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BDS2 Caries Symposium > 2 and 3 > Flashcards

2 and 3 Flashcards

1
Q

what oral disease is more prevalent in younger population?

A

caries

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2
Q

what oral disease is more prevalent in older population?

A

periodontal disease

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3
Q

etiopathology

A

origin of disease

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4
Q

what factors do you need to have caries?

A
  • host (tooth)
  • dental plaque
  • diet (drive, feed bacteria)
  • time
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5
Q

how can time impact caries development?

A

frequency
- how many times eat a diet that generates an acid challenge?

more frequent exposure = shorter caries development time

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6
Q

what are the characteristics of bacteria that is most fit for caries development?

A

Bacteria that is most fit for the procedure of installing itself to surface of tooth is the most successful

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7
Q

how do bacteria adhere to tooth surface?

A

Tooth surface (enamel, Apatite) structure is adapted to receive the first coat of proteins
- Sticky out bits are protein – induced by host to coat the tooth
Necessary because surface is harsh and will damage the mucosa and tongue

Protein Coat is a lubricate – protective mechanism

Bacteria has adapted to that surface.

  • Cannot attached to enamel but can to protein coat
  • Surface of protein exposed to external changes conformation and bacteria recognise this when coating the enamel
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8
Q

secondary elements of aetiology of caries

A
  • Fluoride
  • Diet – what and how frequent
  • Microbial/ bacteria species
  • Buffer capacity – saliva
  • Sugar clearance rate – saliva
  • social class
  • education
  • behaviour and attitude
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9
Q

what is caries?

A

Demineralisation of tooth surface produced by bacteria that produce acid (acidogenic bacteria)

  • Progressive demineralising effect
  • Imbalance generate by acidogenic bacteria causes caries
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10
Q

what are the most common acids made by acidogenic bacteria?

A

lactic acid

acetic acid

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11
Q

how are white spot lesions formed?

A

Lesion is promoted by succession of demineralisation and remineralisation and remineralisation of subsurface takes longer than surface

exchange of acids ions inside is more efficient on sub surface as quicker demineralisation of enamel
- Surface is highly mineralised compared to subsurface

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12
Q

why shouldn’t you probe a white spot lesion?

A

can fracture

in tact surface but highly demineralised subsurface

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13
Q

what is the structure of subsurface enamel lesion?

A

enlarged gaps between rods

  • rod becomes thinner so gaps between them become more present
  • crystallites become thinner (rounder shape)

rod length preserved

interrod region damage but the length of rod is preserved

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14
Q

where is the most common area on tooth to get dental plaque?

A

under contact point

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15
Q

what happens to dentine when a white spot lesion is generated on enamel?

A

initial sclerosis of dentine

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16
Q

sclerotic

A

becomes rigid and unresponsive

losing ability to adapt

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17
Q

what is the second stage in enamel white spot lesion after initial sclerosis of dentine?

A

Demineralisation of enamel causes demineralisation of dentine
- Sclerosis progresses

18
Q

what happens after dentine begins to demineralise in enamel white spot lesion progression?

A

continues to demineralise and get new formation of tertiary dentine

tertiary dentine formation begins before any tissue loss
- only mineral loss currently

19
Q

what happens after tertiary dentine formation in enamel white spot lesion progression?

A

cavitation

  • Sclerotic dentine still progressing
  • Increase in tertiary dentine

Progression to reach dentine of cavity
- Presence of microorganism in dentine

20
Q

what is the appearance of an active white spot lesion?

A

chalk appearance

on gingiva margin (can get inflammation as don’)t brush effectively

21
Q

what is the histological appearance of active white spot lesion compared to remineralise white spot lesions? (on SEM)

A

active lesions has rough surface
- crystallites are there but thinner
- blobby arrangement,
reminerlaistion surface becomes smoother.
- Rough means more SA for plaque build up

22
Q

what happens to the pH of mature plaque when exposed to sucrose?

A

pH of mature plaque drops when exposed to sucrose

  • the organic structure of mature plaque restricts the action of saliva buffer
  • Plaque metabolises the sugar so insoluble in structure so affects buffer in saliva

Lower pH and higher H+

Active lesions pH goes below threshold of 5.5

23
Q

what feature of mature plaque aids demineralisation?

A

the organic structure of mature plaque restricts the action of saliva buffer
- Plaque metabolises the sugar so insoluble in structure so affects buffer in saliva

24
Q

what relationship is broken down between in the case of caries?

A

breakdown of balance between remineralisation and demineralisation

25
Q

what should be aimed for to minimise caries formation?

A

maintain pH in a neutral position by reducing sugar frequency

26
Q

what is ecological shift impact on caries?

A

Streptococcus Mutans
– survives well in acid – other species die.
- Fluoride has the ability to stop pump which allows S.Mutans to live in acid bacteria

Lactobacilli
– only in large carious lesions

Acidogenic bacteria– use sugar to make energy and acid
Not early inducers come along and start making plaque

27
Q

what are acidogenic bacteria?

A

use sugar to make energy and acid

Not early inducers come along and start making plaque
- S.Mutans and Lactobacilli

28
Q

what are proteolytic bacteria?

A

breakdown proteins not sugar for energy

S.sanguinis
S.gordonii

29
Q

how are crystallites organised in fissures?

A

they run perpendicular to surface

30
Q

why are pits and fissures more prone to caries than surfaces?

A

Saliva buffers but more at surface regions

Crystallites organised in fissure differently – run perpendicular to surface

Demineralisation at core central region more than surface
- Specific shape triangle base towards dentine

Interproximal other way round

31
Q

what is the characteristic shape of pits and fissure caries?

A

triangle shape

small lesion on surface and larger damage at base

32
Q

what happens to the pace of demineralisation when caries reaches dentine?

A

takes longer to reach dentine but then spreads quickly

- because dentinal tubules branch at ADJ

33
Q

basic steps of process of caries

A
  • plaque bacteria adhere to surface of enamel
  • sclerosis in dentine
  • demineralisation with tertiary dentine formation
  • bacteria invasion
34
Q

how to detect cavitation?

A

Opaque enamel colour due to white spot

Dark grey shadow under enamel – dentine compromised

Clean the tooth and polish and see if can see lesion = cavitation
- Radiographs can confirm

35
Q

what is the physical difference between demineralised and mineralised dentine?

A

demineralised dentine is soft

mineralised dentine is hard

36
Q

what is an active root caries lesion like?

A

wet surface

whereas non active would be dark and non wet

37
Q

why is it hard to restore an active root caries lesion?

A

surrounding material is not hard and strong enough to glue to material
- lacks enamel at lesion (only some cementum and dentine which are not easy to make a good strong bond)

Poor retention
- Fall off – replace – increase cavity size

Procedure can be more harm than good – need to tell patient likely to fail

38
Q

in order to have fluoroapatite in enamel what needs to occur?

A

demineralisation as F needs to substitute in

39
Q

what happens to F concentration when you go deeper into tooth structure?

A

F concentration decreases with depth of tooth

so demineralisation increases

40
Q

what is the caries case for higher calculus levels?

A

less caries

same factors promote caries and calculus (high Ca and PO4 but less H+ so decreased caries risk)

  • high calculus levels tend to have less caries
  • similar de/remineralisation process
41
Q

what is an important element of caries treatment?

A

patient attitude and behaviours change so improved oral hygiene

  • can lead to restoration failure

BDS2 Caries Symposium (5 decks)

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