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BDS2 CLINICAL Periodontology > Periodontal Immunology > Flashcards

Periodontal Immunology Flashcards

1
Q

What is gingivitis

A

it is inflammation localized to gingival tissues

it is the normal physiological response to infection or injury

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2
Q

what type of inflammation is gingivitis

A

acute

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3
Q

what is periodontitis

A

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

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4
Q

what type of inflammation is periodontitis

A

chronic

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5
Q

is plaque (poor oral hygiene) an etiological factor of periodontitis

A

yes
but it isn’t the full picture
there are other factors that accelerate the disease

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6
Q

describe the oral biofilm composition

A

bacterial interactions modify the environment species

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7
Q

what are the late colonizers typically

A

the late colonizers are typically gram negative anaerobes

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8
Q

what are the early colonizers typically

A

and early colonizers are typically commensal

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9
Q

what are the microbes in the red complex

A

porphyromonas gingival
tannerella forsythia
treponema denticola

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10
Q

what is the red complex

A

these were detonated as periodontal pathogens as their numbers correlate with pocket depth and bleeding on proving.

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11
Q

do specific bacterial species cause periodontal disease?

A

periodontitis cannot occur in the absence of bacteria

it is difficult to establish the role of specific microbes

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12
Q

what are the features of the periodontal pathogens

A

they are present at low numbers in healthy sites

they have increased numbers in diseased sites

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13
Q

what is the difference between colonization and infection

A

colonization does not involve disease - bacteria are present but not actively trying to invade tissues

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14
Q

can commensals become pathogenic

A

yes if the opportunity arises

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15
Q

what is the first stage of infection

A

colonisation

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16
Q

what is the ability to cause disease based on

A

ability to cause disease is not an inherited trait, it is based on the outcome with the human immune system

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17
Q

what do microbes express

A

virulence factors and if there is up regulation to allow invasion the immune system will notice

18
Q

what are the virulence factors of p. gingival

A

asaccharolytic
gingipains
atypical LPS
inflammophilic

19
Q

what does asaccharolytic mean

A

cannot use carbohydrates as an energy source

needs proteins and peptides which it gets from host proteins

20
Q

what are gingipains

A

enzymes
they are proteases which can cleave host proteins and make them available for that bacteria to use as nutrients. they can also activate MMPs

21
Q

what is atypical LPS

A

a TLR4 antagonist

22
Q

what does inflammophilic mean

A

inflammatory environment favors expression of virulence

23
Q

what factors trigger gingival inflammation

A

changes in oral biofilm:
accumulation
composition
expression of virulence

24
Q

what factors determine whether inflammation resolves or progresses

A

periodontal pathogenesis is determined by host bacterial interactions

25
Q

what are the immune defenses in the oral cavity

A

gingival crevicular fluid
oral mucosa
saliva

26
Q

what are present in the oral mucosa that are protective

A

TLRs bind and recognize microorganisms and cells respond by releasing AMPs which trigger release of cytokines and chemokine

27
Q

what is present in saliva that is protective

A 
s-IgA
lysozyme
perioxidase
lactoferrin
mucins
agglutins
cystatins
histamines
28
Q

what is present in GCF that is protective

A 
AMPs
cytokines
chemokines
lactoferrin 
igG
29
Q

what is the predominant cell in gingivitis

A

neutrophils

30
Q

what do monocytes do in gingivitis

A

they move into tissue, activated by cytokines and bacterial components and differentiate into macrophages

31
Q

what do lymphocytes do

A

they are present and they fine tune responses at this stage

32
Q

describes what happens in gingivitis

A

increased TLR stimulation
increased production of pro inflammatory mediators
triggers actue inflammatory response
neutrophils remain the predominant cell type in the initial lesion
monocytes are recruited (macrophages)
lymphocytes are recruited (fine tune the immune response)

33
Q

what is the role of neutrophils in periodontal tissue destruction

A

it is crucial for maintaining healthy periodontium
numbers increase during gingivitis
excessive infiltration associated with chronic inflammation

34
Q

what happens in an immune under reaction

A

there is aggressive periodontitis with leukocyte adhesion deficiency

35
Q

what happens in immune over reaction

A

adult chronic periodontitis

36
Q

why is excessive infiltration of neutrophils associated with chronic inflammation

A 
degradative enzymes (major source of MMPs) 
inflammatory cytokines and oxygen radicals contribute to hypoxic environment 
connective tissue destruction manifests clinically as loss of attachment
37
Q

what is the role of adaptive immunity in periodontal destruction

A

T and B lymphocytes present in the early lesion
aggregates rich in CD4 T cells B cells and dendritic cells evident as lesion progresses
unable to regulate dysbiotic biofilm
b cell/plasma cells predominate advanced lesions
IgG fails to regulate dysbiotic biofilm

38
Q

how is the role of adaptive immunity in periodontal destruction protective

A

it prevents systemic infection

39
Q

how is the role of adaptive immunity in periodontal destruction destructive

A

inflammation induced alveolar bone loss

40
Q

how does inflammation lead to bone loss

A

activated t and b cells in the periodontal lesion secrete RANKL
RANKL binds RANK to induce osteoclast differentiation
OPG prevents RANKL binding RANK
OPG inhibits osteoclast differentiation

41
Q

describe the cellular an molecular events linking bacterial induced inflammation with pathological tissue destruction

A
  1. periodontal pathogens releasing bacterial products which activate TLR on oral epithelium cells and fibroblasts and they respond by releasing chemokine and cytokines
  2. vasodilation and recruitment of cells from the blood, swelling, redness
  3. neutrophils move into tissues and are activated by bacterial products and they also release cytokines so there is amplification within tissues
  4. lymphocyte recruited, they express rank and disrupt homeostatic relationship between OPG and RANKL
  5. osteoclastogenesis that leads alveolar bone resorption
  6. pro inflammatory cytokines can interact with osteoblasts which inhibit bone formation so contribute to bone destruction
  7. MMPs come from excessive neutrophils present and help degrade the ECM leading to loss of attachment

BDS2 CLINICAL Periodontology (17 decks)

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