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Inflammation & Repair

By Dr.
Maha M. Abu-Hashim
Spring 2016
It is local reaction of living tissue to
injurious agents. It is the vascular
response to injury.
Aim of inflammation is to localize and
get rid of the injurious agent.
Inflammation may be acute or chronic.
The suffix “itis” is added to the base word to
state the condition e.g tonsil/tonsilitis….
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Acute inflammation……….Objectives
1. Definition…
2. List 4 cardinal signs of acute inflammation and the
reason for each.
3. Describe the vascular and cellular events of acute
inflammation (Pathogenesis).
4. List the cells of the inflammatory process and
their activity.
5. Define exudate, transudate, and pus.
6. Define the following, fibrinous, serous, suppurative
and catarrhal inflammation, abscess, and cellulitis.

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Acute inflammation
 It is a type of inflammation characterized
1. Sudden onset
2. Short duration
3. Caused by strong irritant
4. Exudative in nature
5. Followed by repair

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Cardinal Signs of acute
1- Redness Hotness
2- Heat Pain
3- Swelling Loss of function

4- Pain
5- Loss of function

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Acute inflammation
Vascular changes

Initial (seconds-5 min.)

arteriolar vasoconstriction.

After that there’s precapillary

arteriolar vasodilatation
resulting in greater blood flow
to the area. This lasts as long
as the acute inflammation
persists (redness and hotness)

Also, there’s increased vascular

permeability (exudate &swelling)
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Exudate and transudate
1- Exudate.. It is a protein rich fluid that occurs in acute inflammation
due to increased vascular permeability.

2- Transudate…It is a protein poor fluid that occurs due to increased

vascular hydrostatic pressure.

 Exudate  Transudate
-Due to increased vascular - Due to increased
permeability. hydrostatic pressure.
- Rich in protein esp. - Low protein content.
fibrin( aspect is turbed) (aspect is clear)
- Coagulates on standing. - Does not.
- High specific gravity - Low specific gravity less
more than 1018). than 1018).
- Contains inflammatory - No( few) inflammatory
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cells. cells
Acute inflammation
Cellular events
1. After vasodilatation,
leukocytes (especially
polymorphes) move from
the vessel into the
interstitial tissue
2. Neutrophils (polymorphes
are the first cells to
emigrate in acute
inflammation followed by
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Cellular events
Vascular and cellular events
1- Emigration

2- Chemotaxis
- It is the directional movement of
leucocytes towards the irritant within the
area of inflammation.

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Cellular events
 Vascular and cellular events

 1- Emigration
 2- Chemotaxis
 3- Phagocytosis
 It is the ingestion and destruction of particulate material
(tissue debris, living or dead bacteria and other foreign
cells) by phagocytic cells mainly neutrophils and monocytes-

 Phagocytosis is facilitated by opsonization which is the

coating of particulate material by substances that
immobilize the particles to the surface of the phagocytes.

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Phagocytosis 3


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Vascular and cellular changes in acute inflammation

 1- Vaso-constriction.
2- Vasodilataion.
3- Increased vascular permeability.
4- Formation of fluid exudate (characters and
differences between it and transudate).
5- Emigration of leukocytes (neutrophils first them
6- Chemotaxis.
7- Phagocytosis (after opsonization).
8- Bacterial destruction.

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Types of acute inflammation
 According to the presence or absence of pus, acute
inflammation is either suppurative or non-suppurative

- Suppurative (purulent)
- Severe acute inflammation with pus formation
- It is caused by pyogenic bacteria e.g. staph.aureus,
strept. Pyogenes, E.coli…..etc.

Pus is a semi fluid, formed of dead and living

neutrophils, micro-organism, necrotic tissue and fluid

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Types of suppurative inflammation

 Localized 1.abscess 2. boil (fruncle) and 3.carbuncle

1 –Abscess:-
* A localized suppurative inflammation characterized by
the formation of an irregular cavity containing pus .

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Types of suppurative inflammation
 2- Boil
Small abscess related to hair follicles, sweat or sebaceous
 3-Carbuncle
Multiple communicating suppurative foci in the subcutaneous
tissue opening to the surface by multiple sinuses.
It is common in diabetic patients
 Diffuse suppurative inflammation…= Cellulitis

Boil Carbuncle

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Non suppurative inflammation
 1- Serous and serofibrinous inflammation…
 2- Catarrhal inflammation…e.g common cold
 3- Pseudomembranous inflammation…e.g diphtheria &
bacillary dysentry.
 4- Hemorrhagic inflammation ….Vascular damage and
 5- Necrotizing inflammation …. Excess tissue necrosis
 6- Allergic inflammation …. From Antigen/Antibody

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1- Serous inflammation

Excess watery fluid


Occurs in burns and

some viral infections
where (blisters) are

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Non-suppurative inflammation
 2- Serofibrionous inflammation…. Exudation of serous
fluid rich in fibrinogen.
 3- Catarrhal inflammation…
Mild acute inflammation of
the mucous membranes with
excess mucin secretion.
 4- Pseudomembranous inflammation…
Acute inflammation characterized
by formation of pseudomembrane
formed of fibrin, desquamated
epithelium and inflammatory cells.

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Outcomes (Fate) of Acute
1-Resolution..complete restoration of normal tissues
2-Abscess (via liquefactive necrosis)
3-Scar (sometimes occurs even if pathogen is eliminated)
4-Persistent inflammation (chronic inflammation) – due to
a failure to completely eliminate the pathological insult

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Chronic inflammation & Repair ……. Objectives

1. Discuss chronic inflammation including definition,

how it arises, its cells , and histology.
2. Distinguish granulomatous inflammation as to causes
and morphology.
3. Define labile, stable and permanent cells relative
to healing. Give tissue examples.
4. Describe the process of wound healing by first
intension and second intension.
5. Describe systemic and local influences that may
modify the quality of the repair process. Define
the following, ulcer, fistula, and sinus.

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Chronic inflammation

A type of inflammation characterized by

1. Gradual onset
2. Long duration
3. Caused by mild irritant
4. Proliferative in nature (excess cells)
5. Associated with repair
- Chronic inflammatory cells include..lymphocytes,
plasma cells and macrophages
- Chronic inflammation may be specific or non specific

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Chronic specific inflammation….
- It is a type of chronic
specific inflammation in
which the histiocytes
play a predominant role .

- It starts as small
granules then fuse to
form a grossly, tumor-
like mass

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Types of granulomas
1- Infective
- Bacterial.. Tuberculosis, syphilis ,leprosy
- Fungal…histoplasma , Candida.
- Viral…lymphogranuloma inguinal.
- Parasitic…. Bilharziasis.
- Suppurative granuloma….actinomycosis
2- Non infective
- Foreign body ..around surgical stitches.
- Allergic…..Rheumatic fever.
 3- Of unknown cause
- Sarcoidosis

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Tuberculous granuloma

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Acute and Chronic inflammation

Acute Chronic
-Sudden onset -Gradual onset
-Short duration -Long duration
-Severe irritant -Mild irritant
- Vascular phenomena -End arteritis obliterans
- Exudative -Proliferative
- Polymorphs -Lymphocytes, plasma
&macrophages cells & macrophages.

-Followed by repair -Associated with repair

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Repair, Regeneration, and Fibrosis
Repair means
Replacement of damaged tissue by a healthy new one.
It occurs when body defense and treatment overcomes
the irritant
Regeneration: (generate, to bring to life).
Replacement of injured cells by cells of the same type,
sometimes with no trace of injury.
- This occurs when the connective tissue infrastructure
remains intact.
- The surviving parenchymal cells must have the
capacity to regenerate.

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Repair, Regeneration, and Fibrosis
According to their proliferative potential, cells of
the body are Three types…..
1-Labile- These are continuously dividing cells
throughout life to replace the damaged cells. -
Examples are epidermis of the skin, and hemopoietic
cells of the bone marrow
2-Stable…cells which do not proliferate under normal
conditions but only when there is need. They include
hepatocytes, renal tubular cells, glandular cells, and
mesenchymal cells e.g smooth muscle, osteoblasts,
cartilage cells,
3-Permanent…cells that do not proliferate in the post
natal life. Permanent cells are found in the central
nervous system and heart. Once they are destroyed,
they cannot regenerate.
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Healing by fibrosis

Fibrosis… It is replacement of the damaged tissue by

granulation tissue which matures to fibrous tissue.
 It occurs if the connective tissue infrastructure is
destroyed or if the cells of the tissue can not divide.
 Granulation tissue:-
It is a transitory tissue formed of capillaries and

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Wound Healing
Wound healing can occur by one of two ways according
to the type of wound

1- Primary intention: the usual case with a surgical

wound, in which there is a clean (sterile) wound with
minimal tissue destruction, well-apposed edges, and
therefore, there’s minimal scar formation.

2-Secondary intention: when wound is infected, with

excessive tissue destruction, edges cannot be apposed,
(e.g., following wound infection), then the wound slowly
fills with granulation tissue from the bottom up. A large
scar usually results.

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Primary intension Secondary intension


- Clean surgical wound. - Gaping wound.

- Minimal tissue loss - Excess tissue loss
- Sterilization, no infection - Infected with tissue debris
- Well opposed edges - Not well opposed edges
- Rapid healing with minimal - Slow healing with many
complications complications

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Factors that influence wound healing

1.Type, size, and location of the wound

2.Vascular supply
3.Infection - delays wound healing and leads to more
granulation tissue and scarring
4.Movement - wounds over joints do not heal well due
to traction
5.Radiation - ionizing radiation is bad, UV is good

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Factors that influence wound healing
6.Overall nutrition: vitamin and protein deficiencies
lead to poor wound healing, especially vitamin C,
which is involved in collagen synthesis,also zink and
calcium are important.
7.Age: younger is definitely better!
8.Hormones - corticosteroids drastically impair wound
healing, because of their profound effect on
inflammatory cells

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Complications of wound healing

I. Defective formation of granulation tissue and fibrous

 1- Wound dehiscence…failure of the wound to heal.
 2- Decreased cellular proliferation , this can lead to
formation of ulcer, sinus, or fistula.
a- Ulcer = discontinuity of the surface epithelium of the
skin or mucous membrane.
b- Sinus = A blind ended tract opening on the surface.
c- Fistula = A tract joining two hollow organs.
 3- Weak scar….incisional hernia.
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Complications of wound healing


Oral ulcer


Oral maxillary
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Complications of wound healing
II. Excessive Formation of granulation tissue &

1- Proud flesh Excessive formation of granulation

tissue above the surface of the wound. - This
prevents epithelialization of the surface. - Surgical
removal or cautery is required for complete healing of
the wound

 2-Keloids (hypertrophy scars) - Are the result of

over-exuberant production of scar tissue, which is
primarily composed of type III collagen
Page- 36Surgical removal is usually followed by recurrence
Complcations of wound healing

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Thank U

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