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Inflammation & Repair ( Endodontics point of view)
- 1. PRESENTED BY DR. METTINA 1st MDS INFLAMMATION & HEALING 1
- 2. CONTENTS • Introduction • Signs of inflammation • Classification • Acute inflammation • Chronic inflammation • Inflammation-Dental implications • Wound healing • Healing – dental implications • Conclusion 2
- 3. INTRODUCTION • INFLAMMATION IS A COMPLEX REACTION TO INJURIOUS AGENT SUCH AS MICROBES & DAMAGED NECROTIC CELLS THAT CONSIST OF VASCULAR RESPONSES, MIGRATION, & ACTIVATION OF LEUKOCYTES & SYSTEMIC REACTION. - ROBIN’S PATHOLOGIC BASIS OF DISEASE 7TH EDITION 3
- 6. ACUTE INFLAMMATION Foreign body Physical/chemical agents Immune reactions Infection – Bacterial/Viral Trauma 6
- 7. ACUTE INFLAMMATION- events • Vascular events • Structural changes in microvasculature • Emigration of leucocytes & accumulation at the focus of injury 7
- 8. HEMODYNAMIC CHANGES/CHANGES IN VASCULAR CALIBRE Transient vasoconstriction Vasodilation Increased permeability of microvasculature Emigration of leukocytes Stasis 8
- 9. VASOCONSTRICTION Arterial vasoconstriction is for 3-5 seconds in mild injury In severe injury -5 seconds 9
- 10. PROGRESSIVE VASODILATION • This vasodilation is seen in the first 30 minutes. • It first involves arteriole other than the capillary bed • Results in increased blood volume. • The mediators are – Nitric oxide • - Histamine 10
- 11. INCREASED PERMEABILITY OF MICROVASCULATURE • IT INVOLVES • Contraction of endothelial cells- Histamine • Retraction of endothelial cells- cytokine IL1, TNF • Direct injury to endothelial cells • Endothelial injury mediated by leukocytes. • Leakage from new blood vessels. 11
- 12. STASIS • Increased vascular permeability leads to loss of fluid from the microvasculature • Concentration of red cells in small vessels • Slower blood flow 12
- 13. LEUKOCYTE MIGRATION & EMIGRATION • Peripheral orientation of leukocytes along vascular endothelium • Leukocytic migration • Movement of leukocytes in extracellular space through gaps between endothelium • Emigration 13
- 14. CELLULAR EVENTS • THE INFLAMMATORY CELLS INVOLVED ARE MACROPHAGE 14
- 15. • Leukocytes are delivered to the site of injury. • They ingest the pathogens • Kill Bacteria • Get rid of necrotic tissue & foreign substance 15
- 16. DELIVERY OF LEUKOCYTES TO THE SITE OF INJURY In the lumen -Margination -Adhesion -Rolling Trans- migration Emigration (into interstitial tissue) Chemotaxis 16
- 17. DELIVERY OF LEUKOCYTES TO THE SITE OF INJURY 17
- 18. TRANSMIGRATION Pseudopodia – Squeeze through inter- endothelial junction. Lie between endothelial cells & basement membrane. 18
- 19. EMIGRATION • Leukocytes lodged between basement membrane & endothelium • Release collegenases- cause localized break in membrane 19
- 20. CHEMOTAXIS • Chemotaxis of neutrophil is along a chemical gradient 20
- 21. CHEMO- ATTRACTANTS • Exogenous substances • Bacterial products • A) Peptides – N- formyl methionine terminal amino acid B) Lipids Endogenous substances a) LTB-4 b) PF-4 c) Components of complement system d) Cytokine: IL-1, 5,6 e) Monocyte chemoattractant f) Chemotactic factor for CD4 cells g) Eotaxin chemotactic factor for eosinophils. 21
- 22. PHAGOCYTOSIS Recognition & attachment of particle Engulfment with formation of phagocytic vesicle Degranulation stage Killing & degradation stage 22
- 23. Recognition and attachment of particle Chemotactic agents MACROPHAGE Mannose receptor Scavenger receptor IgG C3b- OPSONIN Lectins OPSONIN 23
- 24. ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE 24
- 25. DEGRANULATION STAGE • Preformed Polymorphoneutrophils( PMNs ) from the granules are released intpo the phagolysosome. • Mononuclear phagocyte secretes enzymes like • IL-2, 6 TNF • Arachidonic acid metabolites( prostaglandin , leukotriene, platelet activating factor) • Oxygen metabolites. 25
- 26. KILLING AND DEGRADATION STAGE Oxygen dependent bactericidal mechanism Oxygen independent mechanism 26
- 27. OXYGEN DEPENDENT MECHANISM • Production of reactive oxygen metabolites • NADPH oxidase H2O2 27
- 28. OXYGEN INDEPENDENT MECHANISM • Followed by • Lysosomal hydrolases • Permeability increasing factors • Defensins • Cationic proteins 28
- 29. ACUTE INFLAMMATION - VIDEO 29 • HTTPS://WWW.YOUTUBE.COM/WATCH?V=1SVEDG94QUA
- 30. MORPHOLOGY OF ACUTE INFLAMMATION Pseudomembrane formation Ulceration Bacterial infusion of Blood Cellulitis Abscess 30
- 31. SYSTEMIC EFFECTS OF ACUTE INFLAMMATION • FEVER • LEUCOCYTOSIS • LYMPHANGITIS / LYMPHADENITIS 31
- 32. CHEMICAL MEDIATORS OF INFLAMMATION • Chemical mediators are the substances that mediate the process of inflammation. Plasma derived These are present in the plasma in precursor form Should be activated before attaining biological properties. Cell derived Present in intercellular granules. Major cellular sources -Platelets -Neutrophil Monocyte / macrophage 32
- 33. CELL DERIVED MEDIATORS • 1.VASOACTIVE AMINES HISTAMINE 1) Mast cells in the connective tissue adjacent to blood vessels 2) Blood basophils 3) Platelets Stimuli: Injury Immune reactions Fragments of complement Neuropeptides Cytokines-IL 1, 8 SEROTONIN Source: 1) Platelets 2) Enterochromaffin cells Stimuli Platelet aggregation after contact with collagen , thrombin 33
- 34. HISTAMINE & SEROTONIN HELP IN • Dilation of Arterioles & Permeability of vasculature. 34
- 35. 2.ARACHIDONIC ACID METABOLITES • It is obtained from two sources- • Directly through diet. • Conversion of essential fatty acid. ARACHIDONIC ACID cyclo-oxygenase pathway ARACHIDONIC ACID lipo-oxygenase pathway METABOLITES CYCLO-OXYGENASE PATHWAY Prostaglandin- PGD2, E2,F2 Thromboxane A2 Prostacyclin LIPO-OXYGENASE PATHWAY S-HETE Leukotrienes 35
- 36. 3. LYSOSOMAL COMPONENTS • ACID PROTEASE • COLLAGENASE • ELASTASE • PLASMINOGEN ACTIVATOR Primary MPO Acid hydrolases Neutral proteases Secondary Lactoferrin Lysososme Alk. Phosphatase Collagenase 36
- 37. 4.CYTOKINES • These are proteins produced mainly by activated lymphocytes & macrophages, also from endothelium , epithelium & connective tissue cells. TNF & IL 1 • Major cytokines that mediate inflammation. • Produced mainly by activated macrophages • STIMULI • Immune reactions • Physical injury & variety of inflammatory stimuli • Endotoxins & other microbial products 37
- 38. • 5. NITROUS OXIDE • Mediates vascular dilation . 6. OXYGEN METABOLITES • Released by activated neutrophils & macrophages Superoxide, hydrogen peroxide, hydroxyl ion • They mediate- Endothelial cell damage- including vascular permeability • Damage to cells & tissue matrix by activating protease & inactivating anti- protease. 38
- 39. MEDIATORS BRINGING ABOUT ROLLING & ADHESION SELECTINS INTEGRINS IMMUNO- GLOBULIN SUPERFAMI LY ADHESION MOLECUES 39
- 40. PLASMA DERIVED MEDIATORS FACTOR IX KININ SYSTEM COMPLEMENT SYSTEM CLOTTING SYSTEM 40
- 41. FATE OF ACUTE INFLAMMATION ACUTE INFLAMMATION Healing by scarring Progression to suppuration Progression to chronic inflammation Resolution 41
- 42. CHRONIC INFLAMMATION • Inflammation of prolonged duration in which inflammation, tissue destruction & attempt at repair are proceeding simultaneously. • CAUSES • Sequelae of acute inflammation • Benign insidiously as a low grade inflammation • Persistent inflammation by micro-organisms • Prolonged exposure ro toxic agents • Auto immunity 42
- 43. FEATURES OF CHRONIC INFLAMMATION Infiltration with mononuclear cells- macrophages, lymphocytes & plasma cells Tissue destruction Healing by proliferation & connective tissue replacement of damaged tissue. 43
- 44. INFILTRATION WITH MONONUCLEAR CELLS • Macrophages • Lymphocytes • Plasma cells 44
- 47. PROLIFERATION • Helps in healing of damaged tissue. ANGIOGENESIS FIBROBLASTS 47
- 48. INFLAMMATION OF PULP & PERIAPICAL TISSUES • 1. PULPITIS ACUTE PULPITIS CHRONIC PULPITIS 48
- 49. ACUTE VS CHRONIC PULPITIS ACUTE PULPITIS • Continued vascular dilation • Accumulation of oedema fluid in connective tissue. • Margination of PMNLs along the endothelial walls CHRONIC PULPITIS • Progresses from acute pulpitis • Mono nuclear cells predominate • Evident fibroblastic activity • Collagen fibres seen in bundles 49
- 50. UNTREATED PULPITIS • PULPITIS • ACUTE CHRONIC APICAL PERIODONTITIS PERIAPICAL ABSCESS PERIAPICAL GRANULOMA 50
- 51. APICAL PERIODONTITIS • It is the inflammation of periodontal ligament around the tooth, elicits tenderness on percussion. • Could be symptomatic or asymptomatic 51
- 52. PERIAPICAL ABSCESS Periapical abscess is defined as the infection around the root of the tooth, which occurs as a sequelae of dental caries leading to pulpal necrosis. 52
- 53. PERIAPICAL ABSCESS • Characterized by Disintegrating PMNLs Visible leukocytes, lymphocytes, bacterial colonies Dilated blood vessels in adjacent PDL. 53
- 54. ACUTE PERIAPICAL ABSCESS Takes the path of least resistance CHRONIC FORM SINUS TRACT FISTULA 54
- 55. WOUND HEALING • WOUND- Anatomic or functional interruption in continuity of a tissue that is accompanied by cellular damage & death. • HEALING- Series of coordinated processes directed towards restoring the injured tissue of the body to as near normal AS POSSIBLE IS TERMED WOUND HEALING. 55
- 56. • May be a result of Physical injury Chemical injury Biological injury 56
- 57. 57
- 58. GOAL OF WOUND HEALING • 1. To approximate the wound edges • 2. To Re- establish tissue function. •Biologic process by which structure & function of disrupted tissue is restored. REGENERATION •Biologic process by which continuity of disrupted tissue is regained ; the new tissue does not restore structure & functionREPAIR 58
- 59. REGENERATION • It is the healing by proliferation of parenchymal cells. • Results in complete restoration of the original tissues. • GROWTH FACTORS • 1. Epidermal • 2. Fibroblast • 3.Platelet derived • 4. Endothelial • 5. Transforming 59
- 60. REPAIR • Healing by connective tissue fibrosis & scarring Phase of inflammation Phase of clearance Phase of ingrowth of granulation tissue 60
- 61. TYPES OF WOUND HEALING PRIMARY INTENTION SECONDARY INTENTION TERTIAR Y INTENTI ON 61
- 62. HEALING BY PRIMARY INTENTION Healing is said to occur by first intention where • There are clean & uninfected wounds. • Surgical incision has been done • Edges have been approximated. • There is not much loss of tissue. 62 STAGES • Initial haemorrhage • Acute Inflammatory response • Epithelial changes • Organization
- 63. HEALING BY PRIMARY INTENTION 63
- 64. HEALING BY SECONDARY INTENTION • Healing is said to occur by secondary intention when the wound is extensive and involves considerable tissue loss & the edges of the wound cannot be approximated . 64
- 65. CONDITIONS • Open wound with large tissue defects. • Extensive loss of tissue. • Skin is not approximated. 65 Wound contraction Due to the action of myofibroblasts in granulation tissue, wound contracts to almost 1/3rd the original size. This feature is exclusive to healing by secondary intention. Granulation tissue The bulk of healing by secondary intention is by formation of granulation tissue.
- 66. WOUND HEALING - VIDEO 66 • HTTPS://WWW.YOUTUBE.COM/WATCH?V=TLVWELDMDWS
- 67. DENTAL IMPLICATIONS OF HEALING 1. Periapical wound healing after non-surgical Root canal therapy • It follows the general principle of healing, accomplished by regeneration to a large extent & to some degree by fibrosis. 2. Suture tracks • Each suture track is a separate wound which heals by primary intention. 3.Healing after Replantation • Following Replantation, clot forms between the ruptured PDL & the root surface. • Proliferation of fibroblasts & endothelial cells is seen. • Reconnection of PDL is evident by extension of collagen fibers from cementum to alveolar bione. 67
- 69. REGENERATIVE DENTISTRY – SOME CONCEPTS 69 Stem cells DPSC SHED SCAP PDLSCs Platelet Rich Fibrin Ozone CPP-ACP Nanohydroxyapatite Flavonoids Tricalcium phosphate Titanium tetrafluoride MTA Biodentin CaOH
- 70. CONCLUSION 70 • Knowledge of the processes of Inflammation & healing is crucial for the analysis & resolution of Day to Day problems in dentistry. • Innovations in wound healing would enhance the quality of dental treatments offered.
- 71. REFERENCES 71 • Robbin’s Pathologic basis of disease – 6th Edition • Essential Pathology for Dental students by Harsh mohan – 4th Edition • Shafer’s textbook of Oral Pathology- 3rd Edition • Grossman’s Endodontic practice -13th edition • www.wikipedia.org • www.google.co.in • www.pubmed.org
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