Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Periodontics > Pathogenesis > Flashcards

Pathogenesis Flashcards

(49 cards)

Start Studying
1
Q

Describe 4 host defence mechanisms

A
  1. Saliva (general feature)
  2. Epithelial barrier (general feature)
  3. Inflammatory response
  4. Immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe 2 purposes of inflammation

A
  1. Isolate, neutralise and remove cause

2. Initiate healing and repair

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

Describe the role of inflammatory response in periodontal disease

A

Periodontal pathogens release LPS and virulence factors leading to inflammatory response

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

Describe what occurs when the bacterial challenge outweighs the immune response

A
  • Bacterial insult overwhelms inflammatory response
  • Dysbioitic biofilm forms from periodontal pathogens
  • State of chronic inflammation occurs
  • Tissue destruction due to chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the inflammatory response of the body

A
  • Rapid
  • Non-specific
  • Soluble effectors and cellular component
  • Cytokines important in the regulation
  • Degree of bystander damage is likely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the stages of the initial inflammatory response

A
  1. Fluid exudate
  2. Soluble effectors from plasma
  3. Complement system
  4. Cellular exudate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe how fluid exudate occurs

A
  • Dilatation of blood vessels
  • Increased vascular permeability
  • Fluid exudate dilutes causative agent and carries plasma protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describ 2 soluble effectors from plasma

A

Complement System - Group of 20 proteins which have key roles in mediating inflammation
Kinin System - Peptides of 9-11 amino acids e.g bradykinin

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

Name 2 components exudate

A
  1. Neutrophils (PMNs)

2. Macrophages

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

What does PMNs stand for?

A

Polymorphonuclear Leucocytes

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

Describe the production, lifespan and function of PMNs

A
  • Produced in bone marrow
  • Lifespan of 2-3 days
  • Phagocytose foreign agents
  • Cytokine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe how neutrophils move from the blood stream to have an effect on inflammation

A
  • Vasodilatation facilitates this
  • LFA-1 receptor on neutrophil and ICAM-1 on endothelium bind
  • This stops the neutrophil from moving through lumen
  • Allows neutrophil to squeeze between endothelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does LAD-1 stand for?

A

Leucocyte adhesion deficiency

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

Describe LAD-1

A
  • Rare genetic disorder
  • Lack of CD-18 expression on PMNs, required for adhering to endothelial cell wall
  • Recurrent RTIs, mucosal infections and aggressive periodontitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cyclic neutropenia?

A

Neutrophil numbers drop cyclically which can lead to serious furcation in deciduous teeth

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

Describe the production, lifespan and function of macrophages

A
  • Derived from blood monocytes
  • Lifespan of 2-3 months
  • Phagocytosis
  • Antigen processing and presentation
  • Cytokine and prostaglandin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name 3 examples of cytokines

A
  1. interleukins
  2. Tumour necrosis factor alpha
  3. Prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the function of cytokines?

A

Cell-cell communication in a paracrine / autocrine fashion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the difference between autocrine and paracrine function?

A

Autocrine affects the same cells where paracrine is communication with other cells in the same area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the general function of interleukins?

Study These Flashcards
A

Family of cytokines which regulate the inflammatory and immune responses

21
Q

Name 4 sources for IL-1

Study These Flashcards
A
  1. Macrophages
  2. Epithelial cells
  3. Fibroblasts
  4. PMNs
22
Q

Name 3 effects of IL-1

Study These Flashcards
A
  1. Activates neutrophils and macrophages
  2. Activates B and T lymphocytes
  3. Induces cytokine release
23
Q

Name 2 ways IL-1 can cause bystander damage

Study These Flashcards
A
  1. Induce matrix metalloproteinase (MMP) release

2. Induces osteoclast activation and bone resorption

24
Q

Describe MMPs

Study These Flashcards
A
  • Family of proteases with zinc ion in active centre
  • Capable of degrading ECM molecules
  • Secreted as inactive pro-MMP
  • Inhibited by TIMP (tissue inhibitor of Metalloproteinases)
25
Describe the production and function of IL-6
- Produced by lymphocytes, monocytes and fibroblasts - Stimulates plasma cell proliferation - Stimulation osteoclast activation - Higher levels in GCF from periodontitis site
26
What is the function of IL-8?
- Chemoattractant for neutrophils - Higher levels in GCF from periodontitis sites - Stimulates MMP expression
27
What is the function of prostaglandins?
- Proinflammatory mediators | - Induce bone resorption via the RANK ligand signalling pathway
28
What does RANK ligand stand for?
Receptor Activator of Nuclear factor Kappa B ligand
29
Describe the relationship of RANK ligand and osteoprotegerin (OPG) and bone resorption
- RANKL is a member of TNF superfamily - Expressed on surface of osteoblasts and binds to RANK receptor on osteoclast precursor cells, stimulating osteoclast activation - RANKL inhibited by OPG - Osteoclastogenic molecules stimulate expression of RANKL while inhibiting OPG
30
Describe active immunity
- Memory cells produced and highly specific - Soluble effectors and cellular components - Cytokines important in regulation - Bystander damage less likely
31
What is the soluble effector of the adaptive immune response?
Antibody
32
Name 4 cellular components of the adaptive immune response
1. T lymphocytes 2. B lymphocytes 3. Plasma cells 4. Macrophages
33
Describe humoral immunity
- Protection against extracellular infectious agents | - Production of antibodies by B-cells under influence of activated T-helper cells
34
Describe cell-mediated immunity
- Protection against intracellular infectious agents - Mainly through release of toxic agents by cytotoxic T-cells, stimulated by IFN gamma, produced by activated T-helper cells
35
Describe the initiation of the humoral immune response in periodontal tissues
- Bacterial antigen - Macrophage - Local lymph node - Presented to B-lymphocyte - Plasma cell created - Secretes antibody - Antibody reaches gingival tissues via circulation - Interacts with specific antigen
36
Name 4 biological activities of IgM (pentamer)
1. Toxic neutralisation 2. Agglutination 3. Opsonisation 4. Activates complement IgM and IgG
37
Name 3 biological activities of IgA
1. Major Ig in secretions 2. Surfaces protection 3. Toxin neutralisation
38
Name a biological activity of IgE
Histamine release from mast cells
39
Name a biological activity of IgD
Receptor on B-cells
40
What is the function of T-helper cells?
Required for maturation of B cells and activation of phagocytes
41
What is the function of T-suppressor cells?
Inhibit immune response
42
What is the function of T-killer cells?
Cytotoxic
43
Describe the antibacterial effects of saliva
- Inhibition of attachment of bacteria (sIgA) - Killing bacteria by peroxidase system - Killing bacteria by lysozyme and histatins
44
Name 3 causes of xerostomia
1. Drug induced (antihypertensives and antidepressants) 2. Head and neck radiation 3. Salivary disease
45
Describe the epithelial barrier
- Barrier against invading microbes - Release of pro-inflammatory cytokines - Produces antimicrobial peptides - Bacterial proteases from P.gingivalis break down barrier function
46
Describe the early lesion at the junctional epithelium
- Increased PMN migration - Macrophage and lymphocytic infiltrate - Localised collagen degradation - Localised fibroblast degeneration - Clinically normal
47
Describe the established lesion (gingivitis) at the junctional epithelium
- PMNs walling off plaque - Increased lymphocytic infiltrate - 60-70% collagen destruction - Lateral proliferation of JE with micro-ulceration - Gingival redness and swelling
48
Describe periodontitis at the junctional epithelium
- Apical migration of JE - Loss of periodontal ligament attachment - Loss of alveolar bone - Micro-ulceration of JE - True pocket formation
49
What is the most commonly accepted theory of the progression of periodontal disease?
Burst hypothesis - Relatively short period of time patient will lose some attachment - Attachment loss is slow following this before another burst - Loss does not occur at same rate constantly for years

Periodontics (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions