CARIES- final exam Flashcards
1
Q
name some bacteria involved in the caries process?
A
- streptococcus mutans
- lactobacillus
- actinomyces
- streptococcus sobrinus
- streptococcus salivarius
2
Q
can fungi be associated with dental caries?
A
- yes, cariogenic fungi include Candida albicans.
- C. albicans has been known to cause the expression of S.mutans virulence genes, enhancing the toxicity of the biofilm.
3
Q
what are the properties of streptococcus mutans?
A
- gram positive
- facultative anaerobe (can survive in O2 or de-O2 environment and use O2 if present.
- acidogenic
- acidoduric
- adhesion- by produce EPS for more bacteria to adhere to
- found in early plaque
4
Q
what are the properties of lactobacilli?
A
- gram positive
- acidogenic
- acidoduric
- aerotolerant anaerobe ( can tolerate O2 but do not use it to grow)
- late colonisers
- dentine caries
5
Q
what are the properties of actinomyces?
A
- gram positive
- facultative anaerobe
- sticky branched network (hard to remove)
- seen in root caries
- acidogenic
- acidoduric
6
Q
what are the properties of streptococcus sobrinus?
A
- gram positive
- facultative anaerobic bacteria
- acidogenic
- acidoduric
- early colonisers
7
Q
what are the properties of streptococcus salivarius?
A
- gram positive
- facultative anaerobe
- acidogenic
- acidoduric
- early colonisers
8
Q
what 4 things are needed to cause caries?
A
- time
- sugar (fermentable carbohydrate)
- tooth surface
- plaque biofilm (dysbiotic)
9
Q
what is the main acid produced by cariogenic bacteria?
A
lactic acid
10
Q
what is the process of sugars to lactic acid known as?
A
fermentation
11
Q
describe the vipeholm study.
A
- Vipeholm study was an experiment conducted in a Swedish psychiatric hospital.
- patients were split into groups including those given different forms of sugar at mealtimes, those given sugar between meals, those given sticky sugars at meal times and during meal times.
12
Q
what were the results from the vipeholm study?
A
- sugar causes caries.
- frequency of sugar consumption is important for caries.
- form of sugar is important for caries.
13
Q
what was the issue with the vipeholm study?
A
- highly unethical
- patients did not give consent, and would not have had the capacity to give consent.
- introduced disease into healthy tissues.
14
Q
describe the hopewood house study.
A
- study conducted on 12 year olds at Hopewood house boarding school in Australia.
- consumed a controlled lacto-vegetarian diet (low in sugar)
- 46% of 12 yo were caries-free compared to the 1% of caries free 12 yo at state schools.
- after 12 years of age, when the children left school and had access to sugar- caries rate increased to the same levels of those at state schools.
15
Q
describe the Turku study.
A
- 3 groups were observed over two years in Turku, Finland.
- 3 groups included those consuming sucrose, fructose and xylitol in gum form.
- caries incidence was increased in the S and F groups.
- caries incidence was greater in the S group that F.
- there was an 85% decrease in caries incidence in the X group- suggesting a therapeutic effect on dental caries (remineralisation).
16
Q
describe the alaskan Inuit study.
A
- alaskan inuit eskimos consumed food they hunted- low caries incidence.
- post office and shop were then established in the area.
- this led to a 50% increase in refined carbohydrates.
- causing a 90% increase in DMFT and all previous caries free children developed caries.
17
Q
describe the Tristan da Cuhna sugar study.
A
- Tristan da Cunha is a remote island in the south Atlantic.
- consumed home-grown foods.
- very low caries rate
- volcanic eruption in 1961- inhabitants evacuated to England.
- upon their return caries incidence increased had increased to up to 80% due to consumption of a western diet, high in fat and sugar.
18
Q
what is the specific plaque hypothesis? is this likely?
A
- small number of specific microorganisms leads to disease. If absent, no disease.
- unlikely- as those without caries have cariogenic bacteria in their biofilm, and those with caries have cariogenic bacteria missing from biofilm.
19
Q
what is the non-specific plaque hypothesis? and is it likely?
A
- all microorganisms within a plaque biofilm cause disease.
- unlikely as this would mean those without caries would have 0% plaque- very hard to achieve. Would be higher levels of caries.
20
Q
what is marsh’s ecological plaque hypothesis?
A
- cariogenic bacteria is ubiquitous within a biofilm.
- but at low levels- no disease.
- an ecological shift caused by a local environmental factor (sugar) leads to adaptation and selection of the biofilm to a more acidogenic/acidoduric biofilm e.g S. Mutans
21
Q
describe the histopathology of enamel caries ?
A
- surface zone- highly mineralised and intact.
- body of the lesion- largest part of lesion- greatest demineralisation- seen of RG
- dark zone- demineralisation and remineralisation occurring here.
- translucent zone- 1st carious change.
22
Q
what kind of product is enamel?
A
epithelial product
23
Q
what are the properties of enamel?
A
hard and brittle
24
Q
what is the basic structural unit of enamel?
A
enamel prisms/rods
25
what are enamel prisms composed of?
hydroxyapatite- calcium, phosphate and hydroxyl ions.
26
what are clinical signs of caries?
- WSL
- Cavitation
27
what are the clinical signs of a WSL that is:
- active?
- arrested?
active- rough frosty appearance
arrested- smooth glossy appearance
28
how do you treat WSL?
- OHI
- Diet advice
- Fluoride application- Duraphat if over 16 yo (5000ppm)
29
what can happen to a WSL?
- reverse
- arrest
- cavitate
30
what symptoms can WSL's cause?
31
describe the histopathology of dentine lesions
- advancing front zone- no bacteria but acid demineralisation (lactic acid)
- zone of bacterial invasion- affected dentine- dentine tubules invaded by bacteria- loss of mineral but collagen matrix keeps shape.
- zone of destruction - infected necrotic dentine- collagen matrix has been completely broken down.
32
what do active dentine caries look like clinically?
soft carious dentine
33
what do arrested dentine caries look like clinically?
dark, hard, glossy dentine
34
what are the clinical signs of initial, mod and extensive occlusion lesions?
35
what are the clinical signs of initial, mod and extensive proximal lesions?
36
what are the clinical signs of initial, mod and extensive anterior lesions?
37
what is pulpitis and what causes it?
inflammation of the pulp due to:
- caries
- trauma
- deep restorations
- toothier
38
what is reversible pulptitis?
inflammation of the pulp caused by a noxious stimulus, where the pulp can return to normal state following removal of the causative agent.
39
what are the signs of reversible pulpitis?
- NOT TTP
- caries into dentine
- early carious lesion
40
what are the symptoms of reversible pulpitis?
- sharp pain from stimulus (hot, cold, sweet)- resolved upon removal of stimulus
- short duration
- often occurs when eating
41
what is irreversible pulptitis?
inflammation of the pulpal tissue is more severe and bacteria invades the pulp leading to pulpal necrosis. This cannot be resolved even after removal of the causative agent.
42
what are the signs of irreversible pulpitis?
- mobile tooth
- sinus
- fever
- lymphadenopathy
- extensive marginal ridge destruction
- caries close to pulp on radiograph
- TTP
43
what are the symptoms of irreversible pulpitis?
- pain that keeps you awake at night
- pain even when stimulus is removed
- spontaneous, continuous and prolonged pain
- relieved only by analgesics
44
what does a vital tooth have?
a blood supply
45
how does saliva protect against caries?
- washes plaque and food away
- alkaline and acts as a buffer to maintain pH above critical pH
- contains calcium and phosphate for remineralisation of the tooth surface
- lubricant- deters plaque bacteria from adhering to surface
- contains antibacterial factors such as enzymes and antibodies.
- delivers fluoride to the tooth surface
46
how does fluoride affect the critical pH?
- when fluoride is applied, the OH ions of hydroxyapatite are replaced with fluoride ions.
- this makes enamel more resistant to acid dissolution
- this is because fluorapatitie has a critical pH of 4.5 instead of 5.5 meaning a more acidic env is needed to cause demineralisation, and allows remineralisation to occur at 5.5 pH.
47
what does fluoride do to the salivary composition?
increases calcium and phosphate ions in the saliva which help to remineralise the tooth
48
what else can fluoride do which helps protect against caries?
- bacteriostatic- meaning fluoride inhibits the growth of caries.
- can change the morphology of the tooth- which can result in more rounded cusps and shallow fissures.
- reduces the number of streptococcus mutans.
49
what is the difference between systemic and topical fluoride?
- systemic fluoride is delivered to the circulatory system
- topical fluoride is applied locally to the intended target.
50
what are topical forms of fluoride?
- toothpaste
- mouthwash
- varnish
- drops
- gels
51
what are systemic forms of fluoride?
- fluoridated water
- fluoridated milk
- fluoride tablets
- fluoridated salt
52
what factors contribute to caries or put individuals in the high risk category?
- poor OH
- diet high in sugar
- socio-economic status
- irregular attender
- previous extractions
- history of caries
- family members with caries
- medical hx- cariogenic medications
- xerostomia
- smoking
- disabilities
- fluoride use
- radiotherapy (damages salivary glands causing xerostomia)
- tooth anatomy (deep fissures)
-plaque retentive areas (overhangs, crowding)
- braces
53
how can you detect caries?
- radiographs (bitewings)
- separators
- clinical examination- DRY AND CLEAN TOOTH ALWAYS.
- transillumination
- caries dyes
- fluorescence
54
how often should you be taking radiographs for everyone over 6yo with a
- high caries risk
- mod caries risk
- low caries risk
high- 6 months or until lower risk category
mod- 12 monthly until no active lesions
low- 2 years
55
how are carious lesions classified?
- severity
- location
- active/arrested
- primary/secondary
56
what are rampant caries? where are they normally found? what is a likely cause
- fast progressing caries
- anterior buccal caries
- bottle mouth caries
