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CARIES - FINALS PREP > CARIES > Flashcards

CARIES Flashcards

1
Q

what is the aetiology of caries - VENN DIAGRAM

A

BACTERIA, TIME, TOOTH SURFACE, SUGAR

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2
Q

how does caries occur/how does it form

A

FERMENTATION PROCESS, lactic acid produced as a by-product of dietary carbohydrate metabolism by plaque bacteria resulting in drop of pH at tooth surface.

Calcium and phosphate ions (hydroxyapatite) diffuse out of enamel resulting in demineralisation

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3
Q

What PREVENTION METHODS ARE THERE/WAYS CAN WE PREVENT the development of carious lesions (4)

A

OHI
fissure sealants
fluoride
dietary advice

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4
Q

why do we place fissure sealants ?

A

to create shallower fissures to remove the stagnation area for plaque to accumulate within the fissures

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5
Q

describe the clinical process when placing a fissure sealant

A

firstly, etch placement - orthophosphoric acid (37%) for 15 SECONDS
wash and dry until frosty appearance
apply fissure sealant resin and cure

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6
Q

Why might we not place a fissure sealant / contraindications to placing a fissure sealant (3)

A
  • moisture control an issue - need effective moisture control here due to nature of material / longevity of it
  • no pt co-operation
  • partial eruption - stagnation area for plaque due to operculum etc
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6
Q

Describe the 1901 mcKay fluoride theory

A

The McKay Fluoride Theory, introduced in 1901 by Dr. Frederick McKay was a postgrad dentist wanting to set his own business up in Colorado Springs when we notices that natives of the area had brown discoloured teeth. This made him want to investigate this further and in conclusion of his research, he proposed that fluoride naturally present in water could prevent tooth decay by strengthening tooth enamel. This discovery emerged from McKay’s investigation into the cause of “Colorado Brown Stain,” a discoloration on teeth in certain regions. McKay’s findings paved the way for further research into fluoride’s dental benefits and eventually led to the implementation of water fluoridation programs worldwide to improve dental health.

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6
Q

describe what etch does to enamel

A

it ALTERS THE SHAPE OF THE PRISMS 3 WAYS
1. removes the CORE
2. removes the PERIPHERY
3. ‘haphazard’ effect - can go either way

the changes of the prisms creates micromechanical retention on the surface of enamel (finger like projections that allow the material to bond to the enamel)

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6
Q

Describe the modes of action that fluoride can have on teeth/enamel etc (4)

A
  1. Calcium fluorapatite forms when fluoride is present and changes the structure of calcium hydroxyapatite (during the remin process)
    Fluoride ions replace the OH (hydroxyl) ions. this makes calcium fluorapetite
    Fluorapatite is LESS soluble than Hyroxyapatite under acidic conditions meaning it can withstand further acidic attacks.
    Because of the replacement of the ions we get calcium fluorapatite CRYSTALS - this has a critical pH of 4.5 (can withstand more of an acidic environment!)
    REMEMBER critical pH of mouth is 5.5! (when the pH drops below this point, your teeth start to demineralise)
  2. has an effect on plaque bacteria - fluoride has bacteriostatic (inhibits growth) and bactericidal properties (kills bacteria)
  3. fluoride PROMOTES REMINERALISATION
  4. can have an effect on tooth morphology - can get more rounded cusps, flatter fissures meaning that there is a decrease in stagnation areas for plaque. This would have to be given when teeth are developing!
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7
Q

what can methods of fluoride delivery be broken down into?

A

SYSTEMIC DELIVERY AND TOPICAL DELIVERY

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8
Q

Describe some SYSTEMIC ways of delivering fluoride (5)

A
  • water
    -drops
    -tablets
    -milk
    -salt
    ALL OF THESE ARE FLUORIDATED.
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9
Q

Describe some TOPICAL ways of delivering fluoride

A
  • fluoride varnish (22600 ppm SODIUM FLUORIDE)
  • Mouthwashes
    -APF gels (Acidulate Phosphoric Fluoride)
    -toothpastes
    -salt
    -milk
    -water
    -tabs
    -drops
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10
Q

speaking of caries and DIET, what evidence is there to show that sugar causes caries

A

Turku, Vipeholm, Hopewood House, Inuit, tristan da cunha

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11
Q

what 3 conclusions came from the Vipeholm caries study

A
  1. type of foodstuff is important (consistency) ie sticky consistencies higher probability of causing caries
  2. sugar causes caries
  3. FREQUENCY of sugar intake
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12
Q

What is important when we are giving our patients diet advice (what things do we want to be looking out for)

A
  • HIDDEN SUGARS (people may mis-interpret this for being low in sugar)
  • acidic foods/drinks
  • alcohol (this also provides an increased risk of getting oral cancer)
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13
Q

how can we classify caries / what are the different classification systems? (4 diff according to)

A

ACCORDING TO SEVERITY WE HAVE:
- ICDAS (international caries detection assessment system)
- e1,e2,e3 etc
- d1, d2, d3 etc
- DMFT (decayed, missing and filled teeth)

ACCORDING TO LOCATION:
- surface
- tooth substance (enamel or dentine)
- is it anterior or posterior

ACCORDING TO PRIMARY/SECONDARY CARIES:
- initial lesion (primary)
- around existing restoration (secondary)

ACCORDING TO ACTIVE/ARRESTED

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14
Q

what are the different factors that may make someone incur a high caries risk (8)

A

previous caries/restorations
siblings that have had caries/have caries
high sugar diet
poor/inadequate OH
SIMD (Scottish index of multiple deprivation)
fluoride/water/toothpaste
medically compromised
quantity/quality of saliva present

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15
Q

what can MANAGEMENT of caries be split up into? - 2 ways

A

PREVENTITIVELY (on a wsl - white spot lesion) or OPERATIVELY (into dentine)

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16
Q

In terms of OPERATIVELY managing caries, when should we ALWAYS restore?

A

always restore OCCLUSAL caries - this is due to the way/pattern it spreads

nowadays we can restore proximal lesions. WE ONLY INTERVENE in more than or equal to 50% of dentine is affected or if it is VISIBLY cavitated (hence why we place separators)

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17
Q

list the 4 stages within the histopathology of ENAMEL caries

A
  1. translucent zone
  2. dark zone
  3. body of lesion
  4. surface zone
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18
Q

describe the translucent zone

A

1st carious change, FEW large pores due to loss of prism periphery which can be penetrated by quinoline

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19
Q

describe the dark zone

A

turns dark brown w quinoline, consists of large and small pores, NOT penetrated by quinoline, de-mineralisation and re-mineralisation occur here

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20
Q

describe the body of lesion

A

this is the largest part and centre of the lesion - area of greatest demineralisation, enamel is relatively TRANSLUCENT here, corresponds to the radiographic appearance (what we see on rads)

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21
Q

Describe the surface zone

A

this zone appears almost unaffected !
minimal demineralisation and greater fluoride concentration

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22
Q

what are primary caries

A

lesions on UNRESTORED TOOTH SURFACE

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23
Q

what are secondary caries

A

lesions that developed NEXT TO A FILLING

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24
Q

what is residual caries

A

demineralised tissue that has been left behind before a filling has been placed - by the operator

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25
Q

how can we describe rampant caries

A

This is the name given to multiple active carious lesions occurring in the same patient. this frequently involves surfaces of teeth that do not usually experience dental caries eg bottle or nursing caries, drug-induced caries.

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26
Q

what are the 3 way to classify dentine

A
  1. developmental : mantle and circumpulpal dentine
  2. primary, secondary, and tertiary
  3. tubule : peri-tubular or intra-tubular
    inter-tubular dentine
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27
Q

Describe the histopathology of dentine caries

A

3 zones:
1. Zone of destruction (necrotic dentine here)
2. Zone of bacterial invasion (lactic acid)
3. Advancing front of lesion (closest to pulp - only acid here! - no bacteria)

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28
Q

describe the definition cariogenic

A

ability to CAUSE disease/caries

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29
Q

describe the definition ACIDOGENIC

A

ability to produce acid (lactic acid in this case for caries)

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30
Q

what are the different bacteria causing caries

A

streptococcus mutans - Gram positive aerobic which is aciduric and acidogenic
lactobacilli - Facultative anaerobe
actinomyces - ROOT CARIES
staphylococcus aureus
staphylococcus anginoses

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31
Q

Describe the systemic fluoride dosages that we should follow

A
  • no fluoride supps from 0-6months
  • give 0.25mg for 6months-2years
  • give 0.50mg for 2years-6years
  • 1mg for 6years +
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32
Q

Describe the turku sugar study

A
  • Turku, Finland, main aim was to compare the cariogenicity of sucrose fructose and xylitol.
  • results of the study showed that both sucrose and fructose were cariogenic. - sugars caused caries
33
Q

Describe the Hopewood house study

A

An Australian boarding school for delinquant children.
They had a very strict lacto-vegetarian diet (low in sugar) compared to state schools.
When they left there was a massive increase in caries due to the high sugar diet they were now eating.

34
Q

Describe the process that caries management can be viewed as a process of? (5 R’S)

A

RECOGNITION of the disease and contributory factors
RE-ORIENTATION of contributory life-style factors
REMINERALISATION of all lesions - visible and not visible, cavitated and non cavitated
REPAIR where no other treatment option is possible
REVIEW of the oral health and situation

35
Q

What happens if you ingest too much fluoride ?

A
  • nausea and vomiting associated with the ingestion of topical fluorides
  • dental fluorosis while tooth enamel is developing until about age 6 due to daily ingestion of fluoride
  • can develop rapidly
36
Q

Describe the ways we can clinically detect caries

A

Radiographs
Spacers so we can see ID
transillumination
caries detection dyes
dry the tooth well with 3 in 1
clinically
fluorescence wans

37
Q

What role does saliva play in PREVENTION of caries?

A

90% of saliva is produced by THREE pairs of major glands: parotid, submandibular and sublingual.
- its FLOW helps to clear the mouth of food and cellular and bacterial debris
- regulates the pH of the oral cavity
- helps to maintain integrity of teeth due to its calcium and phosphate content. Meaning tooth dissolution is prevented
- saliva has antibacterial and antiviral properties too.

38
Q

Describe how caries occurs (stages rather than histopathology) 4

A
  1. plaque covered surface
  2. acid production in plaque
  3. acid penetration into enamel
  4. initial response of dentine to acid - retreat of odontoblast process, laying down of peri-tubular dentine, translucent appearance to dentine
39
Q

what is the SEQUELAE of enamel caries

A

= arrest or remineralisation - pre clinical lesion, pre-white spot
= cavitation - non cavitated white spot or brown spot!

40
Q

List the 3 principals (primary, secondary, tertiary) of prevention in caries management

A

PRIMARY PREVENTION - diet and fluoride - active remin) this prevents the disease from ocurring or REVERSE the disease that has ocurred

SECONDARY PREVENTION - (arrest lesions, seal lesions, cut out caries and seal) -this stops the disease from progressing

TERTIARY PREVENTION (extraction) - this is removal of the diseased part to prevent further complications

41
Q

describe the role that saliva plays in caries

A

saliva = intra-oral antacid, due to alkali pH at high flow rates, and buffering capacity.
- it decreases plaque accumulation: antacids clear foodstuffs
- acts as a resivour of calcium, phosphate and fluoride ions FAVOURING REMINERALISATION
- antibacterial action due to diff immune cells, enzymes etc
- sugar fre gum regularly after meals appears to reduce caries, but reduction is small!

42
Q

Describe some properties of Lactobacilli (6)

A
  • After streptococci, lactobacilli are the most important group of bacteria involved in dental caries
  • Lactobacilli are gram POSITIVE
  • facultative anaerobe
  • acidogenic/aciduric
  • adheres/sticks to DENTINE
  • over represented in ADVANCED carious lesions
43
Q

Describe some properties of Actinomyces(6)

A
  • Gram POSITIVE pleomorphic rods
  • Found approximal and within gingival crevice on tooth surface, also found in supra and sub-gingival plaque
  • historically reported as being associated with root surface caries, where the roots of the teeth are exposed and become carious therefore increase IF GINGIVA HAVE RECEEDED EXPOSING THE ROOT
  • Arranged in pairs, short chains or clumps
  • Facultative anaerobe
  • NON-MOTILE
44
Q

Describe the structure of enamel

A

enamel is made up of enamel prisms - an arrangement of hydroxyapatite crystals
these prisms consist of a prism core and a prism sheath
core= tightly bound hydroxy crystals
sheath = crystals less tightly packed, more space for organic components

45
Q

What path do enamel prisms follow?

A

FOLLOW THE PATH OF THE AMELOBLASTS

46
Q

What does the gnarled enamel do for the cusps of teeth / how does it become gnarled

A

provides strength
due to the prisms taking an undulating course, twisting around one another

47
Q

CLINICAL APPEARENCE OF ENAMEL CARIES/
SIGN OF ARRESTED ENAMEL CARIES

A

WHITE SPOT LESION, requires clean and dry teeth to be seen, matt appearence too
ARRESTED = SHINY AND GLOSSY

48
Q

What is in the dentinal tubules

A
  1. no cell process, just fluid
  2. odontoblast process
  3. odontoblast process and nerves
49
Q

Describe the classifications of dentine

A
  1. Developmental:
    - mantle dentine
    - circumpulpal dentine
  2. Primary, Secondary, Tertiary
  3. Tubule:
    - Peri-tubular
    - inter-tubular
50
Q

Describe the histopathology of dentine caries

A

Advancing front
Zone of bacterial penetration
Zone of destruction

51
Q

what occurs at the advancing front

A
  • zone of demineralised dentine
  • acid demineralisation, no bacteria here
52
Q

what occurs at the zone of bacterial penetration

A

AFFECTED DENTINE - dentine tubules are invaded by bacteria/demineralised but holds shape as collagen matrix is not broken down ie it is firm

53
Q

what occurs at the zone of destruction

A

infected dentine, collagen breakdown loses its shape resulting in soft carious dentine

54
Q

What 3 types of diagnosis do we have

A
  1. provisional - formed on the initial info gathered , still need to conduct special tests and investigate further eg rads
  2. differential - a list of possible conditions or diseases that present with similar signs/symptoms
  3. definitive - the FINAL diagnosis , an accumulation of the history etc etc
55
Q

What considerations should we take into account when treatment planning? (8)

A
  • the patient/dentist relationship - deally a match between what the patient wants and what the patient needs!
  • patients understanding and attitude about dental care / there prev exp
  • consider a simple procedure first to gain the patients trust
  • the pts age eg if young consider tooth eruption, larger pulp chambers ets
  • caries risk!
  • pts ability to tolerate treatment and maintain treatment provided
  • pts attendance record
  • pts financial considerations. cost of treatment should be discussed at the treatment planning phase.
56
Q

What are some DENTAL CONSIDERATIONS to take into account when treatment planning (5)

A
  • OH status, and patient cooperation and motivation
  • control of dental caries, tooth wear and perio disease
  • pulpal status of individual teeth
  • aesthetics of the dentitions
  • restorability of the teeth
57
Q

the aim of treatment is to provide 3 things:

A
  1. functional dentition
  2. dentition that is free from discomfort and disease
  3. dentition that is aesthetically pleasing
58
Q

Describe how dental plaque can occur on a tooth

A
  • the formation of a PELLICLE - this is an acellular protinaceous film, derived from saliva which forms on the ‘naked’ tooth surface
  • within hours, single bacterial cells colonise on the pellicle - a large portion at this point are streptococci
  • within 1-14 days, the streptococcus DOMINATED plaque changes to a plaque dominated by actinomyces
59
Q

What does MICROBIAL SUCCESSION mean

A
  • this is when the bacterial species become more DIVERSE eg actinomyces is more harmful than streptococci and the microbiome continue to grow
60
Q

What is the NON-SPECIFIC plaque hypothesis?

A

considered the carious process to be caused by the overall activity of the total plaque microflora. A consequence of this approach is that all plaque should be disturbed by MECHANICAL plaque control.

61
Q

Describe the specific plaque hypothesis?

A

only a few organisms out of the diverse collection in the plaque flora were actually involved in the disease

62
Q

what is the ecological plaque hypothesis

A
  • this is a process that the organisms associated with disease may be present at SOUND sites.
  • Demineralisation will result from a shift in the balance of these microflora driven by a CHANGE in the local environment .
63
Q

Describe the term bottle caries or nursing caries

A
  • names used to describe a particular form of RAMPANT caries in the primary dentition of infants and young children.
  • problem is found in an infant or toddler who falls asleep sucking a bottle which has been filled with sweetened fluids
64
Q

briefly describe the vipeholm study

A
  • Sweden 1939, vipeholm hospital and institution for MENTALLY HANDICAPPED individuals
  • was a study on the relationship between DIET AND DENTAL CARIES
  • the patients were divided into one control and six experimental groups
  • 4 meals were eaten daily and for one year patients received a diet relatively low in sugar. during this time the no of new carious lesions was assessed and found to be very low.
  • the experimental groups, had a marked increase in caries except when sugary foodstuff was taken at MEAL times.
65
Q

Describe an animal study that showed plaque causes caries/oral microflora needed to be also present for the aetiology rather than just sugar alone…

A
  • rats under GERM-FREE conditions was taken out
  • these rats had no bacteria in mouth, were fed a cariogenic diet, caries did not develop
  • this showed that a cariogenic ORAL MICROFLORA (plaque bacteria) is essential for the development of dental caries
66
Q

What do we mean by INTRINSIC sugars?

A

Sugars that are INtegrated into the cellular structure/vesicle of food eg fruit

67
Q

What do we mean by extrinsic sugars?

A

these are sugars present in free form eg table sugar or added to food eg sweets/biscuits

68
Q

What may a low grade, long-lasting stimulus result in regarding the pulp?

A

CHRONIC inflammation

69
Q

What type of inflammation is present when there is a severe stimulus

A

ACUTE pulpitis / pulp inflammation

70
Q

Clinically, what do actively progressing lesions look like in dentine?

A

they are SOFT and WET - infected dentine here (zone of destruction!)
because of the SPEED of development of the lesion, the defence reactions will not be well developed.

71
Q

Clinically, what does arrested/slowly progressing caries look like

A
  • a hard and leathery consistency (affected dentine - zone of penetration) - slower progression
  • arrested - dark in colour and firm to probe with - ONLY USE BALL ENDED PROBE
72
Q

Why is diagnosis of caries important? - 3 reasons

A
  • forms the basis for a treatment decision (active lesions require some form of active management whereas arrested lesions do not)
  • we are informing the patient - the patient is the central to the management of the carious process.
  • advising health service planners - epidemiological surveys inform the politicians who commission the state of health and disease of the population.
73
Q

Describe the ‘iceberg of dental caries’

A

NAC (no active care advised) to PCA (preventitive care advised)

PCA to P&OCA (prevenitive care advised to preventitive and operative care advised

74
Q

Describe the flossing technique (3)

A
  • fingers holding the floss should not be more than half an inch apart
  • the floss should be guided slowly through the contact point then wrapped around the interproximal surface of each tooth in turn into anatomical width of gingival crevice
  • a clean SECTION of floss should be used for each IP space
75
Q

What are the PRINCIPAL strategies for managing caries in the PRIMARY dentition - 4 STRATS

A
  • NO caries removal - SEAL with a crown using the Hall Technique
  • no caries removal and fissure seal
  • selective caries removal and restoration (walls prepared to hard/scratchy dentine with adequate depth for restorative material)
  • pulpotomy - vital radicular pulp
76
Q

When a restoration involves the distal of an E (primary dentition), what may be the best technique especially if the 1st permanent molar is growing in.

A

to avoid iatrogenic damage to the adjacent proximal surface of the tooth, we would possibly indicate the hall crown technique as this is minimally invasive.

77
Q

What if a child is not able to tolerate any type of sealant to seal in initial occlusal caries- even gi

A

HALL TECHNIQUE

78
Q

What does cavitation/shadowing indicate on a tooth

A

the lesion has extended into dentine and is an indication to check radiographically the extent of the lesion and adjacent teeth

79
Q

what is the aim when treating reversible pulpitis

A

to remove pain and avoid the disease progressing to pulpitis with irreversible symptoms

80
Q

treatment in a primary tooth with reversible pulpitis symptoms…. is….

A

place a crown using the Hall Technique
IF an OCCLUSAL lesion - carry out SELECTIVE caries removal, avoiding the pulp, and restore using composite, GI.

81
Q

What is the treatment option in a primary tooth for irreversible pulpitis symptoms

A

THE PULP HERE IS STILL VITAL but it is inflammed/coronal portion of the pulp - trying to keep the radicular pulp vital here!
- treatment may be a pulpotomy or xla. (if coop allows and if tooth necrotic)

82
Q

what does site-specific prevention involve?

A

demonstrate effective brushing of the lesion
give diet advice
apply fluoride varnish to the lesion four times a year

83
Q

what are the 4 main lactic acid producing oral microbes?

A

ORAL STREP - REMEMBER THE 3 MAIN TYPES
LACTOBACILLI
ACTINOMYCES (historical link to root surface caries)
ROTHIA DENTICARIOSA

84
Q

what is the importance of air drying a tooth to detect caries?

A
  • sound enamel is translucent and microporous
  • where an enamel lesion is seen when wet it has greater porosity than a lesion seen only when dehydrated
  • first sign of carious change in enamel is a change in translucency seen only on dehydrated surface! - hence why we dry!

CARIES - FINALS PREP (4 decks)

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