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INDIAN
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acute inflammation

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit 
www.indiandentalacademy.com

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit 
www.indiandentalacademy.com

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acute inflammation

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing Dental Education www.indiandentalacademy.com
  2. 2. REFERENCES • Robbins,Kumar,Abbas,Mitchell,Fausto. Textbook of Basic Pathology ,8th Edition. • Harshmohan.Textbook of Essential pathology, 5th Edition. •Walter and Isreal. General pathology 6th edition. www.indiandentalacademy.com
  3. 3. Learning objectives: At the end of the seminar learner should be able to: 1. Define inflammation. 2. Enumerate cardinal signs, causes of inflammation. 3. Describe events in acute inflammation . 4. Describe inflammatory mediators. 5. Describe outcomes, morphological patterns of inflammation. 6. Describe the clinical importance of inflammation. www.indiandentalacademy.com
  4. 4. History:  Signs of inflammation were described in an Egyptian papyrus, (3000 B.C.)  Celsus, a roman writer, in 1st century A.D., first listed four signs of inflammation  Rubor - Redness Tumor - Swelling Calor - Heat Dolor - Pain  Rudolf virchow (1858), added fifth sign, Loss of function (functio laesa) www.indiandentalacademy.com
  5. 5. SIGNS OF INFLAMMATION www.indiandentalacademy.com
  6. 6. Definitions : “The local response of living mammalian tissue to injury due to any agent”. “Inflammation is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.” www.indiandentalacademy.com
  7. 7. CAUSES 1. Physical agents 2. Chemical agents 3. Infective agents 4. Immunological agents heat, cold, radiation and mechanical trauma. organic and inorganic poisons. bacteria, viruses and their toxins. cell-mediated and antigen- antibody reactions. www.indiandentalacademy.com
  8. 8. Inflammation Acute Chronic Acute versus chronic inflammation are distinguished by the duration and the type of infiltrating inflammatory cells www.indiandentalacademy.com
  9. 9. “It is a rapid response to injury or microbes and other foreign substances that is designed to deliver leucocytes and plasma proteins to sites of injury.” www.indiandentalacademy.com
  10. 10. • The changes in acute inflammation can be described under the following headings- 1 ) Vascular changes - Changes in vascular caliber and flow. - Increased vascular permeability. 2) Cellular events - Exudation of leucocytes - Phagocytosis www.indiandentalacademy.com
  11. 11. VASCULAR CHANGES www.indiandentalacademy.com
  12. 12. Vascular events Alteration in the microvasculature is the earliest response to tissue injury, they are:  Hemodynamic changes  Increased vascular permeability www.indiandentalacademy.com
  13. 13. Haemodynamic changes The earliest feature of inflammatory response results from change in vascular flow and caliber of small blood vessel in injured tissue. www.indiandentalacademy.com
  14. 14. 1) Transient vasoconstriction of arterioles: -Immediate vascular response irrespective of the type of injury. -Vasoconstriction in mild to moderate injury: 3-5 seconds -In severe injury : lasts upto 5 minutes www.indiandentalacademy.com
  15. 15. 2) Persistent progressive vasodilatation : -Mainly involves arterioles, venules . - Changes are seen within half an hour. - Vasodilatation results in increased blood volume in the area responsible for heat and redness. www.indiandentalacademy.com
  16. 16. Vascular dilatation www.indiandentalacademy.com
  17. 17. 3) Elevation of local hydrostatic pressure : Results in transudation of fluid into extracellular space causing swelling at the site of inflammation. www.indiandentalacademy.com
  18. 18. 4)Slowing or stasis of the microcirculation  Caused by prolonged vasodilatation and increased permeability of microvasculature  Increased concentration of red cells  Increased blood viscosity www.indiandentalacademy.com
  19. 19. 5) leukocyte margination ( peripheral orientation)  Leukocytes mainly neutrophils stick to the vascular endothelium  moves and migrates through endothelial gaps into extracellular space called as emigration. www.indiandentalacademy.com
  20. 20. www.indiandentalacademy.com
  21. 21. Triple response: It demonstrates features of haemodynamic changes in inflammation www.indiandentalacademy.com
  22. 22. The Triple Response  Red line, Flare& Wheal (Lewis, 1927)  Take a blunt instrument and draw a line on your forearm. • Red line appears due to vasodilatation of capillaries and venules in response to injury. • Flare is red irregular zone or flush surrounding the red line, that develops due to arteriolar dilation. • Wheal a zone of edema due to fluid exudation. www.indiandentalacademy.com
  23. 23. ALTERED VASCULAR PERMEABILITY www.indiandentalacademy.com
  24. 24. Vascular changes & fluid leakage during acute inflammation lead to Edema in a process called Exudation Transudate •Result of hydrostatic imbalance •Low protein content •Specific gravity < 1.015 Exudate •Result of inflammation Vascular permeability •High protein content •specific gravity >1.020 www.indiandentalacademy.com
  25. 25. STARLING’S HYPOTHESIS  Fluid balance is maintained by 2 opposing sets of forces: 1) Intravascular hydrostatic pressure & interstitial osmotic pressure – Causes outward movement of fluid from circulation. 2) Intravascular osmotic pressure & interstitial hydrostatic pressure – Causes inward movement of fluid. www.indiandentalacademy.com
  26. 26. Increased vascular permeability is due to :- • Reduced osmotic pressure in the vasculature • Increased osmotic pressure in the interstitium www.indiandentalacademy.com
  27. 27. Mechanism of increased vascular permeability: www.indiandentalacademy.com
  28. 28. • Short – lived. (15-30 min.) • Reversible process. • For e.g. Mild thermal injury www.indiandentalacademy.com
  29. 29. •Endothelial cell contraction occurs rapidly after binding of mediators to specific receptors , is called the immediate transient response. •A slower and more prolonged contraction of endothelial cells, resulting from changes in the cytoskeleton, may be induced by cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1). •This reaction may take 4 to 6 hours to develop after the initial trigger and persist for 24 hours or more. www.indiandentalacademy.com
  30. 30. • It is usually seen after severe injuries (burns and some infections). www.indiandentalacademy.com
  31. 31.  In most cases leakage begins immediately after the injury and persists for several hours (or days) therefore, this reaction is known as the immediate sustained response.  Venules, capillaries, and arterioles can all be affected, depending on the site of the injury.  Direct injury to endothelial cells may also induce a delayed prolonged leakage that begins after a delay of 2 to 12 hours, lasts for several hours or even days, and involves venules and capillaries. www.indiandentalacademy.com
  32. 32. • Accumulated leucocytes release toxic oxygen species & proteolytic enzymes. www.indiandentalacademy.com
  33. 33. CELLULAR EVENTS -The cellular phase of inflammation consists of 2 processes: 1) Exudation of leucocytes. 2) Phagocytosis. www.indiandentalacademy.com
  34. 34. The sequence of extravasation of Leukocytes from blood to tissues: Margination and pavementing Adhesion and Rolling Emigration and Diapedesis Chemotaxis www.indiandentalacademy.com
  35. 35. Exudation of leukocytes  Changes in the formed elements of blood  Margination: Due of stasis of blood flow, leukocytes assumes a more peripheral position along the endothelial surface because of loss of plasma by exudation and it is called as margination. Pavementing: The neutrophils rests and adheres to the endothelium resembling pebbles and it is known as pavementing. www.indiandentalacademy.com
  36. 36. Margination & pavementing www.indiandentalacademy.com
  37. 37. www.indiandentalacademy.com
  38. 38. • Rolling and adhesion: Pavemented neutrophils slowly rolls over the endothelial cell lining the vessel wall this is followed by firm adhesion. 4 type of distinct adhesion molecule:  Selectins  Addresins  Integrins  Immunoglobulin super family adhesion molecule www.indiandentalacademy.com
  39. 39. www.indiandentalacademy.com
  40. 40. Emigration  After adhesion, neutrophils throw out their cytoplasmic pseudopods. It gets lodged between endothelial cells and basement membrane. Damages basement membrame with secreted collagenases. Escapes out into extravascular space. www.indiandentalacademy.com
  41. 41. Leukocyte adherence www.indiandentalacademy.com
  42. 42. CHEMOTAXIS  The Chemotactic factors mediate transmigration of leukocytes to reach interstitial tissue.  The factors are:  Leukotriene B4  Platelet factor 4  Complement system  Cytokines  Soluble Bacterial products  MCP-1  Chemotactic factor for CD4 +T cells & eosinophils. www.indiandentalacademy.com
  43. 43. The concept of chemotaxis is well illustrated by Boyden’s chamber experiment. www.indiandentalacademy.com
  44. 44. Phagocytosis : “Phagocytosis is defined as the process of engulfment of solid particulate material by the cells(cell-eating)”. Steps in phagocytosis: 1. Attachment stage 2. Engulfment stage 3. Secretion (Degranulation stage) 4. Killing/ Degradation www.indiandentalacademy.com
  45. 45. Stages in phagocytosis:  1) Attachment or opsonisation:  In order to establish a bond between microorganism and phagocytic cell ,the microorganism gets coated with opsonins.  And their corresponding receptor is present on the phagocyte. www.indiandentalacademy.com
  46. 46. The two main opsonins present in the serum and their corresponding receptor on the surface of phagocytic cell are: 1) IgG opsonin : Its receptor on Fc fragment of immunoglobulin on surface of phagocytic cell. 2)C3b opsonin : Is a fragment of complement and corresponding receptor for C3b on the surface of phagocytic cells. www.indiandentalacademy.com
  47. 47. 2) ENGULFMENT STAGE:  The opsonised particle is engulfed by formation of cytoplasmic pseudopods around the particle, enveloping it in phagocytic vacuole.  The lysosome of the cell fuses with the phagocytic vacuole and forms phagolysosome. www.indiandentalacademy.com
  48. 48. 3) DEGRANULATION:  PMNs discharge granules into phagosomes and extracellular environment.  Primary granules (azurophilic granules) fused with phagosomes.  Secondary granules are discharged. www.indiandentalacademy.com
  49. 49. 4) KILLING OR DEGRADATION STAGE:  The microorganism after being killed by anti bacterial substance are degraded by hydrolytic enzymes.  The antimicrobial agent acts by the following mechanism :  1) Oxygen dependent bacterial mechanism.  2) Oxygen independent bacterial mechanism.  3) Nitric oxide mechanism. www.indiandentalacademy.com
  50. 50. KILLING OF MICRO-ORGANISMS www.indiandentalacademy.com
  51. 51. Stages in phagocytosis www.indiandentalacademy.com
  52. 52. Stages of phagocytosis of a foreign particle www.indiandentalacademy.com
  53. 53. TO BE CONTINUE………. www.indiandentalacademy.com
  54. 54. Presented by: Sadaf Alvi Guided by: Dr. Minal Chaudhary Dr. Madhuri Gawande Dr.Swati patil Dr. Alka Hande www.indiandentalacademy.com
  55. 55. Learning objectives: At the end of the seminar learner should be able to: 1. Describe inflammatory mediators. 2. Describe outcomes, morphological patterns of inflammation. 3. Describe the clinical importance of inflammation. www.indiandentalacademy.com
  56. 56. CHEMICAL MEDIATORS OF INFLAMMATION www.indiandentalacademy.com
  57. 57. Cell-derived mediators CELL- DERIVED Mast cells, basophils, platelets Platelets Inflammatory cells Histamine Serotonin •PGs •Leukotriens •PAF •Cytokines •Nitric oxide & o2 metabolite Permeability & vasodilatation Permeability & vasodilatation Vasodilatation .fever, pain Permeability, chemotaxis, ,leukocytic adhesion Fever , pain Tissue damage www.indiandentalacademy.com
  58. 58. CELL-DERIVED MEDIATORS www.indiandentalacademy.com
  59. 59. 1. VASOACTIVE AMINES: Two important pharmacologically active amines that have role in the early inflammatory response , they are so named as they have important action on blood vessels . They are: A.HISTAMINE. B.SEROTONIN (5- HYDROXYTRYPTAMINE). www.indiandentalacademy.com
  60. 60. Histamine:  It is stored in the granules of mast cells, basophils and platelets.  Various factors responsible for the release of it :  Stimuli or substances inducing acute inflammation e.g. heat, cold, irradiation, trauma, irritant chemicals.  Anaphylatoxins like fragments of complement C3a , and C5a,  Histamine-releasing ptoteins from leukocytes.  Neuropeptides such as substance P.  Interleukins IL-1 IL-8. It causes:- • Vasodilatation of arterioles.  Increased vascular permeability of venules , itching and pain. www.indiandentalacademy.com
  61. 61. Serotonin (5-Hydroxytryptamine)  It is present in tissues like chromaffin cells of GIT, spleen, nervous tissue, mast cells and platelets. .  Actions :-  increased vascular permeability  vasodilatation . www.indiandentalacademy.com
  62. 62. Arachidonic acid metabolites (eicosanoids )  Arachidonic acid is a 20 carbon Polyunsaturated fatty acid derived from dietary sources or by conversion from the essential fatty acid linoleic acid. • It is present in esterified form as a component of cell membrane phospholipids. • It is released from membrane phospholipids through the action of cellular phospholipases. www.indiandentalacademy.com
  63. 63. www.indiandentalacademy.com
  64. 64. www.indiandentalacademy.com
  65. 65. 3. LYSOSOMAL COMPONENTS  Neutrophils and monocytes contain lysosomal granules, which when released, may contribute to the inflammatory response. These are as under: 1. Granules of neutrophils Specific/ Secondary. Azurophil/ Primary. 2. Granules of monocytes and tissue macrophages & eosinophils. www.indiandentalacademy.com
  66. 66. • Large azurophil ( primary) granules contains myeloperoxidase, bactericidal factors ( lysozymes, defensins), acid hydrolases & variety of neutral proteases. •Different granule enzyme serves different functions acid proteases act within the cell to cause destruction of bacteria and neutral proteases attack on extra cellular components. • Smaller specific ( secondary) granules contains lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histamine & alkaline phosphatase. a. Granules of neutrophills: www.indiandentalacademy.com
  67. 67. b. Granules of monocytes and tissue macrophages: • Releases mediators of inflammation like acid proteases, collagenase and plasminogen activator. • More active in chronic inflammation. www.indiandentalacademy.com
  68. 68. Eosinophil granule proteins Following activation by an immune stimulus, eosinophils degranulate to release an array of cytotoxic granules that are capable of inducing tissue damage and dysfunction. These include: •Major basic protien (MBP) •Eosinophil cationic protein (ECP) •Eosinophil peroxidase (EPO) •Eosinophil-derived neurotoxin (EDN) c. www.indiandentalacademy.com
  69. 69. 4. Platelet-Activating Factor Generated from membrane phospholipids of neutrophils, monocytes, basophils, mast cells, endothelium and platelets.  Actions:  vasoconstriction .  Bronchoconstriction.  Increased vascular permeability.  Enhanced leukocyte adhesion.  Chemotaxis and Degranulation. www.indiandentalacademy.com
  70. 70. 5. CYTOKINES • Cytokines are polypeptide substances produced by activated lymphocytes and activated monocytes. • TNF and IL-1, IL-6 are major cytokines that mediate inflammation . • Action in inflammation: • 1) Local effects: • Endothelium • Leukocytes • Fibroblasts • 2)Systemic effects www.indiandentalacademy.com
  71. 71.  Chemokines are proteins that act primarily as chemoattractants to specific types of leukocytes. They are classified into four major groups :-  C-X-C Chemokine: Act primarily on neutrophils.  C-C Chemokine : chemotactic for all leukocytes except neutrophils.  C Chemokine: specific for leukocytes.  CX3C Chemokine: Act on monocyte and T-cells. www.indiandentalacademy.com
  72. 72. 6. NITRIC OXIDE  Nitric oxide (NO) is described as vascular relaxation factor produced by endothelial cells, macrophages and neurons in the brain.  Various functions of NO :-  Vasodilatation.  Anti-platelet activating agent.  Microbicidal action. www.indiandentalacademy.com
  73. 73. 7. OXYGEN DERIVED FREE RADICAL  They are released extracellularly from neutrophils and macrophages after exposure to microbes and include superoxide oxygen (0‘2), H202, OH' .  These oxygen-derived free radicals have the following action in inflammation:  Endothelial cell damage and thereby increased vascular permeability.  Activation of protease and inactivation of antiproteases causing tissue matrix damage.  Damage to other cells like RBC. www.indiandentalacademy.com
  74. 74. PLASMA-DERIVED MEDIATORS www.indiandentalacademy.com
  75. 75. Plasma derived mediators PLASMA- DERIVED FIBRINOLYTIC SYSTEM KININ SYSTEM COMPLEMENT SYSTEM Fibrin split products Kinin/ Bradykinin Anaphylotoxins C3a, C4a, C5a permeability Permeability, pain Permeability ,chemotaxis www.indiandentalacademy.com
  76. 76. A. Kinin system ◦ The kinins are vasoactive peptides derived from plasma protein (kininogens) by the action of specific proteases called Kallikreins. ◦ Bradykinin is the most important Kinin . www.indiandentalacademy.com
  77. 77. ACTIVATION OF KININ SYSTEM ACTIVATION OF KININ SYSTEM www.indiandentalacademy.com
  78. 78. www.indiandentalacademy.com
  79. 79. Functions of Bradykinin: - Increases vascular permeability. - Causes contraction of smooth muscle. - Vasodilatation. - Pain www.indiandentalacademy.com
  80. 80. • This system is activated by plasminogen activator. • The sources of which include kallikrein of the kinin system, endothelial cells and leucocytes. • Plasminogen activator acts on plasminogen present as component of plasma proteins to form plasmin. • Further breakdown of fibrin by plasmin forms fibrinopeptides or fibrin split products . B.FIBRINOLYTIC SYSTEM www.indiandentalacademy.com
  81. 81. Fibrinolytic system www.indiandentalacademy.com
  82. 82. The actions of plasmin in inflammation are: •Splits off complement C3 to form C3a which is a permeability factor. • fibrin split products which increase vascular permeability and are chemotactic to leucocytes. www.indiandentalacademy.com
  83. 83. C. COMPLEMENT SYSTEM  It is a cascade system of enzymatic proteins.  function in both innate and adaptive immunity.  consists of more than 20 proteins.  complement proteins are present in inactive forms in the plasma .  many of them are activated to become proteolytic enzymes that degrade other complement proteins. www.indiandentalacademy.com
  84. 84.  The critical step in complement activation is proteolyis of C3.  Cleavage of C3 occurs by one of the three pathways: 1. Classical pathway 2. Alternative pathway 3. Lectin pathway www.indiandentalacademy.com
  85. 85. The activation and functions of the complement system. www.indiandentalacademy.com
  86. 86. The biologic functions of complement system fall into 3 general categories 1) Inflammation – C5a,C3a and C4a(lesser extent) 2) Phagocytosis-C3b acts as opsonins and promote phagocytosis. 3) Cell lysis - deposition of MAC(membrane attack complex)makes cells permeable to water and ions results in cell death. www.indiandentalacademy.com
  87. 87. Vasodilatation Prostaglandins Nitric oxide Histamine Serotonin, Increased vascular permeability Vasoactive amines C3a and C5a Bradykinin Leukotrienes PAF Substance P Chemotaxis C5a Leukotriene B4 Chemokines Fever IL-1, TNF Prostaglandins Pain Prostaglandins Bradykinin, substance p Tissue damage Neutrophil and macrophage lysosomal enzymes Oxygen metabolites Nitric oxide Role of Mediators in Different Reactions of Inflammation www.indiandentalacademy.com
  88. 88. Outcomes of acute Inflammation  Complete resolution.  Healing by connective tissue replacement (fibrosis).  Progression to chronic inflammation. www.indiandentalacademy.com
  89. 89. Outcomes of Acute Inflammationwww.indiandentalacademy.com
  90. 90. MORPHOLOGIC PATTERNS OF INFLAMMATION 1. Serous inflammation. 2. Fibrinous inflammation 3. Suppurative or Purulent inflammation (Abscess formation) 4. Ulcers www.indiandentalacademy.com
  91. 91. Serous inflammation www.indiandentalacademy.com
  92. 92. www.indiandentalacademy.com
  93. 93. Fibrinous inflammation www.indiandentalacademy.com
  94. 94. Purulent inflammation www.indiandentalacademy.com
  95. 95. ULCERS www.indiandentalacademy.com
  96. 96. APPLIED ASPECTS www.indiandentalacademy.com
  97. 97. SYSTEMIC EFFECTS OF ACUTE INFLAMMATION  Fever - Occurs due to bacteraemia. - In response to infection various chemical mediators releases like prostaglandins, interleukin-1, TNF are released. •Leucocytosis Neutrophilia points to bacterialinfection. Lymphocytosis points to viral infection. Eosinophilia points to allergy or parasitic infection. www.indiandentalacademy.com
  98. 98.  Lymphangitis- Lymphadenitis: • Manifestation of localized inflammatory injury. • The lymphatics and lymph nodes that drain the inflamed tissue show reactive inflammatory changes in the form of lymphangitis and lymphadenitis. www.indiandentalacademy.com
  99. 99. Benign (reactive) lymphadenopathy There are three distinct patterns of benign lymphadenopathy: •Follicular hyperplasia - Seen in infections, autoimmune disorders. •Paracortical hyperplasia - Seen in viral infections, skin diseases. •Sinus histiocytosis - Seen in inflammatory lesions and malignancies. www.indiandentalacademy.com
  100. 100. Shock: • Occur in severe cases. • Massive release of cytokine TNF- alpha in response to severe tissue injury or infection results in profuse systemic vasodilatation, increased vascular permeability and intravascular volume loss. •The net effect of these changes is hypotension and shock. www.indiandentalacademy.com
  101. 101. CONCLUSION:  The survival of all organism requires that they should eliminate foreign invaders such as, infectious pathogens and damaged tissues.  These functions are mediated by a complex host response called inflammation.  Inflammation accomplishes its protective mission by, destroying or otherwise neutralizing harmful agents.  The body attempts to heal the damage with some changes by the process of repair.  The repair begins almost as soon as the inflammatory changes have started and involves several processes, including cell proliferation and differentiation. www.indiandentalacademy.com
  102. 102. THANK YOU THANK YOU www.indiandentalacademy.com

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