This document discusses inflammation and healing. It defines inflammation as the local response of living tissues to injury. The causes of inflammation can be exogenous, such as physical or chemical agents, or endogenous like circulation disorders or metabolic products. The classic signs of inflammation are redness, swelling, heat, and pain. Acute inflammation involves rapid onset and short duration, while chronic inflammation has insidious onset and longer duration. Acute inflammation is characterized by increased blood flow, vascular permeability, and leukocyte infiltration. Chronic inflammation features infiltration by mononuclear cells like macrophages and lymphocytes, along with simultaneous tissue destruction and healing.

1. INFLAMMATION
AND
HEALING
Mohammad Muztaba Khan
Assistant professor(Jr.)
Department of Pharmacology Bhavdiya
institute sibar Sohawal Ayodhya

2. DEFINITION:
Inflammation is defined as the local response of living
tissues to injury due to any agent.
inflammation, a process by which the body's immune
system malfunctions.( failure to function normally.
Eg. diseases, like arthritis, diabetes, myasthenia gravis

3. The causes of inflammation are many and varied:
 Exogenous causes:
 Physical agents
 Mechanic agents: fractures, foreign corps, sand, etc.
 Thermal agents: burns, freezing
 Chemical agents: toxic gases, acids, bases
 Biological agents: bacteria, viruses, parasites
 Endogenous causes:
 Circulation disorders: thrombosis, infarction, hemorrhage
 Enzymes activation – e.g. acute pancreatitis
 Metabolic products – uric acid, urea
ETIOLOGY:

4. INFLAMMATION
INTRODUCTION
TYPES
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
CHRONIC INFLAMMATION

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

6. TYPESOF INFLAMMATION
ACUTE
Rapid onset
Short duration
Fluid accumulation, plasma protein exudation
Neutrophils
CHRONIC
Onset- insidious
Longer duration
Lymphocytes, macrophages, plasma cells as inflammatory
cells

7. Pathogenesis: Three main processes occur at the site of
inflammation, due to the release of chemical mediators
● Increased blood flow (redness and warmth).
● Increased vascular permeability (swelling,
pain & loss of function).
● Leukocytic Infiltration.

8. Mechanism of Inflammation
1. Vasodilatation
2. Exudation ‐
Edema
3. Emigration of
cells
4. Chemotaxis

9. ACUTE INFLAMMATION
VASCULAR EVENTS CELLULAR EVENTS
1. HAEMODYNAMIC CHANGES
2. ALTERED VASCULAR PERMEABILITY
1. EXUDATION OF LEUKOCYTES
2. PHAGOCYTOSIS

10. VASCULAREVENTS
1. HAEMODYNAMIC CHANGES:
1. TRANSIENT VASOCONSTRICTION
2. VASODILATATION (arterioles, venules and capillaries)
obvious within half an hour of injury
Increase blood volume in microvascular bed Redness
and warmth
3. Elevation of HYDROSTATIC PRESSURE
Results in transudation of fluid in the extracellular space
swelling

11. 4. Slowing or stasis
Increased vascular permeability
Increased concentration of RBCs
Raised blood viscosity
Slower blood flow

12. slowing followed by
LEUCOYTE MIGRATION (neutrophils mainly) to the
vascular endothelium
Leukocytes then move and migrate
through gaps between the endothelial
cells in the extravascular space.
EMIGRATION

13. 2. 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 cause INWARD MOVEMENT of interstitial fluid
into circulation are intravascular osmotic pressure and hydrostatic
pressure of interstitial fluid.

14. • Accumulation of fluid - interstitial compartment
which comes from blood plasma by its escape
through the endothelial wall of peripheral vascular
bed.
• Escape of fluid is due to vasodilatation and
consequent elevation in hydrostatic pressure -
transudate.
• Subsequently, the characteristic inflammatory
oedema, appears by increased vascular
permeability of microcirculation – exudate.

16. MECHANISMS OF
INCREASED VASCULAR
PERMEABILITY

17. 1. Endothelial cell contraction
reversible process
mediated by histamine, bradykinin, leukotrienes
short duration: 15-30 min.
2. Structural re-organisation of the
cytoskeleton of endothelial cells -
Reversible retraction at the intercellular
junctions.
• Mediated by cytokines such as
interleukin-1 (IL-1) and tumour
necrosis factor (TNF)-α.c

18. 3. Endothelial injury or Direct injury to endothelial cells
Causes
Cell necrosis and appearance of physical gaps.
Process of thrombosis is initiated at the site of damaged
endothelial cells.
Affects all levels of microvasculature.
immediate sustained response, lasts for
several hours or days

19. 4. Leukocyte-mediated endothelial injury
• Adherence of leucocytes to the endothelium at the site of
inflammation.
• Activation of leucocytes - release proteolytic enzymes and
toxic oxygen.
• Cause endothelial injury and increased vascular
leakiness.
• Newly formed capillaries under the influence of vascular
endothelial growth factor (VEGF).
• Process of repair and in tumours are excessively
leaky
5. Neo vascularisation

20. CELLULAREVENTS
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, polymorphonuclear neutrophils comprise
the first line of defense, followed later by the monocytes and
macrophages.

21. CHANGES LEADING TO MIGRATION
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 the vessel
wall
PAVEMENTING

23. 2. ROLLING ANDADHESION:
Peripherally marginated and pavemented neutrophils slowly roll
over the endothelial cells lining the vessel wall.
ROLLING PHASE
Transient bond between the leucocytes and the endothelial cells
becoming firmer.
ADHESION PHASE

24. ADHESION MOLECULES:
SELECTINS :
E-selectin
P-selectin
(cytokine-activated Endothelial cells)
(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 leucocytes.
IMMUNOGLOBULIN SUPER FAMILYADHESION
MOLECULE: ICAM-1,2

25. 3. EMIGRATION

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

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

28. 4. CHEMOTAXIS
The chemotactic factor mediated transmigration of leucocytes
after crossing several barriers to reach the interstitial tissues is
called CHEMOTAXIS.
Well illustrated by BOYDEN’S CHAMBER EXPERIMENT.

29. In this, a millipore filter separates the suspension of leucocytes
from the test solution in tissue culture chamber.
If the test solution contains chemotactic agent, the leucocytes
migrate through the pores of filter towards the chemotactic agent.

30. CHRONIC INFLAMMATION
It is a prolonged process in which tissue destruction and
inflammation occurs at the same time.
Time course:
 > 48 hours (weeks, months, years)
 Cell type
 Mononuclear cells (Macrophages, Lymphocytes, Plasma cells)
Can be caused by 1 of the following 3 ways:
1. Chronic inflammation following acute inflammation
2. Recurrent attacks of acute inflammation
3. Chronic inflammation starting de novo

31. FEATURES OF CHRONIC INFLAMMATION
 Infiltration with mononuclear
cells – macrophages,
lymphocytes & plasma cells
CHRONIC
INFLAMMATION
Tissue
destruction
Healing by Proliferation &
connective tissue replacement of
damaged tissue

32. INFILTRATION WITH MONO-NUCLEAR CELLS

33. • Incr. lysosomal enzymes
• Greater abilityto
phagocytose
55
ACTIVATION OF MACROPHAGE
Cytokine
IFN - ɤ
Endotoxin ,
fibronectin
chemical mediators

34. MACROPHAGE
IN ACUTE
INFLAMMATION
Irritant eliminated-
macrophagedisappears
IN CHRONIC
INFLAMMATION
Persistent macrophage accumulationby
following mechanisms :
1. )Recruitment from circulation–
Chemotactic stimuli include:
a) C5a
b) Platelet derived growthfactor
c) Transforming growthfactor
s
2.) Local proliferation of macrophage
3.) Immobilization of macrophages
56

35. 57
TISSUE DESTRUCTION OR NECROSIS
• ACTIVATED
MACROPHAGES
Elastase
Protease
Collagenase
Reactive oxygen
radical
Cytokine IL-1,8

36. 58
PROLIFERATION
Small BLOOD
VESSELS
FIBROBLAST
Resulting in the formation of granulation tissue

37. REACTIONS OF PULP TO BACTERIAL INVASION
ᶲ Vascular changes take place
inside blood vessels.
ᶲ PMNLs reach the area of
inflammation
ANATOMICAL FEATURES OF PULP THAT TEND TO
ALTER THE RESPONSE
Enclosure of pulp in rigid calcified walls - PREVENTS EXCESSIVE
SWELLING.. Thus more painful.
Pressure leads to decrease Blood supply and Ischaemia – does not get
corrected since collateral circulation cannot develop through tiny apical59
foramina

38. HISTOLOGIC FEATURES OF PULPITIS
ACUTE CHRONIC
60
 MONONUCLEAR CELLS
PREDOMINATE - chiefly
plasma cells &
lymphocytes.
 Fibroblastic activity is
evident
 collagen fibres seen in
bundles
• Continued vascular
dilation
• Accumulation of oedemal
fluid in connective tissue
• Pavementing of PMNLs
along endothelial wall

39. • Inflammation of periodontal ligament around root apex..
Changes localised around root
apex…..since richly vascular.
Vascular changes , infiltration of
PMNLs , and exudate
accumulation
Resorption of bone –
ABSCESS FORMATION
61

40. 1) Robbin’s & Cotron Pathological basis of diseases
2) Essential pathology for dental students - Harsh mohan
3) Text book of oral pathology - Shafers
References……..

41. THANKYOU