Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation

2. Contents :
 Introduction
 History
 Types of Inflammation
 Acute Inflammation

3. Introduction to
Inflammation:
Definition: Inflammation is defined as the local
response of living tissues to injurious agents.

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

9. Vascular events :
Changes in vascular flow and caliber
Altered vascular permeability

10. Changesin vascular flow
and caliber

11. Transient vasoconstriction
 It occurs in arterioles
 Lasts from 3-5 seconds to 5 minutes

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

16. Altered vascular
permeability

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

21. Exudation of leukocytes
Phagocytosis

22. Exudation of leukocytes

23. NORMAL AXIAL BLOOD FLOW

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

28. Phagocytosis

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.

32. Degranulation stage
 Preformed granule – stored products of PMN’s are
discharged into the phagolysosome.

33. Degradation stage
 Micro-organisms after being killed by antibacterial
substances are degraded by hydrolytic enzymes.

34. MORPHOLOGY OF ACUTE
INFLAMMATION

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.

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 .

41. Leukocytosis
 It accompanies the acute inflammatory reaction
 Bacterial infections – Neutrophilia
 Viral infections – Lymphocytosis
 Parasitic infections – Eosinophilia

42. Lymphangitis and
Lymphadenitis
 Lymphatics and lymph nodes show reactive
inflammatory changes

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

44. Fate of acute
inflammation

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

50. Acute lesions seen in orofacial region:
Bacterial
• Pulpitis
• Acute necrotizing ulcerative gingivitis
• Acute herpetic gingivo stomatitis
• Cellulitis
• Ludwig’s angina
• Osteomyelitis
• Pericoronitis
• Diphtheria

51. Viral
• Herpes Zoster
• Mumps (Parotitis)
Fungal
• Pseudomembraneous Candidiasis
• Median Rhomboid Glossitis
Immune related
• Recurrent Apthous Stomatitis
• Angioedema
• Contact Stomatitis
• AIDS

52. References :
1) Robbins Basic Pathology ,7th edition
2) Essential pathology, Harsh Mohan ,3rd edition
3) Wheater’s Basic Pathology ,5th edition
4) Inflammation by Trowbridge and Emling ,5th edition
5) Shafer’s Textbook of Oral Pathology, 6th edition

53. Part 2 of Inflammation
 Chronic inflammation
 Mediators of inflammation
 Intervention in inflammation