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BDS2 BAMS > Hostbacterial interactions in periodontal disease > Flashcards

Hostbacterial interactions in periodontal disease Flashcards

1
Q

What is gingivitis?

A
  • Inflammation localised to gingival tissues
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2
Q

What type of inflammation is present in gingivitis and what is this?

A
  • Acute inflammation

- Normal physiological response to infection or injury

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3
Q

What type of inflammation is present in gingivitis and what is this?

A
  • Chronic Inflammation

- Pathological inflammatory response associated with tissue destruction

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4
Q

What is periodontitis?

A
  • Inflammation of the gingival tissues and supporting periodontal structures
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5
Q

Is poor oral hygiene an aetiological factor in periodontitis?

A
  • Tes, BUT it is not the full picture
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6
Q

What are late colonisers of the oral biofilm usually?

A

Typically Gram negative anaerobes

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7
Q

What are early colonisers in the oral biofilm usually?

A

Typically commensal species

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8
Q

What are 3 examples of microbes that have been strongly identified to be a part of periodontitis?

A
  • Porphyromonas gingivalis
  • Tannerella forsythia
  • Treponema denticola
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9
Q

Can periodontitis occur in the absence of bacteria?

A
  • No
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10
Q

Can periodontal pathogens be present at low numbers in healthy sites?

A

Yes

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11
Q

Can periodontal pathogens increase in numbers in diseased sites?

A

Yes

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12
Q

Can periodontal pathogens be absent from diseased sites?

A
  • Yes
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13
Q

Are specific bacterial species an aetiological factor in periodontitis?

A

Yes, But it is not the full picture

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14
Q

What is colonisation?

A
  • Microbial presence on a body surface without clinical signs of inflammation or disease
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15
Q

What time of microbes are present in colonisation?

A

Commensal

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16
Q

Can commensal organisms become pathogenic?

A

Yes… if conditions favour expression of virulence

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17
Q

What is infection (in relation to microbes)?

A
  • Microbial invasion of host tissues
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18
Q

What type of microbes are present in infection?

A
  • Pathogens
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19
Q

Can pathogens behave like commensals?

A
  • yes… if conditions DO NOT favour expression of virulence
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20
Q

P. gingivalis is an asaccharolytic. What does this mean?

A
  • Can’t use carbs as an energy source

- Gets nutrients from breakdown of proteins and peptides

21
Q

P. gingivalis has gingipains. What are these and what do they do? (3 points)

A
  • Proteases with broad-specificity

They:

  • Degrade host proteins
  • Activate MMP’s
22
Q

P. Gingivalis is an atypical LPS, what is this?

A

an TLR4 antagonist (doesn’t signal through TLR4)

23
Q

P. Gingivalis is an inflammophilic. What is this?

A
  • Inflammatory environment favours expression of virulence
24
Q

What factors trigger gingival inflammation? (4 points)

A

Changes in oral biofilm

  • Accumulation
  • Composition
  • Expression of virulence
25
Q

What factors determine whether inflammation resolves or progresses?

A
  • Periodontal pathogenesis is determined by host-bacterial interacitons
  • Interaction between bacteria present and the host immune system
26
Q

What are 3 examples of immune defences in the oral cavity?

A
  • Gingival Crevicular fluid
  • Oral mucosa
  • Saliva
27
Q

In gingivitis there in an increase in TLR stimulation and increased production of pro-inflammatory mediators. What does this trigger? (3 points)

A

Triggers acute inflammatory response:

  • Redness, swelling, bleeding
  • Increased vasodilation, cell migration
28
Q

What type of cell remains the predominant cell type in the initial lesion of gingivitis?

A
  • Neutrophils
29
Q

Monocytes are recruited in gingivitis, when they are activated what do they differentiate into?

A

Monocytes

30
Q

What type of cell is recruited to fine tune the immune response in gingivitis?

A
  • Lymphocytes
31
Q

What is dysbiosis?

A
  • An imbalance between the types of organism present in a person’s natural microflora, though to contribute to a range on conditions of ill health
32
Q

What are possible causes of dysbiosis of the oral biofilm? (9 points)

A
  • Genetic differences
  • Activity of salivary protein s
  • Salivary flow rates
  • Innate/adaptive immune factors
  • Oral hygiene
  • Diet
  • Smoking
  • Antibiotics/antimicrobial agents
  • Diseases e.g. diabetes
33
Q

Does gingivitis have true or false pocketing?

A

False

34
Q

Does periodontitis have true or false pocketing?

A

Attachment loss so true pocket

35
Q

What is the role of neutrophils in periodontal tissue destruction crucial for?

A
  • Crucial for maintaining a healthy periodontium
36
Q

What is aggressive periodontitis associated with?

A

Leukocyte adhesion deficiency

37
Q

The numbers of neutrophils increases during gingivitis. What happens of they can contain the infection?

A

Then will return to health

38
Q

The numbers of neutrophils increases during gingivitis. What happens of they are unable to contain the infection?

A
  • The are predisposed to disease progression
39
Q

What is excessive infiltration of neutrophils associated with?

A
  • Chronic inflammation
40
Q

Excessive infiltration of neutrophils is associated with chronic inflammation. How is this the case? (3 points)

A
  • Degradative enzymes (major source of matric metallo-proteinases (MMP’s))
  • Inflammatory cytokines and oxygen radicals contribute to hypoxic environment
  • Connective tissue destruction manifests clinically as loss of attachment
41
Q

What is the role of adaptive immunity in periodontal destruction? (7 points)

A
  • T and B lymphocytes present in early lesion
  • Aggregates rich in CD4 T cells, B cells and dendritic cells evident as lesion progresses
  • Unable to regulate dysbiotic biofilm
  • B cells/ plasma cells predominate advanced lesions
  • IgG fails to regulate dysbiotic biofilm
  • Protective - prevents systemic inflammation
  • Destructive - inflammation indices alveolar bone loss
42
Q

What does an osteoblast do?

A

Synthesises and secretes bone tissue

  • Bone formation
43
Q

What does an osteoclast do?

A
  • Resorbs bone
44
Q

What are osteoclasts derived from?

A

Derived from monocyte/macrophage lineage

45
Q

In health are formation and bone resorption coupled?

A
  • Yes
46
Q

What are osteoclasts regulated by?

A

RANKL/RANK/OPG triad

47
Q

What is the process of bone formation and resorption? (4 points)

A
  • Activated T and B cells in periodontal lesion secrete RANKL
  • RANKL binds RANK to induce osteoclast differentiation
  • OPG prevents RANKL binding to RANK
  • OPG inhibits osteoclast differentiation
48
Q

How does inflammation lead to bone loss? (4 points)

A
  • High levels of sRANKL
  • Low levels of OPG
  • Inflammation induced bone resorption
  • Pathological bone destruction
49
Q

What are the cellular and molecular events linking bacterial-induced inflammation with pathologic tissue destruction? (7 points - long)

A
  1. Bacterial products bind TLR’s on epithelium, stimulating secretion of cytokines, chemokines and AMP’s
  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, RANK/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-7, TNFa) contribute to bone resorption by inhibiting bone formation
  7. Elevated and dysregulated MMP activation contributes to a connective tissue destruction

BDS2 BAMS (57 decks)

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