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Inflammation and Healing

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Pathology

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Inflammation and Healing

  1. 1. INFLAMMATION AND HEALING Seminar by: RUHEENA KHAN PG 1st year DEPARTMENT OF ORAL MEDICINE AND RADIOLOGY
  2. 2. INFLAMMATION INTRODUCTION TYPES ACUTE INFLAMMATION CHEMICAL MEDIATORS OF INFLAMMATION CHRONIC INFLAMMATION DENTAL ASPECTS OF INFLAMMATION
  3. 3. DEFINITION: Inflammation is defined as the local response of living tissues to injury due to any agent. ETIOLOGY: The causes of inflammation are many and varied:  Exogenous causes:  Physical agents  Mechanic agents: fractures, foreign corps, sand, etc.  Thermal agents: burns, freezing  Chemical agents: toxic gases, acids, bases  Biological agents: bacteria, viruses, parasites  Endogenous causes:  Circulation disorders: thrombosis, infarction, hemorrhage  Enzymes activation – e.g. acute pancreatitis  Metabolic products – uric acid, urea
  4. 4. CELSUS in 1st century A.D named the famous 4 cardinal signs of inflammation as:  rubor (redness)  tumor (swelling)  calor (heat)  dolor (pain) To these, 5th sign functio laesa, or loss of function was later added by VIRCHOW SIGNS OF INFLAMMATION
  5. 5. TYPES OF INFLAMMATION ACUTE Rapid onset Short duration Fluid accumulation, plasma protein exudation Neutrophils CHRONIC Onset- insidious Longer duration Lymphocytes, macrophages, plasma cells as inflammatory cells
  6. 6. ACUTE INFLAMMATION VASCULAR EVENTS CELLULAR EVENTS 1. HAEMODYNAMIC CHANGES 2. ALTERED VASCULAR PERMEABILITY 1. EXUDATION OF LEUKOCYTES 2. PHAGOCYTOSIS
  7. 7. VASCULAR EVENTS 1. HAEMODYNAMIC CHANGES: 1. TRANSIENT VASOCONSTRICTION 2. VASODILATATION (arterioles, venules and capillaries) obvious within half an hour of injury Increase blood volume in microvascular bed Redness and warmth 3. Elevation of HYDROSTATIC PRESSURE Results in transudation of fluid in the extracellular space swelling
  8. 8. 4. Slowing or stasis Increased vascular permeability Increased concentration of RBCs Raised blood viscosity Slower blood flow
  9. 9. slowing followed by LEUCOYTE MIGRATION (neutrophils mainly) to the vascular endothelium Leukocytes then move and migrate through gaps between the endothelial cells in the extravascular space. EMIGRATION
  10. 10. LEWIS EXPERIMENT:  Lewis induced the changes in the skin of the inner aspect of forearm by firm stroking with a blunt point. The reaction so elicited is known as TRIPLE RESPONSE or RED LINE RESPONSE consisting of : RED LINE- local vasodilatation of capillaries and venules FLARE - vasodilatation of adjacent arterioles WHEAL - transudation of fluid into the extravascular space
  11. 11. STARLING’S HYPOTHESIS 2. ALTERED VASCULAR PERMEABILITY  In normal circumstances fluid balance is maintained by 2 opposing set of forces: 1. Forces that cause OUTWARD MOVEMENT of fluid from microcirculation are intravascular hydrostatic pressure and osmotic pressure of interstitial fluid. 2. Forces that cause INWARD MOVEMENT of interstitial fluid into circulation are intravascular osmotic pressure and hydrostatic pressure of interstitial fluid.
  12. 12. Normally whatever little fluid is left in the interstitial compartment is drained by the lymphatics and thus no oedema results.
  13. 13.  In inflamed tissues, the endothelial lining becomes leaky. Consequently, the intravascular osmotic pressure decreases and osmotic pressure of the interstitial fluid increases resulting in excessive outward flow of fluid into the interstitial compartment. EXUDATIVE INFLAMMATORY OEDEMA
  14. 14. 1. Endothelial cell contraction reversible process mediated by histamine, bradykinin, leukotrienes short duration: 15-30 min. 2. Retraction of EC TNF and IL-1 onset of response takes 4-6 hrs after injury and lasts for 2-4 hours or more
  15. 15. 3. Endothelial injury immediate sustained response, lasts for several hours or days 4. Leukocyte-mediated endothelial injury activation of leucocytes release proteolytic enzymes and toxic oxygen species. Late response 5. Neovascularisation under the influence of VASCULAR ENDOTHELIAL GROWTH FACTOR during the process of repair are leaky
  16. 16. MECHANISM MICROVAS- CULATURE RESPONSE TYPE PATHOGENESIS EXAMPLES CELL CONTRACTION Venules Immediate 15-30 min Histamine Bradykinin Mild thermal injury CELL RETRACTION Venules Delayed 24 hrs or more IL-1, TNF In vitro only DIRECT CELL INJURY Arterioles Venules Capillaries Immediate or delayed Cell necrosis and detachment severe Burns, Bacterial infections, radiation injury LEUCOCYTE- MEDIATED Venules Capillaries Delayed Leucocyte activation Pulmonary venules NEOVASCULARI SATION All Any type VEGF tumours
  17. 17. CELLULAR EVENTS 1. EXUDATION OF LEUCOCYTES Most important feature of inflammatory response. The escape of leucocytes from lumen of microvasculature to the interstitial tissue. In acute inflammation, polymorphonuclear neutrophils comprise the first line of defense, followed later by the monocytes and macrophages.
  18. 18. CHANGES LEADING TO MIGRATION 1. CHANGES IN THE FORMED ELEMENTS OF BLOOD VASODILATATION subsequently, SLOWING of BLOOD STREAM The central stream of cells widens and peripheral plasma zone becomes narrower because of loss of plasma by exudation. MARGINATION The neutrophils of the central column come close to the vessel wall PAVEMENTING
  19. 19. 2. ROLLING AND ADHESION: Peripherally marginated and pavemented neutrophils slowly roll over the endothelial cells lining the vessel wall. ROLLING PHASE Transient bond between the leucocytes and the endothelial cells becoming firmer. ADHESION PHASE
  20. 20. ADHESION MOLECULES: SELECTINS : E-selectin (cytokine-activated Endothelial cells) P-selectin (Preformed and stored in endothelial cells) L-selectin (expressed on surface of Lymphocytes and neutrophils) INTEGRINS: Activated during the process of loose and transient adhesions between the endothelial cells and leucocytes. IMMUNOGLOBULIN SUPER FAMILY ADHESION MOLECULE: ICAM-1,2
  21. 21. 3. EMIGRATION
  22. 22. Neutrophils move till a suitable site is reached CYTOPLASMIC PSEUDOPODS Subsequently, crosses the basement membrane by damaging it locally with secreted collagenases and escape out into the extravascular space. EMIGRATION
  23. 23. DIAPEDESIS Simultaneously escape of RBCs takes place through the gaps between the endothelial cells. DIAPEDESIS Diapedesis gives Hemorrhagic appearance to the inflammatory exudate.
  24. 24. 4. CHEMOTAXIS The chemotactic factor mediated transmigration of leucocytes after crossing several barriers to reach the interstitial tissues is called CHEMOTAXIS. Well illustrated by BOYDEN’S CHAMBER EXPERIMENT.
  25. 25. In this, a millipore filter separates the suspension of leucocytes from the test solution in tissue culture chamber. If the test solution contains chemotactic agent, the leucocytes migrate through the pores of filter towards the chemotactic agent.
  26. 26. AGENTS ACTING AS CHEMOTACTIC SUBSTANCES EXOGENOUS SUBSTANCES ENDOGENOUS SUBSTANCES a) Peptides – N – formyl methionine terminal amino acid b) Lipids a) LT-B4 b) PF-4 c) Components of complement system c3,c5 d) Cytokine : IL – 1, 5 , 6 e) Monocyte chemoattractant protein f) Chemotactic factor for CD-4 cells g) Eotaxin chemotactic factor for eosinophils
  27. 27. 2. PHAGOCYTOSIS ENGULFMENT of solid particulate material by the cells (cell eating). The cells performing this function are PHAGOCYTES. There are two main types of cells: 1. PMNs which appear early in acute inflammatory response and are called as MICROPHAGES. 2. Circulating monocytes and fixed tissue mononuclear phagocytes called as MACROPHAGES. The process of phagocytosis is same for both polymorphs and macrophages and involves 4 steps:
  28. 28. 4 STEPS: RECOGNITION AND ATTACHMENT OF PARTICLE ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE DEGRANULATION STAGE KILLING & DEGRADATION STAGE
  29. 29. Opsonins are naturally occuring factors in the serum. 1. IgG opsonin: Fc fragment of immunoglobulin G. It is naturally occuring antibody in the serum that coats the bacteria while PMNs possess receptors for the same. 2. C3b opsonin: fragment of complement. It is generated by the activation of complement pathway. 3. Lectins: carbohydrate binding proteins in the plasma which bind to the bacterial cell wall.
  30. 30. The opsonised particle is ready to be engulfed. formation of cytoplasmic pseudopods around the particle enveloping in the phagocytic vacuole Eventually, the plasma membrane breaks from the cell surface and the lysosomes of the cell fuse with the phagocytic vacuole PHAGOLYSOSOME or PHAGOSOME
  31. 31. Preformed granule stored products of PMNs are released into phagolysosome. Mononuclear phagocyte also secrete enzymes eg • IL-2 and 6,, TNF • Arachidonic acid metabolites (Prostaglandins , leukotrienes , platelet activating factor) • Oxygen metabolites (superoxide oxygen, hydrogen peroxide, hypochlorous acid) DEGRANULATION STAGE
  32. 32. KILLING OR DEGRADATION STAGE The micro-organisms after being killed are degraded by hydrolytic enzymes. The antimicrobial agents act by 2 mechanisms: OXYGEN - DEPENDENT BACTERICIDAL MECHANISM OXYGEN - INDEPENDENT MECHANISM
  33. 33. OXYGEN DEPENDENT BACTERICIDAL MECHANISM An important mechanism of microbicidal killing is by production of reactive metabolites (O2, H2O2, HOCl, HOI, HOBr) This type of activity is carried out either through enzyme MYELOPEROXIDASE (MPO) present in the granules of neutrophils and monocytes, or independent of enzyme MPO.
  34. 34. MPO – DEPENDENT KILLING MPO – INDEPENDENT KILLING H202 HOCl, Cl, Br, I HOBr, HOI + H2O MORE POTENT ANTIBACTERIAL AGENT MPO H2O2 O2 Fe++ HYDROXYL RADICALS
  35. 35. Few agents released from the granules of phagocytic cells do not require oxygen. These include:  Lysosomal hydrolases  Permeability increasing factors  Defensins  Cationic proteins OXYGEN INDEPENDENT BACTERICIDAL MECHANISM
  36. 36. CHEMICAL MEDIATORS OF INFLAMMATION Also called as PERMEABILITY factors or ENDOGENOUS factors. The substances acting as chemical mediators of inflammation may be released from the cells, the plasma, or damaged tissue itself. Classified into 2 groups: Mediators released by CELLS Mediators originating from PLASMA
  37. 37. HISTAMINE  SOURCE : 1) Mast cells in C.T adjacent to blood vessels 2) Blood basophils 3) Platelets  STIMULI : Injury Immune reactions Fragments of complement - C3a , C5a Neuropeptides such as substance P Cytokines IL – 1 , 8 • SEROTONIN  SOURCE : 1) Platelets 2) Enterochromaffin cells 3) nervous tissue 4) mast cells  STIMULI : Platelet aggregation after contact with collagen , thrombin Action: vasodilatation, increased vascular permeability, itching and pain VASOACTIVE AMINES
  38. 38. A fatty acid with 2 main sources : Directly through diet Through conversion of essential fatty acid, linoleic acid to arachidonic acid ARACHIDONIC ACID ARACHIDONIC ACID METABOLITESLipo-oxygenase Pathway Cyclo-oxygenase pathway CYCLO – OXY- GENASE PATHWAY Prostaglandin - PGD2 , E2 , F2 Thromboxane A2 Prostacyclin LIPO – OXY – GENASE PATHWAY 5 – HETE Leukotrienes ARACHIDONIC ACID METABOLITES
  39. 39. Action: Cyclooxygenase Pathway • PGD2, PGE2, PGF2α Vasodilatation Potentiates Edema formation • PGI2 (prostacyclin) Vasodilatation, Inhibits Platelet aggregation • TxA2 Vasoconstriction & stimulates platelets aggregation Lipoxygenase Pathway Vasoconstriction Bronchoconstriction Increased vascular permeability
  40. 40. GRANULES OF NEUTROPHILS: MPO ACID HYDROLASES NEUTRAL PROTEASES GRANULES OF MONOCYTES AND TISSUE MACROPHAGES: LACTOFERRIN LYSOZYME ALKALINE PHOSPHATASE COLLAGENASE PRIMARY SECONDARY ACID PROTEASE COLLAGENASE ELASTASE PLASMINOGEN ACTIVATOR LYSOSOMAL COMPONENTS
  41. 41. produced mainly by: activated lymphocytes & macrophages , also from endothelium, epithelium & connective tissue cells. TNF and IL-1 • major cytokines that mediate inflammation. Produced mainly by activated macrophages • Immune reactions, • physical injury & variety of inflammatory stimuli. • endotoxins & other microbial products STIMULI CYTOKINES
  42. 42. • TNF & IL-1 – Endothelial effects • Endothelial activation • WBC binding & recruitment • Procoagulant activity – Fibroblast effects • Activates tissue fibroblasts • Increases proliferation • Production of collagen & ECM
  43. 43. mediates in vascular dilation Anti-platelet activating agent Possibly microbicidal action Released by activated neutrophils and macrophages Superoxide oxygen, hydrogen peroxide , hydroxl ion ACTION : Endothelial cell damage and thereby increasing vascular permeability Damage to cells and tissue matrix by activating protease and inactivating anti protease. NITRIC OXIDE OXYGEN METABOLITES
  44. 44. CLOTTING SYSTEM KININ SYSTEM COMPLEMENT SYSTEM FIBRINOLYTIC SYSTEM
  45. 45. FACTOR XII contact FACTOR XIIa FIBRINOLYTIC CLOTTING KININ PLASMIN FIBRIN BRADYKININ FIBRIN SPLIT PRODUCTS COMPLEMENT SYSTEM Permeability factors C3a, C4a, C5a
  46. 46. ANAPHYLOTOXINS : 1. Release of histamine from mast cells and basophils 2. Increased vascular permeability causing odema in tissues 3. Phagocytosis 4. Chemotactic agent
  47. 47. FATE OF ACUTE INFLAMMATION ACUTE INFLAMMATION RESOLUTION HEALING BY SCARRING PROGRESSION TO SUPPURATION PROGRESSION TO CHRONIC INFLAMMATION
  48. 48. CHRONIC INFLAMMATION It is a prolonged process in which tissue destruction and inflammation occurs at the same time. Time course:  > 48 hours (weeks, months, years)  Cell type  Mononuclear cells (Macrophages, Lymphocytes, Plasma cells) Can be caused by 1 of the following 3 ways: 1. Chronic inflammation following acute inflammation 2. Recurrent attacks of acute inflammation 3. Chronic inflammation starting de novo
  49. 49. FEATURES OF CHRONIC INFLAMMATION  Infiltration with mononuclear cells – macrophages, lymphocytes & plasma cells CHRONIC INFLAMMATION Tissue destruction Healing by Proliferation & connective tissue replacement of damaged tissue
  50. 50. INFILTRATION WITH MONO-NUCLEAR CELLS
  51. 51. • Incr. lysosomal enzymes • Greater ability to phagocytose 55 ACTIVATION OF MACROPHAGE Cytokine IFN - ɤ Endotoxin , fibronectin chemical mediators
  52. 52. MACROPHAGE IN ACUTE INFLAMMATION IN CHRONIC INFLAMMATION Irritant eliminated- macrophage disappears Persistent macrophage accumulation by following mechanisms : 1. )Recruitment from circulation – Chemotactic stimuli include : a) C5a b) Platelet derived growth factor c) Transforming growth factor 2.) Local proliferation of macrophages 3.) Immobilization of macrophages 56
  53. 53. 57 TISSUE DESTRUCTION OR NECROSIS • ACTIVATED MACROPHAGES Elastase Protease Collagenase Reactive oxygen radical Cytokine IL-1,8
  54. 54. 58 PROLIFERATION Small BLOOD VESSELS FIBROBLAST Resulting in the formation of granulation tissue
  55. 55. REACTIONS OF PULP TO BACTERIAL INVASION ᶲ Vascular changes take place inside blood vessels. ᶲ PMNLs reach the area of inflammation ANATOMICAL FEATURES OF PULP THAT TEND TO ALTER THE RESPONSE Enclosure of pulp in rigid calcified walls - PREVENTS EXCESSIVE SWELLING.. Thus more painful. Pressure leads to decrease Blood supply and Ischaemia – does not get corrected since collateral circulation cannot develop through tiny apical foramina 59
  56. 56. HISTOLOGIC FEATURES OF PULPITIS ACUTE CHRONIC 60  MONONUCLEAR CELLS PREDOMINATE - chiefly plasma cells & lymphocytes.  Fibroblastic activity is evident  collagen fibres seen in bundles • Continued vascular dilation • Accumulation of oedemal fluid in connective tissue • Pavementing of PMNLs along endothelial wall
  57. 57. • Inflammation of periodontal ligament around root apex.. Changes localised around root apex…..since richly vascular. Vascular changes , infiltration of PMNLs , and exudate accumulation Resorption of bone – ABSCESS FORMATION 61
  58. 58. WOUND HEALING
  59. 59. WOUND HEALING INTRODUCTION REGENERATION AND REPAIR HEALING BY PRIMARY AND SECONDARY INTENTION FACTORS AFFECTING HEALING HEALING IN ORAL TISSUES
  60. 60. WOUND: A circumscribed injury which is caused by external force and it can involve any tissue and organ. It can be classified based on: Origin of the wound. Contamination of the wound. Depth of the wound.
  61. 61. BASED ON ORIGIN Mechanical 1. Abraded wound 2. Punctured wound 3. Incised wound 4. Cut wound 5. Crushed wound 6. Torn wound 7. Bite wound 8. Shot wound Chemical Acid & base Radiation Thermal Burning & freezing Special Toxins & venoms
  62. 62. BASED ON CONTAMINATION 1. Clean wound 2. Clean & contaminated wound 3. Contaminated wound
  63. 63. BASED ON THE DEPTH 1. Superficial wound = only epidermis. 2. Partial thickness wound = epidermis + dermis. 3. Full thickness wound= epidermis + dermis + subcutaneous fats 4. Deep wound = epidermis + dermis + subcutaneous fats + exposed muscles, bone connective tissue, organs etc.
  64. 64. HEALING Healing is the body’s response to injury in an attempt to restore normal structure and function. The process of healing involves 2 distinct processes: a. REGENERATION b. REPAIR
  65. 65. REGENERATION  Regeneration : Is when healing takes place by proliferation of parenchymal cells and usually results in complete restoration of the original tissues.  To maintain proper structure of tissues, these cells are under constant regulatory control of the cell cycle.
  66. 66. REPAIR  Is when healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring.  Two processes are involved in repair: a. Granulation tissue formation b. Contraction of wound Cells involved in the process of repair; 1. Mesenchymal cells 2. Endothelial cells 3. Macrophages 4. Platelets 5. Parenchymal cells of injured organs
  67. 67. GRANULATION TISSUE PHASE OF INFLAMMATION Following injury blood clots at the site of injury.There is acute inflammatory response with exudation of plasma, neutrophils, and some monocytes within 24 hours. PHASE OF CLEARANCE Proteolytic enzymes liberated from neutophils, autolytic enzymes from dead tissue and phagocytic activity of macrophages, clear off the necrotic tissue, debris and red blood cells. PHASE OF GROWTH OF GRANULATION TISSUE This phase consists of two main processes a. ANGIOGENESIS OR NEOVASCULARISATION b. FIBROGENESIS
  68. 68.  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.  The newly formed blood vessels are more leaky accounting for the more edematous appearance of new granulation tissue.  Soon these blood vessels differentiate into muscular arterioles, thin-walled venules and true capillaries. Angiogenesis takes place under the influence of : 1. Vascular endothelial growth factor 2. Platelet derived growth factor 3. Transforming growth factor- β 4. Fibroblast growth factor
  69. 69. FIBROGENESIS  The newly formed blood vessels are present in an amorphous ground substance. The new fibroblasts originate from the fibrocytes as well as by mitotic division of fibroblasts.  Some of these fibroblast has functional and structural similarities to smooth muscles cell called as myofibroblast.  Collagen fibrils appear by about 6th day. As maturation proceeds, more and more of collagen is formed the number of active fibroblasts and the number of new blood vessels decreases.  This result in the formation of inactive looking scar known as cicatrisation.
  70. 70. GRANULATION TISSUE
  71. 71. CONTRACTION OF WOUND  The wound starts contracting after 2-3 days and the process is completed by 14th day. During this period the wound is reduced by approximately 80% of its original size.  Contraction of wound helps in rapid healing. Factors responsible for wound contraction: 1. Dehydration due to removal of fluids by drying. 2. Contraction of collagen 3. Discovery of myofibroblasts.
  72. 72. TYPES OF WOUND HEALING  HEALING BY FIRST INTENTION also called as PRIMARY UNION.  HEALING BY SECOND INTENTION also called as SECONDARY HEALING.
  73. 73. HEALING BY FIRST INTENTION Healing of wound with following characteristics:  Clean and uninfected  Surgically incised  Without much loss of cells and tissue  Edges of wound are approximated by surgical sutures.
  74. 74. STEPS IN PRIMARY WOUND HEALING  INITIAL HEMORRHAGE: Immediately after injury, the space between the surfaces of incised wound is filled with blood which soon clots, and prevent further infection.  ACUTE INFLAMMATORY RESPONSE: This occurs within 24 hours of appearance of polymorphs from the margins of incision.  EPITHELIAL CHANGES: The basal cells of epidermis from both cut margins starts proliferating and migrating towards incisional space in the form of epithelial spurs.  A well approximated wound is covered by a layer of epithelial cell in 48 hrs. The migrated epithelial cell separates the necrotic cells and clot forming a scab which cast off. The basal cells continues to divide. By 5th day new epidermis is formed.
  75. 75.  ORGANISATION : by 3rd day, fibroblasts also invades the wound area. By 5th day new collagen fibrils start forming which dominate till healing is completed. In 4 weeks a scar tissue with scanty cellular and vascular elements, a few inflammatory cells and epithelialised surface is formed.
  76. 76. HEALING BY SECONDARY INTENTION This is defined as the healing of a wound with following features. i. Open with large tissue defects, at times infected ii. Having extensive loss of cells and tissues, and iii. The wound is not approximated by sutures but is left open. STEPS IN HEALING OF SECONDARY WOUND:  Initial haemorrhage: as a result of injury the wound space is filled with blood and fibrin clot which dries.  Inflammatory phase: there is initial acute inflammatory response followed by appearance of macrophages which clear off the debris.
  77. 77.  EPITHELIAL CHANGES: The epidermal cells from both the margins proliferate and migrate into the wound in the form of spurs till they meet in the middle and re-epithelialise the gap completely.  However, the proliferating epithelial cells do not cover the wound completely until the granulation tissue from the base has started fill the wound space.  GRANULATION TISSUE: The main bulk of secondary healing is by granulation. Granulation tissue is formed by proliferation of fibroblasts and neovascularisation. The newly formed granulation tissue is deep red, granular and very fragile. With time, it becomes pale white due to increased in collagen and decreased blood supply.  WOUND CONTRACTION: This phase is not seen in primary healing. Due to the action of myofibroblasts present in granulation tissue, the wound contracts to one-third of its original size. It occurs during the formation of active granulation tissue.
  78. 78. 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 FRQUENT FREQUENT
  79. 79. FACTORS AFFECTING WOUND HEALING Local factors Systemic factors INFECTION NUTRITIONAL FACTORS LOCATION OF THE WOUND AGE OF THE PATIENT IMMOBILISATION SYSTEMIC INFECTION PHYSICAL FACTORS ADMINISTRATION OF GLUCOCORTICOIDS UNCONTROLLED DIABETES
  80. 80. FACTORS AFFECTING WOUND HEALING LOCAL FACTORS  INFECTION: It has been demonstrated that wounds which is completely protected from bacterial irritation heal considerably more rapidly than wounds which are exposed to bacteria or other mild physical irritation.  LOCATION OF THE WOUND: wounds in the area in which there is a good vascular bed heal considerably more rapidly than the area in which is relatively avascular.
  81. 81.  IMMOBILISATION: If the wound is in an area which is subjected to constant movement so that formation of new connective tissue is continuously distrupted (e.g.: corner of the mouth), it will result in delayed wound healing.  PHYSICAL FACTORS: severe trauma to tissues is obviously a determinant in rapid wound healing. local temperature in the area of wound influences the rate of healing. Thus, in environment hyperthermia, wound healing is accelerated while in hypothermia it is delayed. circulatory factors: anemia has been reported to delay wound healing. Similarly dehydration also delays wound healing.
  82. 82. SYSTEMIC FACTORS  NUTRITIONAL FACTORS: Delay in the healing of wounds may occur in a person who is deficient in variety of essential foods such as proteins, vitamins, especially vitamin A, D and B complex.  AGE OF THE PATIENT: Wounds in younger persons heals more rapidly than wounds In elderly persons and the rate of wound healing appears to be in inverse proportion to the age of the patient.
  83. 83.  SYSTEMIC INFECTION Delays healing of the wound.  ADMINISTRATION OF GLUCOCORTICOIDS It has an anti-inflammatory effect thus it delays wound healing.  UNCONTROLLED DIABETES Diabetics are more prone to develop infections thus delayed wound healing takes place.  HAEMATOLOGIC ABNORMALITIES There is delayed wound healing
  84. 84. HEALING OF EXTRACTION WOUND IMMEDIATE REACTION FOLLOWING EXTRACTION  After the extraction, the blood which fills the socket coagulates, red blood cells being entrapped in the fibrin meshwork.  The resultant fibrin meshwork containing entrapped red blood cells seals off the torn blood vessels and reduces the size of the extraction of wound.  Within the first 24-48 hours after extraction there are alterations in the vascular bed. There is vasodilation and engorgement of blood vessels in the remnants of the periodontal ligament and the mobilization of leucocytes to the immediate area around the wound.
  85. 85. FIRST WEEK WOUND  Within the first week after tooth extraction, proliferation of fibroblasts from connective tissue cells in the remnants of the periodontal ligament is evident, and these fibroblasts have begun to grow into the clot around the entire periphery.  This clot forms the scaffold on which the cells associated with healing process may migrate. It is the temporary structure.  The epithelium at the periphery of the wound grow over the surface of the organizing clot.
  86. 86.  Osteoclasts accumulate along the alveolar bone crest setting the stage for active crestal resorption.  Angiogenesis proceeds in the remnants of the periodontal ligaments.
  87. 87. SECOND WEEK WOUND  During the second week, the blood clot continues to get organized through fibroplasia and new blood vessels that penetrate towards the center of the clot.  Trabeculae of the osteoid slowly extend into the clot from the alveolus, and osteoclastic resoption of the cortical margin of the alveolar socket is more distinct.  The remnants of the periodontal ligament gradually undergo degeneration and are no longer recognizable.
  88. 88. THIRD WEEK WOUND  As healing continues into the third week , the original clot appear completely organized by mature granulation tissue and poorly calcified bone at the wound perimeter.  The surface of the wound is re-epithelised with minimum or no scar formation.  Very young trabeculae of osteoid bone forms around the entire periphery of the wound from the socket wall.
  89. 89.  The original cortical bone of the alveolar socket undergoes remodeling so that it is no longer consist of such a dense layer.  The crest of the alveolar bone is rounded off by osteoclastic resoption.
  90. 90. FOURTH WEEK WOUND  During the fourth week the wound begins the final stage of healing, in which there is continued deposition and remodeling resorption of the bone filling the alveolar socket.  Much of this early bone is poorly calcified, as is evident from its general radiolucency on the radiograph.  Radiographic evidence of bone formation does not become prominent until the sixth or eighth week after tooth extraction.
  91. 91. HEALING AFTER EXTRACTION OF TOOTH 1- immediate reaction after extraction 2-second week after extraction 3-third week after extraction 4-six to eight weeks after extraction (complete healing)
  92. 92. COMPLICATION OF HEALING OF EXTRACTON WOUND  DRY SOCKET  FIBROUS UNION DRY SOCKET  The most common and painful complication in the healing of human extraction wound is alveolar osteitis or dry socket.  It is basically a focal, in which the blood clot has disintegrated or been lost.  The condition is extremely painful without suppuration and the presence of foul odor.
  93. 93.  The condition derives its name from the fact that after the clot is lost the socket has a dry appearance because of the exposed bone.  It is more commonly associated with difficult and traumatic extractions like the removal of impacted third molars.  Destruction of the clot is caused by the proteolytic enzymes produced by bacteria or local fibrinolytic activity.
  94. 94. DRY SOCKET
  95. 95. FIBROUS HEALING OF EXTRACTION WOUND  It occurs more frequently when the extraction is accompanied by the loss of both the buccal and the lingual cortical plates of bone and the loss of periosteum as well.  On a radiograph the lesion appears as a well circumscribed radiolucent area in the site of a previous extraction wound .  There is no certain way of differentiating fibrous healing from the residual infection like residual cyst or granuloma.  The areas of fibrous healing consists of dense bundles of collagen fibrils with occasional fibrocytes and few blood vessels. The lesion is a fibrous scar tissue with little or no evidence of ossification.
  96. 96. HEALING OF FRACTURE IMMEDIATE EFFECTS OF FRACTURE  When fracture of a bone occurs, the haversian vessels of the bone are torn at the fracture site along with the vessels of the periosteum and the marrow cavity. This evokes acute inflammation in the soft tissue adjacent to the fracture line.  Because of the disruption of the vessels, there is considerable amount of blood in this general area and at the same time there is loss of circulation and blood supply.
  97. 97.  Three major phase occurs: 1) Reactive phase: -fracture and inflammation -granulation tissue formation 2) Reparative phase: -callus formation -lamellar bone deposition 3) Remodelling phase:
  98. 98. REACTIVE PHASE  Soon after fracture the blood vessels constrict, stopping any further bleeding.  Within a few hours after fracture, the extravascular blood cells forms a blood clot called as Hematoma.  All of the cells within the blood clot degenerate and die.  Some of the cells adjacent to the fracture site also die, but fibroblast survive and replicate forming a loose aggregates of cells interspersed with small blood vessels known as Granulation tissue.
  99. 99. REPARATIVE PHASE  Days after fracture, the cells of the periosteum replicates.  The Periosteal cells proximal (close) to the fracture gap develops into chondroblasts which forms hyaline cartilage.  Periosteal cells distal (far away ) from the fracture gap develops into osteoblasts which forms woven bone.  The fibroblast with in the granulation tissue develops in to chondroblasts which also forms hyaline cartilage.
  100. 100.  The two new tissue grow in size until they meet their counter part from other part of fracture. This process is called as Callus formation. Callus in Latin means overgrowth of hard skin.  Composed of varied amounts of fibrous tissue, cartilage and bone.  The external callus consists of the new tissue which forms around the outside of two fragments of bone.  The internal callus is the new tissue arising from the marrow cavity.
  101. 101. The next step is deposition of lamellar bone by replacing hyaline cartilage and woven bone.  The replacement process is called endochondral ossification.  The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized.  The new bone is formed in the form of trabecular bone.
  102. 102. REMODELLING PHASE  In this, the trabecular bone is replaced by compact bone.  It takes 3-5 yrs depending on factors like type of fracture, age of patient, or general condition of patients.
  103. 103. STAGES IN HEALING OF FRACTURE
  104. 104. COMPLICATIONS OF FRACTURE HEALING  DELAYED UNION OR NON UNION This results when the calluses of the osteogenic tissue over each of the two fragments fail to meet and fuse or when endosteal formation of bone is inadequate.  FIBROUS UNION The Fractured ends of fragments are united by fibrous tissue, but there is failure of ossification.  LACK OF CALCIFICATION This may occur in unusual circumstances of dietary deficiency or mineral imbalance which is seldom seen clinically.
  105. 105. HEALING AFTER REPLANTATION  Following replantation the clot forms between the root surface and ruptured periodontal ligament.  Proliferation of the fibroblasts and the endothelial cells occurs in the periodontal ligament remnants on the side of the alveolar bone.  The reconnection of the periodontal ligament is evident by the extension of collagen fibers from the cementum to the alveolar bone.
  106. 106.  The epithelium is reattached to the tooth at the end of the first week.  Complete regeneration of the periodontal ligament takes place between two to four weeks.  In the course of time, a number of teeth results in resorption or ankylosis.
  107. 107. COMPLICATIONS OF WOUND HEALING  INFECTION Wounds may provide a portal of entry to microorganisms. Infections of the wound delay the healing process. Systemic conditions such as diabetes mellitus, immunosuppressive state etc. make the individual prone to infection.  KELOID AND HYPERTROPIC SCAR Keloids are overgrown scar tissues with no tendency for resolution. They occur in wound, which heal without any complications.
  108. 108. Hypertrophic scar occur in wounds where healing is delayed. These scars are more cellular and vascular. Keloid and hypertropic scars are not seen in the wounds of the oral cavity. PIGMENTARY CHANGES These are common in healing of wounds on skin and may appear and may appear as hyperpigmented and hypopigmeted areas. In oral cavity hypopigmented scars are less common but some lesions leave hyperigmentation while healing e.g. lichenplanus, lichenoid reactions.
  109. 109.  CICATRIZATION Cicatrization refers to late reduction in the size of the scar in contrast to immediate wound contraction. It a complication due to burns on the skin.  IMPLANTATION CYSTS Epithelial cysts may slide and get entrapped in the wound and later may proliferate to form implantation cysts.
  110. 110. Healing – NEW CONCEPTS Healing of chronic wound can be enhanced by one of the following methods 1. Topical application of growth factors. 2. Hyperbaric oxygen therapy. Systemic Local 3. Electrical stimulation for wound healing Direct current Low frequency pulsed current (LFPC) High voltage pulsed current (HVPC) 4. Topical application of cultured keratinocytes. 5. Vacuum assisted closure of the wound.
  111. 111. 1) Robbin’s & Cotron Pathological basis of diseases 2) Essential pathology for dental students - Harsh mohan 3) Text book of oral pathology - Shafers References……..
  112. 112. THANK YOU

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