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Resto > Caries (2) > Flashcards

Caries (2) Flashcards

1
Q

Define Caries:

A

Infectious microbiologic disease of the teeth that
results in localized dissolution and destruction of the calcified tissues.

caries is formed due to the acid

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2
Q

Epidemiology:

A
  1. Sex, race, geography
  2. Diet
  3. Hygiene
  4. Socioeconomics status
  5. Age
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3
Q

Incidence 4-8 years

A

Immature enamel

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4
Q

Incidence 11-18 years

A

more sugar/ more hygiene

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5
Q

Incidence more 55 years

A

Gingival retraction

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6
Q

Distribution

A
  1. Bilateral and symmetric often on both sides on the same tooth
  2. Teeth
  3. Surfaces
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7
Q

What are the most affected teeth?

A
  • molars
  • premolars
  • incisors and canines

(most affected the molars and premolars)

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8
Q

Which surfaces are affected?

A
  • occlusal 40-45%
  • proximal 40-45%
  • buccal and lingual 10%
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9
Q

Pathogenesis:

A
  • microbes (plaque)
  • substrate (diet)
  • Host (individual characteristics, tooth surface)
  • time
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10
Q

Whats the keyes triad?

A
  1. Microflora
  2. tooth
  3. diet
  4. tooth decay
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11
Q

When do we have a problem?

A

If those 3 things are not in the balance, we get caries

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12
Q

Whats the process of caries?

A

ph reduces, the acid produces caries in the mouth

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13
Q

On what does caries depend on?

A

It depends if we use fluoride toothpaste and how much fluoride the patient has

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14
Q

What are the primary cariogenic factors?

A
  1. Microorganism
  2. Diet
  3. Saliva
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15
Q

What do the microorganisms include?

A
  • biofilm composition

- activity

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16
Q

What does the diet include?

A
  • number exposures to sugar per day

- number of acidic exposures per day

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17
Q

What does the saliva include?

A
  • consistency of unstimulated saliva
  • ph of unstimulated saliva
  • buffering capacity of stimulated saliva
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18
Q

What are secondary modifying factors?

A
  • Past and present of dental status
  • Past and present medical condition
  • Accordance with advice on oral hygiene and diet • Lifestyle
  • Socioeconomic status
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19
Q

Multifactorial disease

A
  1. Microbes (plaque)
  2. Substrate (Diet)
  3. Host (individual characteristics)
  4. Time
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20
Q

Biofilm

A

microbial community adhered to a substrate trough an extracellular polymeric matrix.

(in the plaque we have many types of bacterials, but not always it produces caries)

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21
Q

Bacterial dental plaque

A

Microbial community on the tooth’s surface in the form of a biofilm. Determinants in their composition: nutrients, oral hygiene, retentive surfaces.

(the bacteria produces some metabolic products, that other bacterial use)

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22
Q

Define Caries

A

PH alteration, composition and metabolic activity of the biofilm

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23
Q

Nutritional bacterial plaque factors:

A
  • Endogenous
  • Exogenous
  • Inter bacterial
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24
Q

Endogenous

A

Saliva, gingival fluid, mucous.

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25
Q

Exogenous:

A

carbohydrates from diet

  • sugar fermentation > acidity in plaque
  • critical value of pH= 5.5 = enamel demineralisation
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26
Q

Inter-bacterial

A

metabolism products of some bacteria are used as

nutrients by other bacteria.

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27
Q

Bacterial plaque. Composition:


A

Exogenous acquired film (covers tooth surface, allows
bacteria to adhere)

Matrix: proteins, long chain polysaccharides and lipids

Bacteria. Acidogenic bacteria

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28
Q

Bacteria. Acidogenic bacteria implicated:

A
  1. Streptococcus mutans (mutans streptococci)-main bacterium contributor to tooth decay related to caries start, s.sobrinus, s.salivarius: that participate actively in caries developing.
  2. Lactobacillus, bifidobacterium, prevotella: mainly in cavitated caries, have co-aggregation with other species: caries progression.
  3. Actinomyces: primary teeth and root caries in adults.
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29
Q

When is the biofilm formed?

A

right after we eat, the biofiom is fprmed which also protects the tooth, in the biofilm the biofilm does not produce caries, but if we eat all the time, the streptococcus produces caries

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30
Q

Diet

A
  1. Type of food
  2. Highly cariogenic carbs
  3. > 20% sugar in diet = > caries incidence
  4. Frequency (Stephan curve)
  5. Poor dietary habits
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31
Q

What includes the type of food?

A

carbohydrates (glycolysis: drop PH), physical qualities of the food (stickiness, texture and solubility)

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32
Q

What problem do highly cariogenic carbohydrates have?

A

Diet of highly cariogenic carbohydrates is easily metabolized by plaque to produce acids.

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33
Q

What food do contain sucrose?

A

Sugary food, fruit juices, fizzy drinks… high molecular weight Polysaccharid. Easy solubility, quick diffusion.

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34
Q

Whats the Stephens curve?

A

The curve on a graph, first described by Robert Stephan in 1943, showing the fall in pH below the critical level of pH 5.5, at which demineralization of enamel occurs following the intake of fermentable carbohydrates, acidic liquids, or sugar in the presence of acidogenic bacteria.

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35
Q

Whats the usual pH?

A

5,5

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36
Q

What happens with the pH if we have breakfast?

A

If we have breakfast, the pH drops

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37
Q

Whats the aim of the healthy Stephens curve?

A

in this graph, the graph is more time in the healthy zone than in the ill zone

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38
Q

Whats the most acidic during the day?

A

Coffe

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39
Q

What happens if we brush our teeth right after having a meal?

A

if we brush our teeth right after, the pH goes up faster due to the fluoride

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40
Q

Individual hist characteristics:

A
  1. Tooth
  2. Saliva
  3. Fluoride
  4. Other factors
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41
Q

What refers to the tooth host?

A

Morphology, maturation, position, composition of dental tissues (fluorapatite)

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42
Q

What do we understand under position?

A

If the tooth is rotated etc.

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43
Q

What do we understand under composition?

A

How much fluoride the tooth contains

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44
Q

And Saliva what do we understand?

A

What components does the saliva contain

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45
Q

What contains the saliva?

A

Anticariogenic power

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46
Q

What is Anticariogenic power?

A
  1. Mechnical removal of residues
  2. Buffer power
  3. Reduction enamel solubility
  4. Remineralized enamel
  5. Bactericidal and bacteriostatic power
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47
Q

Whats a buffer power?

A

Saliva ph= 6.75

Neutralizes plaque acids

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48
Q

What plaque acids does it neutralise?

A 
– carbonic acid-bicarbonate system
– Phosphate-phosphoric acid system
– salivary urea
– salivary proteins
– Ph elevator peptide or sialin
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49
Q

What is reduction enamel solubility?

A

forms the acquired pellicle, contains fluoride, calcium and phosphate ions.

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50
Q

Whats remineralised enamel?

A

calcium, phosphorus, fluoride, salivary proteins

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51
Q

Bactericidal and bacteriostatic power

A

lisozime, lactoferrin, lactoperoxidase, phosphoproteins, IgA

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52
Q

Whats remineralisation?

A

in saliva we have calcium and phosphate ions, when they get in touch with the hydroxide

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53
Q

When do we have remineralisation?

A

Saliva + hydroxyapatite= remineralization

  • Calcium/phosphate ions in supersaturated solution.
  • Neutralizing buffer systems.
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54
Q

Wats deminerlaization?

A

we eat, produce acid and touch the hydroxyapatite

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55
Q

When do we have Demineralization?

A

Acids + hydroxyapatite= decalcification.

  • Dissociation of phosphate groups
  • Release of calcium ions
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56
Q

Describe the concept of demineralisation and reminerlation:

A

After an acid attack ph decreases: Ca and P ions are released after the HAp’s dissolution, just in a few minutes, there will be an increase in the ph due to the formation of new HAp crystals thanks to saliva and fluoride.

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57
Q

How does fluoride work?

A

– Contact with the hydroxyapatite in enamel: replaces the hydroxyl ions with
fluoride, forming fluorapatite, less soluble (OH- !F-)

> rate of remineralization
< colonization and growth of the bacterial plaque, increases resistance of enamel to acid attack.

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58
Q

Other host factors?

A
  • genetic
  • chronic diseases or with low immunity
  • oral hygiene habits
  • xerestomia
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59
Q

What other factor does affect the oral fluoride?

A

due to any drugs, when we have a patient who takes many drugs, it affects the saliva and the fludity of the saliva
so might apply fluoride

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60
Q

What induces Xerestomia?

A
  • Systemic diseases: Sjögren Sd.
  • Radiation therapy.
  • Drugs:psychotropic drugs, cytostatic…
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61
Q

What factors do we include as the time?

A
  1. Chronological
  2. Posteruptive maturation
  3. Period demineralisation/ remineralisation
  4. Development of immunity
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62
Q

What do we refer as chronological?

A

Dental plaque accumulation

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63
Q

What do we refer to posteruptive maturation?

A

Immature enamel

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64
Q

What do we refer to demineralisation and reminerlaization period?

A

2/22 h proportion

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65
Q

Whats the best zone?

A

22 hours healthy zone, 2 hours ill zone

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66
Q

What are Pathological factors?

A
  • acid producing bacteria
  • sub normal saliva flow and or function
  • frequent eating/ drinking of fermentable carbs
  • poor oral hygiene
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67
Q

What are protective factors?

A
  • sliva flow and components
  • demineralisation (fluoride, calcium, phosphate)
  • good oral hygiene
  • strategies that maintain a healthy microbiome (probiotics, probiotics, arginine, pH modifiers, erythritol and xylitol)
  • strategies that modulate a dysbiotic microbiome (silber, peptides, tin, antimicrobials)
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68
Q

Whats the caries balance?

A

The caries balance, the balance between demineralisation and demineralisation is illustrated in terms of pathologic factors (ex. those favouring demineralisation) and protective factors (ex. those favouring reminerlaization)

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69
Q

Types of caries regarding the depth of the lesion:

A

1- Enamel caries

  1. Dentin caries (dentin pulp complex)
  2. Cement caries
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70
Q

Enamel caries:

Macroscopically

A
  • Opacity
  • White Lesion
  • Brown lesion
  • Cavitation

(first we note it as the opacity, then white lesion etc.)

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71
Q

What alway we have to do and why?

A

from the surface we can only see the white lesion, if its deeper or not
we can also have caries with no cavitation, thats why its importat to take an xray

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72
Q

Enamel caries:

Microscopically

A
  1. Surface zone
  2. Body of the lesion
  3. Dark zone
  4. Translucent zone
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73
Q

Surface zone

A

20-50Um

Loss of mineral content 5-10%

74
Q

Body of the lesion

A

– Largest portion of the lesion
– Loss of mineral content 10-15%
– Porosity 5-25%
– Selective demineralization (striae of Retzius and prism cores)

75
Q

Dark zone

A

– Dark brown band
– Loss of mineral content 5-8%
– Porosity 2-4%
– Represents process of demineralization and remineralization

76
Q

Translucent zone

A

– The deepest zone
– Loss of mineral content 1-5%.
– Porosity 1% (x10 normal enamel)

77
Q

Dentin caries:

Macroscopically

A

Dentin pulp complex

  1. Infected dentin
  2. Affected dentin
78
Q

Infected dentin

A

cavity, caseous tissue, soft texture, easy to remove.

79
Q

Affected dentin

A

hard texture, dark color.

80
Q

What 2 options do we have if the caries reaches the dentin?

A
  1. reaches on the top

2. reaches on the bottom

81
Q

What dentin we do just remove?

A

We just remove the infected dentin, the one on the top

82
Q

Dentin pulp complex active caries
Microscopically
(exam)

A
  1. Infected dentin
  2. Affected dentin
  3. Hyper mineralised dentin
  4. Pulp reaction
83
Q

Infected dentin

A
  • Necrotic/destruction zone

* Outer demineralized dentin zone

84
Q

Affected dentin:

A
  • Inner demineralized dentin zone

* Outer sclerotic dentine zone

85
Q

Hyper mineralised dentin

A

• Inner sclerotic or translucent laye

86
Q

Pulp reaction

A
  • 3ry dentin Reparative dentin

* Pulp inflammation

87
Q

Main character of the root surface caries?

A

very common, problem has a quick progession, since all the rest is close its affected but they dont fell anything

88
Q

Root surface caries:

A

– Concave anatomic surface contours
– Roughness at the termination of the enamel –cementum
– Dentin exposure to the oral environment (gingival recession)
– U-shaped with quick progression

89
Q

Classification:

A
  1. Location
  2. Activity
  3. Development stage
  4. Mode of appearance
  5. Location and size
90
Q

Location

A
  • Fissures, grooves, pits

* Free enamel surfaces: Proximal, buccal, lingual • Root

91
Q

Activity

A
  • active
  • arrested
  • rampant
92
Q

Development stage:

A
  • White spot- incipient caries
  • Dentin affected, no cavity
  • Cavity
  • Pulp exposure
  • Crown destruction
93
Q

Mode of appearance:

A
  • Primary
  • Recurrent, secondary
  • Residual
94
Q

Location and size:

A
  • Hume&Mount classification.

- Black classification (disused)

95
Q

Caries classification

- based on location

A
  • occlusal surface
  • proximal surface
  • root
96
Q

Caries in occlusal surface:

A

• Located in pits, grooves and fissures

• Caries progress:
– Starts in the lateral walls of the cavity
(Expands laterally).
– Easy access
– Fluoride in early detection
97
Q

Proximal caries

A
  • Located in the most cervical and buccal part of the contact area.
  • Slow progress. We could try non invasive methods depending on the patient’s diet, fluoride…

(always located most cervical and buccal)

98
Q

Caries progress

In pits and fissures

A

it spreads in triangular pattern with base towards DEJ.

99
Q

Caries process:

in proximal caries

A

apex towards DEJ.

When caries passes through enamel, it spreads laterally along the DEJ: cone shaped lesion with its apex towards the pulp

100
Q

Whats the 1st manifestation of enamel caries?

A

white spot

101
Q

Based on activity:

Arrested- Enamel

A 
Enamel:
- Non cariogenic activity
- Remineralized affected enamel:
hard and bright
- and feels hard if a sharp probe
is gently drawn across it.
102
Q

Based on activity

Arrested- dentin

A

Dentin:

- Marked brown pigmentation and hard, shiny.

103
Q

Based on activity:

Active- enamel

A

Enamel:

- White mark, chalk appearance

104
Q

Based on activity.

Active- Dentin

A

Dentin:

  • Caseous, wet, soft tissue
  • Light brown/ grey or yellow
105
Q

Based on activity

Active- Rampant/ Early childhood caries

A
  • quick process

- > teeth in not common surfaces

106
Q

According to the development stage:

A
  1. No cavitation
  2. Cavitation
  3. Pulp exposure
  4. crown destruction
107
Q

According to development stage:

No cavitation

A
  • Active enamel caries lesion (white spot- incipient caries)
  • Inactive enamel caries lesion
  • Lesion with involvement of the dentin without cavitation : dentin affected but intact enamel. Hidden caries
108
Q

Active enamel caries lesion (white spot- incipient caries):

A

Opaque, rough, difficult cleaning areas, gingivitis

109
Q

Inactive enamel caries lesion

A

– pigmented or clear spot

– Enamel surface shiny smooth and polish

110
Q

According to development stage:

Cavitation

A
  • Active caries lesion with cavity

- inactivecaries lesion with cavity

111
Q

Active caries lesion with cavity:

A

– Clear color, soft texture

– Active withe spot in around

112
Q

Inactive caries lesion with cavity:

A

– Dark color, hard texture

– Well limited edges, without active white spot halo.

113
Q

What else can we find in the no cavitation area?

A

normally gingivitis in this area as well cause the patient cant clean well in this area

114
Q

Whats a hidden caries?

A

the enamel doesnt have a cavitation, but the dentin has a caries cause its inside the root: hidden caries

115
Q

Main difference of active and inactive caries:

A

active: softer
inactive: harder

116
Q

Based on mode of appearance:

A
  1. primary caries
  2. Recurrent or secondary caries
  3. Residual caries
117
Q

Primary caries:

A

Carious lesions on unrestored tooth surface

caries that appear on the topth surface, there is no treatment necessary

118
Q

Recurrent or secondary caries:

A

Carious lesions that develop adjacent to an obturation.
Formed around the margins and under the obturation, usually on rough areas and margins or fractured dental tissue.

we can see caries around it

119
Q

Residual caries

A

Remaining caries that has been left behind in a prepared cavity on which an obturation is placed.

(caries left in the cavity, left in the obturation)

120
Q

Location:

site 1

A

pits and fissures

not only occlusal, can also be on the lateral pits

121
Q

Location:

site 2

A

Proximal surfaces

122
Q

Location:

site 3

A

cervical areas

123
Q

Stage 0:

A

the earliest lesion that can be identified as the initial stages of demineralization

(we can use fluoride to demineralise it)

124
Q

Stage 1:

A

Minimal surface cavitation with involvement of dentine just beyond treatment by mineralization

(dentin is already affected, we cant remineralise it)

125
Q

Stage 2:

A

moderate involvement of dentine. The remaining tooth is sufficiently strong to support the restoration.

(tooth is still strong enough to remain)

126
Q

Stage 3:

A

the lesion is enlarged beyond moderate. Remaining tooth structure is weakened to the extent that cusps or incised edges are split, or are likely to fail if left exposed to occlusal load.

(cavitation is bigger, cusps are weak)

127
Q

Stage 4:

A

extensive caries or massive loss of tooth structure e.g. loss of a complete cusp or incisal edge has already occurred.

(cup is completely broken on edge)

128
Q

Hume & Mount Classification

A

This classification: helps to make decisions about the treatment to establish protocols for each case:

129
Q

Hume and Mount:

stage 0

A

A white spot lesion, stage 0: remineralized techniques

130
Q

Hume and Mount:

Stage 1:

A

Stage 1: Minimally invasive restorative treatment

131
Q

Hume and Mount:

Stage 2, 3, 4

A

Stage 2, 3, and 4 more complex restorative treatment

132
Q

Why do we have the Hume and mount classification?

A

In order to know how we treat them

133
Q

Diagnosis:

A
  • Patient history (how painful etc)
  • Clinical examination
  • Radiographic assessment
  • Nutritional analysis
  • Salivary analysis
134
Q

Patients history:

A

– Asymptomatic. – Symptomatic:

• Hyper sensitivity? • Pain?

135
Q

Visual

A

Detection of white spot, discoloration, cavity, opacity under an evidently sound or stained pit or fissure

136
Q

Visual and tactile examination

A
  1. Examination wet and dry teeth surfaces.
  2. Plaque-free (clean surfaces)
  3. Mirror and not sharped explorer!
  4. Sound enamel refractive index (R.I)=1,62
  5. Demineralized enamel
137
Q

Demineralized enamel:

A

– > porosity
– > Water accumulation (r. i = 1,33)
– After water dry: r.i = 1,0 = opaque lesion.

138
Q

What can you conclude is the tooth we and you see the white spot?

A

no caries

139
Q

What can you conclude if it is dry and you see white spot?

A

caries

140
Q

Visual inspection:

A

Low sensitivity technique –
high number of not diagnosed caries

but more specific
low number of false +.

141
Q

if we have stain, does it indicate caries?

A

No, Stain doesn’t always indicate caries.

142
Q

What diagnosis is analysed in 55% caries=

A

55% caries diagnosis in

sound teeth.

143
Q

What do we have to analyse close to the fissure?

A

Opacity changes

144
Q

If we have a cavitation, how is the exam tester seen?

A

hard or soft

145
Q

If we have a shiny surface, is it an indication for caries?

A

if the surface is shiny around we have caries, an indication at least

146
Q

Tactile:

A
  1. Explores
  2. Dental floss
  3. probe
147
Q

What do we use on the occlusal surface?

A

explorer

148
Q

What do we use interproximal and what’s the consequence?

A

dental floss, if it breaks caries

149
Q

What does the explorer do?

A

if retentive area in the tooth, the probe could easily enter the space. We can evaluate softness/ hardness of walls and floors

150
Q

When do we NOT use the explorer?

A

When cavity is not cavitated, we dont use explorer

151
Q

What we shouldn’t do after exploration a caries?

A

if we probe a large caries and with that probe we touch an obturation, we transfer the caries

152
Q

What kind of probes do we use?

A

we only use sharp prrobes if its cavitated, otherwise round probe

153
Q

When do we use sharp probes?

A

if its cavitated

154
Q

What consequences do sharp probes have?

A
  • Damage the sound enamel and convert remineralized lesions in irreversible lesions.
  • Microorganism transmission from carious surfaces to sound surfaces
  • Risk of fracture surface of the enamel, prevents future remineralization
  • Transport cariogenic bacteria from a tooth with carious lesion to a sound piece
155
Q

Regarding the radiograph: when can we ONLY see caries?

A

Only visible when there has been enough demineralization (>40%)

Only advanced lesions are detected.

so if we see smth= warn

156
Q

Whats the percentage in detecting carious lesion?

A

50-70% sensitivity in detecting carious lesions

  • high number of false + and false – in small caries
157
Q

When do we often think it might be caries?

A
  • overlapping of proximal surfaces

- cervical burnout

158
Q

With what cervical burnout is often confused?

A

With root caries

159
Q

What do we always have to do?

A
  • xray

- visual

160
Q

Occlusal caries xray

A
  • Occlusal caries xrays

    Theanatomyoftheocclusalsurfaceofposterior teeth leaves a lot of enamel covering the dentin of the buccal and lingual cusps , which , in an X-ray helps to mask any incipient occlusal demineralization in the occlusal fissures decreasing sensitivity.
  • In addition, the enamel - dentin line separation is difficult to appreciate at the occlusal level when we take a bitewing, leading to false positives.
161
Q

What can also be confused on the xray because its seen dark?

A

Enamel dentin junction

162
Q

Advantages of Radiograph:

A
  1. detection of lesion development
  2. Identification of caries in areas of difficult acess (intraproximal and sub gingival)
  3. Hunden occlusal caries diagnosis and pre- eruptive caries diagnosis
  4. Recurrent caries
  5. To monitor preventive therapies and monitoring already diagnosed injuries
  6. Legal document
  7. Bitewing radiographs to improve sensitivity of detection on proximal surfaces
163
Q

Detection of lesion development:

A

– Evaluation of the depth of the injury in relation to the pulp and the biological space.
– See changes occurring at the dentin and pulp chamber (Tertiary dentin)

164
Q

Biological criteria for the removal of advanced carious lesion

A
  1. How much carious tissue should I remove?
  2. How do I remove it?
  3. Are viable microorganisms into the dentin that we leave?
  4. Could these microorganisms be recurrent?
165
Q

We have 2 ways of cleaning:

A
  1. Leaving remnant affected carious dentin: the caries
    will stop progressively once it is isolated from the oral cavity
  2. Removing all the carious dentin
166
Q

Fusayama y cols, Ogawa y cols distinguish

A
  1. infected dentin

2. affected dentin

167
Q

Due to Fusayama:

infected dentin

A
  • Denatured superficial dentin
  • Can’t be remineralized
  • Must be removed

(infected dentin always have to be removed=

168
Q

Due to Fusayama:

Affected dentin

A
  • Deep
  • Denatured but reversible.
  • Can be remineralised
  • Must be kept.

(we can leave it)

169
Q

How to remove carious tissue?

A
  1. Removal method

2. Acid method

170
Q

Removal method

A

Turbine, contra angle, excavator use of caries detector dyes hardness lesions

171
Q

Acidic method:

A

Dyes (Fusayama).
Fucsina (0,5% propilenglicol)
Red acid 1% propolinglicol

Has to be washed really well cause otherwise it could affect other lesions

172
Q

What dentin is stained in theory?

A

disorganized

173
Q

What dentin is stained due to studies?

A

Some studies have shown that it also stains deep intertubular dentin

174
Q

Caries detector:

A

Maltz & cols: dyes have great affinity for:

  • areas of lower concentration of minerals
  • surrounding-pulp deep dentin
  • high degree of porosity areas (white spot)
  • Intact areas

This can lead to an excessive removal of the dental structure.
in anterior teeth staining may compromise the aesthetics
It is important to associate it with the criteria of surface hardness

175
Q

When do we not use a caries detector?

A

As soon as we know how caries feel like

176
Q

What might leave stains if we dont wash it?

A

anterior teeth staining

177
Q

Dentin hardness:

Advantages

A
  • Most used method.

* Removal of infected dentin

178
Q

Dentin hardness

Disadvantages

A
  • no differences between infected and affected dentin

- sharp excavator eliminates non infected dentin

179
Q

What main character does the affected dentin have?

A

Affected dentin: 35-40% softer than normal dentin

180
Q

Maltz y cols: Study in 32 patients with partial removal of caries. After 6-7 m

A

– Color alteration
– Hardness 80%
– Significative decrease of streptococcus and lactobacillus

Resto (9 decks)

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