Introduction DR SANJIV KUMAR HEALING OCCURS BY 1 HEALING BY REGENERATION 2 HEALING BY REPAIRSUBSTITUTION DR SANJIV KUMAR DR SANJIV KUMAR DR SANJIV KUMAR DR SANJIV KUMAR Labile cells ID: 916156
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WOUND HEALING
DR SANJIV KUMAR
Slide2Introduction
DR SANJIV KUMAR
Slide3HEALING OCCURS BY
1. HEALING BY REGENERATION2. HEALING BY REPAIR/SUBSTITUTIONDR SANJIV KUMAR
Slide4DR SANJIV KUMAR
Slide5DR SANJIV KUMAR
Slide6DR SANJIV KUMAR
Slide7Labile cells - Continuously dividing cells. e.g. epidermis, epithelial cells, bone marrow cells
Stable cells/Quiescent cells• Undergoes division occasionally• Liver, kidney pancreas, fibroblasts, endothelial cellsPermanent cells
• Non–dividing cells• Neurons, muscle cells (cardiac, skeletal)DR SANJIV KUMAR
Slide8Types of Wound Healing
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Slide9Healing by first Intention
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Slide10Stages of Wound Healing
INFLAMMATORY PHASE PROLIFERATIVE PHASE MATURATION AND REMODELING PHASE
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Slide11DR SANJIV KUMAR
Slide120 hour
Clot filling the incised area
3-24 hour
Neutrophilic infiltration
48 hour
Basal cell proliferation and epithelial closure takes place by 24-48 hours
72 hours
Macrophages replace neutrophils. Granulation tissue begins to appear. Collagen is arranged vertically
120 hours
Incised space is filled with granulation tissue. Neovascularisation is maximal. Collagen fibre begin to appear and epithelial proliferation is maximal
2 weeks
Proliferation of fibroblast with continuous collagen accumulation producing a scar. Type III collagen is deposited early in scar tissue and is replaced by adult type I collagen which accounts for wound strength. Newly formed blood vessels disappear.
8 week
Scar tissue consists of granulation tissue which is devoid of inflammation covering intact epidermis.
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Slide13Angiogenesis
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Slide14Maturation Phase
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Slide15Inflammation subsidesDecreased fibroblasts & EC Myoid differentiation of fibroblasts leading to wound contraction Crosslinking of collagen into thicker bundles
Proteolysis Further contraction Further crosslinking…Remodeling & ScaringDR SANJIV KUMAR
Slide16The wound involved shows extensive loss of cells and tissue. e.g. infarction, ulceration, abscesses, surface wound with large defects.
The wound is filled with tissue debris, a few erythrocytes and bacteria. Abundant granulation tissue (soft, pink, granular appearance of wound surfaces) grows in from the margin to fill the defect but at the same time the wound contracts i.e., the defect is marked by depression and decrease from its original size.
Microscopically granulation tissue consists of new capillaries, fibroblasts, collagen and proteoglycan rich ground substance.
Initially granulation tissue is soft and spongy due to leaky blood vessels.
Healing by Second Intention
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Slide17Difference b/w Primary and Secondary intention
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Slide18Exuberant granulation or proud flesh
Sometimes the granulation continues to grow in abnormally large amount due to irritant, movement or trauma which prevents healing. This condition is called proud flesh or excess granulation tissue.
KeloidKeloid is another condition. The connective tissue below the epithelial covering continues to proliferate. This is found in horses and black people having some genetic or familial predisposition.
Complication
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Slide19Systemic factors
NutritionalVitamins – vitamin C is required for collagen synthesisProteins deficiency – starvationSulphur containing amino acids (methionine and cystine) are important and required for intermediate forms of collagen
Zinc – as metalloenzyme, it is essential for remodelling of extracellular matrixMetabolic factorsDiabetes mellitus – delays healing
Hyperadrenocortism
Circulatory stasis or adequacy of blood supply
Inadequate blood supply – delays healing
Hormones – concurrent glucocorticoid therapy hinders inflammatory and reparatory process
Systemic and local factors influencing wound healing
DR SANJIV KUMAR
Slide20Local factors Infection can delay healing Mechanical – movements directly affect wound healing
Foreign bodies impede healing Size, location and type of wound Cold inhibits wound healingOthersOld age-Healing is slower than young ones.Chemotherapeutic agentsRadiationImmunodeficiency
DR SANJIV KUMAR