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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
what determines periodontal pathogenesis
host bacterial interactions
26
what is the consequence of excessive biofilm accumulation
not accessible to cell mediated immune responses
27
what protect function and integrity of teeth
vast array of enzymes, MMPs, protect function and integrity of teeth physcial barrier to prevent microbes invading underlying tissue
28
role of TLR in immune defence in oral cavity
TLR will bind to and recognise pathogens | - respond by release of cytokines and chemokines
29
neutrophils role in immune defence in oral cavity
neutrophils traverse through gingival tissue | - degranulate and release histamine
30
why is the immune system active in health in the oral cavity
to maintain the biofilm
31
symbiotic means
benefit us and benefits itself by pleasant environment - Exists with host tissue in health
32
is the oral biofilm easily disrupted
yes sensitive
33
what is the basic description of periodontal pathogenesis
accumulation and acquisition of virulent pathogens causes change in immune response
34
immune response in gingivitis
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
what causes there to be a resolution in inflammation
elimination of the pathogen tissue returns to health
36
what happens if unable to control infection
progression of disease process inflammation persists give bacterial species a competitive advantage over commensal organisms as incompatible with inflammation dysbiotic biofilm
37
competitive advantage of periodontal pathogens
give bacterial species a competitive advantage over commensal organisms as incompatible with inflammation
38
9 environmental and genetic risk factors that alter ecological pressure exerted on oral biofilm
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
what are the levels of symbiotic to pathogenic species of MO in health
pathogenic species are present in health but not clinically relevant
40
how can ecological pressures alter the levels of bacteria in the biofilm
can upregulate virulence factor predominate and drive inflammation further
41
what is the effect of inflammatory response on symbiotic (avirulent) species?
more susceptible numbers and proportions become diminished
42
what is the effect of inflammatory response on pathogenic species?
they are capable of evading immune response periodontal pathogens
43
how can it be that periodontal pathogens are present in health but not causing disease
because conditions don’t favour expression of virulence
44
clinical appearance of healthy gums
small periodontal pocket
45
clinical appearance of gingivitis
pocket increases slightly due to increase swelling of tissues
46
periodontal disease
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
what are host-bacterial interactions like in periodontal disease?
they are disrupted so become destructive
48
what is the effect of host-bacterial interactions on perio disease pathogenesis
Immune response continues and inflammation continues Acute protective response in gingivitis To destructive and associated with tissue destruction
49
neutrophil function
crucial for maintaining healthy periodontium
50
what is a deficiency associated with aggressive periodontitis
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
what is the outcome if neutrophils are increased and able to contain infection
return to health
52
what is the outcome if neutrophils are increased but unable to contain infection
predispose to disease progression ineffective neutrophil action at controlling biofilm
53
excessive neutrophil infiltration associated with...
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
role of adaptive immunity in periodontal destruction
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
osteoblast
synthesis and secretion of bone tissue (osteoid) bone formation
56
osteoclast
resorbs bone (recyclers) derived from monocyte/macrophage lineage in health, bone formation and bone resorption are coupled - bone volume maintained
57
healthy relationship of bone formation/resorption
bone formation and bone resorption are coupled | - bone volume maintained
58
what triad regulated bone formation/resorption
RANK/RANKL/OPG
59
microbial composition of periodontal lesion
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
how does inflammation lead to bone loss
High levels of RANKL Low levels of OPG - Not balanced Inflammation induced bone resorption Pathological bone destruction
61
7 stages of cellular and molecular events linking bacterial induced inflammation with pathologic tissues destruction
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
what determines the severity and progression of periodontal disease
interaction between bacteria challenge and host immune response
63
what governs patient susceptibility to periodontal disease
immune-inflammatory mechanisms governs pt susceptibility and is modified by environmental factors

BDS2 BAMS (54 decks)

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