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BDS1 BAMS: Pathology > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

Name 3 examples of chronic inflammation

A

Periodontitis, Autoimmune diseases (e.g. rheumatoid arthritis), Orofacial Granulomatosis

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2
Q

Name the 3 classes of chronic inflammation

A
  1. Non-specific chronic inflammation
  2. Specific (primary) chronic inflammation
  3. Chronic granulomatous inflammation (a subset of specific chronic inflammation)
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3
Q

What is the infiltrate dominated by in non-specific chronic inflammation?

A

Tissue macrophages, T cells and B cells

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4
Q

What is non-specific chronic inflammation characterised by?

A

A dynamic balance between tissue destruction and repair

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5
Q

Describe the ‘initiation’ stage in gingivitis/periodontitis

A

Microbes in dental plaque recognised by gingival epithelial cells via pattern recognition receptors (TLRs)

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6
Q

Describe the ‘progression’ stage in gingivitis/periodontitis

A

Containment of microbes by innate immune cells and antimicrobial compounds (e.g. AMPs and secretory IgA)

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7
Q

Describe the ‘amplification’ stage in gingivitis/periodontitis

A

Recruitment and activation of innate immune cells via chemokine/cytokine activity and vascular dilation

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8
Q

What are the 2 types of specific chronic inflammation?

A

Granulomatous or non-granulomatous

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9
Q

What is specific chronic inflammation characterised by?

A

Excessively activate macrophages

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10
Q

What can specific chronic inflammation be induced by?

A

Non-immunological agents (foreign body reactions, inert noxious materials such as asbestos), or immunological agents (infective organisms that grow in cells, hypersensitivity reactions, autoimmune reactions, infection by fungi, protozoa or parasites)

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11
Q

What is an autoimmune disease?

A

An example of specific chronic inflammation. An unwanted response to body’s own cells and tissues or commensal bacteria. Loss of tolerance to self antigens or commensal bacteria.

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12
Q

What usually prevents autoimmunity?

A

Multiple mechanisms of tolerance (checkpoints)

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13
Q

Describe the autoimmune disease ‘rheumatoid arthritis’

A

Autoreactive T cells against antigens found in joints in the body

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14
Q

Describe the autoimmune disease ‘Crohn’s disease’

A

Autoreactive T cells against commensal bacteria found within the intestines

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15
Q

Describe the autoimmune disease ‘Diabetes Type I’

A

Autoreactive T cells that target the islet cells within the pancreas, leading to the destruction of insulin producing beta-cells

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16
Q

Describe the proposed link between rheumatoid arthritis and periodontitis

A

P. gingivalis infection in periodontitis produces PAD enzymes which convert arginine to citrulline. This leads to loss of tolerance. Citrulline is not a naturally occurring amino acid. Host will target citrulline containing proteins. This occurs in the joints in arthritis.

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17
Q

How does chronic granulomatous inflammation differ from normal chronic inflammation?

A

The predominant cell types are macrophages known as epithelioid macrophages

18
Q

What are epithelioid macrophages?

A

Modified activated macrophages that can fuse to form giant multinucleate cells. They are more secretory than phagocytic. Found in chronic granulomatous inflammation.

19
Q

What are the causes of chronic granulomatous inflammation?

A

Immunological - delayed hypersensitivity type reaction or invading pathogens
Non-immunological - foreign body in tissues e.g. asbestos
Unknown causes

20
Q

What is the precursor to macrophages?

A

Monocytes. They circulate in the blood and migrate to the tissues where they differentiate into macrophages.

21
Q

What is the main aim of macrophages?

A

To phagocytose and present antigen

22
Q

Which macrophages are pro-inflammatory and which are anti-inflammatory?

A

Pro-inflammatory = M1
Anti-inflammatory = M2
Need a balance between M1 and M2

23
Q

What are the functions of M1 macrophages in tissue injury?

A

Release toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, amino acid metabolites, nitric oxide

24
Q

What are the functions of M2 macrophages in tissue repair?

A

Process of fibrosis, growth factors (PGDF, FGF, TGF-beta), fibrogenic cytokines, angiogenesis factors, remodelling collagenases

25
Q

What are granulomas?

A

Clustering of macrophages and adaptive immune cells characterised by the formation of giant cells - epithelioid macrophages clustered together.

26
Q

What are the stages involved in the formation of a granuloma?

A
  1. Macrophages present antigen to lymphocytes (T cells and B cells).
  2. T cells produce IL-12, IL-2 and IFN-gamma.
  3. This induced the formation of epithelioid macrophages.
  4. Contribute further to giant cell formation (epithelioid macrophages aggregate)
  5. Giant cell is formed - engulfs foreign material
27
Q

Name an example of chronic granulomatous inflammation.

A

Orofacial Granulomatosis (OFG)

28
Q

Describe the features of orofacial granulomatosis (OFG).

A

Granulomas present in oral cavity
Swelling
If patient has intestinal Crohn’s - termed Oral Crohn’s
If not Crohn’s - termed OFG

29
Q

Describe features of chronic periodontitis

A 
Apical migration of the epithelial tissue and formation of a periodontal pocket 
Soft tissue (gingival tissue) destruction 
Hard tissue (alveolar bone) destruction 
Presence of inflammatory infiltrate consisting of defence cells
30
Q

What are the 7 stages of tissue destruction in periodontitis?

A

1) Initiation of immune response
2) Recruitment of immune cells
3) Immune cell activation
4) RANKL production
5) Activation of osteoclasts
6) Reduced function of osteoblasts
7) Activation of MMPs

31
Q

What are matrix metalloproteinases (MMPs)?

A

Enzymes produced by fibroblasts and other immune cells. MMPs remodel/degrade the extracellular matrix (ECM). This allows immune cells to move through tissue to site of infection.

32
Q

What is the extracellular matrix (ECM)?

A

A complex structure that supports cells. It provides a scaffold for immune cells moving through the tissue.

33
Q

What are the functions of MMPs?

A 
Remodel the ECM
Drive angiogenesis (formation of new blood vessels)
34
Q

What is osteoblastogeneis?

A

Bone formation

35
Q

What is osteoclastogenesis?

A

Bone resorption

36
Q

How often is the human skeleton completely remodelled?

A

Every 10 years

37
Q

What are the precursors for osteoclasts?

A

Macrophages

38
Q

What is RANKL?

A

Receptor Activator of Nuclear Factor Kappa-B Ligand. RANKL is produced by osteoblasts.

39
Q

What does RANKL do?

A

RANK-L, produced by osteoblasts, is a ligand that activates the RANK receptor on osteoclasts. This will lead to bone resorption.

40
Q

What is osteoprotogerin (OPG)?

A

Osteoprotogerin (OPG) is secreted by osteoblasts inhibits RANKL function, therefore controlling bone resorption.

41
Q

RANKL and OPG are secreted by…

A

Osteoblasts

42
Q

An increase in the RANKL/OPG ratio results in what?

A

An excessive immune response. Balance is tipped towards more bone resorption.

BDS1 BAMS: Pathology (11 decks)

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