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BDS2 BAMS > Periodontal Immunology > Flashcards

Periodontal Immunology Flashcards

1
Q

2 stages of periodontal diseases

A

gingivitis

periodontitis

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2
Q

gingivitis

A

Inflammation localised to gingival tissues
Acute inflammation
Normal physiological response to infection or injury

  • Active normal physiological responses
  • Repair tissue to return to homeostasis
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3
Q

periodontitis

A

Inflammation of the gingival tissues and supporting periodontal structures
- extended

Chronic inflammation
- If acute inflammation unsuccessful descend into this

Pathological inflammatory response associated with tissue destruction

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4
Q

gum appearance in health

A

pink

scalloped shaped knife edge margin

stippling

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5
Q

gingivitis appearance of gums

A

gingival swelling

redness

inflammation

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6
Q

periodontal diseases are triggered by

A

plaque

amount of plaque correlates to amount of inflammation in gums

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7
Q

composition of the oral biofilm

A

All microbes on teeth and oral surfaces

  • 150-200 different species
  • Types and proportions differ between individuals

Late colonisers typically Gram negative anaerobes

Bacterial interactions

Modify the environment

Early colonisers typically commensal species

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8
Q

most virulent complex in sub-gingival plaque

A

red (periodontal pathogens)

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9
Q

3 bacterial in red complex

A

porphyromonas gingivalis

tannerella forsythia

treponema denticola

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10
Q

what is the orange complex of pathogens virulence in comparison to red pathogens

A

lesser extent than red but still associated

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11
Q

proportion of periodontal pathogens in healthy sites

A

present in low numbers

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12
Q

proportion of periodontal pathogens in diseased sites

A

usually increased numbers

but in some complex situations can be absent

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13
Q

colonisation

A

microbial presence on a body surface without clinical signs of inflammation or disease
commensal
- doesn’t involve disease

can become pathogenic if conditions favour the expression of virulence
- oppurtunistic

1st stage of infection

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14
Q

infection

A

Microbial invasion of host tissues

Pathogens

Can behave like commensals if conditions do not favour expression of virulence

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15
Q

how is pathogenicity portrayed by different bacteria

A

Pathogenicity is not an Inherent microbial trait

Host immune system actively suppresses overt expression of virulence factors

Wait for opportunity to strike

Some microbes are more virulent so easier to overcome host defences

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16
Q

describe technique used by P.gingivalis as its virulence factor

A

immune invasion and subversion

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17
Q

4 virulence factors of P.gingivalis

A

Asaccharolytic

Gingipains

Atypical LPS - TLR4 antagonist

Inflammophilic

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18
Q

Asaccharolytic

A

virulence factor of P.gingivalis

nutrients from breakdown of proteins and peptides
- Cannot use carbohydrates for energy

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19
Q

gingipains

A

virulence factor of P.gingivalis

proteases with broad-specificity

Degrade host proteins
- Make available for nutrient use

Activate MMPs

  • Help in tissue repair by removing damaged tissue
  • Cleave host proteins – hi jacked
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20
Q

atypical LPS - TLR4 antagonist

A

virulence factor of P.gingivalis

Doesn’t signal through TLR4
- Different way to survey immune system

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21
Q

inflammophilic

A

virulence factor of P.gingivalis

Inflammatory environment favours expression of virulence
- Like inflammation

In this environment they are able to express their virulence factors

In healthy environment present but not actively doing anything

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22
Q

what modifies pathogens virulence factors ability

A

internal and external factors

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23
Q

what is a more systemic factor which can cause a bacteria to have increased virulence

A

medical conditions

  • Weaken immune system
  • Lesser pathogens more able to cause disease in this situation

Meaning periodontal pathogens can be absent from disease as lesser pathogens are involved

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24
Q

3 factors which trigger gingival inflammation

A

changes in oral biofilm

  • accumulation
  • composition
  • expression of virulence
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25
Q

what determines periodontal pathogenesis

A

host bacterial interactions

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26
Q

what is the consequence of excessive biofilm accumulation

A

not accessible to cell mediated immune responses

27
Q

what protect function and integrity of teeth

A

vast array of enzymes, MMPs, protect function and integrity of teeth

physcial barrier to prevent microbes invading underlying tissue

28
Q

role of TLR in immune defence in oral cavity

A

TLR will bind to and recognise pathogens

- respond by release of cytokines and chemokines

29
Q

neutrophils role in immune defence in oral cavity

A

neutrophils traverse through gingival tissue

- degranulate and release histamine

30
Q

why is the immune system active in health in the oral cavity

A

to maintain the biofilm

31
Q

symbiotic means

A

benefit us and benefits itself by pleasant environment

  • Exists with host tissue in health
32
Q

is the oral biofilm easily disrupted

A

yes

sensitive

33
Q

what is the basic description of periodontal pathogenesis

A

accumulation and acquisition of virulent pathogens

causes change in immune response

34
Q

immune response in gingivitis

A

Increased TLR stimulation
- Greater level in gingivitis

Increased production of pro-inflammatory mediators
- More inflammation

Triggers acute inflammatory response

  • Redness, swelling, bleeding
  • Increased vasodilation, cell migration

Neutrophils remain the predominant cell type in the initial lesion

Monocytes are recruited, activated and differentiate into macrophages
- Activated by cytokines and chemokines present

Lymphocytes are recruited
- To fine-tune the immune response

35
Q

what causes there to be a resolution in inflammation

A

elimination of the pathogen

tissue returns to health

36
Q

what happens if unable to control infection

A

progression of disease process

inflammation persists

give bacterial species a competitive advantage over commensal organisms as incompatible with inflammation

dysbiotic biofilm

37
Q

competitive advantage of periodontal pathogens

A

give bacterial species a competitive advantage over commensal organisms as incompatible with inflammation

38
Q

9 environmental and genetic risk factors that alter ecological pressure exerted on oral biofilm

A

diseases e.g. diabetes

genetic differences

activity of salivary proteins

salivary flow rates

innate/adaptive immune factors

oral hygiene

diet

smoking

antibiotics/antimicrobial agents

39
Q

what are the levels of symbiotic to pathogenic species of MO in health

A

pathogenic species are present in health but not clinically relevant

40
Q

how can ecological pressures alter the levels of bacteria in the biofilm

A

can upregulate virulence factor

predominate and drive inflammation further

41
Q

what is the effect of inflammatory response on symbiotic (avirulent) species?

A

more susceptible

numbers and proportions become diminished

42
Q

what is the effect of inflammatory response on pathogenic species?

A

they are capable of evading immune response

periodontal pathogens

43
Q

how can it be that periodontal pathogens are present in health but not causing disease

A

because conditions don’t favour expression of virulence

44
Q

clinical appearance of healthy gums

A

small periodontal pocket

45
Q

clinical appearance of gingivitis

A

pocket increases slightly due to increase swelling of tissues

46
Q

periodontal disease

A

attachement loss
biofilm to new sites
descend deeper into pocket

alveolar bone loss and deeper pocket depth is caused by host immune response to bacterial biofilm

47
Q

what are host-bacterial interactions like in periodontal disease?

A

they are disrupted so become destructive

48
Q

what is the effect of host-bacterial interactions on perio disease pathogenesis

A

Immune response continues and inflammation continues

Acute protective response in gingivitis

To destructive and associated with tissue destruction

49
Q

neutrophil function

A

crucial for maintaining healthy periodontium

50
Q

what is a deficiency associated with aggressive periodontitis

A

leukocyte-adhesion deficiency – IMMUNE UNDER-REACTION
- Neutrophils are trapped in blood

Cannot traverse through BV wall to tissue

  • Present with aggressive perio from young age
  • Absence of neutrophils in gum tissue causes them to run riot

Need neutrophils to maintain healthy periodontium

51
Q

what is the outcome if neutrophils are increased and able to contain infection

A

return to health

52
Q

what is the outcome if neutrophils are increased but unable to contain infection

A

predispose to disease progression

ineffective neutrophil action at controlling biofilm

53
Q

excessive neutrophil infiltration associated with…

A

Degradative enzymes (Major source of matrix metallo-proteinases [MMPs])

Inflammatory cytokines and oxygen radicals contribute to hypoxic environment
- unhealthy

Connective tissue destruction manifests clinically as loss of attachment
- Too many degradative enzymes, sources of MMPs, contribute to attachment loss

54
Q

role of adaptive immunity in periodontal destruction

A

T and B lymphocytes present in early lesion

  • Present in gingivitis
  • Eliminate the pathogen and return to health

Aggregates rich in CD4 T cells, B cells and dendritic cells evident as lesion progresses
- Infiltrate tissue

Unable to regulate dysbiotic biofilm

B cell/plasma cells predominate advanced lesions

  • From innate to adaptive immune response
  • Still unable to regulate dysbiosis biofilm
  • Descends deeper into pocket

IgG fails to regulate dysbiotic biofilm
- Plasma cells release high affinity IgG

Protective – prevents systemic infection

Destructive – inflammation induced alveolar bone loss

55
Q

osteoblast

A

synthesis and secretion of bone tissue (osteoid)

bone formation

56
Q

osteoclast

A

resorbs bone (recyclers)

derived from monocyte/macrophage lineage

in health, bone formation and bone resorption are coupled
- bone volume maintained

57
Q

healthy relationship of bone formation/resorption

A

bone formation and bone resorption are coupled

- bone volume maintained

58
Q

what triad regulated bone formation/resorption

A

RANK/RANKL/OPG

59
Q

microbial composition of periodontal lesion

A

Activated T and B cells in periodontal lesion Release and secrete RANKL into environment

  • RANKL Binds to RANK on pre osteoclasts
  • —Induce osteoclast differentiation
  • Monocytes recruited into tissue
  • OPG Bind to RANK and inhibits pathway
  • —-Prevent RANKL binding to RANK
  • —Inhibits osteoclasts differentiation
60
Q

how does inflammation lead to bone loss

A

High levels of RANKL

Low levels of OPG
- Not balanced

Inflammation induced bone resorption

Pathological bone destruction

61
Q

7 stages of cellular and molecular events linking bacterial induced inflammation with pathologic tissues destruction

A
  1. Bacterial products bind TLRs on epithelium, stimulating secretion of cytokines, chemokines and AMPs
  2. Vasodilation and selective recruitment of leukocytes (predominantly neutrophils, also monocytes and lymphocytes)
  3. Bacterial products activate neutrophils, further release of pro-inflammatory mediators. Amplification loop of neutrophil infiltration.
  4. Activated lymphocytes express RANKL. RANKL/OPG balance disrupted
  5. RANKL binds RANK on osteoclast precursors (monocytes). Activates osteoclastogenesis leading to alveolar bone resorption
  6. Pro-inflammatory cytokines (IL-1, IL-6, IL-17, TNFa) contribute to bone resorption by inhibiting bone formation (osteoblast)
  7. Elevated and dysregulated MMP activation contributes to connective tissue destruction
    - Excessive neutrophils present
    - Degrade ECM leads to loss of attachment
62
Q

what determines the severity and progression of periodontal disease

A

interaction between bacteria challenge and host immune response

63
Q

what governs patient susceptibility to periodontal disease

A

immune-inflammatory mechanisms governs pt susceptibility and is modified by environmental factors

BDS2 BAMS (54 decks)

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