WOUND HEALING.pptx

The variety of wounds present challenges to the physician to select the most appropriate management to facilitate healing.

A complete wound history along with knowledge of the healing potential of the wound, as it relates to the specific medical and environmental considerations for each patient, provides the basis of decision making for wound management.

It is essential to consider each wound individually in order to create the optimal conditions for wound healing.
Understanding of wound healing is as important as knowing the pathogenesis of disease, because satisfactory wound healing is the ultimate goal of treatment.


If we are able to understand the mechanism of wound healing, we can design treatment approaches that maximize favorable conditions for wound healing to occur.

1. 1 WOUND HEALING DEPARTMENT OF PERIODONTOLOGY RAMA DENTAL COLLEGE HOSPITAL AND RESEARCH CENTRE, KANPUR, UTTAR PRADESH- 208024

2. CONTENTS Introduction History Regeneration and Repair Phases of wound healing Types of wound healing Mediators of wound healing Factors affecting wound healing Wound healing in specialized tissue Complications of wound healing Advances in wound healing Future strategies Conclusion References 2

3. INTRODUCTION Wound is a disruption of the normal structure and function of the skin and underlying soft tissue. Wound healing  is the body’s response to injury in an attempt to restore normal structure and function. Wound healing involves two distinct processes : - Regeneration - Repair 3

4. 4 a. Tidy wounds ► They are wounds like surgical incisions and wounds caused by sharp objects. ► It is incised, clean, healthy wound , without any tissue loss. ► Usually primary suturing is done. Healing is by primary intention. CLASSIFICATION OF WOUNDS I. RANK & WAKEFIELD CLASSIFICATION

5. 5 They are due to: Crushing. Tearing. Avulsion. Devitalised injury. Vascular injury. Multiple irregular wounds. Burns. b. Untidy wounds Fracture of the underlying bone may be present. Wound infection, delayed healing are common. Liberal excision of devitalised tissue and allowing to heal by secondary intention is the management. Secondary suturing, skin graft or flap may be needed.

6. 6 CLASSIFICATION BASED ON THE THICKNESS OF WOUND Superficial wound- involving only epidermis and dermal papillae. Partial thickness wound- with skin loss up to deep dermis with only deepest part of the dermis, hair follicle shafts and sweat glands are left behind. Full thickness wound- with loss of entire skin and subcutaneous tissue causing spacing out of the skin edges. Deep wound- are the one extending deeper, across deep fascia into muscles or deeper structures. Complicated wound - are one associated with injury to vessels or nerves. Penetrating wound- are one which penetrates into either natural cavities or organs.

7. 7 CLASSIFICATION BASED ON THE INVOLVEMENT OF STRUCTURES Simple wounds- are one involving only one organ or tissue. Combined wounds- are one involving mixed tissues.

8. 8 Acute wounds in normal, healthy individuals heal through an orderly sequence of physiological events that include hemostasis , inflammation, epithelization , fibroplasia , and maturation. Acute wound is upto 8 hours of trauma. When this process is altered, chronic wound may develop and is more likely to occur in patients with underlying disorders . Chronic wounds are generally associated with physiological impairments that slow or prevent wound healing. Chronic wound develops after 8 hours from the trauma. CLASSIFICATION BASED ON THE TIME ELAPSED

9. HISTORY 9 The earliest accounts of wound healing dates back to about 2000 B.C Galen of Pergamum emphasized the importance of maintaining a moist environment to ensure adequate healing. Ambriose Paré found that simply dressed gunshot wounds heal faster and are less painful than when treated with boiling oil, the previously accepted method. Ignaz Philipp Semmelweis advocated need for washing hands before any treatment. Joseph Lister began soaking his instruments in phenol and spraying the operating rooms, reducing the mortality rates close to 50%.

10. REGENERATION 10 It is the natural renewal of a structure, produced by growth and differentiation of new cells and intercellular substances to form new tissues or parts. It takes place by proliferation of parenchymal cells and usually results in complete restoration of the original tissue. In order to maintain proper structure of tissues ,these cells are under constant regulatory control of their cell-cycle.

11. REPAIR 11 Repair simply restores the continuity of the diseased tissue and re-establishes normal margins. This process is also called “ Healing by Scar ”. It takes place by proliferation of connective tissue elements resulting in fibrosis and scarring . 2 processes are involved in repair: a) Granulation tissue formation. b) Contraction of wounds.

12. 12 INFLAMMATORY PHASE Objective:- Leukocytes and macrophages destroy bacteria, cleaning the wound of cellular debris. Duration:- Immediately following the Hemostasis Phase from 0 to 3 days post injury. Cells Involved:- Host cells infiltrate the wound site, such as leukocytes and marcophages . Bacteria are destroyed by leukocytes. Macrophages cleanse the wound of cellular debris. Signs & Symptoms:- Swelling, Increased fluid, profusion of blood, Redness, Release of Epinephrine, Histamine response, Heat, Pain. PHASES OF WOUND HEALING

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14. PROLIFERATIVE PHASE 14 Proliferative phase is categorized by : Fibroblast migration Collagen synthesis Angiogenesis Granulation tissue formation Epithelisation What happens:- The major activity focuses on angiogenesis and granulation tissue formation. Duration:- 3 to 21 days post injury. Cells Involved:- Macrophages, fibroblasts, immature collagen, blood vessels, and ground substance make up granulation tissue, which fills the wound’s cavity

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16. 16 REMODELING AND MATURATION PHASE What happens:- For the final phase of healing, the collagen fibers in the scar are reorganized to improve tensile strength. Duration:- 21 days post injury and upto 1 years later. Cells Involved:- Fibroblasts, MMPs, growth factors are critical in this phase.

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18. 18 GRANULATION TISSUE FORMATION: Has 3 phases— A. PHASE OF INFLAMMATION – - Following trauma, blood clots at the site of injury. There is acute inflammatory response within 24 hours. B. PHASE OF CLEARANCE – - Neutrophils and phagocytic activity of macrophages clear off the necrotic tissues , debris and RBC. C. PHASE OF INGROWTH OF GRANULATION TISSUE — Consist of 2 main process:-- I)Angiogenesis II) Fibrogenesis

19. 19 ANGIOGENESIS – -Formation of new blood vessels at the site of injury takes place by proliferation of endothelial cells . -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 .

20. 20 FIBROGENESIS – - The newly formed blood vessels are present in an amorphous ground substance or matrix. -The new fibroblasts originate from fibrocytes or by mitotic division of fibroblasts. -Collagen fibrils begin to appear by about 6 th day . -As maturation proceeds, more collagen is formed while the number of active fibroblasts and new blood vessels decreases and results in inactive looking scar known as cicatrisation .

21. 21 CONTRACTION OF WOUNDS : - - It starts after 2-3 days and the process is completed by the 14 th day. -The wound is reduced by approximately 80% of its original size. -Contracted wound results in rapid healing since lesser surface area of the injured tissue has to be replaced.

22. 22 TYPES OF WOUND HEALING Primary intention healing Secondary intention healing Tertiary intention healing

23. 23 PRIMARY INTENTION HEALING Wound healing by primary intention is typical for non-complicated surgical wounds. It can be characterized by— Cleaned and uninfected. Surgically incised. Without much loss of cells and tissues. Edges of wound are approximated by surgical sutures. Events occuring in primary intention are— INITIAL HAEMORRHAGE. ACUTE INFLAMMATORY RESPONSE. EPITHELIAL CHANGES. ORGANIZATION. SUTURE TRACKS.

24. 24 Each suture track is a separate wound and have same phenomenon as in healing of primary wound . On removal of suture around 7 th day, much of epithelialized suture track is avulsed and remaining epithelial tissue gets absorbed. Sometimes suture tract gets infected and resulting in STITCH ABSCESS or when epithelial cells may persists in the tract it causes- IMPLANTATION or EPIDERMAL CYST. Suture Tracks

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27. 27 SECONDARY INTENTION HEALING Healing takes place from the base upwards as well as from the margins inwards. Healing is slow and results in a large, at times ugly, scar as compared to primary intention. Occur in wounds having the following characteristics: – Open with a large tissue defect, at times infected. Having extensive loss of cells and tissues. These wounds are not approximated by surgical sutures but are left open. Events occuring in secondary intention are— INITIAL HAEMORRHAGE. INFLAMMATORY PHASE. EPITHELIAL CHANGES. GRANULATION TISSUE. WOUND CONTRACTION. PRESENCE OF INFECTION.

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29. 29 The open wound is filled with blood clot and there is inflammatory response at the junction of viable tissue Epithelial spurs from the margins of wound meet in the middle to cover the gap and separate the underlying viable tissue from necrotic tissue at the surface forming scab After contraction of the wound ,a scar smaller than the original wound is left A B C

30. Difference between 1˚ & 2˚ union of wound FEATURES PRIMARY SECONDARY CLEANLINESS CLEAN NOT CLEAN INFECTION NOT INFECTED INFECTED MARGINS SURGICALLY CLEAN IRREGULAR SUTURES USED NOT USED HEALING SMALL GRANULATION TISSUE LARGE GRANULATION TISSUE OUT COME LINEAR SCAR IRREGULAR WOUND COMPLICATION NOT FREQUENT FREQUENT

31. 31 TERTIARY INTENTION HEALING Wounds that are too heavily contaminated for primary closure but start appear clean and well vascularized after 4-5 days of open observation can be dealt with tertiary intention healing. When resolution has occurred, the wound edges can be brought together (approximated) and the wound proceeds to heal. Most commonly indicated in:- -infected wounds with high bacterial content, -wounds with a long time lapse since injury, or -wounds with a severe crush component with significant tissue devitalization .

32. 32 MEDIATORS OF WOUND HEALING Growth factors PDGF FGF TGF EGF KGF IGF-I, IGF-II Vascular endothelial factor Cytokines TNF ᾳ IL-1,2, 4,6, 8, 10 IFN-ƴ

33. : Growth Factors and Cytokines Affecting Various Steps in Wound Healing Monocyte chemotaxis PDGF, FGF, TGF-ß Fibroblast migration PDGF, EGF, FGF, TGF-ß, TNF, IL-1 Fibroblast proliferation PDGF, EGF, FGF, TNF Angiogenesis VEGF, Ang, FGF Collagen synthesis TGF-ß, PDGF Collagenase secretion PDGF, EGF, FGF, TNF, TGF-ß inhibits PDGF- platelet-derived growth factor FGF- fibroblast growth factor TGF- transforming growth factor EGF- epidermal growth factor IL- interleukin TNF- tumor necrosis factor VEGF- vascular endothelial growth factor

34. 34 FACTORS AFFECTING WOUND HEALING LOCAL FACTORS Infection Movement Poor Blood Supply Ionising Radiation Foreign Bodies Shearing Forces

35. 35 SYSTEMIC FACTORS Nutrition Age Systemic Infection Glucocorticoids Uncontrolled Diabetics Hematologic Abnormalities

36. 36 WOUND HEALING IN SPECIALIZED TISSUES FRACTURE HEALING Healing of fracture by callus formation depends upon some clinical considerations whether the fracture is- Traumatic or pathologic Complete or incomplete Simple or comminuted or compound However, basic events in healing of any type of fracture are similar and resemble healing of skin wound to some extent .

37. 37 Primary Union of Fractures Occurs in a few special situations when the ends of fracture are approximated. Bony union takes place with formation of medullary callus without periosteal callus formation. Patient can be made ambulatory early but there is more extensive bone necrosis and slow healing. Secondary union of Fractures Is a more common process of fracture healing. Though it is a continuous process, secondary bone union is described under the following 3 headings: Procallus formation Osseous callus formation Remodelling

38. A. PROCALLUS FORMATION : Steps involved are: 38

39. . B. OSSEOUS CALLUS FORMATION: Procallus act as scaffolding on which osseous callus composed of lamellar bone is formed. Woven bone is cleared away by osteoclasts and calcified cartilage disintegrates. Newly-formed blood vessels and osteoblasts invade, laying down osteoid and lamellar bone is formed by developing haversian system concentrically around blood vessels. C. REMODELLING: During the formation of lamellar bone, osteoblastic laying and osteoclastic removal take place  remodelling the united bone ends, which become indistinguishable from normal bone. 39

40. 40 Complications Of Fracture Wound Healing : Fibrous union- when immobilization of fractured bone is not done. False joint develop at fracture site.(pseudo- arthrosis ) Non-union may result if some soft tissue is interposed between fractured ends. Delayed union may occur from to delayed wound healing due to infection, inadequate blood supply, poor nutrition, movement and old age. Pseudo- arthrosis of Tibia

41. 41 Periodontal wound healing H EALING FOLLOWING SCALING & ROOT PLANING Immediately after Scaling of Teeth the epithelial attachment will be severed, junctional & crevicular epithelium partially removed Numerous polymorphonuclear leucocytes can be seen between residual epithelial cells & crevicular surface in about 2 hrs There is dilation of blood vessels, oedema & necrosis in the lateral wall of the pocket The remaining epithelial cells show very little pre-mitotic activity at that time. 24 hrs after scaling a widespread & intense labeling of the cells have been observed, in all areas of the remaining epithelium & in 2 days the entire pocket is epithlialized .

42. 42 In 4-5 days a new epithelial attachment may appear at bottom of sulcus . Depending on the severity of inflammation & the depth of the gingival crevice, complete epithelial healing occurs in 1-2 weeks Immature collagen fibers occur within 21days. Following scaling, root planning & curettage procedure healing occurs with the formation of a long thin junctional epithelium with no connective tissue attachment.

43. 43 A blood clot forms between the root surface & the lateral wall of the pocket, soon after the curettage - Large number of polymorphonuclear leucocytes appear in the area shortly after the procedure - This is followed by rapid proliferation of granulation tissue. - Epithelial cells proliferate along the sulcus . HEALING FOLLOWING CURETTAGE - Epithelisation of the inner surface of the lateral wall is completed in 2-7 days - The junctional epithelium is also formed in about 5 days - Healing results in the formation of a long junctional epithelium adherent to the root surface.

44. 44 HEALING AFTER SURGICAL GINGIVECTOMY Initial response after gingivetomy is the formation of a protective surface clot Underlying tissue becomes acutely inflamed with some necrosis Clot is then replaced by granulation tissue By 24 hours there is an increase in new connective tissue cells, mainly angioblasts just beneath the surface layer of inflammation and necrosis

45. 45 By the 3 rd day numerous young fibroblast are located In the area The highly vascular granulation tissue grows coronally , creating a new free gingival margin and sulcus Capillaries derived from the blood vessels of the periodontal li g a m e n t mig r a t e in t o the g r an ul a tion tissue a n d within 2 weeks they connect with gingival vessels. After 12 to 24 hours ,epithelial cells at the margins of the wound start to migrate over the granulation tissue, seperating it from the contaminated surface layer of the clot Epithelial activity at the margins reaches peak in 24 to 33 hours The new epithelial cells arise from the basal and deeper spinous layers of the wound edge epithelium and migrate over the wound over a fibrin layer that is later resorbed and replaced by a connective tissue bed The epithelial cells advances by tumbling action,with cell becoming fixed to the substrate by heidesmosomes and a new basement lamina

46. 46 After 5 to 14 days, surface epithelization is generally completed During the first 4 weeks after gingivectomy , keratinization is less than it was before surgery Complete epithelial repair takes about one month Vasodilation and vascularity begin to decrease after fourth day of healing and appear to be almost normal by the sixteenth day Complete repair of the connective tissue takes about 7 weeks The flow of gingival fluid in humans is initially increased after gingivectomy and diminishes as healing progresses Maximal flow is reached after 1week,coinciding with the time of maximal inflammation In patients with physiologic gingival melanosis the pigmentation is diminished in the healed gingiva .

47. 47 There appears to be little difference in the results obtained after shallow gingival resection with electrosurgery and that with periodontal knives. However, when used for deep resection close to bone, electrosurgery can produce gingival recession, bone necrosis and sequestration, loss of bone height, furcation exposure, and tooth mobility, which do not occur with the use of periodontal knives. HEALING FOLLOWING ELECTROSURGICAL GINGIVECTOMY

48. 48 HEALING FOLLWING DEPIGMENTATION OF GINGIVA Healing after surgical depigmentation : After surgery it was found necessary to cover the exposed lamina propria with periodontal packs for 7 to 10 days. The wound healed uneventfully. After 6 weeks the attached gingiva regenerated by only a delicate scar present. The newly formed gingiva was clinically non-pigmented . Healing following cryosurgical depigmentation : At 2 nd to 3 rd day: superficial necrosis becomes apparent and a whitish slough could be separated from the underlying tissue, leaving a clean pink surface. In 1-2 weeks: normal gingiva In 3-4 weeks: keratinization completed. No postoperative pain, hemorrhage , infection or scarring seen in patients .

49. 49 Healing following depigmentation by laser : During laser procedure, gingiva gets covered with a yellowish layer, that could be easily removed by a wet gauze. After 1-2 weeks: completion of re- epithelization . At 4 th week: gingiva is similar to normal untreated gingiva i.e., lacking melanin pigmentation completely

50. 50 HEALING FOLLOWING FLAP SURGERY Immediately after suturing of the flap against tooth surface a clot forms between the 2 tissues The clot consists of fibrin reticulum with many polymorphonuclear leukocytes, erythrocytes & remnents of injured clots At edge of flap numerous capillaries are seen 1-3days after surgery space between flap & tooth surface & bone appears reduced & the epithelial cells along border of the flap start migrating By 1 week after surgery epithelial cells have migrated & established an attachment to root surface by means of hemidesmosomes

51. 51 The blood clot is replaced by granulation tissue proliferating from the gingival connective tissue, alveolar bone and periodontal ligament By 2 nd week collagen fibers begins to appear. Collagen fibers gets arranged parallel to root surface rather than at right angles. The attachment between soft tissue & tooth surface is weak By end of one month following surgery the epithelial attachment is well formed & the gingival crevice is also well epithealised There is beginning functional arrangement of supracrestal fibres. In cases where Mucoperiosteal Flap has been reflected, superficial bone necrosis have been observed during first 3 days Osteoclastic Resorption occurs in that area which reaches its peak at 4-6 days Osteoblastic Remodelling occurs subsequently Loss of alveolar bone height by about 1 mm may be expected after healing.

52. 52 HEALING OF PEDICLE AUTOGRAFTS ADAPTATION SATAGE(0-4 days): Clot & thin fibrinous exudate between flap and root surface -PMNLs in clot and connective tissue -Epithelium at margins of flap starts to proliferate-may contact tooth surface PROLIFERATION STAGE(4-21 days): Connective tissue invades the fibrin layer - 6-10 days- fibroblasts apposed against root surface -Collagen within the flap- oriented parallel to root surface -Thin collagen fibers adjacent to root(no fibrous union) -Apical proliferation of epithelium-peaks at 10- 14 days. - Osteoclastic resorption (peaks at 6 th day)- decreases by 14 th day. - Slight cemental resorption

53. 53 ATTACHMENT STAGE(21-28 days): Collagen fibers insert into new cementum - Cementoid deposition(by 28 th day- along the entire root) -Connective tissue attachment - New gingival margin, sulcus and epithelial attachment - Osteoblastic activity MATURATION STAGE(28-90 days): Continuous formation of collagen fibers -Completely formed gingival sulcus and epithelial attachment -Bone apposition at alveolar crest

54. 54 HEALING OF FREE GINGIVAL GRAFT INITIAL PHASE(0-3 days): Thin layer of exudate between graft and recipient bed - Avascular plasmatic circulation (Forman 1960; Reese & Stark 1961) - Epithelium of free graft gets desquamated REVASCULARISATION(2-11 days): Anastomosis between graft and recipient site blood vessels - Capillaries proliferate in the graft tissue - Fibrous union between graft and connective tissue bed - Re- epithelization of the graft TISSUE MATURATION(11-42 days): Decrease in the no. of blood vessel to normal by the 14 th day - Epithelium maturation- formation of keratin layer -Functional integration-by 17 th day - Morphologically distinguishable for several months

55. 55 DONOR SITE Granulation tissue fills the donor site. Initial healing is usually complete within 2-3 weeks after the removal of a 4to 5mm thick graft. Patients should wear the surgical stent for about 2 weeks to protect the healing wound. Palate returns to its pre surgical contour after about 3 months.

56. 56 RECIPIENT SITE First week- Postoperative swelling The epithelium of the graft will slough Epithelial cells together with fibrin form a white film on the surface of the grafts The “white stage” passes in 4-7 days. Epithelium will not cover the grafted tissue until a functional capillary circulation has been re-established. Therefore- Red stage(2 nd & 3 rd week) -Normal colour as epithelialization is completed - Epithelium thickens via stratification. The graft reverts to its original volume or remains slightly larger as the swelling subsides. Tissue form is usually stable after 2 months, but some shrinkage may occur between the 2 nd and 4 th months after surgery. Final restorative measures should be initiated until after 4-6 months.

57. 57 HEALING OF CONNECTIVE TISSUE GRAFTS Healing is similar to Free Gingival Graft. 2 nd day- Epithelialization commences 7-10 days- Initial epithelialization completed 4 weeks- Keratinization commences HEALING FOLLOWING FRENECTOMY -Initial hemorrhage Acute inflammatory response- within 24 hours Epithelial changes- completes by 48 hours Organization of fibroblasts- starts around 3 rd day Wound maturation- starts after 1 week and completes around 4 weeks.

58. 58 HEALING FOLLOWING OSSEOUS RESECTION Osseous surgery initiates a inflammatory response Elevation of Mucoperiosteal Flap results in temporary loss of nutrient supply to the bone In additition surgical resection of bone also contributes to inflammatory changes. Necrosis of the alveolar crest & osteoclastic resorption of the bone takes place initially The osteoclastic resorption is followed by bone deposition & remodeling .

59. 59 The initial loss in bone height is compensated to some extent by the repair and remodeling . Thus final loss in bone height is clinically insignificant Osteoblastic activity is even seen after 1 yr. post-operatively As mucoperiosteum is sutured back on to alveolar process the osteoclastic activity doesn’t last for long

60. 60 HEALING AFTER IMPLANT PLACEMENT The interface area consists of bone, marrow tissue, and a hematoma mixed with bone fragments from the drilling process. In the early phase of healing, woven bone is formed by osteoblasts at the surfaces of trabecular and endosteal cortical bone surrounding the implant. The newly formed bone approaching the implant surface leads to bone condensation into both, the implant threads and towards the implant surface. Consequently, the amount of bone in the threads and the degree of bone-implant contact increase with time. In the late phases of healing, lamellar bone replaces woven bone in a process of creeping substitution.

61. 61 STAGES OF HEALING OF IMPLANTS . Woven Bone Formation : When bone matrix is exposed to extra-cellular fluid, non- collagenous proteins & growth factors are set free & initiate repair. Woven bone is first formed & bridge a gap within a few days. Woven bone formation dominates the first 4-6 weeks Lamellar Bone Formation : From 2 nd month post-operatively the microscopic structure of bone changes to lamellar or parallel fibered bone Bone Remodelling : It begins around 3 rd month post- operatively.Initially rapid remodeling occurs which slows down & continuos for rest of the life Thus complete healing probably takes longer than 3 to 6 months

62. 62 HEALING IN NERVOUS TISSUES Central Nervous System: The nerve cells of brain, spinal cord and ganglia once destroyed are not replaced. Damaged neuroglial cells, however, show proliferation of astrocytes called gliosis . 2. . Peripheral Nervous System: Cells of peripheral nervous system show regeneration, mainly by proliferation of Schwann cells and fibrils from distal end.

63. 63 HEALING OF MUSCLE All 3 types of muscle have limited capacity to regenerate: SKELETAL MUSCLE : Regeneration is similar to peripheral nerves. On injury cut ends retract but are held together by stromal connective tissue  injured site is filled with fibrinous material, polymorphs and macrophages. It is then regenerated either: If muscle is intact- sarcolemmal tubes containing histiocytes appear and in about 3 month time restores properly. If muscle sheath is damaged- it forms a disorganized multinucleate mass and scar composed of fibrovascular tissue. SMOOTH MUSCLE : Non-striated muscle has limited regenerative capacity e.g., appearance of smooth muscle in the arterioles in granulation tissue. However, in large destructive lesions, the smooth muscle is replaced by permanent scar tissue. CARDIAC MUSCLE : Destruction of heart muscle is replaced by fibrous tissue. However, in cases where endomysium of individual cardiac fiber is intact regeneration of cardiac fibers may occur in young patients

64. 64 HEALING OF MUCOSAL SURFACES The cells of mucosal surfaces have very good regeneration and are normally being lost and replaced continuously. This occurs by proliferation from margins, migration, multilayering and differentiation of epithelial cells in the same way as in epidermal cells in healing of skin wounds .

65. 65 COMPLICATIONS OF WOUND HEALING 1. Wound infection Wound infection result from gross bacterial contamination of susceptible wounds, where the bacterial burden of replicating microorganisms actually impair healing. Continual presence of a bacterial infection stimulates the host immune defenses leading to production of inflammatory mediators, such as prostaglandins and thromboxane . These cause wound hypoxia , leading to enhanced bacterial proliferation and continued tissue damage. Neutrophil proteases and endotoxins released by the breakdown of bacteria by the host defense mechanism cause further destruction of newly formed cells and their collagen matrix, resulting in impaired wound healing. Clinical manifestation of wound infection include : erythema , warmth, swelling, pain, odor, and pus.

66. 66 2. Deficient scar formation– This may occur due to inadequate formation of granulation tissue . 3 . Wound dehiscence- Dehiscence result from tissue failure rather than improper suturing techniques. The dehisced wound may be closed again or left to heal by secondary intention, depending upon the extent of the disruption and the surgeon’s assessment of the clinical situation. 4 . Implantation (epidermal) cyst- formation may occur due to persistence of epithelial cells in the wound after healing.

67. 67 5. Proliferative scarring- The two common forms of hyperproliferative healing are hypertrophied scars and keloids . These are characterized by hypervascularity and hypercellularity . It results from altered apoptotic behaviour , which leads to scarring , persistent inflammation, and an overproduction of extracellular matrix components, including glycosaminoglycans and collagen type I. Keloid

68. 68 Pigmentation- Healed wounds may at times have rust like colour due to staining with haemosiderin . 7. Excessive contraction– An exaggeration of wound contraction may result in formation of contractures or cicatrisation .

69. 69 ADVANCES IN WOUND HEALING Advances in wound care include : Growth factors :   Currently, PDGF-BB is used for the treatment of cutaneous ulcers, specifically diabetic foot ulcers. Recombinant KGF-2 enhance the formation of granulation tissues in rabbits and wound closure in human meshed skin grafts. rhBMP-2 and rhBMP-7 induce undifferentiated mesenchymal cells to differentiate into osteoblasts Platelet - rich fibrin  (PRF) is a second-generation PRP where autologous   platelets  and leucocytes are present in a complex  fibrin  matrix to accelerate the healing of soft and hard tissue and is used as a tissue-engineering scaffold for filling the intrabony defects and furcation defects.

70. 70 2 . Dermal and Mucosal substitutes : Immediate coverage protects the wound from water loss, drying and mechanical injury and so accelerates wound healing . Autologous grafts remains standard for replacing dermal mucosal surfaces , a no. of bioengineered substitutes can be used in surgical practice. Engineered skin contains all the components necessary to modulate healing and allow healing that replicates native tissue and limits scar formation .

71. 71 Bioengineered Skin Living bioengineered skin equivalents provide a living supply of growth factors and cytokine and a collagen matrix to build upon. The mechanism of action is not fully understood on how these skin equivalents initiates wound healing, but it has been studied extensively with the Apligraf product. The cells contained in the Apligraf grow and proliferate, producing growth factors, collagens, and extracellular matrix proteins, which stimulate re- epithelization , formation of granulation tissue, angiogenesis, and neutrophil and monocyte chemotaxis . Apligraf acts as a potent cellular remedy that can provide a different and adaptable response in acute and chronic wounds.

72. 72 3. Hydrotherapy Hydrotherapy supports wound healing by debriding the wound, warming the injured extremity, and providing gentle limb resistance for physical therapy. New forms used are pulsed lavage and the VersaJet . Pulsed lavage delivers an irrigating solution under pressure (4 to 15 psi) and the rate of granulation tissue formation was greater in patients receiving pulse lavage compared with those receiving conventional Hydrotherapy. The VersaJet Hydrosurgery System is a water jet–powered surgical tool designed to efficiently debride a wound by removing damaged tissues and contaminants precisely, without the collateral trauma associated with traditional surgical modalities .

73. 73 4. Hyperbaric Oxygen: -Dividing cells in a wound require an oxygen tension of at least 30 mmHg. -Tissues in wounds that are not healing have partial pressure of oxygen values of 5 to 20 mmHg - Many reports in the literature have demonstrated benefit from hyperbaric oxygen treatment for a variety of conditions, including amputations, osteoradionecrosis , surgical flaps, and skin grafts. In addition to simply providing more oxygen to the wound site, hyperbaric oxygen therapy also increases expression of nitric oxide, which is crucial for wound healing.

74. 74 5. Lasers Lasers for open wound management are low-energy lasers capable of raising tissue temperature 0.1°C to 0.5°C. This is called as bio-stimulation. It is caused by the stimulation of ascorbic acid uptake by cells, stimulation of photoreceptors in the mitochondria respiratory chain, changes in cellular ATP and cell membrane stabilization. It increase healing (especially when combined with hyperbaric oxygen treatments) of ischemic, hypoxic, and infected wounds. The 2 most common lasers used clinically are helium-neon lasers and gallium-arsenide lasers.

75. 75 6. Electrostimulation In 1982, Barker described the “skin battery.” He found that the skin surface was always negatively charged (compared with the deeper skin layers), and he measured transcutaneous voltages up to 40mV. Electrostimulation is believed to restart or accelerate the wound-healing process by imitating the natural electrical current that occurs in skin when it is injured. Electrical current applied to wounded tissue increases the migration of cells vital to the wound-healing process (i.e., neutrophils , macrophages, and fibroblasts). Electrostimulation may also play a role in wound healing through improved blood flow.

76. 76 7. Negative Pressure Therapy Negative pressure therapy (or vacuum-assisted closure), uses a sub-atmospheric pressure dressing to convert an open wound into a controlled closed wound. The negative pressure removes interstitial fluid and edema to improve tissue oxygenation. It also removes inflammatory mediators that suppress the normal progression of wound healing. Granulation tissue forms more rapidly and 5 days of therapy decreases the wound bacterial count.

77. 77 FUTURE STRATEGIES Gene Therapy : Gene therapy is the future for wound-healing strategies. Current research is aimed at inserting growth factor genomes into the wound. Inserting the desired genome can be accomplished through several different vehicles: biologic (viral) techniques, chemical methods via cationic liposomes , and physical insertion: hypodermic needle, microseeding , particle-mediated transfer (using a gene gun), and electroporation

78. 78 CONCLUSION The variety of wounds present challenges to the physician to select the most appropriate management to facilitate healing. A complete wound history along with knowledge of the healing potential of the wound, as it relates to the specific medical and environmental considerations for each patient, provides the basis of decision making for wound management. It is essential to consider each wound individually in order to create the optimal conditions for wound healing. Understanding of wound healing is as important as knowing the pathogenesis of disease, because satisfactory wound healing is the ultimate goal of treatment. If we are able to understand the mechanism of wound healing, we can design treatment approaches that maximize favorable conditions for wound healing to occur.

79. 79 REFERENCES Pathology By Harsh Mohan - 4 th edition. Peterson's Principles of Oral and Maxillofacial Surgery, Third Edition 3rd Edition by Michael Miloro  , GE Ghali  , Peter Larsen , Peter Waite  . Carranza’s Clinical Periodontology - By Newman, Takei, Klokkevold , Carranza 10 th Edition. Wound Healing: An Overview. George Broughton. Plast. Reconstr. Surg. 117: 1e-S, 2006 Biology of wound healing. Ikramuddin Aukhil. Perio 2000, vol. 22. 2000 -44-50. Polypeptide growth factors and attachment proteins in periodontal wound healing and regeneration. Raul G. Caffesse & Carlos R. Quinones. -Perio 2000, vol.1 1993- 69-79 - Perio 2000, vol 24:connective tissue of periodontium (cell biology of wound healing) Journel of dental rsearch 2010 march ,89(3),219-229 (factors affecting wound healing)

80. 80 THANK YOU