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Inflammation
Inflammation is a protective , rapid host response that serves to deliver
leukocytes and plasma proteins, such as antibodies, to sites of infection or
tissue injury that intend to eliminate the initial cause of cell inj ury, as we ll
as the necrotic cells , and to initiate the process of repair.

Divide to two types

] -Acute inflammation

2- Chronic inflammation
What are the differences between acute and chronic inflammation?
Onset Fast :few minutes or hours Slow :days
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Cellular infiltration Mainly neutrophils Monocytes /microphage & 1

lymphocyte
. .
Tissues mJury Usually mild and self- Often sever and
fibroses limited progressive I
Local and systemic Prominent Less prominent -may be
sign subtle
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Factors that can stimulate inflammation

• Including:- microorganisms (bacterial and viral infection )
• Physical agents, injury, trauma, bu111s.
• Radiation.
• And corrosive chemicals such as acids, alkalis, and oxidizing agents.
• Inappropriate immunological responses .
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ardinal signs of acute inflammation

1-Rcdness:- caused by vasodilation of the blood capillaries

2-Hcat (increased temperature ):-caused by arterial di lat ion and increase
blood flow with production of chemical mediator (endogenous or
exogenous) .
3-Swelling:- caused by vascular dilation and accumulation of
inflammatory fluid and cellular exudate.
4-Pain : - caused by in-itation of the nerve endings by a toxins and pressure
of the inflammatory exudate on the sensory nerve.
5-Loss of function :-due to the destruction of tissue or to ovoid pain.
Changes that com binc with inflammatory process including:-

1-Vascular changes

When tissue is first injured, the small blood vessels in the damaged area
constrict momentarily, a process called vasoconstriction. Following
this transient event, which is believed to be of little importance to the
inflammatory response, the blood vessels dilate (vasodilation), increasing
blood flow into the area. Vasodilation may last from 15 minutes -to several
hours.

2-Cellular changes
-
• The most important feature of inflammation is the accumulation of white
blood cells at the site of injury. Most of these cells are phagocytes, certain
"cell-eating" leukocytes that ingest bacteria and other foreign particle.s and
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also clean up cellular debris caused by the injury. The 111ain phagocyte's
involved in acute inflammation are the neutrophils, a type of white blood
cell that contains granules of cell-destroying enzymes and pr_otei11s__. ~~ ---_-_ -=-.,. ~ -

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ype of i11jlammatio11
1- Serous inflammation: - an effusion of non -viscous scrou~ fluid under
condition of acute inflammation, commonly produced by mcsothelial ce lls of serous
membrane .TI1c exudation of this inflammation is clear fluid with no WBC. or PMNs.

Serous inflanunation of skin

Low power view of cross section of the skin blister shows the epidermis separated from the
dermis hy the foe.al collection of serous infusion
 __ Fihrinous inflammation:-gcncral morphological pattern of
inflammation, it occur when there is more extensive leakage of Ouid from
vascuJature, thus alJowing for passage of plasma protein .cspcciaJJy
fibrinogen in to the tissue.if the leakage is small much of the escaped
fibrinogen will be removed during the resolution phase of inOammation
.however if the leakage is extensive the mass of fibrinogcn is left in place
and remodeled, ultimately evolving in to fibrosis .

A;Deposits of fibrin on the pericardium.

B; A pink meshwork of fibrin exudate

 -Purulent inflammation- An acute form of exudativc inflammation in
which the enzymes produced by white blood cell s cause liquefaction of the
affected tissues, resulting in pus formation .

Multiple bacterial abscesses m the lung (arrow) m lung disease

(bronchopneumonia)

Chronic inflammation
*Occur more by adaptive immunity
*Last for weeks or months
The causes
1- Persistent infection :- Viral or parasite infection
2- Immune mediated: - auto-immune disease (self-antigen trigger
inflammatory response).
3- Persistent exposure to injurious agent :-silicosis in the lung
Main cells (macrophage, lymphocytes, and plasma cells).
Main effect -more tissue destruction, cellular infiltrates, blood vessels
proliferation, connective tissue deposition.

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 orphological pattern including:-
Granuloma fonnation which is an inflammation found in many diseases.
It is a collection of immune cells known as macrophages. Granulomas
fonn when the immune system attempts to wall off substances, it perceives
as foreign but is unable to eliminate such substances include infectious
organisms ( bacteria and fungi) , as well as other materials such
as keratin and suture fragments .

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typical granulom~ resulting from infection with Mycobacterium

tuberculosis showing central area of caseous necrosis, activated
epithelioid macrophages, giant cells, and a peripheral accumulation of
lymphocytes.

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 Repair, sometimes called Healing. refers to the restorntion of ti ssue arc.: hitcc.: tu rc
and function after an injury.

It occurs by two types of reactions :

• Rege11eratio11.
* Some tissues are able to replace the damaged cells and essentially return to a
nonnal state.
* Regeneration occurs by proliferation of residual (uninjured) cell s that retain the
capacity to divi de and by replacement from ti ssue stem cells.
* It is the typical response to injury in the rapidly dividing cpithcl ia of the skin and
intestines, and some parenchymal organs, notably the liver.

• Scar formation.
* If the injured tissues are incapable of regeneration, or if the supporting structures of
the tissue are severely damaged, repair occurs by the laying down of connective
(fibrous) tissue, a process that results in scar fonnation.

Keio id scar(excess collagen deposition 1n the skin forming a raised

scar)
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A, early Granu lation tissue showing numerous blood vessels, edema, and
a loose ECM containing occasional inflammatory ce11s. Collagen is
stained blue by the trichrome stain; minimal mature co11agen can be seen
at this point.

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B, Trichrome stain of mature scar, showing dense collagen with only

scattered vascular channels. ECM, extracellular matrix