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Inflammation-1
Inflammation-1

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Shashi-12/02/13
Shashi-Mar 2000
Inflammation-2

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

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Shashi-Mar 2000
Inflammation-3

"Opportunities are usually
disguised by hard work, so
most people don't recognize
them."
- Ann Landers
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Shashi-Mar 2000
Inflammation-4







“Inflame” – to set fire.
Inflammation is “dynamic response of
vascularised tissue to injury.”
Is a protective response.
Serves to bring defense & healing
mechanisms to the site of injury.
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Shashi-Mar 2000
Inflammation-5





Flush: capillary dilatation.
Flare: arteriolar dilatation.
Weal: exudation, edema.

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Inflammation-6

(Flare, Flush & Weal – Lewis)

Triple response

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Inflammation-7

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Inflammation-12








Rubor : Redness – Hyperaemia.
Calor : Warm – Hyperaemia.
Dolor : Pain – Nerve, Chemical
med.
Tumor: Swelling – Exudation
Loss of Function:
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Inflammation-13

1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis

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Inflammation-14

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Inflammation-16

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





Chemical substances synthesised or released
which mediate the changes in inflammation.
Histamine by mast cells - vasodilatation.
Prostaglandins – Cause pain & fever.
Bradykinin - Causes pain.

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Shashi-Mar 2000
Inflammation-20



Acute:
Exudative Inflammation: excess fluid. TB lung.
 Suppuration/Purulent – Bacterial - neutrophils
 Fibrinous – pneumonia – fibrin
 Serous – excess clear fluid – Heart, lung
 Haemorrhagic – b.v.damage - anthrax.




Chronic inflammation: with healing.


Grannulomatous – clusters of epitheloid* cells eg. TB,
Fungus, Foreign body.

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Shashi-Mar 2000
Inflammation-21

“Never let the competition define you.
Instead, you have to define yourself
based on a point of view you care
deeply about.”
– Tom Chappel

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Shashi-Mar 2000
Inflammation-22

Fibrosis/Scar
Resolution
Injury

Acute
Inflammation

Chronic
Inflammation

Abscess

Fungus
Virus
Cancers
T.B. etc.

Ulcer
Fistula

Sinus

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Inflammation-23

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







Flush, Flare &
Weal
Acute
inflammatory cells
- Neutrophils
Vascular damage
More exudation
Little or no fibrosis









Little signs Fibrosis,
Chronic
inflammatory
cells –
Lymphocytes
Neovascularisation
No/less
exudation
Shashi-Mar 2000

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Inflammation-34

"People who soar, are those
who refuse to sit back and
wish things would change."
Charles R. Swindoll
Author and Pastor
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Inflammation-35

Heat

Redness Swelling
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Pain Loss Of Func.
Shashi-Mar 2000
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Inflammation-36

Dr. Venkatesh M. Shashidhar.
Associate Professor of Pathology
Fiji School of Medicine
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Inflammation-37







Hemorrhage
Inflammation
Granulation tissue (soft callus)
Scar – Fibrosis (hard callus)
Remodeling & Wound strength

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Shashi-Mar 2000
Inflammation-38






Regeneration of injured tissue by parenchymal
cells of the same type
Replacement by connective tissue
In other words
Regeneration
 Scar


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Shashi-Mar 2000
Inflammation-39



Labile cells - continuously dividing




Stable cells - low level of replication




Epidermis, mucosal epithelium, GI tract epithelium
etc
Hepatocytes, renal tubular epithelium, pancreatic
acini

Permanent cells - never divide


Nerve cells, cardiac myocytes, skeletal mm

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Shashi-Mar 2000
Inflammation-40







Most Important Mediators affecting Cell Growth
Present in serum or produced locally
Exert pleiotropic effects; proliferation, cell
migration, differentiation, tissue remodeling
Regulate growth of cells by controlling
expression of genes that regulate cell
proliferation

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Shashi-Mar 2000
Inflammation-41






Occurs when repair by parenchymal
regeneration alone cannot be accomplished
Involves production of Granulation Tissue
replacement of parenchymal cells with
proliferating fibroblasts and vascular
endothelial cells

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Shashi-Mar 2000
Inflammation-42






Angiogenesis - New vessels budding from old
Fibrosis, consisting of emigration and
proliferation of fibroblasts and deposition of
ECM
Scar remodeling, tightly regulated by
proteases and protease inhibitors

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Shashi-Mar 2000
Inflammation-43






Induction of acute inflammatory response by
an initial injury
Parenchymal cell regeneration
Migration and proliferation of parenchymal
and connective tissue cells

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Shashi-Mar 2000
Inflammation-44






Synthesis of ECM proteins
Remodeling of parenchymal elements to
restore tissue function
Remodeling of connective tissue to achieve
wound strength

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Inflammation-45

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Inflammation-46

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Inflammation-47





After sutures are removed at one week, wound
strength is only 10% of unwounded skin
(Walker’ Law)
By 3-4 months, wound strength is about 80% of
unwounded skin (Walker’s Law)

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





Systemic
Age
Nutrition
Vitamin def.
Immune status
Other diseases








Local
Infection
Size or extent.
apposition
Blood supply
Mobility
Foreign body

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Shashi-Mar 2000
Inflammation-52








Healing – Proliferation & Differentiation.
Labile, Stabe & Permanent cells
Stages of Healing: 1-2-3-4….
Healing by First or Second intention.
Skin wound healing - bone healing.
Factors affecting healing – Local / Systemic

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Shashi-Mar 2000
"Each time you are honest and conduct
yourself with honesty, a success force will
drive you toward greater success. Each
time you lie, even with a little white lie,
there are strong forces pushing you
toward failure."
Joseph Sugarman
Author and Marketing Specialist
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Inflammation-54

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Leader in continuing dental education

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Shashi-Mar 2000

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