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WOUND HEALING REPAIR + REGENERATION REPAIR + REGENERATION NEW EPITHELIUM GROWTH NEW EPITHELIUM GROWTH.

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Presentation on theme: "WOUND HEALING REPAIR + REGENERATION REPAIR + REGENERATION NEW EPITHELIUM GROWTH NEW EPITHELIUM GROWTH."— Presentation transcript:

1 WOUND HEALING REPAIR + REGENERATION REPAIR + REGENERATION NEW EPITHELIUM GROWTH NEW EPITHELIUM GROWTH

2 TISSUE REPAIR Replacement of injured or dead cells is critical to survival. Replacement of injured or dead cells is critical to survival. Repair involves mainly two processes Repair involves mainly two processes 1. Regeneration 2. Replacement by connective tissue or fibroplasia.

3 Wound healing is an intricate process where the skin (or another organ-tissue) repairs itself after injury. In normal skin, the epidermis and dermis exist in a steady-state equilibrium, forming a protective barrier against the external environment. Once the protective barrier is broken, the normal (physiologic) process of wound healing is immediately set in motion. Wound healing is an intricate process where the skin (or another organ-tissue) repairs itself after injury. In normal skin, the epidermis and dermis exist in a steady-state equilibrium, forming a protective barrier against the external environment. Once the protective barrier is broken, the normal (physiologic) process of wound healing is immediately set in motion.epidermisdermisepidermisdermis

4 Steps in wound healing wound healing is divided into three or four sequential phases: (1) hemostasis (not considered a phase by some authors) wound healing is divided into three or four sequential phases: (1) hemostasis (not considered a phase by some authors)hemostasis, (2) inflammation, (2) inflammation, (3) proliferation and, (3) proliferation and (4) remodeling. (4) remodeling. Upon injury to the skin, a set of complex biochemical events takes place to repair the damage. Upon injury to the skin, a set of complex biochemical events takes place to repair the damage.

5 Cells are divided into three types based on their proliferative capacity: Cells are divided into three types based on their proliferative capacity: 1. Labile cells 2. Stable cells 3. Permanent cells

6 Labile cells: Labile cells: –This sub-population of cells is constantly turned over. The best examples are found in the epithelial cell population of the skin or gut, and the hematopoetic cells in the bone marrow. These cells have a short, finite life span, die via apoptosis, and are rapidly replaced. Permanent cells: Permanent cells: –Permanent cells are found in the CNS (neurons) and heart (Cardiac muscle). Once they are destroyed, they cannot regenerate.

7 Stable cells characteristically undergo few divisions. These cells are capable of regeneration following injury. Stable cells characteristically undergo few divisions. These cells are capable of regeneration following injury. Includes hepatocytes, renal tubular cells, parenchymal cells of many glands and numerous mesenchymal cells( sm, endo. CT,cartilage, osteoblasts) Includes hepatocytes, renal tubular cells, parenchymal cells of many glands and numerous mesenchymal cells( sm, endo. CT,cartilage, osteoblasts)

8 CLINICAL SURGICAL CORRELATES OF WOUND HEALING PRIMARY UNION HEALING BY “FIRST INTENTION” HEALING BY “FIRST INTENTION” SUTURED SURGICAL INCISION SUTURED SURGICAL INCISION SECONDARY UNION HEALING BY “SECONDARY INTENTION” HEALING BY “SECONDARY INTENTION” LARGE DEFECTS, ULCERS LARGE DEFECTS, ULCERS

9 W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company Slide 4.17

10 WOUND CONTRACTION IN A CENTRIPETAL FASHION WOUND CONTRACTION IN A CENTRIPETAL FASHION

11 WOUND CONTRACTION BY ACTION OF MYOFIBROBLASTS

12 WOUND CONTRACTION

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15 First 24 hrs; Neutrophils’ migration towards fibrin clot. ACUTE INFLAMMATORY RESPONSE ACUTE INFLAMMATORY RESPONSE ERYTHEMA, EDEMA ERYTHEMA, EDEMA Basal cells exhibit mitotic activity Basal cells exhibit mitotic activity 24-48 hrs: Epithelial cell from edges migrate and proliferate along dermis. Epithelial cell from edges migrate and proliferate along dermis. PLATELET/FIBRIN COVERING PLATELET/FIBRIN COVERING MIGRATION TO MIDLINE MIGRATION TO MIDLINE

16 WOUND HEALING SEQUENCE

17 Day 3: Neutrophils replaced by macrophages and granulation tissue INVADES WOUND SPACE Neutrophils replaced by macrophages and granulation tissue INVADES WOUND SPACE Collagen fibres formation. Collagen fibres formation. CONTINUED EPITHELIAL THICKENING CONTINUED EPITHELIAL THICKENING Day 5: Neovasularization. Neovasularization. Bridging of incision by collagen fibres Bridging of incision by collagen fibres MAXIMAL ANGIOGENESIS AND GRANULATION TISSUE MAXIMAL ANGIOGENESIS AND GRANULATION TISSUE EPITHELIUM RESTORED EPITHELIUM RESTORED

18 Second week: Continue collagen deposition and fibroblast proliferation. Continue collagen deposition and fibroblast proliferation. “BLANCHING” “BLANCHING” DECREASED VESSELS, EDEMA DECREASED VESSELS, EDEMA RESOLUTION OF INFLAMMTORY INFILTRATE RESOLUTION OF INFLAMMTORY INFILTRATE After one month: Scar tissue without inflammatory cells. Scar tissue without inflammatory cells. CELLULAR CONNECTIVE TISSUE CELLULAR CONNECTIVE TISSUE PROGRESSIVE INCREASE OF TENSILE STRENGH OVER NEXT SEVERAL MONTHS PROGRESSIVE INCREASE OF TENSILE STRENGH OVER NEXT SEVERAL MONTHS

19 Remodeling phase 3 week to 2 year 3 week to 2 year New collagen forms which increase tensile strength to wound New collagen forms which increase tensile strength to wound Balance of matrix degradation and collagen synthesis Balance of matrix degradation and collagen synthesis Scar tissue is only 80% as srtong as original tissue. Scar tissue is only 80% as srtong as original tissue.

20 HYPERTROPHIC SCAR HYPERTROPHIC SCAR linear, red, RAISED,PRURITIC LESIONS, confined to the original injury site Common affect under constant pressure and stretching area. Usually arise within one month of injury Usually arise within one month of injury

21 CAUSES OF HYPERTROPHIC SCAR FOREIGN BODY IN THE WOUND FOREIGN BODY IN THE WOUND SCRATCHING SCRATCHING HEMATOMA HEMATOMA SECONDARY INTENTION SECONDARY INTENTION EXCESSIVE TENSION EXCESSIVE TENSION INADEQUATE WOUND CLOSURE INADEQUATE WOUND CLOSURE

22 KELOIDS Form, irregularly shape Form, irregularly shape Thin epi. Caused by surgical procedure, burn, trauma, inflamm. Thin epi. Caused by surgical procedure, burn, trauma, inflamm. Spread beyond the limit of original injury Spread beyond the limit of original injury Appear within week or yr. Appear within week or yr. LOCALLY INVASIVE BENIGN NEOPLASTIC TISSUE LOCALLY INVASIVE BENIGN NEOPLASTIC TISSUE Persist over time.RARELY REGRESS Persist over time.RARELY REGRESS

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24 Early lesion: red, tender, rubbery, may be telangiectatic Early lesion: red, tender, rubbery, may be telangiectatic Old lesion: brown, pruritic, pain, hyperesthesia Old lesion: brown, pruritic, pain, hyperesthesia Varying in size and number Varying in size and number Most commo0n in neck, chest, ear, extremities Most commo0n in neck, chest, ear, extremities Rarely on face, palm, sole Rarely on face, palm, sole

25 Complications of wound healing - Deficient scar formation-which can lead to rupture of the wound due to inadequate formation –result in dehiscence and ulceration - Excessive scar formation of the repair components- Keloid & hypertrophic scar

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28 W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company SUMMARY WOUND HEALING


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