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BDS 2: Periodontology > Aetiology & Pathology of Periodontal Disease > Flashcards

Aetiology & Pathology of Periodontal Disease Flashcards

1
Q

What is the appearance of healthy gingivae? (4)

A
  • Pink
  • Firm
  • Stippled
  • “Knife-edge” papillae
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2
Q

What are the clinical features of gingivitis? (7)

A
  • Bleeding from gingivae
  • 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 ? (8)

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

Define the dysbiosis plaque hypothesis

A

Any disruption of the ‘normal’ microbiome content that changes the symbiotic relationship between the host and microbes, a disruption that can result in disease

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5
Q

Define the keystone hypothesis

A

Certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one

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6
Q

Describe the differences in bacteria from healthy periodontal health to periodontitis (3)

Predominant species type?
Ecological changes?
Biofilm Complexity?

A
  • Healthy is gram positive whereas periodontitis is negative
  • Healthy is aerobic, periodontitis is anaerobic
  • Biofilm in healthy is simple and symbiosis, where as in periodontitis its complex and dysbiosis
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7
Q

Define the non specific plaque hypothesis

A

Plaque volume associated with level disease with the precise microbial
composition of dental plaque not critical

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8
Q

Define the specific plaque hypothesis

A

Specific species are associated with level of disease

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9
Q

Define the ecological plaque hypothesis

A

Environmental conditions dictate the balance of the microbial community

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10
Q

What is calculus?

A
  • Mineralised plaque

- Calcified bacterial matrix and pellicle

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11
Q

Where does calculus attach?

A

Attaches to enamel, dentine and cementum

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12
Q

Describe what occurs during an initial periodontal lesion (3)

A
  • Dental plaque accumulation
  • Increased neutrophil migration
  • Gingival crevicular flow increases
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13
Q

Describe what occurs during an early periodontal lesion (4)

A
  • Dental plaque accumulation more extensive
  • Increasing neutrophils followed by macrophages and then lymphocytes
  • Increased vascularity
  • Collagen destruction to create space for infiltrate
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14
Q

Name some bacteria found in a healthy periodontium (3)

A
  • Streptococcus oralis
  • Streptococcus mitis
  • Streptococcus intermedius
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15
Q

Name some bacteria found in a periodontitis biofilm (3)

A
  • Porphyromonas gingivalis
  • Tannerella forsythia
  • Treponema denticola
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16
Q

Describe what occurs during an established periodontal lesion (5)

A
  • Neutrophils continue to migrate into the tissues and into the gingival crevice
  • Extensive subgingival plaque
  • Plasma cell (B cell) predominate in the
    inflammatory infiltrate
  • No loss of CT attachment
  • No bone loss
17
Q

Describe what occurs during an advanced periodontal lesion (6)

A
  • Gingival recession with fibrosis in connective tissue
  • Continued extension of subgingival plaque
  • Extension of inflammatory infiltrate into CT
  • Apical migration and ulceration of junctional epithelium
  • Periodontal ligament loss
  • Alveolar bone resoprtion by osteoclasts
18
Q

What triggers inflammation and immune response? (3)

A
  • Bacterial products secreted
  • Bacterial membrane
  • Metabolic products
19
Q

Give some examples of sentinel cells (3)

A
  • Macrophages
  • Dendritic cells
  • Mast cells
20
Q

What are pattern recognition receptors (PRRs) on sentinel cells are activated by? (2)

A
  • Pathogen Associated Molecular Patterns (PAMPS)

- Damage Associated Molecular Patterns (DAMPS)

21
Q

What do sentinel cells release?

A

Alarm molecules (alarmins) that are pro-inflammatory mediators that trigger inflammation

22
Q

What is type 1 inflammation?

A
  • Activation by histamine (Minutes)
  • Vasodilatation and Endothelial cell contraction
  • Inflammatory exudate move into tissues
  • Leukocyte extravasation
23
Q

What is type 2 inflammation?

A
  • activation by TNF-𝛼 and IL-1𝛽 (Hours)
  • More pronounced type 1 activation
  • Monocyte recruitment (Macrophages in tissues)
24
Q

What is the importance of RANKL on the surface of neutrophils?

A

Contribute to bone destruction

25
Q

Name some neutrophil defects associated with periodontitis (4)

A
  • Leukocyte adhesion deficiency
  • Lazy leukocyte syndrome
  • Neutropenia
  • Cyclic neutropenia
26
Q

What occurs during an acute macrophage response?

A

Interleukin 6 produced by sentinel cells

27
Q

What occurs during an systemic macrophage response?

A

Increased Acute phase response by liver

28
Q

How can you resolve periodontium inflammation? (4)

A
  • Remove plaque
  • Reduction in pro-inflammatory mediators
  • Resolvins (Lipid mediators of inflammation)
  • Repair connective tissue to produce new collagen forming new CT
29
Q

What does the RANKL-OPG pathway control?

A

Bone loss

30
Q

What is the affect of oestrogen on the RANKL-OPG pathway?

A

Limits release of RANKL

31
Q

What is the role of OPG in the RANKL-OPG pathway?

A
  • OPG competes with osteoclasts for the RANKL on osteoblasts
  • So this prevents osteoclasts maturing which prevents bone resorption
32
Q

What are the 2 theories of periodontal progression?

A
  • Gradual destruction model

- Burst theory (Periods of rapid breakdown interspersed with long periods of quiescence)

BDS 2: Periodontology (9 decks)

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