Inflammation, role and types.

Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.

1. INFLAMMATION
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Dr. Ali Yaldrum
B.D.S, M.Sc (London)
Faculty of Dentistry, SEGi University

2. Survival of all organisms requires they
eliminate:
•foreign invaders (infectious pathogens: viruses,
bacteria, fungi)
•damaged tissues
•Achieved via a complex mechanism
called “inflammation”

3. Inflammation is a protective response
intended to eliminate the initial cause of cell
injury as well as the necrotic cells and
tissues resulting from the original insult

4. Diluting
Destroying/
Neutralising
Heal &
Repair
Restoration
of Function

5. A double edge sword?
Although inflammation helps clear infections
and other noxious stimuli and initiates
repair, the inflammatory reaction and the
subsequent repair process can cause
considerable harm.

7. Signs of Inflammation
Cardinal signs are
•Heat (calor)
•Redness (rubor)
•Swelling (tumor)

8. 2 additional signs seen in acute inflammation
•Pain (dolor)
•Loss of function (function laesa)

9. Steps of Inflammation
5R’s
1.Recognition of injurious agent
2.Recruitment of leukocytes
3.Removal of agent
4.Regulation of the response
5.Resolution

10. Types of Inflammation
•Acute
•Chronic

11. Acute Inflammation

12. Acute Inflammation
rapid response to injury or microbes and
other foreign substances that is designed to
deliver leukocytes and plasma proteins to
sites of injury

13. Stimuli
can be triggered by a variety of stimuli
•Infections
•Trauma
•Physical & chemical agents
•Foreign bodies
•Immune reactions

15. Acute inflammation has two major
components
•Vascular changes
•Cellular events

16. Vascular
•Changes in Vascular Caliber and Flow
•Increased Vascular Permeability

17. Changes in Vascular
Caliber and Flow
•Changes in blood vessels begin rapidly
after infection or injury but may develop
at variable rates, depending on the
nature and severity of the original
inflammatory stimulus.

18. transient vasoconstriction
arteriolar vasodilation
increased viscosity & slowing of circulation
stasis
migration
lasting few seconds

20. •Endothelial cell contraction leads to
intercellular gaps in post capillary venules

21. •Histamine, bradykinin, leukotrines
•immediate
•short lived 15 to 30 mins
•called as immediate transient response

22. •IL1 and TNF
•prolonged changes in cytoskeleton of
endothelial cells
•take 4-6 hours to develop
•lasts for up to 24 hours

23. Cellular Events
•an important function of the inflammatory
response is to deliver leukocytes to the
site of injury and to activate them

24. Leukocyte recruitment
Sequence consists of:
1.margination, adhesion to endothelium &
rolling along the vessel wall
2.firm adhesion to endothelium

25. 3.transmigration between endothelial cells;
4.migration in interstitial tissues toward a
chemotactic stimulus

27. Leukocyte activation
•Once leukocytes have been recruited to
the site of infection or tissue necrosis,
they must be activated to perform their
functions

28. •Stimuli for activation include microbes,
products of necrotic cells, and several
mediators

29. Phagocytosis
Consists of 3 distinct but interrelated
steps
1.recognition and attachment of the particle to the
ingesting leukocyte
2.engulfment, with subsequent formation of a phagocytic
vacuole
3.killing and degradation of the ingested material.

30. Patterns of acute
inflammation

31. Patterns of acute
inflammation
•vascular and cellular reactions that
characterize acute inflammation are
reflected in the morphologic appearance
of the reaction

32. •serous inflammation
•fibrinous inflammation
•suppurative inflammation

33. serous
characterized by:
• the outpouring of a watery
•relatively protein-poor fluid that,
depending on the site of injury

34. fibrinous
•occurs as a consequence of more severe
injuries,
•resulting in greater vascular permeability
that allows large molecules (such as
fibrinogen) to pass the endothelial barrier

35. suppurative
•manifested by the presence of large
amounts of purulent exudate (pus)
consisting of neutrophils, necrotic cells,
and edema fluid

36. •Abscesses are focal collections of pus
that may be caused by seeding of
pyogenic organisms into a tissue or by
secondary infections of necrotic foci.

37. Chemical mediators of
inflammation

38. Chemical mediators of
inflammation
•Mediators may be produced locally by
cells at the site of inflammation,
•or may be circulating in the plasma as
inactive precursors that are activated at
the site of inflammation

41. Chronic Inflammation

42. Chronic Inflammation
•is inflammation of prolonged duration
(weeks to months to years) in which
active inflammation, tissue injury, and
healing proceed simultaneously.

43. Characterized by:
•infiltration with mononuclear cells
•plasma cells tissue destruction
•repair
•angiogenesis
•fibrosis

44. When acute inflammation
converts to chronic?

45. Chronic inflammation arises in the following
settings:
1.T lymphocyte-mediated immune
response called delayed-type
hypersensitivity
2.Immune-mediated inflammatory diseases
3.autoimmune diseases

46. Chronic Inflammatory
Cells and Mediators
•fundamental feature of chronic
inflammation is its persistence
•results from complex interactions
between the cells that are recruited to
the site of inflammation and are activated
at this site

47. Macrophages
•dominant cell of chronic inflammation
•derived from circulating blood monocytes
•act as filters for particulate matter,
microbes, and senescent cells, as well as
acting as sentinels

48. •scattered in most connective tissues,
•also found in organs such as the liver
•spleen and lymph nodes
•central nervous system
•lungs

49. •Together these cells comprise the so-
called mononuclear phagocyte system,
also known by the older name of reticulo-
endothelial system

51. Lymphocytes
•mobilized to the setting of any specific
immune stimulus
•as well as non-immune-mediated
inflammation

53. Eosinophils
•characteristically found in inflammatory
sites around parasitic infections
•or as part of immune reactions mediated
by IgE, typically associated with allergies.

54. Mast cells
•sentinel cells widely distributed in
connective tissues throughout the body,
•participate in both acute and chronic
inflammatory responses
•"armed" with IgE antibody specific for
certain environmental antigens

55. •Neutrophils are the classic hallmarks of
acute inflammation, many forms of
chronic inflammation may nevertheless
continue to show extensive neutrophilic
infiltrates

56. References
•Robins, Basic Pathology, 8th Edition.