Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
4. History :
4 cardinal signs of inflammation
Rubor (redness)
Tumor (Swelling)
Calor (heat)
Dolor (pain)
The fifth sign Functio laesa (loss of function) was
later on added by Virchow.
5. Sir Thomas Lewis
Triple response or red line response consists of
Red line
Flare
Wheal
6. Types of Inflammation
Acute inflammation:
• Short duration
• Represents early body reaction
• Usually followed by repair
Chronic inflammation :
Longer duration
Occurs either due to persistence of the causative agent
of acute inflammation for a longer duration, or
The stimulus is such that it induces chronic
inflammation.
7. Definition: It is a rapid response to an injurious
agent that serves to deliver leukocytes and plasma
proteins, such as antibodies to the site of infection or
tissue injury.
Acute Inflammation
8. Stimuli for Acute Inflammation
Infection
Trauma
Physical and Chemical injuries
Tissue necrosis
Foreign bodies
Immune reaction
12. Persistent progressive dilatation
Arterioles dilate
Microvasculature at the site of injury becomes filled
with blood
Immediate response mediated by
Sustained by
13. Increase in local hydrostatic
pressure or Vascular
Permeability
Outpouring of protein-rich fluid into extra vascular tissues
It can occur by 2 different mechanisms
According to type of injury permeability occurs
Mild injury - postcapillary venules
Moderate injury – capillaries and small venules
Severe injury – capillaries, venules and arterioles
14. Slowing or stasis
There is loss of fluid from blood vessels
No loss of other blood cells
Thus increase in viscosity of blood
15. Leukocyte migration
Endothelial cells are activated by mediators and express
increased level of adhesion molecule
Leukocytes adhere to endothelium and migrate through
the vascular wall into the interstitial tissue
Of all the cells mainly
neutrophils
accumulate along the
vascular endothelium
17. Contraction of endothelial cells
Most common mechanism of vascular leakage
Elicited by histamine, bradykinin, leukotriene and
neuropeptide substance P
It is called Immediate Transient Response
18. Direct endothelial injury
Direct injury to endothelial cells causes cell necrosis
and appearance of physical gaps
Neutrophils that adhere the endothelium may also
injure the cells
In most cases leakage starts immediately after the
injury and sustains for several hours
19. Increased Transcytosis
Presence of increased transport of fluids and proteins
through endothelial cells
It may involve channels consisting of inter connected,
uncoated vesicles and vacuoles located close to inter
cellular junction
20. Leakage from new blood vessels
Under the influence of VEGF the new capillaries are
formed
They become excessively leaky
24. Changes in formed elements of blood
With stasis, normal axial flow of blood changes.
Central beam widens and periphery becomes narrow.
Occurrence of
‘Rouleaux formation’
Leucocytes move to the
periphery- Margination
25. Rolling and adhesion
Peripheral neutrophils roll over to the endothelial cells
Transient bond between leucocytes and endothelial cells
occur
This is brought about by various
adhesion molecules
26. Emigration
Neutrophils force their way out by thrusting a pseudo
pod through the intercellular junction
It then squeezes out by amoeboid movement
27. Chemotaxis
Trans migration of leukocytes to reach the interstitial
tissues is known as Chemotaxis
Agents which act as
potent chemotactic
substance are called
Chemokines
29. It is the process of engulfment of solid particulate
material by the cells.
There are two types of cells involved in this→
Microphages
Macrophages
Process of Phagocytosis includes :
30. Recognition and attachment
Bacterial products release chemotactic factors
Phagocytes are recognized and attracted to bacteria
Micro-organisms get coated with Opsonins.
31. Engulfment stage
The opsonized particle is ready to get engulfed.
Cytoplasmic pseudopods are formed around the
particle.
The vacuole then lies free in the cytoplasm.
The lysosome of the cell fuses with the vacuole to form
Phagolysosome.
35. Pseudomembranous
Inflammation
Inflammatory response of mucous surfaces to toxins
Due to denudation of epithelium plasma exudes on the
surface
It coagulates and with necrosed epithelium forms false
membrane
E.g. - Candidiasis
36. Ulcer
Local defect on the surface of epithelium
Acute stage – Infiltration by PMN’s with
vasodilatation
Chronic stage – Infiltration by lymphocytes, plasma
cells and macrophages with scarring
E.g. – Apthous ulcer
Herpetic ulcer
37. Abscess formation
Acute infection + Intense neutrophilic infiltration
Tissue necrosis
Formation of pus filled cavity → Abscess
E.g.
Periodontal abscess
Gingival abscess
Periapical abscess
38. Cellulitis
It is a diffuse inflammation of soft tissues which is not
circumscribed to one area, but which, in contrary to the
abscess, tends to spread through tissue spaces and along
fascial planes.
39.
40. Fever
It is due to release of IL-1 and TNF.
They reach the brain, bind to thermo regulatory
receptors of hypothalamus and through the synthesis
of Prostaglandins cause fever .
43. Shock
It is due to massive release of cytokine TNF-α
Results in vasodilatation, increased vascular
permeability and intra vascular volume loss
Net effect is hypotension and shock
46. Resolution
It means complete restitution of normal tissue
architecture and function
Occurs when tissue is intact and has the capacity to
replace any specialized cells
47. Healing by scarring
It occurs when
Substantial damage to connective tissue framework
Tissue lacks ability to regenerate specialized cells
48. Progression to Suppuration
It occurs when pyogenic bacteria causes severe tissue
necrosis
Firstly there is neutrophilic infiltration
Mixture of neutrophils, bacteria, necrotic tissue, cell
debris and fibrin→ Pus
49. Progression to Chronic
Inflammation
Persistence of injurious agents over a prolonged
period
Process of inflammation and healing proceed side by
side