caries symposium 2 + 3 Flashcards
what are the 3 main things needed for caries to form
- tooth
- dental plaque
- diet
what is a 4th factor that affects caries formation
time - how often is sugar consumed
what kind of patient can’t get any caries
edentulous patients as have no teeth for caries to from on
can baby’s get caries
yes
- if fed with milk with lots of sugar
- if mother has high caries diet then effects baby’s risk of caries too
how is the enamel structure adapted to receive the first coat of proteins
- first coating is coating that appears after brushing
- is a protective lubricant to stop tooth from harming other soft tissues
- when coating attaches to enamel it changes conformation (however bacteria have adapted to detect this change)
what are the secondary elements fro caries
- perhaps more important than primary
- saliva, capacity of buffering, presence of fluoride, diet etc
- these elements drive caries
secondary elements are also driven by external factors = social class, income, knowledge and education, attitudes and behaviour
what is the definition of caries
- demineralisation of tooth surface caused by acid produced by bacteria - acidogenic bacteria
- breakdown of the balance between demineralisation and remineralisation
does caries happen immediately
no, develops over a long time
how deep does caries go
as deep as it progresses
- has nothing to do with a hole, the hole is a consequence of caries
can demineralised tissue be repaired
- if repaired before cavity is there
- prevention is preferred = avoiding restorative procedures gives better quality of life for patient
how is a bigger lesion exposing the inside of the tooth better than a small lesion
- small lesion may have caries growing underneath along the ADJ
- an exposed lesion can still be brushed at least
- can be restored without exposing the pulp
what can affect how long a lesion will last
the environment in the mouth
what are the 4 parts of a white spot lesion
- surface = 1% mineral loss (still intact)
- body = 5% mineral loss
- dark = 10% mineral loss
- translucent = 20% mineral loss
what promotes a white spot lesion
- a succession of demineralisation and remineralisation
- surface is remineralised first which is why it is less demineralised at the surface compared to the deeper enamel even though the plaque is on the surface
- acid works better in subsurface of enamel than surface due to change in pKa
why should you never probe a white spot lesion
it will likely create a cavity
what is the structure of a white spot lesion
- subsurface is lost
- enlarged gaps between rods = rods become thinner and rounder
- rod length is preserved = crystallites running perpendicular to rod instead of parallel are less likely to demineralise
does a white spot lesion from immediately
no
- there is large time scale before cavitation
- doesn’t happen immediately
what is a good way to allow patients to see how to clean their plaque off
- use a staining chemical to allow them to see where the plaque is and then have them clean it
- will give them a better understanding of how to clean properly
what is inter proximal caries
- a lesion underneath the contact point
- plaque forms here so demineralisation occurs
should you be worried about dark spots
- no, should care about ‘active’ white spots
- the more active/demineralised the white spots are, the brighter more chalky white they become
how do you know the white spot is active
- if the white spot lesion is not at the gingival margin then it is not active as plaque is at gingival margin
- need mature plaque to produce acid - plaque that has been present for a long time
what does an active white spot lesion look like under microscope
- is quite rough
- has larger surface area for plaque to build up
what does an inactive white spot lesion look like
little loss of tissue - around 0.1mm
- can’t restore even if you wanted to as lesion so small
- it is not visible
what must you do for inactive white spot lesions
need to protect it, clean it and give fluoride treatment to it
how can you tell if patient is being non-compliant
- if they come in with white spots along the gingival margin but no plaque there
- shows they know what they are meant to do but don’t do it until they come to the dentist
- shows patient wouldn’t take care of a restoration if given one
- would need to see this patient more often = need to make them understand responsibility to look after their teeth
what does it show if a patient has an inter proximal white spot lesion that is not at the gingival margin and with a missing neighbour tooth
- used to have low compliance but now doesn’t
- this gives a good opportunity to look at the mesial side and ensure it is intact and protected before neighbour tooth erupts as then have limited vision
what can you do for patients with very tight contact points
- put an orthodontic band between the teeth for a few days
- will create a space to work with
what happens when a patient is exposed to sugar
- the plaque pH decreases
- how much it decreases depends on the maturity of the plaque
- mature plaque means it has been there for a longer time and has infrastructure for protection = can reach lower pH
how does mature plaque resist salivary buffering
the organic structure of plaque has matured enough to restrict the ability of buffering
what are the 3 types of lesions
- active carious lesions
- inactive carious lesions
- no visible lesion (sound tooth)
- there is very little difference between inactive lesions and no visible lesion = all to do with diet
what is the pH threshold for plaque to actively form
below pH 5.5
how can you ‘beat’ caries
by increasing remineralisation and decreasing demineralisation
how can you maintain pH
- increase fluoride will make enamel stronger
- reduce sugar intake = frequency
- make environmental change
what is the ecological shift that causes caries to form
- mutans streptococci cause demineralisation
- use sugar to produce energy, as a waste there is acid
- survives well in acid = acidogenic
- has a pump that keeps the inside fresh and alive by removing acid from its body = proteogluco pump
- streptococcus sanguines causes remineralisation
- proteolytic - destroys proteins
- not associated with sugar and don’t like acid
how can fluoride kill mutans streptococci
has ability to damage the proteogluco pump so will damage/kill the bacteria
how can you make a patient less at risk of caries
- dietary advice = change habits
- use fo fluoride toothpaste and varnishes
what do you need to do if you spot a white lesion around a pit or fissure
- don’t probe it, it will breach the enamel
- need to try and identify the cavitation
- as plaque receives sugar it produces acid, and buffering occurs more at surface regions which is why white spot lesions disappear more as you move away from pits and fissures
what happens as you have acid production
there is demineralisation of the crystallites at the core central region - higher concentration of acid there
what shape are pits and fissures lesions
triangle shaped
- base of triangle is towards the dentine
- lesion may be small at the surface but it will have more damage extending out underneath
what happens when the lesion reaches dentine
- spread very quickly
- takes a long time to get there but once there is spreads very fast
- dentine has tubules which branch out so once one is affected at ADJ the rest are soon after
when does tertiary dentine form
- once the lesion has reached dentine, tertiary dentine begins to form
- dentine becomes sclerotic (hard) due to bacterial invasion
what does it mean when there is a dark grey shadowing under the enamel
- means the dentine has been breached
- need to clean the tooth and polish
- can see shadowing due to translucency of enamel
which type of dentine is harder
sound dentine is harder than carious dentine
what is the progression of a carious lesion in dentine from the ADJ to the pulp
area with bacterial invasion -> area with a lot of demineralisation -> area with a little demineralisation -> are a with hard dentine
what is the most worrying looking lesion
when it looks wet and soft
- means it is the most active
what is the least worrying looking lesion
when it looks hard and dark
- means it has been there for a long time
- looks the worst but is actually inactive caries (arrested caries) so is least worrying
what is arrested caries
caries that is no longer active
why is it difficult to restore the very active caries at the gingival margin of the tooth
- usually when resting we use the surrounding material but don’t have a lot of that here
- mainly just dentine there which is hard to work with
- can restore with some sort of retention but it will likely just fall off
- restoration here do more harm than good so just need to try and persuade patient to not have one
where is there a higher concentration of fluoride
on the surface of a tooth
why do we need demineralisation to happen to help remineralisation
- fluoride is on enamel
- need demineralisation of enamel as this will cause the deposition of hydroxyapatite form fluoride to bind to to from fluorapatite instead of HA = fluoride is stronger
what happens to apatite over time
- HA crystals get ion substitutions by Mg2+, CaO3 and Fl|-
- structure changes over time
- as apatite is converted, you lose areas of carbonated apatite
do patients with a high concentration of calculus have high or low amount of caries
- low amount
- have a higher concentration of PO4 and a higher acid concentration so not suitable conditions for caries to form, just calculus
what does caries show up as on a radiograph
grey shadowy areas
- dark/black areas on radiograph is not caries, these are spaces
why are radiographs not perfect
they are 3D projections condensed into 2D images
- they should only be used as supporting elements
how can changing the aspect of a radiograph help see caries
can help see the depth of the damage caused by caries
