Wound healing

1. TISSUE RENEWAL/WOUND HEALING
Dr. ANAND

2. HEALING VS REPAIR

3. • Healing is body’s response to injury in an
attempt to restore normal structure and
function.
• It involves
• A. Regeneration
• B. Repair

4. • Regeneration is restoration to original tissue
by proliferation of parenchymal cells
• Repair is healing of proliferation of connective
tissue resulting in fibrosis and scaring

5. • WHAT ARE THE ORGANS IN THE BODY WHICH
REGENERATES

6. TYPES OF CELLS

7. TYPES OF CELLS IN BODY
• LIABLE CELLS— epidermis, endometrium,
blood cells
• STABLE CELLS--- decrease proliferation after
adolescence– bone cartilage, liver, pancreas
• PERMANENT CELLS– stop proliferation after
birth– neurons, skeletal mucles, cardiac
muscles

9. Why ??
• Each of these cells have separate wound
healing process

10. FACTORS

11. • CELL CYCLE SIGNALLING PATHWAYS[UBIQUINTIN
PATHWAYS]
• CDK
• ANGIOGENESIS[ Formation of new blood vessels]
• NEOVASCULARISATION– Formation of new blood
vessels
• GROWTH FACTORS-TGF, FGF, PDGF

12. • NEUTROPHILS
• MACROPHAGES
• PLASMA CELLS

13. TABLE 3-4 -- Growth Factors and Cytokines
Affecting Various Steps in Wound Healing
Monocyte chemotaxis Chemokines, TNF, PDGF,
FGF, TGF-β
Fibroblast
migration/replication
PDGF, EGF, FGF, TGF-β,
TNF, IL-1
Keratinocyte replication HB-EGF, FGF-7, HGF
Angiogenesis VEGF, angiopoietins, FGF
Collagen synthesis TGF-β, PDGF
Collagenase secretion PDGF, FGF, TNF; TGF-β
inhibits

14. HOW WOUND IS
STRENGTHENED??

16. • FIBROSIS HAS OCCURRED
• EXTRACELLULAR MATRIX COMPONENTS

17. • COLLAGEN
• FIBRONECTIN
• ELASTIC FIBRES
• PROTEOGLYCANS

19. REPAIR
• Repair is the replacement of injured tissue by
fibrous tissue.
• Two processes are involved in repair:
• 1. Granulation tissue formation; and
• 2. Contraction of wounds

20. • Repair response takes place by participation of
• mesenchymal cells (consisting of connective
tissue stem cells, fibrocytes and histiocytes),
endothelial cells,
• macrophages,
• platelets,
• parenchymal cells of the injured organ

22. STEP-1 BLOOD CLOT
• Clot is reffered as SCAB…. Forms as a barrier
of wound preventing microbial invasion
• Factors involved:
• - Transforming growth factors[TGF]
• -Platelet derived growth factors[PDGF]
• Source:: Platelets and plasma

24. Step-II Inflammation
• Neutrophils infiltrate the wound to remove the microbes
and necrotic debris
• Plasma derived fibronectin and neutrophil debris acts as
chemoattractants from macrophage and fibroblasts
• Macrophage eats neutrophil debris and release factors for
fibrogenesis and angiogenesis
• Factors: TGF
• Source: Neutrophils

25. III--Granulation tissue formation
• It is transient specialised organ of repair
• Composed of:
• Erythrocytes and fibroblasts
• Single cell lined capillaries
• Factors involved: FFG, TGF
• Source:: Macrophages , fibroblasts

26. IV– Fibroblast proliferation and matrix
accumulation
• 2 or 3 days after injury, fibroblasts start
secreting collagen
• 5-7 days later,, collagen is more in amount and
tightly grips the wound
• Source: macrophages, fibroblasts

27. STEP—V ANGIOGENEIS

28. i) Angiogenesis (neovascularisation). Formation of new
blood vessels at the site of injury takes place by
proliferation of endothelial cells from the margins of
severed blood vessels.
• Initially, the proliferated endothelial cells are solid buds but
within a few hours develop a lumen and start carrying
blood.
• The newly formed blood vessels are more leaky, accounting
for the oedematous appearance of new granulation tissue.
Soon, these blood vessels differentiate into muscular
arterioles, thin-walled venules and true capillaries

29. • FACTORS INVOLVED: Vascular endothelilal
growth factors[VEGF]
• Source Macrophages, monocytes

30. VI– WOUND CONTRACTION
– It is done by specialize type of fibroblasts called as
– MYOFIBROBLASTS[ MYO + FIBROBLASTS]
MF contains actin – contractile
Forms a tight junctions and contract leading to wound
contraction
Factors involved: TGF
Source: Platelets, macrophages

31. VII- Accretion of tensile strength and
remodelling
• Remodelling is done cross linking of collagen
fibres
• Occurs as wound site devascularies
• Factors; PDGF, FGF MMP
• Source: platelets, fibroblasts

34. Mechanism of Wound healing
Macrophages
Cytokines
Free
radicals
Enzymes
NO
TGF-B
FGE +
EGF
AngiogenesisFibrosis
Granulation tissueHealing
Activation
TH
© Dr.yasir 2oo7

35. GRANULATION TISSUE

36. • Granulation tissue= granular and pink
appearance
• Granule stands for histologically proliferation
of small sized blood vessels

38. • DOES GRANULATION TISSUE NORMALLY
PRESENT IN BODY??

40. • WHAT IS THE DIFFERENCE BETWEEN
• GRANULATION TISSUE
VS
• BLOOD VESSEL

44. TYPES OF WOUND HEALING
• PRIMARY INTENTION
• SECONDARY INTENTION

45. • Healing by First Intention (Primary Union)
This is defined as healing of a wound which has the
• following characteristics:
• i) clean and uninfected;
• ii) surgically incised;
• iii) without much loss of cells and tissue; and
• iv) edges of wound are approximated by surgical
sutures.

46. • 1. Initial haemorrhage
• 2.Acute inflammatory response.-Neutrophils
• 3. Epithelial changes– Granulation tissue
• 4. Organisation- fibroblasts
• 5. Suture tracks- fibrous union

48. Healing by Second Intention
(Secondary Union
• This is defined as healing of a wound having the
following characteristics:
• i) open with a large tissue defect, at times
infected;
• ii) having extensive loss of cells and tissues; and
• iii) the wound is not approximated by surgical
sutures but is left open.

52. HEALING IN SPECIALISED
TISSUES

53. FRACTURE HEALING
• CALLUS FORMATION

54. • Fracture Healing
• Healing of fracture by callus formation
depends upon some
• clinical considerations whether the fracture is:
• traumatic (in previously normal bone), or
pathological (in previously diseased bone)

55. • Primary union of fractures occurs in a few
special situations when the ends of fracture
are approximated as is done by application of
compression clamps

56. • Secondary union is the more common process of fracture
healing. Though it is a continuous process,
Secondary bone union is described under the 3headings:
• i) Procallus formation
• ii) Osseous callus formation
• Remodelling

60. FACTORS AFFECTING WOUND
HEALING
• LOCAL FACTORS
• SYSTEMIC FACTORS

61. • BLOOD SUPPLY
• INFECTION
• FOREIGN BODY
• MECHANICAL STRESS

62. • SYSTEMIC FACTORS
• AGE
• ANAEMIA
• DIABETES
• SEPTICEMIA
• COLLAGEN GENETIC DISEASES
• DRUGS

63. • DIABETES MELLITUS

64. COMPLICATION OF WOUND HEALING
• DEFICIENT SCAR FORMATION
• KELOID
• CONTRACTURES

68. OVERVIEW OF WOUND HEALING MECHANISM

70. THANKU