1. Periodontitis Flashcards

1
Q

Pathogenesis of gingivitis (2)

A

Microbial challenge (plaque) leads to clinical disease (gingivitis)

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2
Q

Types of local plaque retention factors (4)

A

Calculus
Restoration margins
Crowding
Mouth breathing

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3
Q

Types of systemic modifying factors (2)

A

Sex hormones

Medication

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4
Q

Features of gingival health (6)

A
Knife-edge, scalloped gingival margin
Stippling (in about 30% of cases)
Pink/pale colour
Firm and flat gum tissues
Painless
No bleeding
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5
Q

Specific features of health (6)

A

Intact barrier provided by junctional epithelium
Shedding of oral epithelial cells
Flow of GCF
Antibodies in GCF
Phagocyte function and lymphocyte infiltrate
Complement activity

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6
Q

Definition of gingivitis (2)

A

Inflammation of the gingiva

Commonly occurs because of films of bacteria that accumulate on the teeth (plaque)

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7
Q

Signs of gingivitis (8)

A
Red or bluish red (chronic inflammation) colour
Bleeding on provocation/probing
Loss of stippling
Pus
Inflammation (oedema - swollen gums)
Bad breath
Receding gingiva
Occasionally painful
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8
Q

Features of gingivitis (7)

A

Altered microbial colonisation
Increased flow of GCF
Influx of neutrophils, increased lymphocytes and monocytes
Increased flow of GCF
Influx of neutrophils, increased lymphocytes and monocytes
Plasma cell infiltrate
Proliferation and ulceration of epithelium

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9
Q

Biofilm features in health (2)

A

Biofilm is gram-negative

Biofilm is aerobic

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10
Q

Biofilm features in disease (2)

A

Biofilm is gram-positive

Biofilm is anaerobic

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11
Q

Removal of microbial challenge leads to

A

A return to health

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12
Q

Definition of periodontitis

A

Inflammation of the gums and supporting structures of the teeth

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13
Q

Causes of periodontitis (2)

A

Certain bacteria

Local inflammation triggered by those bacteria

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14
Q

Definition of biofilm

A

One or more communities of micro-organisms, embedded in a glycoalyx, attached to a solid surface

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15
Q

How is a biofilm removed

A

Mechanical disruption

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16
Q

Function of biofilm (3)

A

Provide protection for colonising species from competing organisms and environment (host defences, antibiotics)
Facilitate uptake of nutrients and removal of metabolic products
Allow for development of appropriate physiochemical environment (pH, O2 conc.) and allow for communication between bacteria

17
Q

Features of late colonisers (2)

A

Associated with periodontal disease

Require a fairly established biofilm before being able to colonise

18
Q

Definition of bacterial virulence (2)

A

Ability to colonise and compete in an ecological niche
The ability to evade host defences by degrade host Ig and complement leukotoxin production, tissue invasion and inhibition of antibody synthesis

19
Q

Evidence for specific bacterial causation (4)

A

Presence in elevated numbers at diseased sites
Reduced number following periodontal therapy
Presence of an elevated specific immune response
Evidence from animal models

20
Q

What is required for periodontitis to occur

A

Presence of bacteria

21
Q

Host immune response mechanisms in the mouth (4)

A

Saliva
Epithelium (physical barrier, shedding of cells, production of inflammatory mediators)
GCF
Inflammatory and immune responses (inflammatory cells, PMNs, etc.)

22
Q

Protective functions of the antibody (4)

A

Inhibition of adhesion/invasion
Complement activation
Neutralisation of toxins
Opsonisation and phagocytosis

23
Q

How does CT matrix degradation occur

A

Through MMPs

24
Q

What are MMPs (2)

A

Matrix metalloproteinases are a family of Zn and Ca-dependent proteolytic enzymes (including collagenases)
In periodontitis, matrix degradation is largely a result of MMPs secreted by host inflammatory cells

25
Q

Definition of leukocyte adhesion deficiency (LAD)

A

A rare autosomal recessive disorder characterised by immunodeficiency resulting in recurrent infections

26
Q

LAD process (6)

A

No neutrophils –> no bacterial phagocytosis –> increased inflammation –> increased tissue destruction –> increased bone loss –> loss of teeth

27
Q

Effects of smoking (5)

A

Vasoconstriction of gingival vessels and increased gingival keratinisation
Impaired antibody production
Depressed numbers of Th lymphocytes
Impaired PMN function
Increased production of pro-inflammatory cytokines

28
Q

Primary etiological agent in inflammatory periodontal diseases

A

Microbial plaque