dermis in terms of
their responsiveness.
 No modality of treatment is predictably
effective for these lesions.

53. Keloids and Hypertrophic Scars

54. KELOID

55. HYPERTROPHIC SCAR