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Microbiology BDS1 > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

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1
Q

what is the difference between acute and chronic inflammation?

A

acute inflammation occurs rapidly whilst chronic inflammation is persistent and occurs over months, years and possibly forever

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2
Q

what is chronic inflammation associated with?

A

greater tissue destruction and generally less fluid build up in infected tissue

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3
Q

what is inflammatory infiltrate?

A

a mixture of macrophages and lymphocytes (neutrophils are not prominent)

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4
Q

what are the three types of chronic inflammation?

A

non-specific chronic inflammation, specific (primary) chronic inflammation, chronic granulomatous inflammation

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5
Q

what is non-specific chronic inflammation

A

failure to resolve, acute inflammation, persistent bouts of acute inflammation, excessive suppuration

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6
Q

what is specific (primary) chronic inflammation

A

arises without prior warning, persistent exposure to agent, autoimmune diseases

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7
Q

what is chronic granulomatous inflammation?

A

subset of specific chronic inflammation

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8
Q

when does chronic inflammation arise from acute inflammation?

A

when the immune system is not sufficient enough to eradicate stimulus

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9
Q

what is the infiltrate of non-specific chronic inflammation dominated by?

A

tissue macrophages, T cells and B cells

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10
Q

what is non-specific chronic inflammation characterised by?

A

a dynamic balance between tissue destruction and repair

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11
Q

what may disease pathogenesis of non-specific chronic inflammation include?

A

repeated acute phases and chronic phases with ongoing repair

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12
Q

give an example of non-specific chronic inflammation

A

periodontitis

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13
Q

is specific chronic inflammation granulomatous or non-granulomatous?

A

either

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14
Q

what is specific chronic inflammation characterised by?

A

excessively activated macrophages

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15
Q

what non-immunological agents induce specific chronic inflammation?

A

foreign body reactions, inert noxious material (silica and asbestos)

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16
Q

what immunological agents induce specific chronic inflammation

A

infective organisms that grow in cells (viruses, mycobacteria), hypersensitivity reactions, autoimmune reactions, infection by fungi, protozoa or parasites

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17
Q

what is specific chronic inflammation induced by?

A

non-immunological agents or immunological agents

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18
Q

what is an autoimmune disease?

A

unwanted response to body’s own cells and tissues or commensal bacteria, loss of tolerance to self antigens or commensal bacteria, sustained immune response that generates cells and molecules that destroy tissues

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19
Q

give an example of an autoimmune disease

A

rheumatoid arthritis

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20
Q

what is the disease mechanism of rheumatoid arthritis?

A

autoreactive T cells against antigens of joint synovium

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21
Q

what is the consequence of rheumatoid arthritis?

A

joint inflammation and destruction causing arthritis

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22
Q

how is periodontal disease associated with rheumatoid arthritis?

A

periodontal disease - porphyromonas gingivalis infection - local and systemic inflammatory syndrome - rheumatoid arthritis OR porphyromonas gingivalis infection - production of enzymes: PAD and proteases - peptide citrullination - loss of tolerance: production of antibodies to citrullinated proteins - rheumatid arthritis

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23
Q

what are PAD enzymes and where are they produced from?

A

peptidyl arginine deiminase and are naturally produced by host cells such as neutrophils but also produced by P. gingivalis

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24
Q

what does PAD enzyme do?

A

citrullinates proteins (arginine conversion to citrulline which is not a normal naturally occurring amino acid)

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25
Q

how does chronic granulomatous inflammation differ from normal chronic inflammation?

A

the predominant cell types are modified activated macrophages

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26
Q

what are the modified activated macrophages in chronic granulomatous inflammation?

A

known as epithelioid macrophages, giant cells (mulit-nucleated formed from fused epithelioid macrophages) and B and T cells present in tissue

27
Q

what are the immunological causes of chronic granulomatous inflammation?

A

delayed hypersensitivity type reaction or invading pathogens

28
Q

what are the non-immunological causes of chronic granulomatous inflammation?

A

foreign body in tissue e.g. asbestos particles

29
Q

what are epithelioid cells?

A

modified macrophages

30
Q

what is the main aim of macrophages?

A

to phagocytose and present antigen

31
Q

what are M1 macrophages?

A

pro-inflammatory

32
Q

what are M2 macrophages?

A

anti-inflammatory

33
Q

what is included in macrophage tissue injury?

A

toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, AA metabolites and nitric oxide

34
Q

what is included in macrophage tissue repair?

A

process of fibrosis, growth factors, fibrogenic cytokines, angiogenesis factors, remodelling collagenases

35
Q

what do fibroblasts do?

A

drive the process of fibrosis - they synthesis the extracellular matrix/collagen that make up the connective tissue

36
Q

what is angiogensis?

A

the formation of new blood vessels

37
Q

what is the process of granuloma formation?

A

1 - macrophages present antigen to lymphocytes, 2 - lymphocytes produce IL-2 IL-12 and IFN - y , 3 - induces formation of epithelioid macrophages, 4 - contribute further to giant cells formation , 5 - giant cell - macrophages engulfing foreign material

38
Q

give an example of chronic granulomatous inflammation

A

orofacial granulomatosis

39
Q

what is orofacial granulomatosis?

A

granulomas in soft tissues of oral cavity and swelling

40
Q

what is orofacial granulomatosis termed if the patient also presents with intestinal crohns?

A

oral crohns

41
Q

what is orofacial granulomatosis termed if the patient does not present with intestinal crohns?

A

orofacial granulomatosis

42
Q

what are the 2 main classes of chronic inflammation?

A

specific and non-specific (specific can be granulomatous or non-granulomatous)

43
Q

what are M1 and M2 macrophages essential in?

A

injury and repair

44
Q

what is the inflammatory infiltrate of chronic periodontitis?

A

defence cells which have been recruited to the tissue in response to microbial biofilm present on the tooth surface

45
Q

what are the steps 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

46
Q

what are the matrix metalloproteinases

A

fibroblast, endothelial cells, macrophage, neutrophil, lymphocyte, dendritic cell, myofibroblast

47
Q

what is the ECM?

A

complex structure that supports cells

48
Q

what is the ECM made of?

A

protein fibres (mainly collagen)

49
Q

what is the ECM remodelled by?

A

matrix metalloproteinases (MMPs)

50
Q

what is osteoblastogenesis?

A

bone formation

51
Q

what is osteoclastogenesis?

A

bone resorption

52
Q

what is osteoclastogenesis mediated by?

A

osteoclasts

53
Q

where do osteoclasts come from?

A

they differentiate from macrophages

54
Q

what are RANKLs produced by?

A

osteoblasts

55
Q

what do RANKLs do?

A

activates the RANK (receptor on osteoclasts)

56
Q

why is RANKL production controlled?

A

so there is no bone resorption

57
Q

what does RANKL mean?

A

receptor activator of nuclear factor kappa-b ligand

58
Q

what is osteoblastogenesis mediated by?

A

osteoblasts

59
Q

what do osteoblasts secrete?

A

osteoprotogerin (OPG)

60
Q

what does OPG do?

A

inhibit RANKL function therefore controlling bone resorption

61
Q

what is excessive immune response in alveolar bone destruction associated with?

A

an increase in the RANKL/OPG ratio and tips the balance towards the bone loss/resorption

62
Q

what does soft tissue destruction involve?

A

matrix metalloproteinases

63
Q

what do MMPs do in periodontitis?

A

remodel the gingival tissue causing soft tissue destruction

Microbiology BDS1 (20 decks)

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