Pathogenesis of periodontal diseases Flashcards

1
Q

Gram positive vs gram negative bacteria

A

Gram positive: only one membrane and a thick peptidoglycan layer which when included in the gram stain method retains the stain in side the cell causing it to appear purple
Gram negative: two membranes with a thin cell wall between the two mems creating a space called the peroiplasm. And have an outer capsule of LPS. Does not retain the stain so appears pink under light microscope

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2
Q

Koch’s postulates

A

traditional view of infection. One organism –> one infection
Not seen as the case anymore

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3
Q

Periodontal progression

A

Health –> gingivitis (inflammation) –> moderate periodontal disease (pocket) –> advanced periodontal disease (bone loss)

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4
Q

Loe longitudinal studies

A

Gingivitis develops when plaque accumulates

Health restored when plaque removed

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5
Q

Germ-free animals

A

No bacteria, no disease
Germ-free plus bacteria –> disease (but not all animals equally)
Periodontitis-causing bacteria ‘transmissable’ (disease may or may not arise)

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6
Q

Layers of organisms in subgingival plaque

A

Firmly attached: deeper layer, predominantly gram+
Loosely attached: more superficial layer, gram- anaerobes and motile bacteria
Exist in close, mixed communities

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7
Q

Disease progression

A

Sporadic and often site specific

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8
Q

What changes a quiescent site to an active one?

A
Change in host - immune status, age, environmental factors (smoking etc)
Change in microbial challenge
-type of organisms
-number of particular organisms
-virulence of organism
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9
Q

Problems with sampling subgingival plaque

A

If tooth is posterior and difficult to access

Might sample supragingival plaque

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10
Q

Instruments to sample subgingival plaque

A

Use a curette or paper point

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11
Q

The idea of the (oral) microbiome

A

The microbiome affects the way that you live
In our bodies we carry around 1kg mass in bacteria (mainly in digestive tract)
Profound influence on our health
-GU health (females)
-GU health > IBD
-GI food processing > obesity

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12
Q

Establishing microbes in subgingival plaque

A

Methods:

  1. Culture up to late 90s
  2. Sequencing 16s rRNA PCR clone libraries/ hybridisation arrays
  3. Mass sequencing of 16s rRNA amplicons
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13
Q

Why do we use 16s rRNA sequencing to identify species?

A

16s rDNA very well conserved due to esssential function
Acts as molecular clock and species signature as evolves slowly in time
We sequence it to speciate bacteria (18s is human/ animal equivalent)

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14
Q

Firmicutes & streps

A

Omnipresent in samples, not contributing to disease

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15
Q

Bacteroidetes

A

Raised in disease

Anaerobic, Gram- bacilli

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16
Q

Unculturables

A

~500 species present

~50% can be cultured

17
Q

Evidence for specific microbial aetiology

A

High numbers of certain bacteria cultured from diseased sites
Can cause disease in certain animal models
Have demonstrable virulence factors

18
Q

Groups of organisms in periodontitis

A

Health: S. mitis, S. oralis
Disease: P. gingivalis, Ta. forsythia

19
Q

P. gingivalis

A

Black pigmented anaerobe
Lipopolysaccharide in outer membrane
Gram negative
Secretes gingipains - virulence factors (proteases which degrade protein)
Epithelial cell invasion - immune evasion and recolonisation after debridement (hides)
Surface proteins key to human-cell interaction

20
Q

Ta. forsythia

A

Anaerobe (not black)
Gram -ve
Unusual structure
Tooth-like S- layer: responsible for aspects of adhesion (glycosylated?)
Fibronectin binding protein
Protease/ toxins
Glycosidases give it competitive advantage

21
Q

Sheffield findings Tannerella

A

Sialic acid is key nutritional source for Tannerella
Acquisition of sialic acid requires cleavage from host proteins
-inhibition with Tamiflu stops growth. New treatment?

22
Q

T. denticola

A

Small, thin spiral shaped bacterium
Few known virulence factors
Difficult to grow and work with

23
Q

Groups of organisms are more important than single pathogens

A

Diff bacteria have diff virulence factors
Combination of these factors more likely to cause disease
Qualitative mixture of pathogens determines disease progression

24
Q

Dysbiosis

A

Move from health to disease

Healthy community –> environmental factors –> disease community

25
Keystone hypothesis
P. gingivalis has been shown to shift whole pop. from non-pathogenic to pathogenic in mouse models even if only present in low numbers Also noticed in obesity
26
Imbalance in innate immunity
Can --> bone loss
27
Mechanisms of tissue damage
Bacteria: | Evasion of host defences, induction of inflammation (cytokines) --> bone resorption, soft tissue damage
28
Necrotising ulcerative gingivitis
Tissue damage Depression of host defences by smoking and modification of response by stress Possibly depression of peripheral blood supply to tips of papillae Selection of specific bacteria by host-derived nutrients Fuso-spirochaetal complex
29
Polymicrobial infections
Caused by interactions between 2 or more organisms leading to disease Sum of parts and their virulence factors cause disease, not one in isolation Interaction with host defences often key