Chronic Inflammation Flashcards

1
Q

What is chronic inflammation associated with?

A

greater tissue destruction

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2
Q

What is inflammatory infiltrate a mixture of?

A

macrophages and B cells/ T cells

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3
Q

Why are neutrophils not as present in chronic inflammation?

A

Neutrophils are short-lived cells that can undergo apoptosis and be cleared by macrophages

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4
Q

What is the time period for chronic inflammation?

A

occurs over months, years and possibly forever

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5
Q

What are the 3 main classes of chronic inflammation?

A

non-specific
specific (primary)
chronic granulomatous

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6
Q

What are the characteristics of non-specific inflammation?

A

usually arises from acute inflammation when immune system does not eradicate infection

infiltrate dominated by tissue macrophages, T cells and B cells

characterised by a dynamic balance between tissue destruction and repair

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7
Q

What is an example of non-specific chronic inflammation?

A

periodontitis

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8
Q

What are characteristics of specific chronic inflammation?

A

can be non-granulomatous or granulomatous

excessively activated macrophages

no acute phase

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9
Q

What are the causes of specific chronic inflammation?

A

non immunological agents (foreign body, inert noxious material like silica and asbestos)

immunological agents (infective organisms that grow in cells, hypersensitivity, autoimmune, infection by fungi protozoa or parasites)

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10
Q

What is an autoimmune disease?

A

unwanted response to body’s own cells

loss (breach of tolerance to self antigens

chronic inflammation generates cells and molecules that destroy tissues

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11
Q

What cells attack what in RA?

A

auto reactive T cells against antigens of joint synovium

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12
Q

What bacteria can RA arise from?

A

porphyromonas gingivalis

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13
Q

What enzyme does P gingivalis create?

A

PAD and proteases (gingipain)

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14
Q

Why does P gingivalis cause an autoimmune reaction?

A

production of enzymes that cause peptide citrullination which causes a breach of tolerance and production of antibodies that attack citrullinated proteins

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15
Q

What are the characteristics of chronic granulomatous inflammation?

A

Differs from normal chronic inflammation as the predominant cell types are modified activated macrophages;
– Known as epithelioid macrophages
– Giant cells (multi-nucleated: formed from fused epithelioid macrophages)
– B and T cells present in tissue.

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16
Q

What are the causes of chronic granulomatous inflammation?

A

– Immunological (delayed hypersensitivity type reaction or invading pathogens)
– Non-immunological (Foreign body in tissue e.g. asbestos particles)

17
Q

What are the subsets of macrophages?

A

M1 - pro inflammatory
M2 - anti inflammatory

18
Q

What do macrophages release to cause tissue injury?

A

– Toxic oxygen metabolites
– Proteases
– Neutrophil chemotactic factors
– Coagulation factors
– AA metabolites
– Nitric oxide

19
Q

What do macrophages release to cause tissue repair?

A

– Process of fibrosis
– Growth factors (PDGF,FGF,TGF beta)
– Fibrogenic cytokines
– Angiogenesis factors (FGF)
– Remodelling collagenases

20
Q

What cells are in and around a granuloma?

A

macrophages
epitheloid macrophages
T cells producing IL-12, IL-2, IFN-Y

21
Q

What is an example of chronic granulomatous inflammation?

A

Orofacial Granulomatosis

22
Q

What is intestinal crohns granulomatosis called?

A

oral crohns

23
Q

Where are the granulomas in the oral cavity?

A

soft tissue

24
Q

What cells produce matrix metalloproteinases (MMPs)?

A

fibroblasts, dendritic cells, lymphocyte, neutrophil, macrophages, endothelial

25
Q

What is ECM?

A

complex structure that supports cells made of protein fibres (mostly collagen)

26
Q

What remodels the ECM in soft tissues?

A

MMPs

27
Q

What do MMPs do?

A

clear pathway for cell migration and angiogenesis

28
Q

What is bone formation?

A

osteoblastogenesis

29
Q

What is bone resorption?

A

osteoclastogenesis

30
Q

When is the skeleton remodelled?

A

every 10 years

31
Q

What do osteoclasts differentiate from?

A

macrophages

32
Q

What do osteoblasts produce?

A

Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL)
osteoprotogerin (OPG)

33
Q

What does RANKL activate?

A

RANK (the receptor) on osteoclasts

34
Q

If RANKL production is controlled, what is prevented?

A

bone resorption

35
Q

What does osteoprotogerin (OPG) do?

A

OPG inhibits RANKL function – therefore controlling bone resorption

36
Q

What ratio is important in preventing bone resorption?

A

RANKL/OPG ratio

37
Q

What is an excessive immune response concerning bone loss associated with?

A

increase in the RANKL/OPG ratio and ‘tips the balance’ toward bone loss/resorption

38
Q

What is the action of RANKL?

A

binds to RANK receptor on the surface of osteoclast precursor cells, stimulating their differentiation into osteoclasts and activating them.