CONTENTS

 DEFINITION
 CAUSES
 SIGNS OF INFLAMMATION
 ACUTE INFLAMMATION
 VASCULAR CHANGES
 CELLULAR EVENTS
 CHRONIC INFLAMMATION
 CHEMICAL MEDIATORS
 CELL- DERIVED CHEMICAL MEDIATORS
 PLASMA DERIVESD CHEMICAL MEDIATORS
 CELLS OF INFLAMMATION
 DISEASES ASSOCIATED WITH ACUTE AND
CHRONIC INFLAMMATION
 ORAL MANIFESTATIONS
 • Inflammation is
defined as protective
response intended
to eliminate the
initial cause of cell
injury as well as the
necrotic cells and
tissue resulting from
original insults
kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.
 IMMUNOLOGICAL
AGENTS

INFECTIVE PHYSICAL
AGENTS
CAUSE AGENTS

INERT CHEMICAL
MATERIALS AGENTS
Signs of Inflammation
(Cardinal Signs)
 ACUTE INFLAMMATION
Acute inflammation is the immediate and early response to
injury,is of relatively short duration,lasting from a few minutes
up to a few days, and is characterized by fluid and plasma
protien exudation and by a predominantly neutrophilic leucocyte
accumulation.
It has three major components:
a) Alteration in vascular caliber
b)Structural changes in microvasculature
c)Emigration of the leucocytes

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 VASCULAR CHANGES
CHANGES IN VASCULAR FLOW AND CALIBER

• Transient vasoconstriction(seconds)

• Vasodilation involving arteriole first

• Local increase in blood flow

redness and warmth(erythema)

• Increased permeability resulting in exudation of protein rich

fluid into the extravascular tissues.

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 Red blood cells become concentrated increasing the
viscosity and slowing the circulation(process called
STASIS)

 Leucocytes (neutrophils) accumulate along the vascular

endothelial surface(process called MARGINATION)

 After adhering to endothelial cells the leucocytes squeeze

between them and migrate through the vascular wall into
interstitial tissue(process called emigration)

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 Leukocyte Cellular Events
Extravasation of leukocytes from vascular lumen to
extravascular space is divided into
Margination and rolling
Adhesion and transmiagration between endothelial
cells
Migration in interstitial tissue toward a chemotactic
stimulus
Chronic Inflammation
 Chronic inflammation is characterized by

1)Inflitration with mononuclear (chronic inflammatory cell)including

macrophages,lymphocytes and plasma cells.

2)Tissue destruction induced by inflammatory cells

3)Repair involving new vessel proliferation(angiogenesis) and

fibrosis.

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 Chronic inflammation may follow acute inflammation

Chronic inflammation arise in following settings:

1)Persistent infections eg Treponema

pallidum(syphilis),mycobacterium (tubercle bacilli), certain fungi

2)Prolonged exposure to potentially toxic agents

eg non-degradable exogenous material (inhaled particulate
silica)silicosis in lungs,endogenous agents such as elevated plasma
lipid components(atherosclerosis).

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

Chemical Mediators of
Inflammation
 CELL DERIVED MEDIATORS

1- VASOACTIVE AMINES

• HISTAMINE
• SEROTONIN

2- ARACHIDONIC ACID METABOLITES

• Metabolites via cyclo-oxygenase pathway

• Metabolites via lipo-oxygenase pathway

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 3- LYSOSOMAL COMPONENTS

• the inflammatory cells – neutrophils and monocytes , contain

lysosomal granules which on release elaborate variety of
mediators of inflammation.
• Granules of neutrophils- these are of two types: specific or
secondary and azurophil and primary.
• Granules of monocytes and tissue macrophages- they are
more active in chronic inflammation.

4- PLATELET ACTIVATING FACTOR

• Released from IgE- sensitized basophils or mast cells, other

leukocytes, endothelium and platelets.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 Actions of PAF are:

a) Increased vascular permeability

b) Vasodilation in low concentration and vasoconstriction
otherwise
c) Bronchoconstriction
d) Adhesion of leukocytes to endothelium
e) Chemotaxis

5- CYTOKINES

• Cytokines are polypeptide substances produced by activated

lymphocytes (lymphokines) and activated monocytes
(monokines)

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
• Currently, main cytokines acting as mediators of inflammation
are :

 interleukin-1 (IL-1),

 tumor necrosis factor (TNF)-alpha and beta,

 interferon (IF)-gamma, and

 chemokines (IL-8, PF-4)

• IL-1 and TNF-alpha are formed by activatd macrophages while

TNF-beta and IF-gamma are produced by activated T cells.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 The actions of various cytokines are:
I. IL-1 AND TNF-alpha, TNF-beta induce endothelial effects
genecity, elaboration of other cytokines, fibroblastic
proliferation and acute phase reactions.

II. IL-gamma causes activation of macrophages and

neutrophils and is associated with synthesis of nitric acid
synthase.

III. CHEMOKINES are a family of chemoattractants for

inflammatory cells and include:

 IL-8 chemotactic for neutrophils

 Platelet factor-4 chemotactic for neutrophils, monocytes and
eosinophils
 MCP-1 chemotactic for monocytes
 Eotaxin chemotactic for eosinophils
Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 6)- NITRIC OXIDE AND OXYGEN METABOLITES

 It was originally described as vascular relaxation factor

produced by endothelial cells.
 NO plays the following role in inflammation:
i) Vasodilation
ii) Anti-platelet activating agent
iii) Possibly microbicidal action

Oxygen-derived metabolites are released from activated

neutrophils and macrophages and include :

• superoxide oxygen (O’2),

• H2O2, OH’ and
• toxic NO products.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 iv) Endothelial cell damage and thereby increased vascular
permeability .

v) Activation of protease and inactivation of antiprotease causing

tissue matrix damage

vi) Damage to other cells.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 PLASMA DERIVED MEDIATORS

These include the various products derived from activation and

interactin of 4 interlinked systems: kinin, clotting, fibrinolytic,
and complement.
 1. THE KININ SYSTEM

Bradykinin acts in the early stage of inflammation and its effects

include:
 smooth muscle contraction
 Vasodilation
 Increased vascular permeability
 Pain

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 2. THE CLOTTING SYSTEM

The actions of fibrinopeptides in inflammation are:

 Increased vascular permeability
 Chemotaxis for leukocyte
 Anticoagulant activity.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 3. THE FIBRINOLYTIC SYSTEM

The actins of plasmin in inflammation are:

 Activation of factor XII to form prekallikrein activator that
stimulates the kinin system to generate bradykinin
 Splits off complement c3 to form c3a which is a permeability
factor
 Degrades fibrin to form fibrin split products which increase
vascular permeability and are chemotactic to leucocytes.

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 4. THE COMPLEMENT SYSTEM

The activation of complement system can occur either:

i) By classic pathway
ii) By alternate pathway

 Complement system yields anaphylatoxins C3a, C4a, C5a and

MAC.

 The actions of anaphylatoxins in inflammation are:

 Release of histamine from mast cells and basophils
 Increased vascular permeability causing edema in tissues.
 C3b => phagocytosis
 C5a => chemotactic for leukocytes

Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
 THE INFLAMMATORY CELLS

PMN (POLYMORPHONUCLEAR
LEUKOCYTES)
EOSINOPHILS
BASOPHILS
LYMPHOCYTES
PLASMA
MONONUCLEAR-PHAGOCYTES
SYSTEM
GIANT CELLS
Mohan H. Essential pathology for dental students. 3rd ed. New Delhi: Jaypee; 2005.
Examples Of Diseases, Conditions, And
Situations Which Can Result In Acute
Inflammation Include:

Acute
infective meningitis
Acute sinusitis

Acute tonsillitis

Acute bronchitis

Acute appendicitis

Acute dermatitis
 SCARRING
RESOLUTION OR FIBROSIS

PROGRESSION
TO CHRONIC
INFLAMMATION

OUTCOMES OF ACUTE INFLAMMATION

33
Chronic Inflammatory Cells And Mediators
▪Macrophages
▪Lymphocytes
▪Plasma Cells
▪Eosinophils
▪Mast Cells

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 Examples Of Diseases And Conditions
With Chronic Inflammation Include

Asthma
Chronic Peptic Ulcer,
Tuberculosis
Rheumatoid Arthritis
Chronic Periodontitis
 Ulcerative Colitis
 Crohn’s Disease

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

 Acute Chronic

Red line, Flare & Wheal. Little signs - Fibrosis

Acute inflammatory cells - Chronic inflammatory cells

Neutrophils – Lymphocytes

Vascular damage Neo-vascularisation

More exudation No/less exudation

Little or no fibrosis Prominent fibrosis

SYSTEMIC EFFECTS OF
INFLAMMATION

Fever
Leucocytosis
Lymphangitis
Lymphadenitis
Shock

kumar v, cotran r, robbins s. Basic pathology. 7th ed. elsevier; 2004.

Allergic reaction induced inflammation
INFLAMMATORY CONDITIONS IN

ORAL CAVITY
GINGIVITIS
PERIODONTITIS
PULPITIS
STOMATITIS
OSTEOMYELITIS
OSTEITIS
GLOSSITIS
PERIIMPLANTITIS
ANGULAR CHEILITIS
APTHOUS STOMATITIS
LUDWIG’S ANGINA
SIALOEDENITIS
PERICORONITIS
TMJ ARTHRITIS
 GINGIVITIS
IT’S AN INFLAMMATION OF
GUM TISSUE
NON-DESTRUCTIVE
PERIODONTAL DISEASE
OCCURS IN RESPONSE TO
BACTERIAL BIOFILMS,
TRAUMA, DRUGS,
PREGNANCY
SIGNS & SYMPTOMS
SWOLLEN GUMS
BRIGHT RED COLOR
BLEEDING GUMS
HALITOSIS
LOSS OF STIPPLING
PERIODONTITIS
IT’S AN INFLAMMTORY
DISEASE AFFECTING THE
PERIODONTIUM
ITS INVOLVES
PROGRESSIVE LOSS OF
ALVEOLAR BONE AROUND
THE TOOTH
CAUSED BY MICROORG
THAT ADHERE ON THE
TOOTH SURFACE ALONG
WITH THE IMMUNE
RESPONSE

SIGNS & SYMPTOMS

DEEP POCKETS
LOOSE TEETH IN LATER
STAGE
 PULPITIS
It’s an inflammation of
dental pulp
Caused by bacterial
infections, trauma,
thermal insults
REVERSIBLE
IRREVERSIBLE
 ANGULAR CHELITIS
It’s the inflammation of
corner of the mouth
Opportunistic fungal and/
bacterial infection with
multiple local and systemic
predisposing factors like
nutrition def, dry mouth,
immunosupression and lip
licking

SIGNS & SYMPTOMS

Erythema at the corner ,
edema ,fissured or
cracked lips
 APHTHOUS
STOMATITIS
Characterised by
formation of mouth ulcer
Caused by t- cell
mediated immune
response, local trauma ,
stress , nutritional def,
hormonal influences etc
 GLOSSITIS
Inflammation with
depaillation of dorsal
surface of the tongue
leaving a smooth and
erythmatous surface.
Caused by nutritional
deficiency , anemia ,
infection , alcoholism ,
AIDS , etc
 PERI IMPLANTITIS
Destructive
inflammatory process
affecting the hard and
soft tissue surrounding
dental implant.
CAUSED BY Implant
structure , microbial
infection , excessive
mech. Stress .

SIGNS & SYMPTOMS

Colour change in the
keratinised gum tissue , BOP ,
increased probing depth and
progressive loss of bone
height.
 PERICORONITIS
Caused by:
Accumulation of
bacteria and debris
beneath the
operculum or by
mech trauma
 OSTEITIS
Alveolar ostetis ,
condensing
osteitis , osteitis
deformans
OSTEOMYELITIS
It’s an Inflammation of
the bone , bone marrow
and surrounding soft
tissues .
Constant bone pain .
Swelling, tenderness,
warmth at infection
site.
Restricted movement
of affected part.
Later signs: drainage
from sinus tracts
SIALOADENITIS
It’s the
inflammation of the
salivary gland

ACUTE
CHRONIC
 TMJ ARTHRITIS
Inflammation of the joint
INFECTIOUS
TRAUMATIC
OSTEOARTHRITIS
RHEUMATOID
SECONDARY
DEGENERATIVE
LUDWIG’S ANGINA
It’s a cellulitic
facial infection
Bilateral
involvement of
submandandibular
Sublingual and
Submental spaces
of the face