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![• CELL CYCLE SIGNALLING PATHWAYS[UBIQUINTIN
PATHWAYS]
• CDK
• ANGIOGENESIS[ Formation of new blood vessels]
• NEOVASCULARISATION– Formation of new blood
vessels
• GROWTH FACTORS-TGF, FGF, PDGF](https://image.slidesharecdn.com/woundhealing-161011095508/85/Wound-healing-11-320.jpg)
![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](https://image.slidesharecdn.com/woundhealing-161011095508/85/Wound-healing-22-320.jpg)
![• FACTORS INVOLVED: Vascular endothelilal
growth factors[VEGF]
• Source Macrophages, monocytes](https://image.slidesharecdn.com/woundhealing-161011095508/85/Wound-healing-29-320.jpg)
![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](https://image.slidesharecdn.com/woundhealing-161011095508/85/Wound-healing-30-320.jpg)
![• CELL CYCLE SIGNALLING PATHWAYS[UBIQUINTIN
PATHWAYS]
• CDK
• ANGIOGENESIS[ Formation of new blood vessels]
• NEOVASCULARISATION– Formation of new blood
vessels
• GROWTH FACTORS-TGF, FGF, PDGF](https://image.slidesharecdn.com/woundhealing-161011095508/75/Wound-healing-11-2048.jpg)
![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](https://image.slidesharecdn.com/woundhealing-161011095508/75/Wound-healing-22-2048.jpg)
![• FACTORS INVOLVED: Vascular endothelilal
growth factors[VEGF]
• Source Macrophages, monocytes](https://image.slidesharecdn.com/woundhealing-161011095508/75/Wound-healing-29-2048.jpg)
![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](https://image.slidesharecdn.com/woundhealing-161011095508/75/Wound-healing-30-2048.jpg)
More Related Content
Wound healing
- 1.
- 2.
- 3. • Healing isbody’s response to injury in an attempt to restore normal structure and function. • It involves • A. Regeneration • B. Repair
- 4. • Regeneration isrestoration to original tissue by proliferation of parenchymal cells • Repair is healing of proliferation of connective tissue resulting in fibrosis and scaring
- 5. • WHAT ARETHE ORGANS IN THE BODY WHICH REGENERATES
- 6.
- 7. TYPES OF CELLSIN 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 ?? • Eachof these cells have separate wound healing process
- 10.
- 11. • CELL CYCLESIGNALLING 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.
- 16. • FIBROSIS HASOCCURRED • EXTRACELLULAR MATRIX COMPONENTS
- 17. • COLLAGEN • FIBRONECTIN •ELASTIC FIBRES • PROTEOGLYCANS
- 19. REPAIR • Repair isthe replacement of injured tissue by fibrous tissue. • Two processes are involved in repair: • 1. Granulation tissue formation; and • 2. Contraction of wounds
- 20. • Repair responsetakes 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 • Neutrophilsinfiltrate 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 proliferationand 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.
- 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 oftensile 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 Woundhealing Macrophages Cytokines Free radicals Enzymes NO TGF-B FGE + EGF AngiogenesisFibrosis Granulation tissueHealing Activation TH © Dr.yasir 2oo7
- 35.
- 36. • Granulation tissue=granular and pink appearance • Granule stands for histologically proliferation of small sized blood vessels
- 38. • DOES GRANULATIONTISSUE NORMALLY PRESENT IN BODY??
- 40. • WHAT ISTHE DIFFERENCE BETWEEN • GRANULATION TISSUE VS • BLOOD VESSEL
- 44. TYPES OF WOUNDHEALING • PRIMARY INTENTION • SECONDARY INTENTION
- 45. • Healing byFirst 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. Initialhaemorrhage • 2.Acute inflammatory response.-Neutrophils • 3. Epithelial changes– Granulation tissue • 4. Organisation- fibroblasts • 5. Suture tracks- fibrous union
- 48. Healing by SecondIntention (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.
- 53. FRACTURE HEALING • CALLUSFORMATION
- 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 unionof fractures occurs in a few special situations when the ends of fracture are approximated as is done by application of compression clamps
- 56. • Secondary unionis 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.
- 64. COMPLICATION OF WOUNDHEALING • DEFICIENT SCAR FORMATION • KELOID • CONTRACTURES
- 68. OVERVIEW OF WOUNDHEALING MECHANISM
- 70.