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Patho inflammation

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Patho inflammation

  1. 1. INFLAMMATION AND HEALING Mohammad Muztaba Khan Assistant professor(Jr.) Department of Pharmacology Bhavdiya institute sibar Sohawal Ayodhya
  2. 2. DEFINITION: Inflammation is defined as the local response of living tissues to injury due to any agent. inflammation, a process by which the body's immune system malfunctions.( failure to function normally. Eg. diseases, like arthritis, diabetes, myasthenia gravis
  3. 3. 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 ETIOLOGY:
  4. 4. INFLAMMATION INTRODUCTION TYPES ACUTE INFLAMMATION CHEMICAL MEDIATORS OF INFLAMMATION CHRONIC INFLAMMATION
  5. 5. 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
  6. 6. TYPESOF INFLAMMATION ACUTE Rapid onset Short duration Fluid accumulation, plasma protein exudation Neutrophils CHRONIC Onset- insidious Longer duration Lymphocytes, macrophages, plasma cells as inflammatory cells
  7. 7. Pathogenesis: Three main processes occur at the site of inflammation, due to the release of chemical mediators ● Increased blood flow (redness and warmth). ● Increased vascular permeability (swelling, pain & loss of function). ● Leukocytic Infiltration.
  8. 8. Mechanism of Inflammation 1. Vasodilatation 2. Exudation ‐ Edema 3. Emigration of cells 4. Chemotaxis
  9. 9. ACUTE INFLAMMATION VASCULAR EVENTS CELLULAR EVENTS 1. HAEMODYNAMIC CHANGES 2. ALTERED VASCULAR PERMEABILITY 1. EXUDATION OF LEUKOCYTES 2. PHAGOCYTOSIS
  10. 10. VASCULAREVENTS 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
  11. 11. 4. Slowing or stasis Increased vascular permeability Increased concentration of RBCs Raised blood viscosity Slower blood flow
  12. 12. 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
  13. 13. 2. ALTERED VASCULAR PERMEABILITY STARLING’S HYPOTHESIS  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.
  14. 14. • Accumulation of fluid - interstitial compartment which comes from blood plasma by its escape through the endothelial wall of peripheral vascular bed. • Escape of fluid is due to vasodilatation and consequent elevation in hydrostatic pressure - transudate. • Subsequently, the characteristic inflammatory oedema, appears by increased vascular permeability of microcirculation – exudate.
  15. 15. MECHANISMS OF INCREASED VASCULAR PERMEABILITY
  16. 16. 1. Endothelial cell contraction reversible process mediated by histamine, bradykinin, leukotrienes short duration: 15-30 min. 2. Structural re-organisation of the cytoskeleton of endothelial cells - Reversible retraction at the intercellular junctions. • Mediated by cytokines such as interleukin-1 (IL-1) and tumour necrosis factor (TNF)-α.c
  17. 17. 3. Endothelial injury or Direct injury to endothelial cells Causes Cell necrosis and appearance of physical gaps. Process of thrombosis is initiated at the site of damaged endothelial cells. Affects all levels of microvasculature. immediate sustained response, lasts for several hours or days
  18. 18. 4. Leukocyte-mediated endothelial injury • Adherence of leucocytes to the endothelium at the site of inflammation. • Activation of leucocytes - release proteolytic enzymes and toxic oxygen. • Cause endothelial injury and increased vascular leakiness. • Newly formed capillaries under the influence of vascular endothelial growth factor (VEGF). • Process of repair and in tumours are excessively leaky 5. Neo vascularisation
  19. 19. CELLULAREVENTS 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.
  20. 20. 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
  21. 21. 2. ROLLING ANDADHESION: 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
  22. 22. ADHESION MOLECULES: SELECTINS : E-selectin P-selectin (cytokine-activated Endothelial cells) (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 FAMILYADHESION MOLECULE: ICAM-1,2
  23. 23. 3. EMIGRATION
  24. 24. 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
  25. 25. DIAPEDESIS Simultaneously escape of RBCs takes place through the gaps between the endothelial cells. DIAPEDESIS Diapedesis gives Hemorrhagic appearance to the inflammatory exudate.
  26. 26. 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.
  27. 27. 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.
  28. 28. 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
  29. 29. 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
  30. 30. INFILTRATION WITH MONO-NUCLEAR CELLS
  31. 31. • Incr. lysosomal enzymes • Greater abilityto phagocytose 55 ACTIVATION OF MACROPHAGE Cytokine IFN - ɤ Endotoxin , fibronectin chemical mediators
  32. 32. MACROPHAGE IN ACUTE INFLAMMATION Irritant eliminated- macrophagedisappears IN CHRONIC INFLAMMATION Persistent macrophage accumulationby following mechanisms : 1. )Recruitment from circulation– Chemotactic stimuli include: a) C5a b) Platelet derived growthfactor c) Transforming growthfactor s 2.) Local proliferation of macrophage 3.) Immobilization of macrophages 56
  33. 33. 57 TISSUE DESTRUCTION OR NECROSIS • ACTIVATED MACROPHAGES Elastase Protease Collagenase Reactive oxygen radical Cytokine IL-1,8
  34. 34. 58 PROLIFERATION Small BLOOD VESSELS FIBROBLAST Resulting in the formation of granulation tissue
  35. 35. 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 apical59 foramina
  36. 36. 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
  37. 37. • 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
  38. 38. 1) Robbin’s & Cotron Pathological basis of diseases 2) Essential pathology for dental students - Harsh mohan 3) Text book of oral pathology - Shafers References……..
  39. 39. THANKYOU

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