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1. ACUTE AND CHRONIC
INFLAMMATION
INDIAN DENTALACADEMY
Leader in continuing Dental
Education
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2. INFLAMMATION :
 Immediate and early response to tissue injury
(physical, chemical, microbiologic, etc.)
 It is body defence reaction in order to
eliminate or limit the spread of injurious
agent as well as to remove the consequent
necrotised cells and tissues
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3. Types of inflammation
 Acute inflammation
 Chronic inflammation
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4. Functions of Inflammation
1. Destroy and remove pathogens
2. If destruction is not possible, to limit
effects by confining the pathogen and its
products.
3. Repair and replace tissue damaged by
pathogen and its products.
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5. Beneficial effects :
 Dilution of toxins
 Entry of antibodies
 Transport of drug to the site of action
 Fibrin formation
 Delivery of nutrients and oxygen
 Stimulation of immune response
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6. Causative Agents :
 Physical agents :
- heat, cold, radiation, mechanical trauma
 Chemical agents :
-Organic & Inorganic poisons
 Infective agents :
-Bacteria,Viruses, andToxins
 Immunological agents :
-Cell mediated &antigen-antibody reactions
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7. LOCAL MANIFESTATIONS
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8.  Fever
 Chills
 Myalgia
 Malaise
ACUTE INFLAMMATION
SYSTEMIC MANIFESTATIONS
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9.  Vasoconstriction
 Vasodilation
 Increased vascular permeability
 Hemoconcentration and stasis
 Leukocyte Adhesion
 Transmigration
 Chemotaxis
 Aggregation
 Phagocytosis
ACUTE INFLAMMATION
STEPS INVOLVED IN INFLAMMATION
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10. Process of Inflammation
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11. ACUTE INFLAMMATIONVASODILATION
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12. Normal flow
Stasis
ACUTE INFLAMMATION
HEMOCONCENTRATION AND STASIS
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13. ACUTE INFLAMMATION
LEUKOCYTE ADHESION
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14. ACUTE INFLAMMATION
EMIGRATION (TRANSMIGRATION)
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15. ACUTE INFLAMMATION
CHEMOTAXIS
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16. ACUTE INFLAMMATION
AGGREGATION
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17. ACUTE INFLAMMATION
PHAGOCYTOSIS - ENGULFMENT
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18. Chemical mediators of inflammation
 Cell derived chemical mediators
-Mast cells, Basophils, platelets
1.Lysosomal enzymes - tissue damage
2.platelet activate factors - Permeability
3.Prostaglandins –Vasodilatation
4.Leukotrienes – increased Permeability
5.Cytokines - fever
6.Nitric oxide &oxygen metabolites –tissue
damage
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19. Contd….
 Plasma derived
1. Clotting & fibrinolytic system
2. Kinin system
3. Complement system
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20. Fate of A.I.
 Resolution
 Healing by scarring
 Suppuration
 Chronic inflammation
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21. Chronic inflammation
 reasons:
 persisting infection or prolonged exposure to
irritants (intracell. surviving of agents -TBC)
 repeated acute inflamations (otitis, rhinitis)
 primary chronic inflammation - low virulence,
sterile inflammations (silicosis)
 autoimmune reactions (rheumatoid arthritis,
glomerulonephritis, multiple sclerosis)
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22. Causes :
 Followed by A.I.
Ex: Osteomylities,pneumonia
 Recurrent attack of A.I.
Ex: A.I. of gall bladder
 C.I. Starting de novo
Ex : tuberculosis
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23. Cells involved :
 Lymphocytes
 Plasma cells
 Eosinophils
 Mast cells
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24. SYMPTOMS :
 Fever
 Anaemia
 Leucocytosis
 ESR
 Amyloiclosins
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25. Types of C.I.
 Non specific
Ex:chronic osteomylitis , chronic ulcer
 Specific
Ex: T.B.
Syphilis
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26. DIAGNOSIS :
 Blood test
 X – ray
 Laproscopy
 Endoscopy
 Morphological changes of perticular body
part
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27. Complications
 A.I. can be lead to C.I.
 Surrounding tissue damage
 Pain persisting for long time
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28. Treatment
 NSAIDS
 STEROIDAL DRUGS
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29. THANKYOU………
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