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BDS2 BAMS infection & immunity > periodontal immunology > Flashcards

periodontal immunology Flashcards

1
Q

what is gingivitis?

A

inflammation localised to gingival tissues
acute inflammation
normal physiological response to infection or injury

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2
Q

what is periodontitis?

A

inflammation of gingival tissues and supporting periodontal structures
chronic inflammation
pathological inflammatory response associated with tissue destruction

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3
Q

describe healthy gingiva

A

stippled

pink

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4
Q

describe gingiva with gingivitis?

A

red

swollen

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5
Q

describe gingiva with periodontitis?

A

significant plaque accumulation

inflammation

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6
Q

what is the trigger for (gingival) inflammation?

A

plaque bacteria

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7
Q

what does supragingival mean?

A

above gum line

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8
Q

what immune components are in saliva?

A 
antimicrobial proteins
peptides
antibodies
S-IgA
lysozyme
peroxidase
lactoferrin
mucins
agglutinins
cystatins
histatins
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9
Q

what is gingival crevicular fluid?

A

subgingival defence- array of microbial factors prevent access to underlying tissues

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10
Q

what antimicrobial components are in gingival crevicular fluid?

A 
AMPs
cytokines
chemokines
lactoferrin
IgG
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11
Q

how does the gingival eptithelium protect?

A

physical barrier

functional barrier- activation of TLR

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12
Q

what antimicrobial components are in oral mucosa?

A

AMPs
cytokines
chemokines

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13
Q

why is poor oral hygiene the predominant aetiological factor in periodontitis?

A

leads to accumulation of plaque bacteria which lead to pro-longed and sustained activation of inflammtaory pathways in gingival tissues

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14
Q

what other factors contribute to periodontitis?

A

type of bacteria present in plaque

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15
Q

what is the ecology of the oral biofilm?

A

early colonisers gram+ , aerobic, commensal species
colonise, modify environment creating new attachment sites for late colonisers
late colonisers gram- , anaerobic

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16
Q

describe periodontal pathogens

A

present in low numbers at healthy sites
increased numbers in diseased sites
can be absent from diseased sites

17
Q

what is polymicrobial dysbiosis?

A

community of micro-organisms that work together to actively disrupt the normal homeostatic balance in the oral cavity for their own benefit

18
Q

how do some bacteria gain a competitive advantage?

A

some succumb to inflammation

accessory and periodontal pathogens eg P gingivalis persist adapting to inflammatory environment

19
Q

what are 4 virulence factors of P gingivalis?

A

asaccharolytic
gingipains
atypical LPS
inflammophilic

20
Q

what does asaccharolytic mean?

A
  • nutrients from breakdown of proteins and peptides

- no carbs meaning inflammatory environment gives access to nutrients

21
Q

what are gingipains?

A

proteases with broad-specificity

-degrade host proteins

22
Q

what is atypical LPS?

A

TLR4 antagonist

23
Q

what does inflammophilic mean?

A

inflammatory environment favours expression of virulence

  • only expresses full range under inflammatory conditions
  • dormant in health
24
Q

what are the main aetiology factors of periodontits?

A

accumulated plaque bacteria
presence of periodontal pathogens
polymicrobial dysbiosis
susceptible host

25
Q

what are the clinical signs of periodontitis?

A

increased pocket depth
-attachment loss
alveolar bone destruction

26
Q

what does increased TLR stimulation cause?

A

increased production of pro-inflammatory mediators
triggers acute inflammatory response
-redness, swelling, bleeding
-increased vasodilation, cell migration

27
Q

what are the main cell type in initial gingivitis?

A

neutrophils

28
Q

what do neutrophils do?

A

recruit monocytes, which are activated and differentiates into macrophages
lymphocytes recruited to fine-tune the immune response

29
Q

what do osteoblasts do?

A

synthesise and secrete bone tissue (osteoid)

bone formation

30
Q

what do osteoclasts do?

A

resorb bone

derived from monocyte/macrophage

31
Q

what are bone formation and resorption regulated by in health?

A

RANKL/ RANK/ OPG triad

32
Q

what is the role of adaptive immunity in periodontal destruction?

A

T and B lymphocytes present in early lesion
aggregate rich in CD4 T & B cells evident
unable to regulate dysbiotic biofilm
B cell/plasma cells predominate advanced lesions
IgG fails to regulate
protective prevents systemic infection
destructive inflammation induced alveolar bone loss

33
Q

what is the role of neutrophils in periodontal tissue destruction?

A

excessive infiltration associated with chronic inflammation
microbial subversion
degradative enzymes
-major source matrix metalloproteinases
inflammatory cytokines and O2 radicals contribute to hypoxic environment
CT destruction manifests clincally as loss of attachment

34
Q

how does inflammation lead to bone loss?

A

activated B + T cells in perio lesion secrete RANKL
RANKL binds RANK to induce osteoclast differentiation
OPG binds to RANKL preventing RANKL binding RANK
inhibiting osteoclast differentiation
low OPG, high RANKL
many monocytes recruited
differentiate into osteoclasts

35
Q

what are the 7 cellular and molecular events linking bacterial induced inflammation w/ pathologic tissue destruction

A
  1. bacterial products bind TLRs on epithelium, stimulating secretion of cytokines, chemokines and AMPs (inflammation)
  2. vasodilation and selective recruitments of leukocytes
    - mainly neutrophils
  3. bacterial products further activate neutrophils, more pro-inflammatory mediators released- loop
  4. activated lymphocytes express RANKL
    - RANKL/OPG balance disrupted
  5. RANKL binds RANK on osteoclast precursors. activates osteoclastogenesis leading to alveolar bone resorption
  6. pro-inflammatory cytokines contribute to bone resorption by inhibiting bone formation
  7. elevated and dysregulated MMP activation contributes to CT tissue destruction

BDS2 BAMS infection & immunity (6 decks)

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