inflammation from Harsh Mohan and Guyton By: Dr. Sunbul Tabrez

1. GOOD MORNING
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2. INFLAMMATION
Presented by-
Dr. Sunbul Tabrez
PG First year
Oral Medicine Diagnosis and Radiology
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3. CONTENTS
 Introduction
 Etiology
 Cardinal signs of inflammation
 Types of Inflammation
 Acute inflammation
 Vascular events
 Cellular events
 Phagocytosis
 Recognition & attachment
 Engulfment
 Killing & degradation
 Mediators of inflammation
 Cell derived
 Plasma protein derived 3

4.  Regulation of inflammation
 Inflammatory cells
 PMN’s, eosinophil, basophils, lymphocytes, plasma cell,
mononuclear phagocyte, giant cells
 Factors affecting acute inflammation
 Fate of acute inflammation
 Chronic inflammation (Definition, Features, Effects and Types)
 Granulomatous inflammation
 Acute VS Chronic inflammation
 Dental implications of inflammation
 Pulpal infections
 Periapical infections & inflammation
 Gingival inflammation
 Periodontal Inflammation
 References
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5. 5

6. INTRODUCTION
 It is defined as the local response of living mammalian
tissues to injury from any agent.
 It is a body’s defense reaction in order to eliminate or
limit the spread of infectious agent, followed by removal
of necrosed cell and tissues
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7. ETIOLOGY
Infective agents like bacteria, virus 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 material such as foreign bodies.
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8. CARDINAL SIGNS OF INFLAMMATION
4 cardinal signs
(Celsus)
– rubor
– tumor
– calor
– dolor
5th sign functiolaesa
-Virchow
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9. TYPES OF INFLAMMATION
Mainly of 2 types i.e. acute and chronic
• Acute Inflammation
– short duration (less than 2 weeks)
– represents the early body reaction- followed by healing.
Sometimes the acute inflammatory response may be quite severe and
termed as ‘fulminant acute inflammation’
• Chronic inflammation
– longer duration.
– causative agent of acute inflammation persists for a long time.
‘Chronic active inflammation’ is the type of chronic inflammation in
which during the course of disease there are acute exacerbation activity.
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10. ACUTE INFLAMMATION
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11. The main features of acute inflammation are:
– accumulation of fluid and plasma at the affected site;
– intravascular activation of platelets;
– polymorphonuclear neutrophils as inflammatory cells.
Acute inflammatory response is a continuous process but for
understanding it is divided into
-vascular events
-cellular events.
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12. VASCULAR EVENTS
Alteration in microvasculature is the earliest response to
tissue injury.
• It includes –
- hemodynamic changes
- vascular permeability
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13. Hemodynamic changes
1. Transient vasoconstriction- immediate vascular response
irrespective of the type of injury, mainly arterioles
Mild injury - 3-5 seconds
Severe injury - 5 minutes
2. Persistent progressive vasodilatation- mainly arterioles, others to
a lesser extent, within half an hour of injury.
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14. 3. Progressive vasodilatation elevates the local hydrostatic
pressure– transudation of fluid into the extracellular space
swelling
4. Slowing or stasis- increased concentration of red cells,
and thus, raised blood viscosity.
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15. 5.Leucocytic margination- peripheral orientation of
leucocytes (mainly neutrophils) along the vascular
endothelium
– stick to the vascular endothelium
– move and migrate through the gaps between the
endothelial cells into the extravascular space
– This is known is emigration.
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16.  LEWIS EXPERIMENT showing TRIPLE
RESPONSE
Lewis induced the changes in skin of inner
aspect of forearm by firm stroking with a
blunt point. The reaction so elicited is known
as triple response or red line response.
RED LINE- appears in few secs due to
arteriolar vasodilatation
FLARE- the flush surrounding the red line due
to arteriolar dilatation of adjacent arterioles
WHEAL- swelling or oedema of the
surrounding skin due to transudation of fluid
into extravascular space
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17. Vascular permeability
The appearance of inflammatory oedema due to increased
vascular permeability is explained on the basis of Starling’s
hypothesis.
It says that fluid balance is maintained by two opposite sets
of forces:
1. Outward movement by intravascular hydrostatic
pressure & colloidal osmotic pressure of interstitial fluid
2. Inward movement by intravascular colloid osmotic
pressure & hydrostatic pressure of interstitial fluid
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18. • Patterns of increased vascular permeability
• Contraction of endothelial cells
• Mild endothelial damage
• Direct injury to endothelial cells
• Leukocyte-mediated endothelial injury
• Leakiness in neovasularisation
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19. CELLULAR EVENTS
There is:
1. Exudation of leukocytes
A. Changes in the formed elements of blood
B. Rolling and adhesion
C. Emigration
D. Chemotaxis
2. Phagocytosis
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21. (A) Changes in the formed elements of
blood
In early stages of inflammation the rate of flow of blood is increased due
to vasodilatation.
Slowing or stasis of blood stream
Changes in the normal axial flow of blood in the microcirculation takes
place.
The central stream of cells widen and peripheral plasma zone becomes
narrower due to loss of plasma by exudation.
This phenomenon is called ‘margination’
Due to this redistribution, neutrophils of the central column come close
to the vessel wall and this is known as ‘pavementing’.
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22. (B) Rolling and adhesion
• The neutrophils roll over the endothelial cells lining the
vessel wall.
• Transient bond formed between lekocytes and endothelial
cells which become firmer and attach via selectins,
integrins and immunoglobulin gene superfamily adhesion
molecule.
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23. (C) Emigration
Adherent leukocytes > pseudopodia
↓
between 2 endothelial cells
↓
Basement memb.& perivascular sheath (damaged by
collagenases & proteases on surface of migrating cells)
This is called as emigration.
First cells involved PMN’s– 1st 24 hrs.
→ Monocytes/macrophages – next 24 hrs.
Followed by diapedesis. 23

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25. (D) Chemotaxis
 The directional movement of leukocytes in response to a chemical
gradient to reach the interstitial tissue mediated by chemotactic
factor is called Chemotaxis.
 Boyden`s chamber experiment:
A Millipore filter(3 micro m) separates suspension of leukocytes from
test solution in tissue culture chamber.
If test solution contains chemotactic agent, the leukocytes migrate
through the pores of filter towards the chemotactic agent
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26. Chemotactic factors for leukocytes
1. Leukotriene B4 (LT-B4)
2. Platelet activating factor (PAF)
3. Components of complement system– C5a & C3a
4. Cytokines (IL-8)
5. Soluble bact. products (formylated peptides)
6. Monocyte chemoattractant protein (MCP-1)
7. Chemotactic factor for CD4 & T cells
8. Eosinophil chemotactic factor of anaphylaxis (ECF – A)
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27. PHAGOCYTOSIS
 Process of engulfment of solid particulate material by the
cells.
 Cells (phagocytes)
1.PMNs (early ac. Inflammation)
2.Circulating monocytes and fixed tissue mononuclear
phagocytes- macrophages
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28. 3 steps
Recognition and
attachment
stage
(opsonisation)
Engulfment
stage
Killing and
degradation
stage
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29. 1.Recognition & attachment stage
 Phagocytosis is initiated by expression of cell surface
receptors on macrophages which recognize micro org.:
mannose receptor and scavenger receptor
 Process of phagocytosis is further enhanced when m.org
are coated with specific proteins, opsonins from the
serum and the process is called opsonisation (preparing
for eating).
 IgG opsonin, C3b opsonin and lectins establish bond
between bacteria and cell membrane of phagocytic cell.
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30. 30Fig: Process of phagocytosis

31. 2.Engulfment stage
 The opsonized particle or microbe bound to the surface of phagocyte
is ready to be engulfed.
 This is accomplished by formation of cytoplasmic pseudopods around
the particle due to activation of actin filaments beneath cell wall,
enveloping it in a phagocytic vacuole/phagosome.
 The phagosome fuses with one or more lysosomes of the cell and form
bigger vacuole called phagolysosome.
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32. 3.Killing & Degradation
 The microorganisms after being killed by antibacterial substances are
degraded by hydrolytic enzymes. There are 2 types of mechanism
involved in the disposal of the microorganism. They are:
 Intracellular mechanism-
 Oxidative bactericidal mech by O2 free radicals
 Oxidative bactericidal mech by lysosomal granules
 Non-oxidative bactericidal mech
 Extracellular mechanism
 Degranulation of macrophages and neutrophils causes
proteolysis inside and outside the cell
 Immune-mediated lysis of microbes by cytolysis, antibody
mediated lysis & cell-mediated cytotoxicity
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33. 33

34. Mediators of inflammation
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35. 35

36. Regulation of Inflammation
1. Acute phase reactants: they protect the normal cells from harmful
effects of toxic molecules generated in inflammation & to clear away
the waste material by means of antioxidants, stress proteins, immune
agents, transport proteins, coagulation proteins, cellular protection
factors
2. Corticosteroids: Act as anti-inflammatory agents. during inf.&trauma
3. Free cytokine receptors in serum correlates with disease activity
4. Anti-inflammatory chemical mediators like PGE2 or prostacyclin
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37. INFLAMMATORY CELLS
PMN’s Eosinophil Basophils &
mast cells
Lymphocytes
Plasma cells Monocyte &
macrophages
Giant cells
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38. Factors affecting acute Inflammation
Factors involving the
organism
1. Types of injury and infection
2. Virulence
3. Concentration of organism
4. Portal of entry
5. Product of organism
Factors involving the host
1. Systemic diseases
2. Immune status of host
3. Congenital neutrophil defect
4. Leukopenia
5. Site or type of tissue involved
6. Local host factors
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39. FATE OF ACUTE INFLAMMATION
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Resolution Regeneration Healing by fibrosis
No tissue loss With tissue loss
Etiological agent removed
Acute inflammation
Persistence of etiological agent
Discharge of pus Recurrence
Suppuration Chronic inflammation

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41. CHRONIC INFLAMMATION
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42. Chronic Inflammation
 It is defined as a prolonged process in which tissue destruction and
inflammation occurs at the same time
 Occurs by one of the following 3 ways:
 Chronic inflammation following acute inflammation
 Recurrent attacks of acute inflammation
 Chronic inflammation starting de novo
 Systemic effects of chronic inflammation include:
 FEVER: mild fever with loss of weight and weakness
 ANAEMIA
 LYMPHOCYTOSIS
 ESR is elevated
 AMYLOIDOSIS
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43. Features of chronic inflammation
 Mononuclear cell infiltration: lymphocytes and macrophages influence
each other and release mediators of inflammation
 Tissue destruction or necrosis: caused by tissue macrophages which
release protease, elastase, collagenase, lipases, cytokines, reactive
oxygen radicals, nitric oxide, angiogenesis growth factor.
 Proliferative changes: Small blood vessels and fibroblasts are
stimulated leading to formation of inflammatory granulation tissue.
Eventually healing by fibrosis and collagen lay down begins
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44. Types of chronic inflammation
Chronic non-specific inflammation:
Irritant substance produces non specific chronic
inflammatory reaction with formation of granulation
tissue and healing by fibrosis.
In chronic suppurative inflammation infiltration by
polymorphs and abscess formation may occur.
Chronic granulomatous inflammation:
Injurious agent causes a histologic
tissue response by formation of
granuloma
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45. Granulomatous inflammation
Granuloma is defined as a
circumscribed, tiny lesion
about 1mm in diameter
composed predominantly
of collection of modified
macrophages called
epitheloid cells and
rimmed at the periphery
by lymphoid cells.
‘Granuloma’ derived from
granule meaning
circumscribed granule like
lesion, -oma which is a
suffix for true tumors but
here it indicates a localized
inflammatory mass or
collection of macrophages.
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CELL INJURY
Failure to digest agent
Weak acute inflammatory response
Engulfment by macrophages
Persistence of injurious agent
T cell-mediated immune response Poorly digested agent
Activation of CD4+ T cells & monocyte chemotactic factor
Accumulation of tissue macrophages & proliferation of T cells
Macrophages activated by IFN Gamma
Transformation to Secretion of fibroblastic
epitheloid & giant cells proliferating cytokines
P
A
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Of
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47. Composition of Granuloma
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Epitheloid
cells
Multinucleate
giant cells
Lymphoid
cells
Necrosis Fibrosis
Modified
macrophages
that are
elongated
cells having
slipper shaped
nucleus.
These are
weakly
phagocytic
Fusion of
adjacent
epitheloid
cells and have
20 or more
nuclei.
These are also
weakly
phagocytic but
cause removal
of invading
agents
As a cell
mediated
immune
response to
antigen.
Loc. area of
death
A feature of
healing by
proliferating
fibroblasts at
the periphery
of granuloma

48. ACUTE VS CHRONIC INFLAMMATION
ACUTE
1. Occurs within short time and lasts
for short duration
2. Cardinal signs present
3. Plasma exudation present
4. Mostly PMN’s and eosinophil's
present
5. High grade fever with
lymphocytosis (N+E)
6. Fated to either resolve, heal or
undergo chronicity
7. Eg: pyogenic abscess, cellulitis
CHRONIC
1. Occurs after delay and lasts longer
2. Generally not detectable
3. Plasma exudation may or may not
be present
4. Mostly lymphocytes, plasma cells,
giant cells and macrophages
5. Mild fever with lymphocytosis
(L+M)
6. Fated to either resolve, heal or
undergo dystrophic calcification
7. Eg: granulation tissue, chronic
osteomyelitis 48

49. APPLIED ASPECT
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50. DENTAL IMPLICATIONS OF INFLAMMATION
 Dental implication of inflammation include inflammation of the pulp
and perapical tissues. These can further spread to the surrounding
spaces presenting as intra-oral and extra-oral swelling.
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Deep dental
caries
Fracture Cracked tooth
syndrome
Physical &
chemical injuries

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53. Pulpitis
 Inflammation of the pulpal tissue is called pulpitis.
 Types: Acute pulpitis, chronic pulpitis, chronic
hyperplastic pulpitis
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54. Apical periodontitis
 Inflammation of the periodontal ligament at the periapex.
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55. Periapical Abscess and Periapical
granuloma
 Abscess is localized collection of pus. An acute case of abscess may
present with swelling and a chronic case of abscess may present with
either a sinus or a fistula opening.
 Abscess can be of 3 types:
 Pyogenic abscess, e.g.- Periapical abscess
 Pyaemic abscess
 Cold abscess, e.g.- tubercular abscess
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56. Rise in pressure with
inflammatory
exudate
Local tissue hypoxia
Localized destruction &
breakdown of
leucocytes, bacteria &
tissue
ABSCESS FORMATION
Acute
infection
Tissue
necrosis
Pus
formation
Abscess
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57. Periapical cyst (Radicular cyst)
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 When the pulp of teeth become necrotic perapical cyst formation may
occur.
 C/F:
 No symptoms unless they are secondarily affected.
 On palpation swelling may feel bony and hard if the cortex is
intact, crepitant as the bone thins and rubbery & fluctuant if the
outer cortex is perforated.
 R/F: Well defined radiolucency with cortical or sclerotic borders (inf.
spreads to surrounding bone)
 D/D: Apical granuloma, periapical pocket cyst, osseous dysplasia,
lateral periodontal cyst

58. Osteomyelitis & Periosteitis
 It is an inflammation of bone which may spread to the marrow,
cortex, cancellous portion and periosteum.
 Cause: Abscessed teeth and post surgical inf.
 Types: acute and chronic
 May present as rarefaction (loss of bone giving a radiolucent app) or
condensation (increased bone formation causing radiopaque app).
 When the inf. spreads to the periosteum of the bone it is called
periosteitis.
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59. Further spread of infection
 When the infection spreads further space infection or cellulitis may develop.
 Cellulitis(phlegmon) is a diffuse inflammation of the soft tissue that tends to
spread through tissue spaces and along facial planes.
 If the sublingual and submandibular spaces get involved then LUDWIG’s
ANGINA may develop where the patient is unable to eat, speak or breathe
which can even lead to death in later stages.
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60. Pericoronitis
 It refers to the inflammation of tissues surrounding the crown of
partially erupted tooth.
 Seen usually in the lower 3rd molars in young adults.
 The gingiva surrounding the erupted portion of the crown becomes
inflamed when food or microbial debris becomes trapped under the
soft tissue and gets secondarily traumatized by the opposing
occlusion.
 C/F: pain, swelling, trismus
 Rx: Removal of the tooth.
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61. Gingivitis
 Inflammation of the gingiva is called gingivitis.
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62. Periodontitis
 When gingivitis progresses to the periodontium it is referred to as
periodontitis.
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63. Treatment
 The main line of treatment to prevent the infection from spreading
into the pulp and periapical tissue is early intervention before any
periapical changes can occur.
 However, if the infection does spread a ROOT CANAL TREATMENT is
the best option unless the prognosis of the tooth is very poor wherein
the tooth needs to get extracted.
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64. REFERENCES
 Essential pathology for Dental students 5th edition by Harsh Mohan and
Sugandha Mohan.
 Robbins Basic pathology 9th edition.
 Oral radiology by White & Pharaoh.
 Shafer’s textbook of Oral Pathology.
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