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Microbiology for Dentists > 17. Dental Caries > Flashcards

17. Dental Caries Flashcards

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1
Q

5 types of caries categories

A
  • anatomical site based
  • primary vs recurrent/secondary
  • residual
  • cavitated/non-cavitated
  • active or inactive/arrested
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2
Q

Define ‘early childhood caries’

A
  • presence of one or more decayed, missing (due to caries) or filled tooth surfaces in any primary tooth of a child between birth and 71 months of age
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3
Q

Possible anatomical sites for caries

A
  • pits and fissures
  • smooth surfaces (enamel or root which start on exposed cementum or dentin)
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4
Q

Root caries affect mainly …

A

older people

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5
Q

Which site of caries is most common?

A

occlusal

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6
Q

Why was there a drastic increase in occlusal caries in the late 19th century?

A
  • sugar and milled wheat
  • now commonplace around 1850
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7
Q

What did the 2010 global burden of disease study find about caries?

A
  • untreated caries in perm teeth is most common global disease
  • 2.4 billion affected
  • untreated caries in deciduous teeth 10th most common (621M affected)
  • marked variation between different pops
  • caries will increase due to greater longevity and pop growth
  • complete tooth loss is decreasing significantly
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8
Q

Even though caries incidence is increasing, what is significantly decreasing?

A

complete tooth loss

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9
Q

Key dental work in 1881

A
  • Underwood and Miles of International Medical Congress
  • observation of germs in affected teeth
  • germs are essential for tooth decay in vitro
  • antiseptics are effective in preventing decay in vitro
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10
Q

Key dental findings in 1890

A
  • The Micro-Organisms of Human Mouth was written
  • Miller’s chemicoparasitic theory (that carbs and bacteria produce acid and affects teeth)
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11
Q

Key dental findings in 1898

A
  • Black and Williams describe ‘gelatinous microbic plaques’
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12
Q

List 6 alternate theories for caries formation other than ‘a result of microbial sugar fermentation’

A
  • worms from ancient Sumerians
  • chymical theory
  • parasitic/septic theory
  • chemico-paarasitic theory
  • proteolytic theory
  • proteolysis-chelation theory
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13
Q

Explain chymical theory of caries

A
  • Parmly in 1819
  • food putrefaction released unidentified chemical agents
  • these dissolve teeth
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14
Q

Explain parasitic/septic theory of caries

A
  • Erdl in 1843
  • described a filamentous parasite in plaque
  • responsible for caries
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15
Q

Explain chemico-parasitic theory of caries

A
  • Miller in 1890
  • stage 1 was decalcification of enamel
  • stage 2 was dissolution of soft residue
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16
Q

Explain proteolytic theory of caries

A
  • Gottleib in 1947
  • microbes invade enamel lamellae
  • initiate caries by proteolysis
  • Pincus in 1950 proposes proteolysis of cuticle
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17
Q

Explain ‘proteolysis-chelation theory’

A
  • Schatz in 1955
  • argued too much emphasis on protons and Miller was misunderstood
  • microbial proteolytic destruction of organic matrix
  • calcium is removed by chelation/organic acids
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18
Q

Proteolysis probably does play a role in … caries

A

root

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19
Q

Bacteria commonly associated with caries

A
  • mutans streptococci
  • lactobacillus spp.
  • actinomyces spp.
  • bifidobacterium spp and others like scardovia wiggsiae
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20
Q

Why do we link certain bacteria to caries?

A
  • elevated at site of caries
  • animal models
  • virulence factors e.g acid production from sugars/acidogenicity and acid tolerance (aciduricity)
  • intracellular storage granules, extracellular polysaccharides etc
21
Q

3 microbiological theories surrounding plaque

A
  • specific plaque hypothesis
  • non-specific plaque hypothesis
  • ecological plaque hypothesis
22
Q

Define ‘specific plaque hypothesis’

A

individual species/pathogen causes disease

23
Q

Define ‘non-specific plaque hypothesis’

A
  • disease is caused by total amount of plaque
  • independent of specific microbes present
24
Q

Define ‘ecological plaque hypothesis’

A
  • individual species are important
  • but disease is due to imbalance/dysbiosis
25
Q

Give Koch’s postulate 1
Can it relate to dental caries?

A
  • the organism must be present in all cases of disease and not in healthy individuals
  • no microbe fills that criteria so it could be amount of organism rather than presence/absence
  • must test abundance of bacteria at site of dental caries
26
Q

Why is it difficult to measure amount of strep mutans and sobrinus?

A
  • basic culture-based approaches can’t distinguish between them
  • so can’t get abundance of both
27
Q

2 methods of inveestigating caries

A
  • cross-sectional (sample at a single time point and compare microbiota in health and disease)
  • longitudinal (sample at multiple time points and compare microbiota to see when health becomes disease)
28
Q

Ads and disads of cross-sectional design for caries

A
  • relatively cheao
  • can sample sites of caries
    BUT
  • can’t show causation
29
Q

Ads and disads of longitiudinal design for caries

A
  • may find changes before detectable caries to develop predictive tests
    BUT
  • relatively expensive
  • can’t predict sites of caries development (sample saliva or pooled plaque)
30
Q

What was found in the study ‘cultivable anaerobic microbiota of severe early childhoof caries’?

A
  • cultured bacteria from 24 children with early childhood caries and from 21 caries-free children (controls)
  • used blood agar (non-selective) and acid agar (5 pH)
  • identified over 5,500 isolates by sequencing 16S rRNA gene
  • bifidobacteria and scardovia wiggsiae were preferentially isolated on acid agar
  • S. mutans and scardovia wiggsiae were significantly associated with caries (over 80% of kids with both has early childhood caries and over 80% with neither were carie-free)
31
Q

What is bifidobacterium?

A
  • anaerobic
  • pleomorphic
  • gram-positive
  • bacilli
32
Q

Why is bifidobacterium linked to caries so highly?

A
  • saccharolytic
  • produce acetic and lactic acid
33
Q

A 2015 study found that S.mutans level did not accurately predict caries. What was found to be much better?

A
  • prevotella spp.
34
Q

Give a study that shows the impact of microbiome imbalance in early life

A
  • sampled saliva in children from a birth cohort (with 16S rRNA gene sequencing)
  • grouped into community states based on dominant taxa
  • followed children over time until caries developed (or matched controls)
  • microbiome differences detected in 12 months between children who went on to develop caries and those who didn’t
35
Q

How are animal models used to investigate caries?

A
  • feed rats sugar and they develop dental caries
  • to test the microbiology, use germfree animals developed in the 1940s
  • proved animals can exist without microbial inhabitants so a clean background to investigate microbial aetiology
36
Q

After indentifying Selemonas sputigena in a study tested in rat caries, what conclusions do we have about it?

A
  • doesn’t cause caries in monocultures
  • enhances cariogenicity of S. mutans
37
Q

How do virulence factors increase cariogenicity?

A
  • adhesins such as antigen I/II, glucosyltransferase
  • mainly acid production/acidogenicity (F-ATPase)
  • aciduricity (DNA repair proteins, protective membrane proteins)
38
Q

Health producing factors

A
  • adhesins of commensal bacteria
  • alkali production
39
Q

How are carbohydrates utilised by caries associated bacteria?

A
  • glucose and sucrose become either intracellular storage polymers or sucrose become an exopolysaccharide
  • exopolysaccharides can join the dental plaque biofilm matrix
  • glucose and sucrose can also produce acid
40
Q

Explain sugar uptake in oral bacteria

A
  • polysaccharides can be digested
  • many different mono/disaccharides can be imported
  • xylitol import leads to a ‘futile cycle’
41
Q

Explain regulation in oral bacteria

A
  • glucose uptake is constitutive/other transporters are regulated
  • in high sugar, lactate is the major product (homofermentation) and glycolysis is accelerated
  • intracellulr polysaccharides are made
  • in low sugar, mixed acid fermentation (heterofermentation) - lactate dehydrogenase is inhibited
  • intracellular polysaccs are degraded
  • oxygen is an important regulator of fermentation - inhibits pyruvate formate lyase
42
Q

Why is oxygen an important regulator of fermentation?

A
  • inhibits pyruvate formate lyase
43
Q

How do intracellular polysaccharides function in oral biome?

A
  • produced by glucose-1-phosphate when carb is in excess
  • glycogen-type glucan
  • broken down and used in glycolysis during starvation
  • role in caries is uncertain
44
Q

How do food webs get used in oral biome?

A
  • end products of metabolism can be recycled by other bacteria
  • several bacteria use lactate - for veillonela spp. it’s essential
45
Q

How is aciduricity an adaptive response?

A
  • bacterial cultures can be treated with weak acid around 5.5 pH for up to 60 mins
  • cultures then added to low pH (4.0) for 60 mins
  • medium was neutralized and surviving bacteria were enumerated by viable counting
  • pre-acidification results in greater acid tolerance, particularly in bacteria that are relatively acid sensitive
46
Q

Mechanisms of acid adaptation

A
  • reduced permeability of cell membrane to hydrogen ions
  • induction of hydrogen ion-translocating ATPase (to expel protons from cell)
  • induction of alkali production systems (arginine deiminase or urease)
  • induction of stress proteins that protect enzymes and nucleic acids from denaturation
47
Q

How is alkali production in oral bacteria important?

A
  • proportion of S. mutans in dental plaque is higher in caries active than caries free subjects
  • salivary arginine deiminase and urease higher in caries free people
  • no correlation between individual ammonia-generating species and caries
48
Q

How does diet affects microbial populations of dental plaque?

A
  • bacterial composition changes from low sugar levels to high sugar levels
  • gleaners at low sugar like P.gingivalis and exploiters at high sugar levels like oral strep
  • if pH then decreases, pH strategists are present like Strep mutans and lactobacillus spp

Microbiology for Dentists (37 decks)

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