Inflammation - Sonu

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inflammation

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Biology of inflammation Submitted by: Sonu M.Pharma 1 st year January 23, 2014 Sonu Baisoya Submitted to: Dr. Silvia Navis

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January 23, 2014 Sonu Baisoya Definition… ‘ ’Protective mechanism by which body deals with an injury or any insult, in which a series of local processes are initiated to contain the offensive agent, neutralise its effect, limit its spread &n hopefully eradicate it ’’

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 History… YEAR SCIENTIST EVENT 3000 BC CELCIUS CARDINAL SIGNS OF INFLAMMATION 1793 JOHN HUNTER INFLAMMATION IS A PROTECTIVE PROCESS 1839-84 JULIUS COHNHEIN UNDERLYING MECHANISM FOR THE CARDINAL SIGNS 1882 ELIE METCHINKOFF PHAGOCYTOSIS 1908 PAUL EHLRICH, METCHKINOFF CELLULAR & HUMOURAL FACTORS IN BODY DEFENSE SIR THOMAS LEWIS CHEMICAL MEDIATORS OF INFLAMMATION

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January 23, 2014 SONU BAISOYA

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Acute inflammation

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January 23, 2014 SONU BAISOYA Acute Inflammation is… The immediate & early response to an injurious agent, designed to deliver leukocytes to the site of injury. . Features : Fluid & plasma protein EXUDATION at the site of injury. 3.Predominantly NEUTROPHILLIC leukocyte accumulation.

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Cardinal signs... Rubor Calor Tumour Dolor Functio laesa

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Game plan for Acute Inflammation... Loosen the vessel & increase ECF fluid Cause stasis of blood & blood cells Recruitment of WBCs out of vessel to the injury site

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Components of acute inflammation…

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Vascular events

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Cellular events

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 1. Margination

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 2. Rolling

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 3. Tight adhesion

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 4.Transmigration

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 5.Diapedesis … This is a process by which the cell moves out of the blood vessel to the ECF. The WBCs secrete proteases to dissolve the basement membrane Leukocytes leave the bloodstream at the level of postcapillary venules ( Marchesi , 1961 ;  Marchesi and Florey, 1960 ).

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC It’s a process in which the WBCs follow the chemical gradient to the injury site. Soluble bacterial products Complement components (C5a) Cytokines ( chemokine family,IL-8) LTB 4 (AA metabolite) 6.Chemotaxis… Chemoattractants

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Chemotaxis …

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 7.Phagocytosis… ‘’Cellular process of engulfment of solid particle by the cell membrane to form a integral phagosome & destruction of that particle (cell eating)’’ Cells involved: Steps : Polymorphonuclear neutrophils Monocytes & Macrophaghes Opsonisation Recognition of opsonised particle Engulfment Degranulation Degradation

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC ontd …

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Chemical mediators

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Definition… ‘’These are endogenous chemical substances that are released from cells or plasma or the damaged tissue itself, to mediate & partake in various processes of acute inflammation like vasodilatation, increased vascular permeability, PMN chemotaxis , fever, pain, tissue damage etc…’’

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Chemical mediators Cell derived Plasma derived Vasoactive amine Eicosanoids Lysosomal contents PAF Cytokines Others Kinins Clotting system Fibrinolytics Complement system

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Vasoactive amines AMINES SOURCE STIMULUS FOR PRODUCTION FUNCTIONS HISTAMINE MAST CELLS BASOPHILS PLATELETS Physical injury Anaphylotoxins (C3a, C5a) Cytokines Histamine releasing factor from WBC When antibody binds mast cells arteriolar dilation Increased vascular permeability Of venule s SEROTONIN PLATELETS ENTERO CHROMAFFIN CELLS Platelet aggregation Same as histamine but less potent

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Eicosanoids Metabolites of ARACHIDONIC ACID ( source: diet/ linoleic acid) Autocoids or local harmones T ypes…

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC E icosanoids - cyclooxygenase products MEDIATORS TX A2 PG I 2 PG E2, D2, F2 SOURCE platelets endothelium Mast cells FUNCTION vaso constriction Platelet aggregation Vasodilator Platelet aggregation inhibitor Vasodilation edema

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Eicosanoids - lipoxygenase products Leukotriene B4 : Chemotaxis, PMN aggregation C4, D4, E4 : Vasoconstriction, increased vascular permeability, bronchospasm

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC EICOSANOIDS

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC C ytokines ‘’ They are polypeptides produced by activated lymphocytes ( LYMPHOKINES) & activated monocytes ( MONOKINES), act on other cells or the cells that produced them ‘’ MONOKINES : IL-1 , TNF alpha , IL-8 LYMPHOKINES : TNF beta , IF gamma CHEMOKINES : IL-8 (monokine) , PF-4

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC C ytokines’ functions…

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC NO & O2 metabolites SUBSTANCE SOURCE FUNCTION NITRIC OXIDE endothelium, activated macrophage vasodilation Microbicidal Anti-platelet activation OXYGEN METABOLITES Metabolic reactions Endothelial cell damage Increased vascular permeability Activation of protease Inactivation of anti protease causing tissue damage

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Neuropeptides These are small peptides that are secreted by the nerve fibres . COMMONEST SITE : GIT, lung EXAMPLE : Substance P FUNCTIONS : - Pain signal -Regulate vessel tone -Modulate permeability Plasma derived mediators These are the 4 inter related plasma derived cascades that are linked by the initial activation of the HAGEMAN FACTOR (Factor 12 of intrinsic coagulation cascade). STIMULUS FOR THE ACTIVATION OF FACTOR 12: When it encounters collagen, basement membrane or activation of platelets. Kininogen in the plasma Kallikrein , plasmin

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Factor 12 Factor 12a Kallikrein Pre- kallikrein Bradykinin kininogen plasminogen plasmin C3 C3a Clotting factors fibrin Fibrin degradation products

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 1. Kinin system This system ultimately leads to the formation of BRADYKININ. Its functions are: increased vascular permeability arteriolar dilation smooth muscle contraction pain. Kallikrein , an intermediade in this system is a potent activator of factor 12.

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC 2. Clotting system FACTOR Xa – increased vascular permeability, WBC emigration. THROMBIN – WBC adhesion to endothelium. FIBRINOPEPTIDES – increased vascular permeability, chemotaxis

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Fibrinolytic system Fibrin degradation products - increased vascular permeability. Plasmin - cleaves the complement C3 to C3a -A ctivates factor 12.

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Complement system ‘’ These are a group of proteins found in plasma & on cell surfaces, whose primary function is defense against microbes by generating a pore-like membrane attack complex that ultimately punches holes in the membranes of microbes’’ Complement components(numbered C1-C9) are present in plasma as inactive forms. Critical step in the elaboration of the biological functions of complement is the activation of the 3 rd complement, C3. C3 cleavage occurs by 2 mechanisms: CLASSICAL PATHWAY ALTERNATE PATHWAY

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC CLASSICAL PATHWAY - triggered by fixation of C1 to antigen-antibody complex. ALTERNATE PATHWAY - Triggered by bacterial polysaccharides ( eg:endotoxin ), complexpolysaccharides or aggregated IgA . C3, C5 can also be activated bt proteolytic enzymes within inflammatory exudate

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Functions of complement VASCULAR EFFECTS: - C3a, C5a ( anaphylotoxins ) increase vascular permeability by inducing histamine release by mast cells. C5a activates lipooxygenase pathway products of arachidonic acid. WBC ACTIVATION, ADHESION, CHEMOTAXIS: - C5a activates WBC & increases the affinity of their integrins . C5a is a potent chemotactic agent for PMN, monocytes , eosinophils , basophils . PHAGOCYTOSIS : - C3b, C3bi act as opsonins augmenting phagocytosis by cells bearing C3b receptors(PMN, Macrophages).

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Outcome of acute inflammation Complete resolution Healing by connective tissue replacement (fibrosis/scar formation) Progression to chronic inflammation

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Chronic inflammation ‘’ An inflammatory response of prolonged duration (weeks – months - years), provoked by the persistence of the causative stimulus & simultaneous presence of acute inflammation, tissue destruction and repair ‘’

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Causes of chronic inflammation Infectious organisms that resist clearance and form a persistent infection in tissue or undrained abscess cavities e.g mycobacterium tuberculosis , actinomycetes , treponema palidum and Staph aureus (in bone and pleural cavities ) Exposure to irritant non-living foreign material that can not be removed implanted materials into wounds (wood splinters), inhaled materials (silica, asbestos), deliberately introduced material (surgical suture material or prosthesis) Potentially normal tissue components as seen in auto-immune diseases Beta islet cell in diabetes mellitus type I , Acetyl cholin receptor in Myastenia gravis

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Characteristics of chronic inflammation Infiltration of mononuclear cells Tissue destruction Healing with scar formation and fibrosis

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC The dominant cellular players in chronic inflammation : Blood monocyte Tissue macrophage (RES) migrate into tissue within 48 hours after injury and differentiate Lymphocyte Plasma cell

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Ulcers Fistulas Granulomatous diseases Fibrotic diseases (Scaring) combinations of the above Outcome of chronic inflammation

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Granulomatous inflammation Granulomas are millimeter size nodules of chronic inflammatory cells that can be isolated or confluent. Granuloma formation is the result of dealing with indigestible substances or pathogens and walls them off The essential component are modified macrophages named epithelioid cell (because of shape). Epithelioid cells can form multinucleated giant cells . Epithelioid cells are surrounded by a collar of lymphocytes and occasionally plasma cells . Fibrous connective tissue often surrounds granulomas (remodeling of tissue) Areas within the granuloma can undergo necrosis (prototype: caseous necrosis in tuberculosis ). Necrosis can lead to calcification or liquefaction and formation of a cavern if drained .

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC Examples of granulomatous inflammation Specific infections (immune granuloma ): Mycobacteria (tuberculosis, lepprosy …) syphilis, brucellosis, … Foreign bodies: endogenous ( keratin, necrotic bone or adipose tissue uric acid crystals) Exogenous (wood, silica, asbestos, silicone…) Specific chemicals: Beryllium Drugs Allupurinol , phenylbutazone , sulphonamides (in liver) Unknown origin Sarcoidosis (although granuloma typically form to defend the host against known injurious agents, they can develop for unknown reasons and become injurious themselves) Hypersensitivity pneumonitis Tuberculosis Foreign body aspiration Berrylliosis

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January 23, 2014 Sonu Baisoya Thank you…

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January 23, 2014 Sonu Baisoya Bibliography Robbin’s & Cotran’s pathologic basis of disease- 7 th edition - Vinay kumar , Nelson fausto , Abul abbas . Rubin’s pathology: clincopathologic correlation of medicine 4 th edition- Emanuel rubins , Fred gorstein , Roland schwarting , David S.Strayer . Essential pathology for dental students 2 nd edition- Harsh mohan . Basic pathology: an introduction to mechanisms of diseases 2 nd edition- Sunil R. Lakhani , susan A. Dilly, Caroline J. http://www.nature.com/labinvest/journal/v82/n5/full/3780446a.html

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January 23, 2014 Dept of Oral & Maxillofacial pathology, TNGDC http://www.telmeds.org/atlas/patologia/patologia-general/inflamacion/inflamacion-aguda/marginacion-y-diapedesis/ http://visualsunlimited.photoshelter.com/image/I0000_MyTlWr2r7Y http://newscenter.lbl.gov/news-releases/2008/11/05/proteomics-study-yields-clues-as-to-how-tuberculosis-might-be-thwarting-the-immune-system/ http://www.sciencephoto.com/images/download_lo_res.html?id=670066706 Reference for pictures

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