This document provides an overview of inflammation. It defines acute and chronic inflammation, describes the signs and causes of inflammation. For acute inflammation, it details the vascular events like increased permeability and cellular events like chemotaxis and phagocytosis. Chronic inflammation is characterized by a mononuclear cell infiltration that can cause tissue destruction. Specific inflammatory disorders of the dental pulp and periradicular tissues are also enumerated. Inflammation forms the basis of many clinical dental pathologies.

1. INFLAMMATION
-Ritu Gupta
PG 1ST YEAR
Dept of Conservative
Dentistry and
Endodontics
PDA, Bhopal (M.P.)

2. CONTENTS
• Introduction
• Etiology
• Signs of inflammation
• Types of inflammation
• Acute inflammation
Definition
Causes
Features
Vascular events
Cellular events
Systemic effects of acute
inflammation
Fate of acute inflammation
• Chronic inflammation
Definition
Causes
Features
Systemic effects of chronic
inflammation
Types of chronic inflammation
• Granulomatous inflammation
• Acute vs Chronic inflammation
• Inflammatory disorders of pulp
and periradicular tissues
• References

3. • Inflammation is defined as the 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, followed by removal of the
necrosed cells and tissues

4. ETIOLOGY
• Infective agents like bacteria , viruses and
their toxins, fungi, parasites
• Immunological agents like cell mediated and
antigen-antibody reactions
• Physical agents like heat, cold, radiation,
mechanical trauma
• Chemical agents like organic
and inorganic poisons
• Inert materials such as
foreign bodies

5. SIGNS OF INFLAMMATION
• The Roman writer CELSUS in 1st century A.D.
named the famous 4 cardinal signs of inflammation
as :
1. rubor (redness)
2. tumor (swelling)
3. calor (heat)
4. dolor (pain)
To these, 5th sign functio laesa (loss of function) was
later added by Virchow

7. TYPES OF INFLAMMATION
• Depending upon the defense capacity of the host
and duration of response, inflammation can be
classified as acute and chronic
• (sub-acute inflammation: state of inflammation
between acute and chronic)
a) Acute Inflammation is of short duration
(lasting less than 2 weeks) and represents the
early body reaction , resolves quickly and is
usually followed by healing

8. • The main features of acute
inflammation are
1. Accumulation of fluid and
plasma at the affected site
2. Intravascular activation of
platelets
3. PMNs as inflammatory
cells
• Sometimes, acute
inflammatory response may
be quite severe and is
termed as fulminant acute
inflammation

9. ACUTE
INFLAMMATION
Vascular events
Hemodynamic
changes
Altered
Vascular
permeability
Cellular events
Exudation of
leukocytes
Phagocytosis

10. b) Chronic inflammation is of longer duration and
occurs either after the causative agent of acute
inflammation persists for a long time, or the
stimulus is such that it induces chronic
inflammation from the beginning
• A variant chronic active inflammation , is the
type of chronic inflammation in which during the
course of disease there are acute exacerbations of
activity.
• Feature :presence of lymphocytes , plasma cells
and macrophages, granulation tissue formation
and in specific situation, as granulomatous
inflammation

11. VASCULAR EVENTS
• HAEMODYNAMIC CHANGES:
1. TRANSIENT VASOCONSTRICTION
2. VASODILATATION(arterioles ,venules and capillaries)
obvious within 30 min of injury
Increase blood volume in microvascular bed –REDNESS &
WARMTH
3. Elevation of LOCAL HYDROSTATIC PRESSURE
Results in transudation of fluid into extracellular space
SWELLING

13. 4. SLOWING /STASIS
Increased vascular permeability
Increased concentration of RBCs
Raised blood viscosity
Slower blood flow

14. slowing followed by
5. LEUKOCYTIC MARGINATION (neutrophils mainly)
to the vascular endothelium
Leukocytes then move and migrate
through gaps between the endothelial
cells in the extravascular space
6.EMIGRATION

15. LEWIS EXPERIMENT
• Lewis introduced the changes
in the skin of the inner aspect
of forearm by firm stroking
with a blunt point. The
reaction so elicited is known as
TRIPLE RESPONSE or RED LINE
RESPONSE consisting of :
RED LINE- local vasodilatation of
capillaries and venules
FLARE –vasodilatation of
adjacent arterioles
WHEAL- transudation of fluid
into the extravascular space

16. • ALTERED VASCULAR PERMEABILITY
STARLING’S HYPOTHESIS
In normal circumstances fluid balance is maintained
by 2 opposing set of forces :
1. Forces that cause OUTWARD MOVEMENT of fluid
from microcirculation are intravascular hydrostatic
pressure and osmotic pressure of interstitial fluid
2. Forces that causes INWARD MOVEMENT of
interstitial fluid into circulation are intravascular
osmotic pressure and hydrostatic pressure of
interstitial fluid

17. • Normally, whatever little fluid is left in the
interstitial compartment is drained by the
lymphatics and thus no edema results.

18. • In inflamed tissues, the
endothelial lining becomes
leaky. Consequently, the
intravascular osmotic
pressure decreases and
osmotic pressure of the
interstitial fluid increases
resulting in excessive
outward flow of fluid into
the interstitial
compartment.
EXUDATIVE
INFLAMMATORY OEDEMA

19. MECHANISMS OF INCREASED
VASCULAR PERMEABILITY
1. Contraction of endothelial cells
• Reversible process
• Mediated by histamine, bradykinin , leukotrienes
• Short duration: 15-30 min
2. Retraction of endothelial cells
• TNFα and IL-1
• onset of response takes 4-6 hours after injury and
lasts for 2-4 hours or more

20. SCHEMATIC ILLUSTRATION OF PATHOGENESIS OF INCREASED
VASCULAR PERMEABILITY IN ACUTE INFLAMMATION

21. 3. Endothelial injury
• Immediate sustained response
• Lasts for several hours or days
4. Leukocyte – mediated endothelial injury
• Activation of leukocytes release proteolytic enzymes
and toxic oxygen species
• Late response
5. Neovascularisation
• Under the influence of VASCULAR ENDOTHELIAL
GROWTH FACTOR during the process of repair and in
tumours are excessively leaky

22. CELLULAR EVENTS
1. EXUDATION OF LEUCOCYTES
• Most important feature of inflammatory
response.
• The escape of leucocytes from lumen of
microvasculature to the interstitial tissue.
• In acute inflammation, PMNs comprise the first
line of defense, followed later by the monocytes
and macrophages.

24. 1. CHANGES IN THE FORMED ELEMENTS OF BLOOD
VASODILATATION
subsequently, SLOWING of blood stream
The central stream of cells widens and peripheral plasma
zone becomes narrower because of loss of plasma by
exudation.
MARGINATION
The neutrophils of the central column come close to
vessel wall
PAVEMENTING

25. 2. ROLLING AND ADHESION
Peripherally marginated and pavemented
neutrophils slowly roll over the endothelial cells
lining the vessel wall
ROLLING PHASE
Transient bond between the leukocytes and the
endothelial cells becoming firmer
ADHESION PHASE

26. • ADHESION MOLECULES
SELECTINS
E-selectin (cytokine activated endothelial cells)
P-selectin (preformed and stored in endothelial cells)
L-selectin (expressed on surface of lymphocytes and
neutrophils)
INTEGRINS
Activated during the process of loose and transient
adhesions between the endothelial cells and leukocytes
IMMUNOGLOBULIN SUPER FAMILY ADHESION
MOLECULE: ICAM-1,2

27. 3. EMIGRATION
neutrophils move till a suitable site is reached
CYTOPLASMIC PSEUDOPODS
Subsequently , crosses the basement membrane by
damaging it locally with secreted collagenase and
escape out into the extravascular space
EMIGRATION

28. Simultaneously escape of RBCs takes place through
the gaps between the endothelial cells
DIAPEDESIS
Diapedesis gives hemorrhagic appearance to the
inflammatory exudate

29. LEUCOCYTIC EMIGRATION

30. 4. CHEMOTAXIS
• The chemotactic factor mediated transmigration
of leukocytes after crossing several barriers to
reach the interstitial tissues is called chemotaxis
• Well illustrated by Boyden’s chamber experiment.
• In this, a millipore filter (3microns pore size)
separates the suspension of leukocytes from the
test solution in tissue culture chamber
• If the test solution contains chemotactic agent,
the leukocytes migrate through the pores of filter
towards the chemotactic agent

31. BOYDEN’S CHAMBER EXPERIMENT

32. • Following agents act as potent chemotactic
substances (chemokines) for neutrophils:
1. Leukotriene B₄ (LT-B₄)
2. C5a and C3a
3. Interleukin-8
4. Formylated peptides
• Chemokine for monocyte: monocyte
chemoattractant protein-1(MCP-1)
• For eosinophils : eotaxin
• For recognising virally infected cells,etc. :
NK cells

33. 2.PHAGOCYTOSIS
• ENGULFMENT of solid particulate material by the
cells (cell eating)
• The cells performing this function are
PHAGOCYTES
• 2 main types of cells:
i. PMNs which appear early in acute inflammatory
response- MICROPHAGES
ii. Circulating monocytes and fixed tissue
mononuclear phagocytes -MACROPHAGES

34. 4 STEPS OF PHAGOCYTOSIS
1.RECOGNITION AND
ATTACHMENT OF
PARTICLE
2. ENGULFMENT WITH
FORMATION OF PHAGOCYTIC
VESICLE
3.DEGRANULATION STAGE
4. KILLING AND
DEGRADATION STAGE

35. STAGE 1 : RECOGNITION AND ATTACHMENT OF PARTICLE
• Opsonins are naturally occuring factors in the serum
• IgG opsonin: Fc fragment of immunoglobulin G. It is
naturally occuring antibody in the serum that coats
the bacteria while PMNs possess receptors for the
same
• C3b opsonin : fragment of complement. It is generated
by the activation of complement pathway
• Lectins : carbohydrate binding proteins in the plasma
which bind to the bacterial cell wall

36. The opsonised particle is ready to be engulfed
Formation of cytoplasmic pseudopods around the
particle
Enveloping in the phagocytic vacuole
Eventually, the plasma membrane breaks from the cell
surface and lysosomes of cell fuse with the phagocytic
vacuole
PHAGOLYSOSOME/ PHAGOSOME

37. STAGE 2: ENGULFMENT WITH FORMATION OF
PHAGOCYTIC VESICLE

38. STAGE 3: DEGRANULATION STAGE
1. Preformed granule stored products of PMNs are
released into phagolysosome
2. Mononuclear phagocyte also secrete enzymes eg:
• IL-2 and 6, TNF
• Arachidonic acid metabolites (prostaglandins,
leukotrienes, platelet activating factor)
• Oxygen metabolites (superoxide oxygen, hydrogen
peroxide, hypochlorous acid)

39. STAGE 4: KILLING OR DEGRADATION STAGE
The micro-organisms after being killed are degraded
by hydrolytic enzymes.
The antimicrobial agents act by 2 mechanisms:
1. Oxygen dependent bactericidal mechanism
2. Oxygen independent mechanism

41. SYSTEMIC EFFECTS OF ACUTE
INFLAMMATION
• Acute inflammation is associated with
systemic effects as well
• These include:
1. Fever
2. Leucocytosis
3. Lymphangitis-lymphadenitis
4. Shock

42. FATE OF ACUTE INFLAMMATION

43. CHRONIC INFLAMMATION
• It is defined as prolonged process in which tissue
destruction and inflammation occurs at the same
time.
• Time course : >48hours (weeks, months, years)
• Cell type: mononuclear cells (macrophages,
lymphocytes, plasma cells)
• Can be caused by 1 of the following 3 ways
1.
Following acute
inflammation
2.
Recurrent attacks of
acute inflammation
3.
Chronic
inflammation
starting de novo

44. Features of
chronic
inflammation
Infiltration with mononuclear cells-
macrophages, lymphocytes & plasma cells
Healing by proliferation &
connective tissue
replacement of damaged
tissue
Tissue destruction
/ necrosis

45. Systemic effects of chronic inflammation
• FEVER: invariably there is mild fever, often with loss
of weight and weakness
• ANEMIA: chronic inflammation is accompanied by
anemia of varying degree
• LEUCOCYTOSIS
• ESR : It is elevated in all cases of chronic
inflammation
• AMYLOIDOSIS : long- term cases of chronic
suppurative inflammation may develop
secondary systemic (AA) amyloidosis

46. CHRONIC
INFLAMMATION
1. NON-SPECIFIC
When irritant substance produces non specific chronic
inflammatory reaction with formation of granulation tissue
and healing by fibrosis
Eg: chronic osteomyelitis, chronic ulcer
2. SPECIFIC
When the injurious agent causes a characteristic histologic
tissue response
Eg : tuberculosis, leprosy, syphilis

47. GRANULOMATOUS INFLAMMATION
• Granuloma is defined as a circumscribed , tiny
lesion, about 1 mm in diameter, composed
predominantly of collection of modified
macrophages called epitheloid cells, rimmed at
periphery by lymphoid cells.
• Formation of granuloma is a type IV granulomatous
hypersensitivity reaction.
• It is a protective defense reaction by the host but
eventually causes tissue destruction because of
persistence of the poorly digestible antigen e.g.
Mycobacterium tuberculosis, M. leprae etc.

49. ACUTE CHRONIC

50. ENNUMERATION OF INFLAMMATORY
DISORDERS IN PULP AND PERIRADICULAR
TISSUES
• Inflammatory diseases of dental pulp
(a) Reversible pulpitis
(b)Irreversible pulpitis
(i) Symptomatic irreversible pulpitis
(ii) Asymptomatic irreversible pulpitis
(iii) Chronic hyperplastic pulpitis
(iv) Internal Resorption

51. • Diseases of Periradicular tissues
1. Symptomatic periradicular disease
(a) Symptomatic apical periodontitis
(i) Vital tooth
(ii) Non-vital tooth
(b) Acute alveolar abscess
(c) Phoenix abscess
2. Asymptomatic periradicular diseases
(a) Asymptomatic apical periodontitis
(b) Chronic Alveolar abscess
(c) Radicular cyst
(d) Condensing osteitis
3. External root resorption
4. Persistent apical periodontitis
5. Diseases of the periradicular tissues of non endodontic origin

52. Inflammation
forms the basis
of most of the
clinical

53. REFERENCES
• Kumar et al. Robbins basic pathology. 7/e.
Pennsylvania:Elsevier;2004
• Rubin E. et al. Rubin’s Pathology:
Clinicopathologic Foundations of Medicine. 4th
ed. Maryland: Lippincott Williams & Wilkins;
2005
• Mohan H. Essential pathology for dental
students. 3rd ed. Noida (India): Jaypee brothers
medical publishers (P) Ltd; 2005
• Grossman’s Endodontic Practice. 13th edition.
New Delhi: Wolters Kluwer (India)Pvt. Ltd ; 2014