This document provides an overview of inflammation. It defines inflammation and describes the signs and types, including acute and chronic inflammation. For acute inflammation, it details the vascular events of altered microvasculature, including hemodynamic changes and increased vascular permeability. It also describes the cellular events of exudation of leukocytes and phagocytosis. It lists the chemical mediators of inflammation released by cells and originating from plasma. It discusses the regulation of inflammation and factors determining the inflammatory response. It outlines the morphology, systemic effects, and fate of acute inflammation. It defines chronic inflammation and describes its causes, features, types, histological features, and systemic effects.

1. DR. MARIYAM MOMIN
I YEAR PG.
DEPARTMENT OF
PERIODONTOLOGY & ORAL
IMPLANTOLOGY.

3. INFLAMMATION

4. CONTENTS
 Introduction
 History
 Definition
 Purpose
 Signs of inflammation
 Types of inflammation
 Acute inflammation
 Vascular events
 Cellular events
 Chemical mediators of
inflammation
 Regulation of inflammation
 Inflammatory cells
 Factors determining
variation in inflammatory
response
 Morphology of acute
inflammation
 Systemic effects of acute
inflammation
 Fate of acute inflammation
 Chronic inflammation
 Definition
 Causes
 General features of chronic
inflammation
 Systemic effects of chronic
inflammation
 Types of chronic
inflammation

5. INTRODUCTION
 Inflammation is normal
protective response against
tissue insults such as
infection, tissue
injury/necrosis, foreign
agents & hypersensitivity
reactions.
 It is the first line of defense
in our body against such
insults.
 Usually promotes healing.
 If uncontrolled, may become
harmful.

6. HISTORY
• “Inflammare”
Means “ to set on fire ”
• But now we know that
burning is only one of the
signs of inflammation.

7. Inflammation Swelling

8. DEFINITION
Inflammation is defined as a local response of
living mammalian tissues to injury due to any
agent.
 It is 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.

9. PURPOSE OF INFLAMMATION
 To eliminate the
injurious agent
 To prevent the spread
of injurious agent
 To remove necrotic
cells & tissues
 To initiate the
repairing process

10. CAUSES
 Physical agents – heat,
cold, radiation, mechanical
trauma.
 Chemical agents – organic
and inorganic poisons.
 Infective agents – bacteria,
viruses and their toxins.
 Immunological agents –
cell-mediated & antigen-
antibody reactions.
Allergic reaction

11. SIGNS OF
INFLAMMATION
4 cardinal signs of
inflammation by
Celsus
 Rubor (redness)
 Tumor (swelling)
 Calor (heat)
 Dolor (pain)
Redness
Pain
Swelling
Warmth

12. 5th sign was later
introduced by Galen
Functio laesa (loss of function)
Rudolf Virchow

13. Terminologies associated with inflammation
 The suffix “-itis” is used to describe the
inflammation.
 Name of Area + “-itis” = nomenclature
associated with describing inflamed part of body.
 For example:
 Appendicitis – inflammation of appendix
 Periodontitis – inflammation of the
periodontium
 Tonsillitis – inflammation of tonsils.

14. TYPES OF
INFLAMMATION
INFLAMMATION
ACUTE
INFLAMMATION
CHRONIC
INFLAMMATION
Features Acute
inflammation
Chronic
inflammation
Onset Fast: minutes to
hours
Innate immune
system
Slow: days
Adaptive immune
system
Duration Hours to days Weeks to months
or years
Cellular infiltrate Mainly
neutrophils,
followed by
macrophages
Macrophages,
plasma cells &
lymphocytes
Vascular changes Prominent
(vasodilation,
increased
permeability)
Not prominent;
angiogenesis
Tissue injury
Self-limited Progressive
Fibrosis Usually mild Often severe
Local and
systemic changes
Prominent Less
Difference between acute and chronic
inflammation

15. ACUTE INFLAMMATION
 The changes in acute inflammation can be conveniently described as:
i) Vascular events
ii) Cellular events

16. VASCULAR EVENTS
 Alteration in microvasculature (arterioles, capillaries and
venules) is the earliest response to tissue injury.
 These alterations include hemodynamic changes and vascular
permeability.

17. Haemodynamic changes
Transient vasoconstriction
Persistant progressive vasodilation
Elevation in local hydrostatic pressure resulting in
transudation of fluid into extracellular space
Slowing or stasis
Leukocytic margination
• The earliest features of inflammatory response result
from changes in the vascular flow and calibre of small
blood vessels in the injured tissue.
Sequence of haemodynamic changes

18. LEWIS EXPERIMENT
 The features of haemodynamic changes in the inflammation are
best demonstrated by the Lewis experiment.
 The reaction so elicited is known as triple response or red line
response.
Fig A:- ‘triple response’elicited by firm stroking of skin of forearm with a pencil
Fig B:- Digrammatic view of microscopic features of triple response

19. Altered vascular permeability
 The appearance of inflammatory oedema due to increased
vascular permeability of microvascular bed is explained
on the basis of Starling’s hypothesis.
 In normal circumstances, the fluid balance is maintained
by two opposing sets of forces:
- Forces that cause outward movement of fluid from
microcirculation are intravascular hydrostatic pressure
and colloid osmotic pressure of interstitial fluid.
- Forces that cause inward movement of interstitial fluid
into circulation are intravascular colloid osmotic pressure
and hydrostatic pressure of interstitial fluid.

22. Mechanism of increased Vascular
Permeability
S.No. Mechanism Microvascu
lature
Response
type
Pathogene
sis
Examples
1 Endothelial cell
contraction
Venules Immediate
transient
(15-30 min)
Histamine,
bradykinin,other
s
Mild thermal injury
2 Endothelial cell
retraction
Venules Somewhat
delayed (4-
6hrs) prolonged
(for 24 hrs or
more)
IL-1, TNF In vitro only
3 Direct endothelial cell
injury
Arterioles,
venules,
capillaries
Immediate
prolonged (hrs
to days), or
delayed (2-12
hrs) prolonged
(hrs to days)
Cell necrosis
and detachment
Moderate to severe
burns, severe
bacterial infection,
radiation injury
4 Leucocyte-mediated
endothelial injury
Venules,
capillaries
Delayed,
prolonged
Leucocyte
activation
Pulmonary venules
and capillaries
5 Neovascularization All levels Any type Angiogenesis,
VEGF
Healing, tumor

23. Schematic illustration of pathogenesis of
increased vascular permeability

24. CELLULAR EVENTS
The cellular phase of inflammation
consists of 2 processes:
1. Exudation of leukocytes
2. Phagocytosis.

25. Exudation of leucocytes
 The escape of leucocytes from the lumen of
microvasculature to the interstitial tissue is the most
important feature of inflammatory response.
 In acute inflammation, polymorphonuclear neutrophils
(PMNs) comprise the first line of body defense,
followed later by monocytes and macrophages.
 The changes leading to migration of leucocytes are as
follows:
1. Margination
2. Rolling and Adhesion
3. Emigration
4. Chemotaxis.

26.  Margination
 Rolling & Adhesion
- Leukocyte rolling – Wagner (1839).
- Sticking and emigration of white cells – Dutrochet (1824).
 Emigration
 Chemotaxis
Sequence of changes in the
exudation of leucocytes
Boyden’s chamber

27. Stages in phagocytosis of a foreign particle
A: Opsonisation of the particle
B: Pseudopod engulfing the opsonised particle
C: Incorporation within the cell & degranulation
D: Phagolysosome formation after fusion of lysosome of the cell.
Phagocytosis

28. SUMMARY OF CELLULAR
EVENTS

29. CHEMICAL MEDIATORS OF
INFLAMMATION
Synonyms: Permeability factors or
endogenous mediators of increased
vascular permeability.
They are broadly classified into 2 groups:
i) Mediators released by cells
ii) Mediators originating from plasma.

30. Chemical Mediators of Acute Inflammation
I. CELL-DERIVED MEDIATORS
1. Vasoactive amines (Histamine, 5-hydroxytryptamine,
neuropeptides)
2. Arachidonic acid metabolites (Eicosanoids)
i) Metabolites via cyclo-oxygenase pathway (prostaglandins, thromboxane A2,
prostacyclin)
ii) Metabolites via lipo-oxygenase pathway (5-HETE, leukotrienes)
3. Lysosomal components
4. Platelet activating factor
5. Cytokines (IL-1, TNF-α, TNF-ᵝ, IFN-ꙋ, chemokines)
6. Nitric oxide and oxygen metabolites

31. Chemical Mediators of Acute Inflammation
II. PLASMA-DERIVED MEDIATORS
(PLASMA PROTEASES)
These are products of:
1. The kinin system
2. The clotting system
3. The fibrinolytic system
4. The complement system

33. Plasma-derived mediators
These include various products
derived from activation and
interaction of 4 interlinked systems:
kinin, clotting, fibrinolytic
and complement.
Hageman factor (factor XII) of
clotting system plays a key role in
interactions of the 4 systems.

34. Interrelatioship between clotting, fibrinolytic,
kinin and complement systems

36. REGULATION OF INFLAMMATION
 The onset of inflammatory responses may have potentially
damaging influence on the host tissues as evident in
hypersensitivity conditions.
 Such self-damaging effects are kept in check by the host
mechanisms so as to resolve inflammation.
 These include the following mechanisms:
i) Acute phase reactants
ii) Corticosteroids
iii) Free cytokine receptors
iv) Anti-inflammatory chemical mediators.

37. INFLAMMATORY CELLS
 The cells participating in acute and chronic inflammation are
circulating leucocytes, plasma cells and tissue macrophages.
Lymphocyte
Plasma cell Eosinophil Basophil
Polymorph Monocyte

38. Giant cells

39. FACTORS DETERMINING VARIATION
IN INFLAMMATORY RESPONSE
The morphologic variation in
inflammation depends on number of
factors and processes.
They are:
1. Factors involving the
Organisms
i) Type of injury & infection
ii) Virulence
iii) Dose
iv) Portal of entry
v) Product of organisms
Boil
Vesicle

40. 2. Factors involving the Host
i) General health of host
ii) Immune state of host
iii) Leukopenia
iv) Site or type of tissue
involved
v) Local host factors.
3. Type of Exudation
i) Serous
ii) Purulent or suppurative
exudate
iii) Fibrinous
iv) Haemorrhagic
v) Catarrhal.

41. MORPHOLOGY OF ACUTE
INFLAMMATION
Morphologic varieties of acute
inflammation are as follows:
1. Pseudomembranous
inflammation
2. Ulcer
3. Suppuration (Abscess
formation)
4. Cellulitis
5. Bacterial infection of the
blood:
i) Bacteraemia
ii) Septicaemia
iii) Pyaemia

42. Sequelae of pyaemia

43. SYSTEMIC EFFECTS OF
ACUTE INFLAMMATION
 Fever
 Leucocytosis
 Lymphangitis-lymphadenitis
 Shock Fever
Lymphangitis-lymphadenitis Shock Leucocytosis

44. FATE OF ACUTE INFLAMMATION
The acute inflammatory process can
culminate in one of the following 4
outcomes:
1. Resolution
2. Healing by scarring
3. Progression to suppuration
4. Progression to chronic
inflammation.

45. CHRONIC INFLAMMATION
Chronic inflammation is defined as
prolonged process in which tissue
destruction and inflammation occur at the
same time.
CAUSES
 Chronic inflammation following acute
inflammation .
 Recurrent attacks of acute
inflammation.
 Chronic inflammation starting de novo. Chronic inflammation

46. FEATURES OF CHRONIC
INFLAMMATION
 Mononuclear cell infiltration
 Tissue destruction or Necrosis
 Proliferative changes
Mononuclear cell infiltration
Necrosis

47. TYPES OF CHRONIC
INFLAMMATION
2 TYPES
NON SPECIFIC:
 Irritant substances produce a non
specific chronic inflammatory reaction
 Formation of granulation tissue and
 Healing fibrosis.
Eg: chronic osteomyelitis, chronic
ulcer
SPECIFIC:
 Injurious agents causes a characteristic
histological tissue response.
Eg: Tuberculosis, Leprosy, Syphilis
Chronic osteomyelitis
Tuberculosis

48. HISTOLOGICAL FEATURES
CHRONIC NON-SPECIFIC
INFLAMMATION:
 Characterised by non specific
inflammatory cell infiltration.
Eg : Actinomycosis
CHRONIC GRANULOMATOUS
INFLAMMATION:
 Characterised by formation of
granulomas .
Eg; Tuberculosis, Leprosy,
Syphilis, Sarcoidosis
Actinomycosis
Leprosy

49. SYSTEMIC EFFECTS OF
CHRONIC INFLAMMATION
 Fever
 Anemia
 Leucocytosis
 ESR
 Amyloidosis

50. Gingivitis
Healthy Gingiva