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Periodontology > ICP-25 Aetiology and Pathogenesis of Periodontal Disease > Flashcards

ICP-25 Aetiology and Pathogenesis of Periodontal Disease Flashcards

(37 cards)

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1
Q

What are the clinical features of good periodontal health

A

Gingiva are:

  • Pink
  • Firm
  • Stippled
  • “knife-edge” papillae
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2
Q

What are the clinical features of gingivitis

A
  • Bleeding from gingiva
  • Marginal redness
  • Gingivae swollen
  • No bone loss/attachment loss
  • No mobility
  • No recession
  • No gaps
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3
Q

What are the clinical features of periodontitis

A
  • Recession
  • Mobility
  • Increased probing depths (pocket formation)
  • Sensitivity
  • Drifting
  • Gaps (black triangles)
  • Bone loss (radiographs)
  • Long teeth
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4
Q

What is the weak point in the periodontal barrier during inflammation

A

the junctional epithelium

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5
Q

What is calculus and where can it be found

A

Mineralised plaque from calcified bacterial matrix and pellicle

Can be found Supra and Subgingivally

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6
Q

Describe Supragingival calculus

A

Creamy/Yellow

Precipitation of mineral salts from saliva (calcium phosphate/hydroxyapatite)

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7
Q

Describe Subgingival calculus

A
  • Brown

- Precipitation of mineral salts from crevicular fluid (whitelockite) - difficult to remove

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8
Q

Where does calculus attach to and what covers it

A

Attaches to enamel, dentine and cementum

Covered by unmineralised bacterial plaque

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9
Q

What are the stages of periodontal lesion and what disease are they associated with

A

Initial lesion - gingivitis
Early lesion - gingivitis
Established lesion - established gingivitis
Advanced lesion - periodontitis

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10
Q

Describe the features of an initial lesion

A

Subclinical

  • Dental plaque accumulation
  • Increased neutrophil migration
  • Gingival crevicular flow increases
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11
Q

Describe the features of Early lesion

A
  • Dental plaque accumulation more extensive
  • Increasing neutrophils followed by monocytes/macrophages and then lymphocytes
  • Increased vascularity
  • Collagen destruction to create space for infiltrate
  • Rete peg proliferation
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12
Q

Describe the features of Established lesion

A
  • Neutrophils continue to migrate into the tissues and into the gingival crevice
  • Extensive sub gingival plaque
  • Plasma cell predominate in the inflammatory infiltrate
  • No loss of CT attachment
  • No bone loss
  • This lesion may remain stable for some time or may progress to a destructive lesion
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13
Q

Describe the feature of an advanced lesion

A
  • Gingival recession with fibrosis in CT
  • Continued extension of subgingival plaque
  • Extension of inflammatory infiltrate into CT
  • Apical Migration and ulceration of JE
  • Periodontal ligament loss
  • Alveolar bone resorption by osteoclasts
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14
Q

What immune cells can be involved with periodontal lesions

A
  • Dendritic cells
  • Macrophages
  • Mast cells
  • Neutrophils
  • Monocytes
  • T cells
  • B cells
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15
Q

What triggers the inflammatory and immune response in periodontitis

A

Bacterial products secreted:
- Enzymes: collagenase, protease, hyaluronidase

Bacterial Membrane:

  • LPS
  • Lipoteichoic acid (LTA)
  • Capsular material

Metabolic Products:

  • Buytric acid
  • Propionic acid
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16
Q

What are some types of Sentinel cells

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A
  • Macrophages
  • Dendritic cells
  • Mast cells
17
Q

What are Pattern Recognition Receptors (PRRs) on sentinel cells activated by

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A

PAMPs - Pathogen Associated Molecular Patterns (on surface of pathogens)
DAMPs - Damage Associated Molecular Patterns (Indicate cell damage - inside of cells externalised)

18
Q

What are released by sentinel cells and what do they do

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A

They release alarm molecules (alarmins) - pro-inflammatory mediators that trigger inflammation

19
Q

What kinds of pro inflammatory mediators are released by sentinel cells

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A
  • Histamine
  • Pro-inflammatory cytokines
  • Prostaglandins
20
Q

What happens when histamine is released

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A
  • Mast cells release histamine - microvasculature produce PGI2, dilates BVs
  • Endothelial contraction - open up vasculature
21
Q

What are some pro-inflammatory cytokines

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A
  • Tumour Necrosis Factor Alpha
  • Interleukin - 1Beta
  • Interleukin - 6
  • Interleukin - 8
22
Q

What are some prostaglandins

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A

Prostaglandins (PGE2)

Prostacyclin (PGI2)

23
Q

Describe type 1 inflammation

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A

Activation by histamine in minutes

  • Vasodilation and endothelial cell contraction (redness and heat)
  • Inflammatory exudate move into tissues (oedema)
  • Leukocyte extravasation - neutrophils brought in from blood into the gingival tissues initially
24
Q

What causes Type 2 inflammation and what happens in it

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A

Activation by TNF-alpha and IL-1B in hours

  • More pronounced type 1 activation
  • Monocyte recruitment (macrophages in tissues)
25
Where are neutrophils recruited from
Recruited early from the blood into the tissues
26
What are the functions of neutrophils
- Phagocytosis Produces: - Chemokines (to attract other immune cells) - Pro-inflammatory cytokines (IL-1B, TNF-a, IL-8) - Anti-inflammatory cytokines (IL-10) - Granule derived antimicrobial molecules and enzymes (lysozymes) - Reactive oxygen species and matrix metalloproteases (MMPs) (enzymes that break down tissues) - Substances that help B cells survival - Neutrophil extracellular traps (NETs) - Express RANKL on surface and contribute to bone destruction - Regulate other immune cells T cells/DCs/NK cells/ Macrophages
27
What are some neutrophil defects that are often associated with periodontitis
- Leukocyte Adhesion Deficiency (LAD) - recruitment deficient - Lazy Leukocyte Syndrome - Neutrophil function affected - Neutropenia - low numbers of neutrophils - Cyclic neutropenia - levels fluctuate over time form normal to low - Produce too many pro-inflammatory cytokines (IL-1B, TNF-a, IL-8)
28
What are the functions of Macrophages
- Antigen presenting cell - Phagocytosis - Produce Proinflammatory cytokines (MI macrophages) - Anti-inflammatory cytokines (M2 macrophages)
29
What is the complement system and what is it activated by
``` Cascade of circulating blood proteins Activated by: - Antigen-antibody complexes - Bacterial endotoxin LPS on bacterial outer membranes - Lectin pathway ```
30
What are the functions of the complement system
- Opsonisation - stick to and mark antigen for phagocytosis - Cell lysis - ruptures bacterial cell walls - Chemotaxis - neutrophils and macrophages attracted to antigen - Mast cell activation - Histamine release
31
What kinds of T helper cells are there and what do they do
Th1 = cytotoxic cells Th2 = mediate humoral immunity (B cells) Th17 - important in mediating bone loss
32
What kinds of T-regulatory cells are there and what do they do
Tregs = anti-inflammatory (IL-10)
33
What do B cells do and when are they predominant in periodontal lesions
- Produce antibodies - Predominate in established and advanced lesions - 60% of lymphocytes in periodontal lesions - Express and produce RANKL - drives bone loss
34
Describe the resolution of inflammation of periodontal tissues
- Removes plaque - Reversal of inflammation - Reduction in pro-inflammatory mediators - Resolvins (lipid mediators of inflammation) - Repair CT to produce new collagen forming new CT
35
What is the RANKL-OPG pathway of bone loss
- Mechanism by which the immune system regulates bone turnover - Balance between RANKL and OPG important in controlling bone loss - Balance between the bone forming and bone resorbing cells
36
Describe how the RANKL-OPG pathway works
- Receptor activator of nuclear factor kappa-B ligand (RANKL) - expressed by osteoblasts - important in osteoclast formation, function and survival - Receptor activator of nuclear factor kappa-B (RANK) - located on osteoclast precursors and mature osteoclasts - Osteoprotegerin (OPG) - binds to RANKL and competitively inhibits RANKL - expressed by osteoblasts and other tissues - protective against bone loss - Oesteogen - limits release of RANKL
37
What ratio of RANKL:OPG causes bone formation/loss
Low RANKL:OPG ratio = bone formation High RANKL:OPG ratio = bone loss

Periodontology (12 decks)

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