inflammation
TRANSCRIPT
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ACUTE INFLAMMATION
Dr.mounika
Fist year MDS
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CONTENTS:
Definition
Acute inflammation.
Inflammatory exudate
Outcome of acute inflammation
Chemical mediators and regulators of inflammation
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DEFINITION
Inflammation is a protective response involving host
cells, blood vessels, and proteins and other
mediators that is intended to eliminate the initial
cause of cell injury, as well as the necrotic cells and
tissues resulting from the original insult, and to
initiate the process of repair.
Inflammare (Latin) : To set on fire
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TYPES OF INFLAMMATION
Acute: rapid onset and short duration.
Chronic: Slowest onset and prolonged duration.
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EXTERNAL MANIFESTATIONS OR
CARDINAL SIGNS
Calor-heat
Rubor-redness
Tumor-swelling
Dolor-pain
Functio laesa- loss of function
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STEPS OF INFLAMMATORY RESPONSE
1)recognition of injurious agent
2)recruitment of leukocytes
3)removal of the agent
4)regulation of response
5)resolution
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ACUTE INFLAMMATION
-Immediate and early response .
-rapidly deliver leukocytes and plasma proteins .
It has two major events:
Vascular events
Cellular events
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STIMULI
Infections
Trauma
Physical and chemical agents
Foreign bodies
Immune reactions
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VASCULAR CHANGES
Altered blood vessel caliber and flow
Vasodilation slowing of flow stasis of blood cells
leukocyte margination
Increased vascular permeability (leakage)
Escape of protein-rich fluid into interstitium altered
osmotic pressure gradient further outflow of fluid
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INCREASED VASCULAR PERMEABILITY
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INFLAMMATORY EXUDATE
Increased vascular permeability: results protein rich fluid accumulation called exudate.
Mechanisms: 1)endothelial cell contraction leading to intercellular gaps in post capillary venules.
2)endothelial injury causing endothelial cell necrosis and detachment.
3)leukocyte mediated vascular injury.
4)leakage from new blood vessels.
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FUNCTION OF INFLAMMATORY EXUDATES
1-Dilution
2-Bring antibodies .
3-Bring leukocytes .
4-Bring fibrinogen .
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RESPONSES OF LYMPHATIC VESSELS:
Lymph flow is increased and helps drain edema
fluid, leukocytes and cell debris from extravascular
space.
Lymphatics and draining lymph nodes may become
secondarily inflamed termed inflammatory
lymphadenitis.
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CELLULAR EVENTS
Emigration of leucocytes ,accumulation .
Activation of leucocytes, enabling them to eliminate
the offending agent
Principal leucocytes are polymorpho nuclear
leucocytes
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CELLULAR EVENTS
LEUKOCYTE RECRUITMENT:
Sequence of events:
1)margination and rolling: as blood flows, circulating
cells are swept by laminar flow against the vessel
wall.
larger LEUCOCYTES are pushed out of central
axial column and thus interact with lining
endothelial cells. = margination.
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If endothelial cells are activated by cytokines and
mediators--express adhesion molecules to which
leukocytes attach loosely.
these cells bind and detach and thus begin to
tumble on endothelial surface, a process called
rolling.
Mediated by selectin family of adhesion molecules.
three members are-
E-SELECTIN-on endothelial cells.
P-SELECTIN-on platelets and endothelium
L-SELECTIN-on surface of most leucocytes
They are induced after stimulation.
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2)ADHESION:
Rolling leucocytes sense changes .
initiate firm adhesion.
mediated by integrins - leukocyte cell surfaces +
ligands - endothelial cells.
Cytokine stimulated increased integrin affinity and
increased expression of integrin ligands provides
stable attachment of leucocytes to endothelial cells
at sites of inflammation.
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3)TRANSMIGRATION:
By squeezing between cells at intercellular
junctions called diapedesis.
mainly in venules of systematic vasculature.
Leucocytes secrete collagenases - pass through
the vascular basement membrane.
Driven by chemokines produced in extravascular
tissues toward their chemical gradient
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4)CHEMOTAXIS
After extravasating from blood, leucocytes move
toward sites of infection or injury along a chemical
gradient by a process called chemotaxis.
Chemotactic substances:
Soluble bacterial products.
Cytokines
Components of complement system,C5
Products of lipooxygenase pathway of arachidonic
acid metabolism, leukotriene B4.
They bind to specific receptors, triggers cytoskeletal
contractile elements for movement.
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LEUCOCYTE LOCOMOTION
Leucocytes move by extending pseudopods that anchor to ECM and then pull the cell in direction of extension.
Neutrophils predominate in inflammatory infiltrate during first 6 to24 hours and are replaced by monocytes in 24 to 48 hours.
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LEUCOCYTE ACTIVATION: cellular receptors - responses in leukocytes -
defensive function =leukocyte activation.
Functions:
Phagocytosis of particles
Intracellular destruction of phagocytosed microbes
and dead cells.
Liberation of substances that destroy extracellular
microbes and dead tissues
Production of mediators.
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PHAGOCYTOSIS
Steps :
1) recognition and
attachment-
opsonization
2) engulfment, with
subsequent formation
of a phagocytic vacuole
3)killing and
degradation of ingested
material.
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RECOGNITION OF MICROBES , NECROTIC
CELLS ,AND FOREIGN SUBSTANCES
Toll like receptors: there are 10 mammalian TlRs
which recognize products of bacteria and other
pathogens located in plasma membranes and
endosomes , so they are able to detect extracellular
and ingested microbes.
provide defense against essentially all classes of
infectious pathogens
Recognition stimulates production of mediators of
inflammation, antiviral cytokines and proteins that
promote lymphocyte activation and even more
potent immune response.
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INFLAMMASOME: multi-protein cytoplasmic
complex that recognizes products of dead cells
such as uric acid and extracellular ATP ,crystals
and some microbial products.
activates enzyme called caspase-1 which cleaves
inflammatory cytokine interleukin-1B into
biologically active form. It recruits leukocyte and
they phagocytose and destroy dead cells.
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FACTORS INVOLVED IN TERMINATION OF
ACUTE INFLAMMATION
- Short half-life of inflammatory mediators.
- Lipoxins
Anti-inflammatory mediators.
Derived from arachidonic acid metabolites.
Inhibit transmigration and chemotaxis.
-Resolvins
Synthesized from omega-3 fatty acids.
Inhibit production and recruitment of
inflammatory cells to the site of inflammation.
-Clearance of neutrophils by apoptosis
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OUT COMES OF ACUTE INFLAMMATION
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CHEMICAL MEDIATORS OF
INFLAMMATION
- Mediators may be circulating in the plasma or they
may be produced locally by cells at the site of
inflammation.
- Most mediators induce their effects by binding to
specific receptors on target cells.
- Mediators may stimulate target cells to release
secondary effector molecules.
- Mediators may act on only one or a very few
targets or they may have widespread activity.
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PREFORMED MEDIATORS
Vaso active amines:
Histamine
serotonin
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ARACHADONIC ACID METABOLITES
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LYSOSOMAL CONSTITUENTS
- Acid proteases - degrade bacteria and debris
within phagolysosome
- Neutral proteases – capable of degrading
various extra cellular components such as
collagen, basement membrane
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PLATELET ACTIVATING FACTOR
. Released by IgE sensitised platelets, mast cells,
basophils, macrophages, endothelial cells.
Functions:
platelet aggregation
low doses – vasodilatation, otherwise
vasoconstriction
increased leukocyte adhesion
chemotaxis
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PLASMA PROTEIN DERIVATED
MEDIATORS
Plasma proteases
- Kinnins
- Clotting system
- Fibrinolytic system
- Complement cascade
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IN DENTISTRY
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ACUTE NECROTISING ULCERATIVE
GINGIVITIS:
A painful, erythematous gingivitis with necrosis of
interdental papillae Most likely caused by both a fusiform bacillus and a
spirochete (Borrelia vincentii)
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ACUTE PERICORONITIS
Inflammation around the crown of a partially
erupted, impacted tooth Most commonly a lower third molar
Trauma from an opposing molar and impacted food
under the soft tissue flap (operculum) may precipitate.
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ACUTE OSTEOMYELITIS
Acute inflammation of the bone and bone marrow Most commonly the result of a periapical abscess
May follow fracture of a bone
May result from a bacteremia
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ACUTE PULPITIS, ACUTE PERIAPICAL
ABSCESS, ACUTE APICAL PERIODONTITIS
Inflammation of dental pulp due to dental caries,
trauma or dental procedures
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Surgical removal of impacted 3rd molars.