Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2 - Infection and Immunity > Periodontal Immunology > Flashcards

Periodontal Immunology Flashcards

1
Q

What are the characteristics of gingivitis?

A

inflammation localised to gingival

acute inflammation

normal physiological response to infection or injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the characteristics of periodontitis?

A

inflammation of gingival tissues and supporting periodontal structures

chronic inflammation

pathological inflammatory response associated with tissue destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What immune factors are found in gingival crevicular fluid?

A
  • AMPs
  • Cytokines
  • Chemokines
  • Lactoferrin
  • IgG
  • Neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What immune factors are found in oral mucosa?

A

AMPs
Cytokines
Chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What immune proteins are found in saliva?

A
  • S-IgA
  • Lysozyme
  • Peroxidase
  • Lactoferrin
  • Mucins
  • Agglutinins
  • Cystatins
  • Histatins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where will neutrophils lyse in normal health?

A

gingival sulcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the early colonisers typically?

A

commensal aerobic (generally gram positive) species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 keystone pathogens implicated in periodontitis?

A

Porphyromonas gingivalis
Tannerella forsythia
Treponema denticola.

gram negative anerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the term coined to describe pathological oral environment?

A

polymicrobial dysbiosis

Disruption of commensal microbial communities in susceptible hosts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the late colonisers typically?

A

gram negative anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What bacterial species reduces as inflammation increases?

A

commensal species that are incompatible with inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the virulence factors of P.gingivalis that evade immunity?

A
  • Asaccharolytic (breakdown of proteins for nutrients)
  • Gingipains (proteases with broad-specificity)
  • Atypical LPS (tlr4 antagonist that blocks signalling)
  • Inflammophilic
  • Drives dysbiosis in susceptible hosts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Is P.gingivalis early or late coloniser?

A

late gram negative anaerobic coloniser

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the aetiology of periodontitis associated with?

A
  • accumulated plaque bacteria
  • presence of periodontal pathogens
  • polymicrobial dysbiosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are hallmark signs of periodontitis?

A

attachment loss
increased pocket depth
bone loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What immune factors increase in gingivitis?

A

increased TLR stimulation

increased production of pro-inflammatory mediators

17
Q

What cell type is predominant in gingivitis?

A

neutrophils

18
Q

What immune under reaction disease can contribute to PD disease?

A

leukocyte adhesion deficiency - patients have neutrophils however they are found in blood and cannot migrate into tissues

(immune under reaction)

19
Q

What is an excessive neutrophil infiltration associated with?

A

chronic inflammation -

source of matrix metalloproteinases

release inflammatory mediators

create hypoxic environment

20
Q

What is the role of adaptive immunity in periodontal destruction?

A

CD4, T and B cells present in early lesions, unable to regulate dysbiotic biofilm, contribute to inflammation and bone loss through RANKL production but also limit infection to site and prevent it becoming systemic

21
Q

Why is there no bone loss in health?

A

in health bone formation and bone resorption are coupled regulated by rankl/rank/opg triad

22
Q

How does inflammation lead to bone loss?

A

activated T/B cells in periodontal lesion secrete RANKL (unbalancing)

RANKL binds RANK to induce osteoclast differentiation

23
Q

What does OPG do?

A

OPG prevents RANKL binding RANK

OPG inhibits osteoclast differentiation

24
Q

What are the molecular events that link bacterial induced inflammation with pathologic tissue destruction

A
  • Bacterial products bind TLRs, stimulating cytokine, chemokine, and AMP production.
  • Vasodilation and leukocyte recruitment (neutrophils, monocytes, lymphocytes).
  • Activated neutrophils release pro-inflammatory mediators, amplifying inflammation.
  • Activated lymphocytes express RANKL, disrupting RANKL/OPG balance.
  • RANKL binds RANK on osteoclast precursors, inducing osteoclastogenesis and bone resorption.
  • Pro-inflammatory cytokines (IL-1, IL-6, IL-17, TNF-α) inhibit bone formation.
  • Dysregulated MMP activation contributes to connective tissue destruction.
25
Q

What are osteoclast precursors?

A

monocytes

26
Q

What are the pro-inflammatory cytokines that contribute to bone resorption?

A

IL-1, IL-6, IL-17. TNF-alpha

2 - Infection and Immunity (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions