WOUND HEALING

1. WOUNDHEALING

2. WOUND is defined as “disruption of normal structure and function”. • HEALINGis response of the body to injury in an attempt to restore normal structure and function.

3. WOUND HEALING: • Closure of a discontinuity in tissue associated with a loss of substance ( wound ) by generation of replacement tissue ( initially granulation tissue, later scar tissue ). • It involves 2 distinct processes. 1. Regeneration. 2. Repair.

4. REGENERATION: • Healing takes place by parenchymal cells & usually results in complete restoration of original tissues. REPAIR: • When healing takes place by proliferation of C / T elements results in fibrosis & scarring.

5. Regeneration involves 2 processes: 1. Proliferation of original cells from the margin of the injury with migration. 2. Proliferation of the migrated cells with subsequent differentiation & maturation.

6. Cell Cycle: • G1 ( gap I ) phase. • S ( synthesis ) phase. • G2 ( gap 2 ) phase. • M ( mitosis phase ). • G0 ( gap 0 ) phase.

8. Duration of the cell cycle: • Can be as less as 8 hrs to 100 days or more.

9. Repair: It Involves 2 processes 1. Granulation tissue formation. 2. Contraction of wounds.

11. Granulation tissue – Trichome stain Mature scar – Trichome stain

12. Wound healing: 1. Primary intention. 2. Secondary intention.

13. Healing by first intention 1. Initial hemorrhage: Wound is filled with blood which then clots and seals the wound against dehydration and infection. 2. Inflammatory phase:

14. 3.Epithelial changes: • Epidermal cells from both the margins proliferate & migrate in the form of epithelial spurs. • A well approximated wound is covered by a layer of epithelium in 48 hrs. • The migrated epidermal cells separate the underlying viable dermis from overlying necrotic material & clot, forming a scab which is cast off.

15. 4. Organization: • By 3rd day fibroblasts also invade the wound area. • By 5th day new collagen fibrils start forming. • In 4 weeks, the scar tissue with scanty cellular & vascular elements, a few inflammatory cells are formed. 5. Suture tracks:

16. Healing by second intention • Initial hemorrhage: • Inflammatory phase:

17. 3. Epithelial changes: Epidermal cells migrate in the form of epithelial spurs but do not cover the surface fully until granulation tissue from base has started filling the wound space.

18. 4. Granulation tissue: The main bulk of secondary healing is by granulation tissue. 5.Wound contraction: Important feature of secondary healing. Wound contracts to one-third to one fourth of its original size

20. Healing skin wound Healed skin wound

21. Wound strength:

22. Factors influencing wound healing: • General factors: 1. Age 2. Anaemia, malnutrition. .

23. Nutrition: deficiency of a.Proteins: • Causes delay in the appearance of new fibroblasts as well as decreased rate of fibroblastic multiplication. • Interfere with granulation tissue formation. • Wound lacks tensile strength.

24. b. Vitamin C deficiency: • Synthesis of pro collagen is hampered. • Results in capillary fragility. • Formation of unstable collagen which is quickly degraded by collagenolysis. c. Vitamin E: • Serves as membrane stabilizer & plays an important role in lysosome function.

25. d.Vitamin A deficiency: - Decreases collagen synthesis and stability.

26. 4. Corticosteroids: - Suppression of immune system. 5. Medicaments: Warferin & heparin decreases formation of fibrin matrix. 6. Depressed general resistance; infection. 7. Systemic infection. 8. Malignancy.

27. Diabetes : a. Increased susceptibility to infections due to decreased phagocytic capacity & neutrophilchemotaxis. b. Hyperglycemia results in production of abnormal collagen. c. Insulin is required for earliest stages of collagen formation.

28. 10. Genetic disorders: Ehler Danlos syndrome. Osteogenic imperfecta. Marfan syndrome. 11. Coagulation disorders: Formation of poor fibrin network & abnormal platelet adhesion.

29. 12.Smoking: Nicotine is potent vasoconstrictor, associated with hypercoaguability & predisposes to micro vascular occlusion.

30. Local factors • Local infection. • Movement. • Poor blood supply. • Presence of foreign bodies. • Type, size & location of injury.

31. COMPLICATION OF WOUND HEALING: 1. Deficient scar formation. 2. Excessive formation of the repair components. 3. Formation of the contracture.

32. i. Deficient scar formation. 1. Ulceration. 2. Bursting open of wounds. -poor surgical technique. -excessive mechanical tension on wound.

33. 2. Excessive formation of repair components: - Hypertrophic scar -Keloid formation - Exuberant granulation ( Proud flesh)

34. 3. Formation of contractures: • Exaggerated contraction in the size of wound.

35. 4. Others: a. Implantation or epidermal cyst. b. Neoplasia. c. Pigmentation.

36. Healing of Extraction Socket 1. Haemorrhage & clot formation. 2. Organization of clot by granulation tissue. 3. Replacement of granulation tissue by C/T & epithelization. 4. Replacement of C/T by coarse fibrillar bone. 5. Replacement of immature bone by mature bone tissue.

37. Events in socket healing: • When a tooth is removed ,socket fills with blood which coagulates to seal it from oral environment. • Vasodilatation & engorgement of blood vessels. • Mobilization of leukocytes to the area around the clot.

38. First week wound: • Proliferation of fibroblasts. • Fibroblasts begin to grow into the clot around the entire periphery. • The clot forms an actual scaffold. • Osteoclastic activity. • Endothelial cell proliferation. • The blood clot begins to undergo organization.

39. Second week wound: • The blood clot becomesorganized by fibroblasts growing into the clot. • New capillaries penetrate to the centre of clot. • The remnants of PDL undergo degeneration. • Epithelial proliferation over the surface of the wound is extensive. • Prominent osteoclasticresorption.

40. Third week wound: • The clot is almost completely organized by maturing granulation tissue. • Very young trabeculae of osteoid or uncalcified bone form around the entire periphery of the wound. • The original cortical bone of the alveolar socket undergoes remodelling. • The surface of the wound may have become completely epithelized.

41. Fourth week wound: • Continued deposition & remodelling resorption of the bone.

42. Complications in the healing of extraction wounds: • Dry socket: A focal osteomyelitis in which the blood clot has disintegrated or been lost, with the production of a foul odor & severe pain of the throbbing type, but no suppuration.

43. Destruction of the clot is caused by the action of: • proteolytic enzymes produced by the bacteria. • local fibrinolytic activity. Activators of fibrinolysins are liberated from the alveolar bone & other oral tissue.

44. Healing of biopsy wound: Primary healing: • Formation of blood clot. • Formation of fibroblasts. • Formation of thin delicate collagen fibrils, which interwine & coalesce in a general direction parallel to the surface of the wound.

45. Endothelial cells proliferate & form new capillaries. • The surface epithelium proliferates rapidly across the line of incision. • The C/T fibrils coalesce into dense bundles & usually contract.

46. Secondary healing: • Heals through granulation tissue formation. • Fibroblasts & capillaries have a greater distance to travel. • As the granulation tissue matures, it becomes more fibrous through condensation of collagen bundles. • The surface of the granulation tissue becomes epithelized.

47. Healing of Fractures • Healing of fractures can be considered in many stages, in fact it is continuous and different stages overlap in different areas. • Integrity of periosteum alone can ensure adequate blood supply. • A. Primary union. • B. Secondary union.

49. Complications of fracture healing: 1. Fibrous healing. 2. Non – union. 3. Delayed union.

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