8/6/23

ACUTE INFLAMMATION

UNDER THE GUIDANCE:

Assoc.Prof.Dr.MANDEEP SINGH
DINGRA
Asst.Prof. Dr. KHUSHBU ADHIKARI
Asst.Prof.Dr.BIKASH KUMAR Dr. SONI BISTA
1ST YEAR PG STUDENT
PERIODONTOLOGY AND ORAL
IMPLANTOLOGY
1. Clinical characteristics of inflammation
2. Stimuli of acute inflammation
3. Reactions of blood vessels in acute
inflammation
4. Cellular processes in acute inflammation
5. Phagocytosis
6. Outcomes of acute inflammation
7. Mediators of inflammation
8. Fate of acute inflammation
 INFLAMMATION

Response of vascularized tissues to infections and

damaged tissues that brings cells and molecules of
host defense from the circulation to the sites where
they are needed, in order to eliminate the offending
agents.
 WITHOUT INFLAMMATION

 Infections would go unchecked

 Wounds would never heal
 Injured tissues might remain permanent festering
sores.
 O LF
D
RU HOW
C
VIR

_CELSUS
 ACUTE INFLAMMATION

 Rapid host response to deliver leukocytes and plasma

protein to the sites of infection or tissue injury.

 Develops within min/hrs; short duration

 Exudation of fluid and plasma proteins (edema)

 Emigration of leukocytes, mainly PMNs

 STIMULI OF
INFLAMMATION
INFECTION
TRAUMA
Bacteria/virus/
fungal/parasitic
Thermal
injury/toxicity

TISSUE FOREIGN
NECROSIS BODIES
ischemia Splinter/dirt/sting

IMMUNE
STEPS OF INFLAMMATORY
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 COMPONENTS

1. VASCULAR CHANGES

2. CELLULAR EVENTS: LEUKOCYTE

EXTRAVASATION AND PHAGOCYTOSIS

3. TERMINATION OF ACUTE INFLAMMATORY

RESPONSE
 1. VASCULAR CHANGES

A) Changes in vascular caliber – Vasodilation with or

without prior Vasoconstriction

B) Vascular leakage – to deliver leukocytes to the area

of insult
A) Changes in vascular caliber

Trauma followed by early vasodilation

Stasis of blood (vascular congestion)

Erythema and increased vascular permeability

Leukocytes arranged in periphery

B) Increased Vascular Permeability
 Hallmark of acute inflammation
 Contraction of endothelial cells resulting in increased
interendothelial spaces is elicited by chemical mediators.
 It is immediate transient response usually short-lived
(15–30 minutes).
 In some mild injuries e.g burns, x or ultraviolet radiation,
certain bacterial toxins, occurs after a delay of 2 to 12
hours lasting for several hours or days, mild endothelial
damage.
  Increased transport of fluids and proteins, called
transcytosis, through the endothelial cell.
VASCULAR LEAKAGE : MECHANISMS
 2. CELLULAR EVENTS: LEUKOCYTE
EXTRAVASATION AND PHAGOCYTOSIS

 Margination , rolling, adhesion to endothelium.

 Migration across endothelium.
 Migration towards chemotactic stimuli.

 Leads to recruitment of leukocytes to sites of

infection and injury and then phagocytosis
MECHANISM

Stasis of blood

Redistribution of
leukocytes
(margination)

Rolling ( selectins)

Adhesion(integrins)
 Leukocyte exudation
 Divided into 4 steps

1. Margination, rolling, and adhesion to endothelium

2. Diapedesis (trans-migration across the endothelium)

3. Migration toward a chemotactic stimuli from the source

of tissue injury.

4. Phagocytosis
The multistep process of leukocyte migration
through blood vessels, shown here for neutrophils
 PHAGOCYTOSIS
 Recognition and attachment : Receptors

 Engulfment :Extension of
cytoplasm(pseudopods)around particle and
Phagosome fuses with lysosomal granules

 Killing or degradation: Oxygen dependent mechanism

(reactive oxygen species)
 Leukocyte mediated tissue injury
 Causes injury to normal cells under several
cirumstances.
 Collateral damage as a part of normal defence against
infectious microbes.
 Inflammatory response is inappropriately directed
against host tissues.
 Host reacts excessively against usually harmless
environmental substances .

Mechanisms involved is same as of antimicrobial

destruction.
 MEDIATORS OF INFLAMMATION
 Properties and principles of mediators
 Are generated either from cells or plasma proteins.
 Active mediators are produced in response to
various stimuli.
 One mediators can stimulate the release of other
mediators.
 Mediators vary in their range of cellular targets.
 Once released from the cell most of these mediators
are short lived.
 OUTCOMES OF ACUTE
INFLAMMATION

1. Complete Resolution

2. Healing by connective tissue replacement (fibrosis)

3. Progression to Chronic Inflammation

 Morphologic PATTERNS
of Acute INFLAMMATION

 Serous (watery)
 Fibrinous (hemorrhagic, rich in FIBRIN)
 Suppurative (PUS)
 Ulcerative
Textbook of pathologic basis of
disease by Robbins and Cotran

Images _ Google