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DS1102 > Week 4 - Intro to the Management and Treatment of Dental Caries and Minimally Invasive Dentistry P1 > Flashcards

Week 4 - Intro to the Management and Treatment of Dental Caries and Minimally Invasive Dentistry P1 Flashcards

1
Q

What are the 2 types of damage to teeth

A
  • carious
  • non carious
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2
Q

What is carious damage

A

damage to tooth structure due to bacteria

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3
Q

What is non carious tooth damage

A

damage to the tooth not due to bacteria

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4
Q

What are the 3 types of non carious damage to teeth

A
  • tooth wear
  • developmental defects
  • trauma
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5
Q

What is tooth Wear

A

it is irreversible loss of surface of dental hard tissues caused by factors other than caries or trauma

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6
Q

What are the 4 types of tooth wear

A
  • Erosion
  • Attrition
  • Abrasion
  • Abfraction
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7
Q

What is erosion

A

irreversible loss of tooth substance brought about by a chemical process that does not involve bacterial action.

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8
Q

What are the causes of erosion

A
  • intrinsic acid (gastric acid)
  • Extrinsic Acid
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9
Q

What are the 2 types of intrinsic acid

A

Involuntary - gastroesophageal reflux, vomiting due to medical conditions

Voluntary - Bulimia nervosa/ other conditions which involve induced vomiting

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10
Q

What are the 2 types of extrinsic acid

A

Dietary - acidic food and drinks e.g. lemonade, fruit juice, fizzy drinks, alcohol

Environmental - acid fumes inhalation

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11
Q

What is attrition

A

the mechanical wear due to tooth to tooth contact

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12
Q

What are the causes of attrition

A
  • functional
  • parafunctional wear
  • Proximal wear
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13
Q

What is the functional cause of attrition

A

Functional wear occurs during normal activities like chewing (mastication). It involves the natural and gradual wearing down of tooth surfaces as part of regular tooth-to-tooth contact

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14
Q

What is the parafunctional wear cause of attrition

A

Parafunctional wear occurs due to abnormal or excessive tooth contact that is not related to normal chewing such as teeth grinding, clenching, nail biting

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15
Q

What is the proximal wear cause of attrition

A

Proximal wear refers to the wear that occurs on the contact surfaces between adjacent teeth. This occurs as teeth naturally move medially causing teeth to rubbed each other during physiological tooth movements and natural aging.

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16
Q

What is abrasion

A

Mechanical/frictional wear due to tooth to non-tooth contact
- leads to more rounded tooth lesions

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17
Q

What are causes of abrasion

A
  • Tooth brushing using coarse abrasive (smooth notches V shaped at the neck of teeth)
  • Habits - nail biting, bottle opening, chewing pen
  • Chewing on abrasive materials/food
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18
Q

What is abfraction (Idiopathic erosion)

A

type of tooth wear that occurs when a tooth is subjected to abnormal mechanical forces, leading to the loss of tooth structure, particularly in the cervical area (the area where the tooth meets the gum). This form of wear typically results in a V-shaped notch at the gum line of the tooth

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19
Q

What are the 2 types of trauma - type of non carious damage

A
  • Accidental e.g. skateboarding, biking
  • Non-accidental (violence)
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20
Q

What are the 2 types of developmental non carious damage

A
  • hereditary developmental defects
  • non hereditary developmental defects
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21
Q

What is amelogenesis and is it hereditary or non hereditary development defects

A
  • hereditary
  • defective enamel in formation/development or calcification
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22
Q

What is Dentinogenesis and is it hereditary or non hereditary development defects

A
  • hereditary
  • Dentin is defective causing early loss of overlying
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23
Q

What is hypoplasia and is it hereditary or non hereditary development defects

A
  • Non hereditary
  • the underdevelopment or incomplete development of enamel, resulting in enamel being thinner than normal
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24
Q

What is hypomineralisation and is it hereditary or non hereditary development defects

A
  • non hereditary
  • where the enamel of the teeth is softer and less mineralized than normal, referring to enamel that forms with a normal thickness but with a deficient mineral content, making it weaker and more susceptible to damage.
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25
Q

What are caries

A

biofilm mediated, sugar driven, multifactorial, dynamic disease process resulting in phasic demineralization and remineralization of the tooth.

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26
Q

What is dental plaque

A

firmly adherent microbial biofilm attached to teeth and is the prime etiological agent of dental caries and periodontal disease.

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27
Q

What can caries be described according to

A
  • location - pit and fissure, smooth surface, root surface, residual (intentional leaving caries behind), secondary
  • direction of progression - forward /backward caries
  • zone - enamel/dentin caries
  • extent - incipient/reversible or cavitated/irreversible
  • progression rate - acute/rampant or chronic/arrested
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28
Q

What are the main sights which plaque forms

A
  1. Margins between the tooth and gum
  2. Fissures in the occlusal surfaces of molars
  3. The approximal or interproximal areas
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29
Q

What are the main factors for caries formation

A
  • Teeth
  • Time
  • Fermentable carbohydrates
  • cariogenic biofilm
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30
Q

What are primary modifying factors for caries formation

A
  • tooth anatomy
  • saliva
  • biofilm pH
  • biofilm composition
  • use of fluoride
  • diet specifics
  • oral hygiene
  • immune system
  • genetic factors
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31
Q

What are secondary modifying factors for the formation of caries

A
  • Socioeconomic status
  • Education
  • life style
  • environment
  • age (lifestyle at certain ages)
  • Ethnic group culture
  • Occupation (chief)
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32
Q

What is stephan’s curve

A

Showcases the decrease in plaque pH followed by remineralisation which occurs after 30-60min

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33
Q

What are factors which increase demineralisation (pathological factors)

A
  • Cariogenic bacteria
  • reduced salivary flow
  • frequent fermentable carbs
  • Poor oral hygeine
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34
Q

What are factors which increase remineralisation (protective factors)

A
  • Good salivary flow and quality
  • goof oral hygeine
  • FI, calcium and phosphate
  • Strategies to maintain healthy microbiome (probiotics, prebiotics)
  • pH modifiers (xylitol)
  • strategies to modulate dysbiotics microbiome
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35
Q

What are rampant caries

A

accelerated rate of caries with multiple carious lesion

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36
Q

Who do rampant caries usually occur in

A
  • Infants - nursing bottles for prolonged periods in the mouth
  • Teenager/young adults - high cariogenic diet and recreational drugs
  • Adult patients - xerostomia due to medication or medical conditions
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37
Q

What are arrested caries

A

lesions that have stopped progressing and are inactive

38
Q

What is caries progression in enamel caries

A
  • Surface demineralization causes enamel prism porosities forming white spot lesions (these are reversible with OH)
  • Progression of caries microscopically occurs in an inverted triangle shape towards the dentin enamel junction
  • White spot lesions are porous hence they can get stained easily and form brown spot lesions
39
Q

What is caries progression with caries at dentine enamel junction

A

Caries lesion extends laterally and then starts penetrating the dentine in another inverted triangle shape.

40
Q

What is the progression of caries in dentine

A
  • One in dentine caries creates a visible gray shadow which can be seen
  • Can cause acute pulpal response (pulpitis) to hot/cold/sweet
41
Q

What is minimal invasive dentistry

A

It is a philosophy or part of Dentistry concerned with the first occurrence, early detection and earlies possible cure of damaged and defective tooth structure on a micro level followed by minimally invasive treatment in order to repair irreversible damages caused by the disease.

42
Q

Does restorative treatment cure the caries process

A

no
Instead identifying and managing the risk factors for caries must be the primary focus, in addition to the restorative repair of damage caused by caries.

43
Q

What is Code 0

A

sound tooth surface, no evidence of caries after 5s of drying

44
Q

What is code 1

A
  • First visual change in enamel
  • opacity or discolouration (white or brown) is visible at the entrance to the pit or fissure seen after prolonged air drying
45
Q

What is code 2

A

Distinct visual change in enamel visible when wet, lesion must be visible when dry

46
Q

What is code 3

A

localised enamel breakdown (without clinical visual signs of dentinal involvement) seen when wet and after prolonged drying

47
Q

What is code 4

A

underlying dark shadow from dentine (with or without enamel breakdown)

48
Q

What is code 5

A

Distinct cavity with visible dentine (less than half the surface)

49
Q

What is code 6

A

Extensive (more than half the surface) distinct cavity with visible dentine

50
Q

What are used to detect caries

A
  • visual and clinical methods (mirror and probe, magnification)
  • radiographs (intraoral e.g. bite wings, extraoral e.g. OPG)
  • Optical/trans illumination (intraoral cameras/LED cams
  • Tooth separators
51
Q

What are the 4 principles of caries management in MID

A
  1. Disease control by reduction in cariogenic bacteria
  2. remineralization of early lesions
  3. avoid removal of tooth structure in excess to absolutely required to restore to their normal conditions
  4. Use of dental material to conserve biological cost of tooth structure.
52
Q

What are the 4 types of caries treatment

A
  • Non-invasive (OHI, Topical Fluoride, Varnish)
  • Micro-invasive (Pit and Fissure sealants)
  • Selectively invasive (partial caries removal to minimise biological cost)
  • Invasive (conventional preps and restorations)
53
Q

What are preventative treatments for caries

A
  • fluoride
  • Casein Phospho peptide-amorphous calcium phosphate (CPP-ACP) has been proven superior to fluoride products for the depth of remineralization (e.g. tooth mouse)
  • Xylitol products have been proven to starve out the cariogenic bacteria and promote the proliferation of good bacteria
  • Dental Ozone
54
Q

What is dental ozone

A

refers to the use of ozone a molecules composed of 3 oxygen atoms O3 in dental treatments

55
Q

What are the functions of dental ozone

A
  • Kills >99% of microorganisms in the carious lesion at a concentration of 2200ppm
  • Oxidizes caries and speeds up remineralization
  • helps to remove organic debris on the carious lesion
  • Potentially whitens discolored caries
  • Decreased treatment time
  • Treatment painless and noiseless
  • Does not cause any allergic reaction
  • Microorganisms do not develop resistance to ozone
56
Q

What are the contradictions for the use of ozone

A

When there is no gas scavenging system available it is highly irritating to eyes and lungs

57
Q

What are alternatives to using drilling tools

A
  • air abrasion
  • Hard tissue laser
  • Chemo mechanical caries removal
58
Q

What are air abrasion tools

A
  • Removes hard substances by impacting abrasive particles in a stream of air or air and water
  • Air prophylaxis units use non abrasive powder (flavored sodium bicarbonate) designed to remove plaque and staining without any damage to tooth structure
  • Doesn’t work on soft structures very well (can cause soft tissue trauma if uncontrolled)
  • Can be quite messy if not properly evacuated
59
Q

What are hard tissue lasers

A
  • Hard tissue laser for accessing enamel/dentine caries
  • Required skills and precision hand control
60
Q

What are chemo mechanical caries removal

A
  • Use of sodium hypochlorite (NaOCl) to dissolve carious dentine
  • Other formulations without NaOCl have also been developed

E.g. Caridex and Papacarie

61
Q

What are the different types of dentine

A
  • Soft Dentine/Infected Dentine
  • Firm Dentin/Affected Dentin
  • Hard Dentin
62
Q

What is soft dentine

A
  • infected dentin
  • necrotic (bacterial contamination)
  • outer most carious dentin
  • low mineral content and irreversibly denatured collagen
  • soft dentin typically does not self-repair
  • Clinically it lacks structure and can be easily excavated with hand and rotary instrumentation
63
Q

What is firm dentin

A

Affected Dentin

  • Inner carious dentine
  • Demineralization of intratubular dentin and of initial formation of intratubular fine crystals at the advancing front of the caries lesion.
  • Transparent appearance
  • Softer than hard normal dentin
  • Clinically it is resistant to hand excavation and can only be removed by exerting pressure
64
Q

What is Hard Dentin

A
  • Deepest zone of a caries lesion - assuming the lesion hasn’t reached the pulp and may include tertiary dentin, sclerotic dentin and sound normal dentin
  • Clinically this dentin is hard and cannot be easily penetrated with a blunt explorer and can only be removed by a bur or a sharp cutting instrument
65
Q

What type of dentin can serve as a template for remineralisation

A

Sclerotic dentin,
Firm (affected) dentin

66
Q

What is reparative dentin

A

The biological regeneration of dentin from new odontoblast-like cells when a dental injury is severe and reaches up to the dental pulp

67
Q

What is the most common denominator in multifactorial tooth wear

A

erosion

68
Q

What type of dentine has a leather like consistency

A

Affected dentine

69
Q

What type of dentine has the consistency of cottage cheese

A

infected dentine

70
Q

What type of dentine has been subject of attack from bacterial metabolites

A

affected
infected dentine would have the bacterial inside the layer

71
Q

At the DEJ what dentin do you remove in caries

A

remove infected dentine, keep affected dentine, in line with minimal invasive dentistry

72
Q

Is the lesion active or inactive if the surface of enamel is whiteish/yellowish; opaque with loss of luster, feels rough when the tip of the ball-ended probe is moved gently across the surface. Lesion is in a plaque stagnation area (e.g. P/F)

A

Active

73
Q

Is the lesion active or inactive if the surface of the enamel is whitish, brownish or black. Enamel may be shiny and feels hard and smooth when the tip of the ball ended probe is moved gently across the surface. For smooth surfaces, the caries lesion is typically located at some distance from the gingival margin. Lesion may not be covered by thick plaque prior to cleaning.

A

Inactive

74
Q

Is the lesion active or inactive if the dentine feels soft or leathery on gentle probing

A

Active

75
Q

Is the lesion active or inactive if the dentine is shiny and hard on gentle probing

A

Inactive

76
Q

Individuals with low risk of caries should be recalled in

A

6-24 months

77
Q

Individuals with a moderate risk of caries should be recalled in

A

3-6 months

78
Q

Individuals with a high risk of caries should be recalled in

A

1-3 months

79
Q

What risk factors classify an individual as high caries risk

A
  • head and neck radiation (patient level risk factor)
  • Hypo-salivation/dry mouth (intra-oral risk factor)
  • PUFA (pulpitis, ulcera, fistula, absess) - Dental Sepsis (intra-oral risk factor)
80
Q

What do the 4 Ds stand for in caries management

A
  1. Determine caries risk (low, moderate, high)
  2. Detect and assess lesions: (What class1,2,3,4,5,6, using radiographs)
  3. Decide personalized patient and tooth surface levels’ care plan - when to recall the patient based on step 1 and 2
  4. Do preventative and tooth preserving care
81
Q

What are patient level risk factors

A
  • Head and neck radiation***
  • dry mouth
  • Inadequate oral health practices
  • deficient exposure to topical fluoride
  • High frequency/amount of sugar consumption
  • Symptomatic-driven attendance
  • Socioeconomic status/Access barriers
  • Mothers high DMF (caries experience)
82
Q

What are Intra Oral Risk Factors

A
  • Hypo-salivation/dry mouth
  • PUFA dental Sepsis
  • Caries experience
  • Thick plaque
  • greater biofilm retention
  • Exposed root surface
83
Q

What are reasons for intervention of noncarious cervical lesions

A
  • inability to eliminate or greatly reduce the rate of lesion progression through elimination of etiological factors
  • lesion is aesthetically unacceptable to the pt
  • significant sensitivity
  • depth of lesion threatens tooth structure (strength of the tooth + integrity of the coronal radicular unit)
84
Q

What are preventative measures for noncarious cervical lesions

A
  • dietary counselling
  • medical attention (gastric reflux/bulimia)
  • antacid lozenges
  • alkaline mouth rinses
  • sugar free gum
  • proper oral hygiene techniques
  • control of occlusal forces
85
Q

What is the clinical prevention method for ICDAS 1

A

remineralisation (secondary prevention)

86
Q

What is the clinical prevention method for ICDAS 2

A

Arrest (secondary prevention)

87
Q

What is the clinical prevention method for ICDAS 3

A

sealant (secondary prevention)

88
Q

What is the clinical prevention method for ICDAS 4

A

minimal surgical (tertiary prevention)

89
Q

What is the clinical prevention method for ICDAS 5

A

traditional surgical (tertiary prevention care)

90
Q

What is the clinical prevention method for ICDAS 6

A

Endodontic treatment or extraction

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