inflammation / dental implant courses by Indian dental academy

SEMINAR ON:

GUIDED BY: PRESENTED
BY:
 Dr. R. R. Bhowate Shruti Sood
 Prof and Guide

 D
INDIAN DENTAL ACADEMY
Leader continuing Dental Education
www.indiandentalacdemy.com

Learning objectives:
At the end of the seminar learner should
be able to:
1. Define inflammation.
2. Enumerate cardinal signs of
inflammation.
3. Describe acute and chronic
inflammation.
4. Enumerate inflammatory mediators.
5. Enumerate cells of inflammation.
6. Describe the clinical importance of

CONTENTS :-
-Definition of inflammation.
-Causes
-Acute inflammation
- Vasular changes
- Cellular changes
-Chemical mediators of inflammation
-Inflammatory cells
-Morphologic patterns of inflammation
-Applied aspects
-Chronic inflammation

 Local response of living mammalian tissues to injury
due to any agent.
 A body defense reaction in order to eliminate or
limit the spread of injurious agent as well as to
remove the consequent necrosed cells and tissues.
INTRODUCTION & DEFINITION
“Inflammation is a protective response intended to
eliminate the initial cause of cell injury as well as the
necrotic cells and tissues resulting from the original
insult “

CAUSES
1. Physical agents
2. Chemical agents
3. Infective agents
4. Immunological
agents
heat, cold, radiation and
mechanical trauma.
organic and inorganic poisons.
bacteria, viruses and their toxins.
cell-mediated and antigen-antibody
reactions.

SIGNS OF INFLAMMATION

Inflammation
Acute Chronic
Acute versus chronic inflammation are distinguished
by the duration and the type of infiltrating inflammatory cells

Acute inflammation
1. Rapid in onset and
of short duration ,
lasts from few
minutes to as long
as few days.
2. Fluid and plasma
protein exudation
(edema).
3. Prominent neutrop-
hilic infiltration.
Chronic Inflammation
1. Insidious and of
longer duration, lasts
for several days to
years.
2. Vascular
proliferation and
fibrosis.
3. Lymphocytic and
macrophagic
infiltration.

“It is a rapid response to injury or microbes
and other foreign substances that is
designed to deliver leucocytes and plasma
proteins to sites of injury.”

Acute inflammation has two major components :-
CELLULAR EVENTS :-
emigration of the
leukocytes from the
microcirculation and
accumulation in the focus
of injury (cellular
recruitment and activation).
The principal leukocytes in
acute inflammation are
neutrophils
(polymorphonuclear
leukocytes).
VASCULAR
CHANGES :-
alterations in vessel
caliber resulting in
increased blood flow
(vasodilation) and
structural changes that
permit plasma proteins
to leave the circulation
(increased vascular
permeability).

 Infections (bacterial, viral, parasitic) and microbial toxins.
 Trauma (blunt or penetrating).
 Physical and chemical agents (thermal injury, irradiation,
burns)
 Tissue necrosis (due to ischemia, physical and chemical
injury ).
 Foreign bodies (dirt, sutures)
 Immune reactions (also called hypersensitivity reactions)

• The changes in acute inflammation can be
described under the following headings-
1 ) Vascular changes
- changes in vascular caliber and flow.
- increased vascular permeabillity.
2) Cellular events
- exudation of leucocytes
- phagocytosis

VASCULAR
CHANGES

A. Changes in vascular flow & caliber :
Arteriolar vasodilatation
Increased blood flow and
engorgement
Increased permeability
Loss of fluid
Increased viscosity of the blood
Stasis
Leukocytes then settle out of
circulation www.indiandentalacdemy.com

A. Changes in Vascular Caliber and Flow :-
• Changes in blood vessels begin rapidly after infection or
injury but may develop at variable rates, depending on the
nature and severity of the original inflammatory stimulus.
•After transient vasoconstriction (lasting only for seconds),
arteriolar vasodilation occurs resulting in locally increased
blood flow and engorgement of the down stream capillary
beds . This vascular expansion is the cause of the redness
and warmth characteristically seen in acute inflammation.

 As the microvasculature becomes more
permeable, protein-rich fluid moves into the
extravascular tissues. This causes the red blood
cells to become more concentrated, thereby
increasing blood viscosity and slowing the
circulation.
As stasis develops, leukocytes (principally
neutrophils) begin to accumulate along the
vascular endothelial surface, a process called
margination.

Vascular changes & fluid leakage during acute inflammation
lead to Edema in a process called Exudation
Transudate
•Result of hydrostatic
or osmotic imbalance
•Ultra filtrate of plasma
•Low protein content
•Specific gravity < 1.015
Exudate
•Result of inflammation
•Vascular permeability
•High protein content
•specific gravity >1.020

STARLING’S HYPOTHESIS
 Fluid balance is maintained by 2 opposing sets of
forces:
1) Intravascular hydrostatic pressure & interstitial
osmotic pressure.
2) Intravascular osmotic pressure & interstitial
hydrostatic pressure.

B. Increased vascular permeability :-
• Loss of protein from plasma leads to edema
• due to reduced osmotic pressure in the vasculature
• and increased osmotic pressure in the interstitium

• Short – lived.
(15-30 min.)
• Reversible
process.
• For e.g. Mild
thermal injury
 Endothelial cell contraction leading to intercellular gaps in
postcapillary venules is the most common cause of increased vascular
permeability.
Endothelial cell contraction occurs rapidly after binding of mediators to specific receptors
, is called the immediate transient response. A slower and more prolonged retraction of
endothelial cells, resulting from changes in the cytoskeleton, may be induced by
cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1). This reaction may
take 4 to 6 hours to develop after the initial trigger and persist for 24 hours or more.

• It is usually seen
after severe injuries
(burns and some
infections).
 Direct endothelial injury results in vascular leakage by causing
endothelial cell necrosis and detachment :-
 In most cases leakage begins immediately after the injury and persists for several hours (or
days) until the damaged vessels are thrombosed or repaired. Therefore, this reaction is known as
the immediate sustained response. Venules, capillaries, and arterioles can all be affected,
depending on the site of the injury. Direct injury to endothelial cells may also induce a delayed
prolonged leakage that begins after a delay of 2 to 12 hours, lasts for several hours or even
days, and involves venules and capillaries. Examples include mild to moderate thermal injury,
certain bacterial toxins, and x- or ultraviolet irradiation

• Accumulated
leucocytes release
toxic oxygen
species &
proteolytic
enzymes.
 Leukocyte- mediated endothelial injury may occur as a
consequence of leukocyte accumulation along the vessel wall

 Increased transcytosis of proteins via an intracellular vesicular
pathway augments venular permeability after exposure to certain
mediators such as Vascular Endothelial Growth Factor (VEGF).

• Tissue repair
involves new blood
vessel formation
(angiogenesis).
• Vessel sprouts remain
leaky until
intercellular junctions
form.
 Leakage from new blood vessels:
 All these described mechanisms may occur in one wound
( e.g. burns) and can be life threatening.

Responses of Lymphatic vessels :-
- As is well known, the small amount of interstitial fluid formed
normally is removed by lymphatic drainage. In inflammation, lymph
flow is increased and helps drain edema fluid from the
extravascular space. Because the junctions of lymphatics are
loose, lymphatic fluid eventually equilibrates with extravascular
fluid.
- In severe inflammatory reactions, especially to microbes, the
lymphatics may transport the offending agent. The lymphatics may
become secondarily inflamed (lymphangitis), as may the draining
lymph nodes (lymphadenitis). Inflamed lymph nodes are often
enlarged, because of hyperplasia of the lymphoid follicles and
increased numbers of lymphocytes and phagocytic cells lining the
sinuses of the lymph nodes.

CELLULAR
EVENTS
-The cellular phase of inflammation consists of 2
processes:
-Exudation of leucocytes; and
-Phagocytosis.

The sequence of extravasation of Leukocytes from
blood to tissues:
Margination and Rolling
Adhesion and Transmigration
Chemotaxis and Activation
Phagocytosis and Degranulation

A. MARGINATION AND ROLLING
 As blood flows from capillaries into postcapillary venules , circulating cells
are swept by laminar flow against the vessel wall. As a result leukocytes are
pushed out of the central axial column and thus have a better opportunity to
interact with lining endothelial cells , as stasis sets in.
• This process of leukocyte accumulation at the periphery of vessels is called
margination. Subsequently, leukocytes tumble on the endothelial surface,
transiently sticking along the way, a process called rolling.

- The weak and transient adhesions involved in
rolling are mediated by the selectin family of
adhesion molecules.
- Selectins are receptors expressed on leukocytes
and endothelium that contain an extracellular
domain that binds sugars.
-The three members of this family are E-selectin
also called CD62E, expressed on endothelial cells;
P- selectin CD62P, present on endothelium and
platelets; and L-selectin CD62L, on the surface of
most leukocytes

• The endothelial selectins are typically expressed at low levels
or are not present at all on normal cells.

B. LEUKOCYTE ADHESION AND TRANSMIGRATION :-
 Eventually leukocytes firmly stick to the endothelial surface ,
called ADHESION. This adhesion is mediated by integrins
expressed on leukocyte cell surfaces interacting with their ligands
on endothelial cells.
 Integrins are transmembrane heterodimeric glycoproteins ,that
also function as cell receptors for extracellular matrix. Integrins
are normally expressed on leukocyte plasma membranes in a low-
affinity form and do not adhere to their appropriate ligands until
the leukocytes are activated by chemokines.

 Chemokines are chemoattractant cytokines that are
secreted by many cells at sites of inflammation and are
displayed bound to proteoglycans on the endothelial
surface.
 When the adherent leucocytes encounter the displayed
chemokines, the cells are activated, and their integrins
undergo conformational changes and cluster together,
thus converting to a high-affinity form.
 At the same time, other cytokines, notably TNF and
IL-1 (also secreted at sites of infection and injury),
activate endothelial cells to increase their expression of
ligands for integrins.

- Adhesion is mediated by members of Ig superfamily on endothelial
cells (ICAM-1, VCAM-1) that interact with leukocyte integrins.
- After being arrested on the endothelial surface ,leukocytes migrate
through the vessel wall primarily by squeezing between cells at
intercellular junctions . This movement of leukocytes, called
diapedesis, occurs mainly in the venules of the systemic vasculature.

• In addition, PECAM-1 (platelet endothelial cell adhesion molecule
1, also called CD31), a cellular adhesion molecule expressed on
leukocytes and endothelial cells, mediates the binding events needed
for leukocytes to traverse the endothelium .

 After extravasating from the blood, leukocytes migrate
toward sites of infection or injury along a chemical gradient
by a process called chemotaxis .
 Chemotactic agent can be:--
~Exogenous agents 
– Soluble bacterial products
- Some peptides possessing N- formylmethionine termini.
~Endogenous agents 
– Components of the complement system (C5a)
– Products of lipoxygenase pathway of arachidonic acid
metabolism (leukotrieneB4)
– Cytokines (chemokines such as IL-8)
C. CHEMOTAXIS AND ACTIVATION

 Chemotactic molecules bind to specific cell surface receptors,
which are members of the seven- transmembrane G-protein
coupled receptor family.
- Binding of the chemoattractants results in G-protein mediated
signal transduction events, some of which lead to increased
cytosolic calcium, which triggers the assembly of cytoskeletal
contractile elements necessary for movement. Leukocytes move
by extending pseudopods that anchor to the ECM and then pull
the cell in the direction of the extension.
- In most forms of acute inflammation, neutrophils predominate
in the inflammatory infiltrate during the first 6 to 24 hours and
are replaced by monocytes in 24 to 48 hours.

D.Phagocytosis &
degranulation :“Phagocytosis is defined as the process of engulfment of
solid particulate material by the cells(cell-eating)”.
Steps in phagocytosis:
1. Attachment stage
2. Engulfment stage
3. Secretion (Degranulation stage)
4. Killing/ Degradation

Stages of phagocytosis of a foreign
particle

Phagocytosis :- Leukocytes bind and ingest most micro
organisms and dead cells via specific surface receptors ,
which recognize either components of the microbes and
dead cells, or host proteins, called opsonins, that coat
microbes and target them for phagocytosis.
-The most important opsonins are antibodies of the
immunoglobulin G class that bind to microbial surface
antigens.
-These opsonins either are present in the blood ready to
coat microbes or are produced in response to microbes.
-Leukocytes express receptors for opsonins that facilitate
rapid phagocytosis of the coated microbes.

-In engulfment, pseudopods are extended around
the object, eventually forming a phagocytic
vacuole. The membrane of the vacuole then fuses
with the membrane of a lysosomal granule,
resulting in discharge of the granule’s contents into
the phagolysosome.
- Killing and Degradation of Microbes :- The
key steps in this reaction are the production of the
microbicidal substances within lysosomes and
fusion of the lysosomes with phagosomes.

- The most important microbicidal substances are
reactive oxygen species (ROS) and lysosomal
enzymes. These ROS act as a free radicals and
destroy microbes.
- However the lysosomes of neutrophils contain the
enzyme myeloperoxidase(MPO) and in the presence
of the halide such as cl- , MPO converts Hydrogen
peroxide to HOCl.
- The dead microorganisms are then degraded by the
action of lysosomal acid hydrolases. Perhaps the
most important lysosomal enzyme involved in
bacterial killing is elastase.

KILLING OF MICRO-ORGANISMS

CHEMICAL MEDIATORS OF INFLAMMATION

Cell-derived mediators
CELL-
DERIVED
Mast cells, basophils,
platelets
Platelets
Inflammatory cells
Histamine
Serotonin
•Lysosomal
enzymes
•PAF
•PGs
•Leukotreines
•Cytokines
•Nitric oxide &
oxygen
metabolites
permeability
permeability
Tissue damage
permeability
vasodialation
permeability
fever
Tissue damage

Plasma derived mediators
PLASMA-
DERIVED
CLOTTING &
FIBRINOLYTIC
SYSTEM
KININ SYSTEM
COMPLEMENT
SYSTEM
Fibrin split
products
Kinin/
Bradykinin
Anaphylotoxins
C3a, C4a, C5a
permeability
permeability
permeability

CELL-DERIVED
MEDIATORS

1. VASOACTIVE AMINES:
Two important pharmacologically active amines that
have role in the early inflammatory response (first one
hour) are:
A.HISTAMINE.
B.SEROTONIN (5- HYDROXYTRYPTAMINE).

Histamin
e: It is stored in the granules of mast cells, basophils and platelets.
 Various factors responsible for the release of it :
 Stimuli or substances inducing acute inflammation e.g. heat,
cold, irradiation, trauma, irritant chemicals, immunologic
reactions etc.
 Anaphylatoxins like fragments of complement C3a , and C5a,
which increase vascular permeability and cause oedema in
tissues,
 Histamine-releasing factors from neutrophils, monocytes and
platelets.
 Neuropeptides such as substance P.
 Interleukins.
It causes:-
• Vasodilatation.
 Increased vascular permeability of venules , itching and pain.

Serotonin (5-Hydroxytryptamine)
 It is present in tissues like chromaffin cells of CTT,
spleen, nervous tissue, mast cells and platelets.
 Release of serotonin is stimulated when platelets aggregate
after contact with collagen, thrombin, Antigen antibody
complexes.
 Actions :-
 It is a less potent mediator of increased vascular
permeability and vasodilatation than histamine.

Arachidonic acid metabolites
(eicosanoids )
 Arachidonic acid is a 20 carbon Polyunsaturated fatty
acid derived from dietary sucrose or by conversion from
the essential fatty acid linoleic acid.
• It is present in esterified form as a component of cell
membrane phospholipids.
• It is released from membrane phospholipids through the
action of cellular phospholipases.

i) Metabolites via cyclo-oxygenase pathway (prostaglandins,
thromboxane A2, prostacyclin):- Prostaglandins and related compounds
are also called autocoids.
- 3 metabolites :-
-Prostaglandins (PGD2, PCE2 and PGF2-a)- PGD2 and PGE2 act on
blood vessels to cause increased venular permeability, vasodilatation and
bronchodilatation and inhibit inflammatory cell function. PGF2-a induces
vasodilatation and bronchoconstriction.
-Thromboxane A2 (TXA2)- It is a vasoconstrictor and bronchoconstrictor
and enhances inflammatory cell function by causing platelet aggregation.
-Prostacyclin (PGI2)-PGI2 induces vasodilatation, bronchodilatation and
inhibits inflammatory cell function by acting as anti-aggregating agent for
platelet.

ii) Metabolites via lipo-oxygenase pathway (5-HETE, leukotrienes).
The enzyme, lipo-oxygenase, acts on activated arachidonic acid to form
hydroperoxy compound, 5-HPETE (hydroperoxy eico-satetraenoic acid)
which on further peroxidation forms the following 2 metabolites .
A) 5-HETE (hydroxy compound) which is a potent chemotactic agent for
neutrophils.
B )Leukotrienes (LT) or slow-reacting substances of anaphylaxis
(SRS-As) are so named as they were first isolated from leucocytes. Firstly,
unstable leukotriene A4 (LTA4) is formed which is acted upon by enzymes
to form LTB4 (chemotactic for phagocytic cells and stimulates phagocytic
cell adherence) while LTC4, LTD4 and LTE4 have common actions by
causing smooth muscle contraction and thereby induce vasoconstriction,
bronchoconstriction and increased vascular permeability.

3. LYSOSOMAL COMPONENTS
 Neutrophils and monocytes contain lysosomal granules, which when
released, may contribute to the inflammatory response.
These are as under:
1. Granules of neutrophills Specific/ Secondary.
Azurophil/ Primary.
2. Granules of monocytes and tissue macrophages.

• smaller specific ( secondary) granules contains
lysozyme, collagenase, gelatinase, lactoferrin,
plasminogen activator, histamine & alkaline
phosphatase.
• large azurophil ( primary) granules contains
myeloperoxidase, bactericidal factors ( lysozymes,
defensins), acid hydrolases & variety of neutral
proteases. Acid proteases act within the cell to cause
destruction of bacteria and neutral proteases attack on
extra cellular components.
1. Granules of neutrophills:
2. Granules of monocytes and tissue macrophages:
• Releases mediators of inflammation like acid
proteases,
collagenase and plasminogen activator.
• More active in chronic inflammation.www.indiandentalacdemy.com

4. Platelet-Activating Factor
-- Generated from membrane phospholipids of
neutrophils,
monocytes, basophils, mast cells, endothelium and
platelets.
 Actions:
 Vasodilatation in low concentration and
vasoconstriction other wise.
 Bronchoconstrictors.
 Increased vascular permeability
 Enhanced leukocyte adhesion

5. CYTOKINES
• Cytokines are polypeptide substances produced by activated lymphocytes
(lymphokines) and activated monocytes (monokines).
 The actions of various cytokines as mediator of inflammation are as under
 IL-1 and TNL-alpha, TNF-beta induce endothelial effects in the form of
increased leucocyte adherence, thrombogenicity, elaboration of other
cytokines, fibroblastic proliferation and acute phase reactions.
 IF-gamma causes activation of macrophages and neutrophils and is
associated with synthesis of nitric acid synthase.

6. CHEMOKINES
 Chemokines are a family of small structurally related proteins
that act primarily as chemoattractants to specific types
of leukocytes.
 They mediate their activity by binding to specific G-
Protein coupled receptors on target cells.
They are classified into four major groups :-
 IL-8 chemotactic for neutrophils.
 platelet factor-4 chemotactic for neutrophils, monocytes
and eosinophils.
 MCP-1 chemotactic for monocytes and
 eotaxin chemotactic for eosinophils.

7. NITRIC
OXIDE
 Nitric oxide (NO) was originally described as vascular
relaxation factor produced by endothelial cells.
 Various functions of NO :-
 Vasodilatation.
 Anti-platelet activating agent.
 Possibly microbicidal action.

8. OXYGEN DERIVED FREE RADICAL
 They are released from activated neutrophils and
macrophages and include superoxide oxygen (0‘2), H202,
OH' and toxic NO products. These oxygen-derived free
radicals have the following action in inflammation:
 Endothelial cell damage and thereby increased vascular
permeability.
 Activation of protease and inactivation of antiprotease
causing tissue matrix damage.
 Damage to other cells.
 The actions of free radicals are counteracted by
antioxidants present in tissues and serum which play a
protective role.

9. NEUROPEPTIDES
• Like vasoactive amines, neuropeptides can also
initiate
inflammatory response.
 They include small protein molecules like Substance
P
and Neurokinin A.
 They - transmit pain signals.
- regulate vessel tone.
- modulate vascular permeability.

PLASMA-DERIVED
MEDIATORS

Plasma derived mediators
PLASMA-
DERIVED
CLOTTING &
FIBRINOLYTIC
SYSTEM
KININ SYSTEM
COMPLEMENT
SYSTEM
Fibrin split
products
Kinin/
Bradykinin
Anaphylotoxins
C3a, C4a, C5a
permeability
permeability
permeability
Each of these systems has its inhibitors and accelerators in the
plasma

INTER-RELATION BETWEEN SYSTEMS

A. KININ SYSTEM
 This system on activation by factor Xlla generates bradykinin, so
named because of the slow contraction of smooth muscle it
induces. First, kallikrein is formed from plasma prekallikrein by
the action of prekallikrein activator which is a fragment of factor
Xlla. Kallikrein then acts on high molecular weight kininogen to
form bradykinin .

Bradykinin:
- Increases vascular permeability.
- Causes contraction of smooth muscle.
- Vasodilatation.
- Pain

B. CLOTTING SYSTEM
 Factor Xlla initiates the
cascade of the clotting
system resulting in
formation of fibrinogen
which is acted upon by
thrombin to form fibrin
and fibrinopeptides.
• The actions of
fibrinopeptides in
inflammation are:
 increased vascular
permeability;
 chemotaxis for leucocyte .
 anticoagulant activity.

C.FIBRINOLYTIC SYSTEM
 This system is activated by plasminogen
activator, the sources of which include
kallikrein of the kinin system, endothelial
cells and leucocytes.
 Plasminogen activator acts on
plasminogen present as component of plasma
proteins to form plasmin. Further breakdown
of fibrin by plasmin forms fibrinopeptides or
fibrin split products .
The actions 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; and
degrades fibrin to form fibrin split products
which jicrease vascular permeability and are
chemotactic to leucocytes.

4. COMPLEMENT SYSTEM
 The activation of complement system can occur either :
 i) by classic pathway through antigen-antibody complexes or
 ii) by alternate pathway via non-immunologic agents such as
bacterial toxins, cobra venoms and IgA.
 Complement system on activation by either of these two
pathways yields anaphylatoxins C3a, C4a and C5a and
membrane attack complex (MAC). The relative potencies of
anaphylatoxins are in the descending sequence of C3a, C5a and
C4a.

 The actions of anaphylatoxins in inflammation
are:
-release of histamine from mast cells andbasophils;
increased vascular permeability causing oedema in
tissues;
- C3b augments phagocytosis; and
- C5a is chemotactic for leucocytes.
The action of MAC is to cause pores in the cell
membrane of the invading microorganisms.

The Inflammatory Cells

A. POLYMORPHORPHONUCLEAR
NEUTROPHILS.
FEATURES
• Called as – Neutrophils /polymorphs
• Referred to as granulocytes.
• Diameter- 10-15µm
• Comprise 40-75% of circulating
leucocytes.
FUNCTIONS
• Initial phagocytosis of bacteria &
foreign body
• Acute inflammatory cell
MEDIATORS
• Primary granules (MPO, lysozyme,
proteases)www.indiandentalacdemy.com

B. MONOCYTE /MACROPHAGE
FEATURES
i. Comprise 4-8% of circulating
leucocytes.
FUNCTIONS
i. Bacterial phagocytosis
ii. Chronic inflammatory cell
MEDIATORS
Acid & neutral hydrolases.
Cationic protein.
Prostaglandin leukotrienes.

C. LYMPHOCYTE
FEATURES
i. Circulating leucocytes 20-45%
ii. Scanty cytoplasm & large nucleus
FUNCTIONS
i. Humoral & cell- mediated immune
responses.
ii. Chronic inflammatory cell
iii. Regulates macrophage response
MEDIATORS
B cells: antibody production
T cells: delayed hypersensitivity,
cytotoxity

D. PLASMA CELL
FEATURES
i. Abundant cytoplasm &
eccentric nucleus
ii. Derived from B cells
FUNCTIONS
i. Chronic inflammatory cells
MEDIATORS
i. Antibody synthesis
ii. Antibody secretion

E. EOSINOPHIL
FEATURES
i. Comprise 1-6% of total
blood leucocytes
ii. Called as granulocytes
FUNCTIONS
i. Allergic states
ii. Parasitic infestations
iii.Chronic inflammatory cell
MEDIATORS
MPL, prostaglandins.

F. BASOPHIL / MAST CELL
FEATURES
i. Comprise 1% of the circulating
leucocytes.
ii. Coarse basophilic granules
iii. Laden with heparin & histamine
FUNCTIONS
i. Receptor for IgE molecules
ii. Electron-dense granules
MEDIATORS
i. Histamine
ii. Leukotrienes
iii.Platelet activating factor

MORPHOLOGIC PATTERNS OF
INFLAMMATION
1. Serous inflammation.
2. Fibrinous inflammation
3. Suppurative or Purulent inflammation
(Abscess formation)
4. Ulcers

1. SEROUS INFLAMMATION
 It is characterized by the outpouring of a watery, relatively
protein-poor fluid.
 The skin blister resulting from a burn or viral infection is a
good example of a serous effusion accumulated either
within or immediately beneath the epidermis of the skin .

2. FIBRINOUS INFLAMMATION
 This occurs due to severe injuries, resulting in greater
vascular permeability that allows large molecules to pass the
endothelial barrier.
 A fibrinous exudate is characterstic of inflammation in the
lining of body cavities such as meninges and pleura
 It undergoes resolution or forms fibrous scar.

3. SUPPURATIVE (PURULENT)
INFLAMMATION
 This is characterized by presence of purulent exudate (pus)
consisting of neutrophils, necrotic cells & edema fluid.
 Certain bacteria(staphylococci) produce this localised suppuration
and are reffered to as pyogenic (pus producing) bacteria.
 Abscesses are focal collections of pus that may be caused by
seeding of pyogenic organisms into a tissue or by secondary
infections of necrotic foci.
 Absceses have central area of necrosis rimmed by a layer of
neutrophils,surrounding it is a layer of dilated vessels and
fibroblastic proliferation which in some time is replaced by
connective tissue.

4. ULCERATION
 An ulcer is a local defect, or excavation, of the surface of an
organ or tissue that is produced by necrosis of cells and
sloughing (shedding) of inflammatory necrotic tissue.
 There is sub-epithelial acute and chronic inflammation.
 The area surrounding the ulcer develops fibroblastic
proliferation, scarring & accumulation of lymphocytes, plasma
cells and macrophages.

APPLIED
ASPECTS

SYSTEMIC EFFECTS OF ACUTE
INFLAMMATION
 Fever
- Occurs due to bacteraemia.
- In response to infection various chemical
mediators releases like prostaglandins,
interleukin-1, TNF are released.
 Leucocytosis
Neutrophilia points to bacterial infection
Lymphocytosis points to viral infection
Eosinophilia points to allergy or parasitic infection

 Lymphangitis- Lymphadenitis
 Manifestation of localised inflammatory injury.
 The lymphatics and lymph nodes that drain the inflammed
tissue show reactive inflammatory changes in the form of
lymphangitis and lymphadenitis.
 This response represents either a nonspecific reaction to
mediators or is immmunologic response to a foreign antigen.
 Shock
 Occur in severe cases.
 Massive release of cytokine TNF- alpha in response to severe
tissue injury or infection results in profuse systemic vasodilatation,
increased vascular permeability and intravascular volume loss. The net
effect of these changes is hypotension and shock.

CHRONIC INFLAMMATION

- DEFINITION
- Chronic inflammation can be considered to be inflammation of
prolonged duration( weeks to months to years) in which active
inflammation, tissue injury and healing proceed simultaneously.
- CAUSES :-
- It can be caused by one of the following :-
1. Chronic inflammation following acute inflammation- When the
tissue destruction is extensive or the bacteria survive and persist in
small numbers at the site of acute inflammation.
2. Recurrent attacks of acute inflammation- When repeated attacks
of acute inflammation culminate in chronicity of the process e.g in
recurrent urinary tract infection leading to chronic pyelonephritis.
3. Chronic inflammation starting de novo- When the infection with
organisms of low pathogenicity is chronic from beginning.

GENERAL FEATURES :-
1. MONONUCLEAR CELL INFILTRATION:-
- Chronic inflammatory lesions are infiltrated by mononuclear
inflammatory cells like phagocytes and lymphoid cells.
- Phagocytes are represented by circulating monocytes, tissue
macrophages, epitheloid cells and multinucleated giant cells.
- Macrophage is the important cell in chronic inflammation.
- The blood monocytes on reaching the extravascular space
transform into tissue macrophages.
- They may get activated in response to stimuli such as
cytokines and bacterial endotoxins.
- On activation, macrophages release active substances like acid
and neutral proteases , cytokines. This products bring about
tissue destruction , neovascularisation and fibrosis.

2. TISSUE DESTRUCTION OR NECROSIS :-
- This is brought about by activated macrophages which
release a variety of biologically active substances e.g. protease,
elastase, collagenase, reactive oxygen radicals and cytokines.
3. PROLIFERATIVE CHANGES :-
- Proliferation of small blood vessels and fibroblast is stimulated
resulting in formation of inflammatory granulation tissue.
- Eventually healing by fibrosis and collagen takes place

SYSTEMIC EFFECTS :-
1. Fever :- there is mild fever, often with loss of weight and
weakness.
2. Anaemia:- it is accompanied by anaemia of varying
degree.
3. Leucocytosis:- there is relative lymphocytosis in these
cases.
4. ESR:- it is elevated in all cases of chronic inflammation.
5. Amyloidosis:- long term cases may develop secondary
systemic amyloidosis.

CONCLUSION:
 The survival of all organism requires that they
eliminate foreign invadors,such as infectious
pathogens,and damaged tissues.
 These functions are mediated by a complex host
response called inflammation.
 Inflammation accomplishes its protective mission by
diluting, destroying or otherwise neutralizing harmful
agents.
 The body attempts to heal the damage with some
changes by the process of repair. The repair begins
almost as soon as the inflammatory changes have
started and involves several processes, including
cell proliferation and differentiation.

REFERENCS
• Robbins,Kumar,Abbas,Mitchell,Fausto. Textbook of
Basic Pathology ,8th Edition.
• Harshmohan.Textbook of Essential pathology, 5th
Edition.
•Textbook of general pathology, S.G.Deodhare,
Y.M.Bhende,
5th Edition.

THANK YOU

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