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IARD > Introduction and Aetiology of Dental Caries > Flashcards

Introduction and Aetiology of Dental Caries Flashcards

1
Q

Dental Caries definition

A

A progressive irreversible bacterial disease of the teeth exposed to the oral environment.

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2
Q

What happens to enamel and dentine?

A
  • Enamel and dentine are destroyed in a demineralisation process.
  • A path to the underlying tissues is opened for bacteria.
  • This causes infection and inflammation of the pulp and periodontal tissues.
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3
Q

Enamel and dentine are not cellular. So?

A
  • They have no blood supply of their own.
  • So no natural repair of decayed tissues.
  • The only way to arrest the decay process is by removing the infected tissue and restoring it with artificial materials.
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4
Q

What is minimal intervention?

A

Using modern dental materials and techniques to arrest early carious lesions in enamel and stabalise more advanced lesions.

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5
Q

W D Miller

A

Showed that lesions similar to dental caries could be produced by incubating teeth in saliva when carbohydrates were added.

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6
Q

Miller’s dental caries conclusion

A

Caries could result from decalcification caused by bacterial acid production, followed by invasion and destruction of any remaining tissue.

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7
Q

Bacteria ferment sugar to…

A

Produce acid or secrete enzymes that digest proteins.

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8
Q

Dental caries develops only in the presence of 4 variables

A
  1. Bacterial plaque containing cariogenic bacteria (Microbial aspects).
  2. Bacterial substrates, especially sugar.
  3. Susceptible tooth surface.
  4. Time.
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9
Q

Bacterial plaque. What is it?

A
  • A soft, non-calcified microbial deposit (biofilm).
  • Develops into a dense mass of colonies which adheres to the acquired pellicle (a glycoprotein film formed from saliva).
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10
Q

Orland 1954

A
  • Completed germ free and gnotobiotic studies.
  • Showed that caries did not develop in germ-free animals.
  • Shows that certain bacteria must be present the plaque for the plaque to be cariogenic.
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11
Q

Gnotobiotes. What are they?

A
  • Animals where the bacterial flora is precisely known or controlled.
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12
Q

Studies involving gnotobiotes

A
  • Animals reared in a sterile environment do not get dental caries even on a diet rich in sugar.
  • To see which bacteria cause dental caries, different types of bacteria are inoculated into the mouths of the animals.
  • Studies show that the most potent mediators of dental caries are strains of acid producing streptococci.
  • Other strains do not cause caries, even in the presence of sugar.
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13
Q

Types of bacteria important in caries

A
  1. Streptococci.
  2. Streptococcus Mutans.
  3. Lacto Bacilli.
  4. Strains of Actinomycetes
  • Bacteria vary depending on the stage of the carious lesion.
  • Attack on enamel is a different process than destruction of dentine.
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14
Q

Streptococci

A
  1. Strep Mutans
  2. Strep Salivarius
  3. Step Mitis
  4. Strep Sangui
  • Commonest inhabitants of the mouth.
  • Common in bacterial plaque and occlusal pits where caries is active.
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15
Q

Strep Mutans

A
  • Involved in the initiation of caries.
  • Strongly acidic.
  • Favourable conditions - Low pH, freely available sugars - the Strep Mutans store a glycogen like reserve polysaccharide.
  • The glycogen can be used as a substrate for acid production when there is no food in the mouth.
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16
Q

Lacto Bacilli

A
  • Acidogenic (ability to produce acid).
  • Present in large numbers in saliva, and present in small number in dental plaque.
  • Numbers increase in plaque after caries has developed, so it is important in progression of the lesion.
  • It was thought to have been the main cause of dental caries because of its large presence in mouths where caries was active. But now we know it becomes more common after caries.
17
Q

Strains of Actinomycetes

A
  • Found when caries is rampant.

- Not been show to be cariogenic in germ free animals EXCEPT in root surface lesions.

18
Q

Pit and fissure caries

A
  • Strep Sangui and Lactobacilli produce some polysaccharides, but not the ones needed to produce caries in smooth surface lesions.
  • In germ free animals, organisms of low cariogenicity have been shown to be able to produce caries in pits and fissures.
19
Q

Acid production in plaque

A

Bacteria produce the enzyme lactic dehydrogenose which converts sugars into lactic acid.

20
Q

Bacterial subtrate

A
  • In a high carbohydrate diet, the microbial composition can change and become acidogenic.
  • This means it is able to produce acid from the fermentable carbohydrates found in the biofilm.
  • Resting pH is lowered because of the acidic products of fermentation.
  • Lower pH favours Step Mutans and Lactobacillus.
21
Q

Step Mutans ability to polymerise sucrose into high molecular weight (long-chains) extracellular polysaccharides appears to be related to…

A
  • Step Mutans ability to initiate smooth surface caries in animals.
  • Strep Mutans ability to form large amounts of adherent plaque.
  • The polysaccharides are referred to as Dextrans and Levans.
22
Q

Dextrans

A
  • Help the Streptococci to adhere to each other on the tooth surface.
  • Important in initiating the attachment of Strep Mutans to the teeth,
  • Major role in building up larger masses of plaque.
23
Q

Sticky insoluble extra-cellular polyglucan produced by…

A
  • Strep Mutans.

- Associated with cariogenicity.

24
Q

Diet studies

A
  • Vipeholm (1945 - 1953).
  • Hopewood House (1948 - 1963).
  • Tristan De Cuna.
25
Q

Vipeholm (1945 - 1953)

A
  • Mentally disabled hospital in Sweden.
  • Investigated the relationship between caries and the ingestion of sugar.
  • Patients were fed large amounts of sugar.
  • Concluded that the risk of sugar increasing caries activity is greatest if the sugar is consumed between meals, and if the food is sticky (stays on the teeth for longer).
26
Q

Hopewood House (1948 - 1963)

A
  • Australian childrens home.
  • Children fed very little refined carbohydrates.
  • Low caries rate in the home compared to other children.
27
Q

Tristan De Cuna

A
  • A remote group of people were evacuated to England after a volcanic eruption.
  • Caries rates increased.
28
Q

Stephans Curve (1940)

A
  • Recorded pH values in the mouth before, during, and after a glucose rinse.
  • After exposure to sugar, pH drops rapidly (in minutes) to pH 5.5.
  • Demineralisation takes places at this pH.
  • After surplus sugar is washed away by saliva, pH does not return to normal.
  • pH stays low for 15-20 minutes.
  • Returns to resting level after an hour.
  • This forms the evidence to avoid sugary snacks between meals.
  • Foods with sticky consistency have a longer clearance time.
29
Q

Susceptible tooth surfaces

A
  • Pits and fissures.
  • Smooth surfaces.
  • Interproximally.
  • Root surfaces.
30
Q

Lesion Types

A
  • Primary.
  • Secondary.
  • Residual.
  • Rampant.
  • Cavitated/Non-cavitated.
  • Active/Inactive.
31
Q

Primary caries

A

Initial lesions developing on intact, natural tooth surfaces.

32
Q

Secondary/recurrent caries

A
  • Occurs underneath or surrounding an existing filling.
  • Can be a primary carious lesion next to an existing filling.
  • Occurs cervically and interproximally due to plaque stagnation.
33
Q

Residual caries

A
  • Demineralised tissue left behind when a filling is placed.
  • Can be active or arrested.
  • Can become remineralised.
34
Q

Rampant caries

A
  • Dental caries in more than 10 teeth.

- Rapidly growing cavities.

35
Q

Cavitated or Non-cavitated

A
  • Early lesion.
  • White spot lesion.
  • Demineralised lesion without evidence of cavitation.
36
Q

Active or Inactive

A
  • Progressing or remineralised.

IARD (6 decks)

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