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Operative (week 1) > Cariology (Exam I) > Flashcards

Cariology (Exam I) Flashcards

1
Q

What are the 5 guiding principles of caries management?

A

1) Assess caries risk status
2) Diagnose disease early
3) Treat disease by remineralizing tooth surface & controlling infection
4) Avoid or delay operative intervention
5) Restore “active” disease ONLY

(Note: ADT-AR)

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2
Q

1908- GV Black ?

A
  • 1908 developed caries pathology prevention and appropriate restorative dentistry protocols
  • Still used in many dental schools today
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3
Q

What events occurs in the 1940s-1950s?

A
  • Rampant and recurrent carries lead to development of operative dentistry
  • Role of diet and bacteria lead to development of the study of cardiology
  • Effects of fluoride lead to development of public health dentistry
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4
Q

What occurred in 2007 pertaining to Dental Caries?

A

Dental caries philosophy changes
The disease and its clinical management
CAMBRA: Caries Management By Risk Assessment

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5
Q

What is the Dental Caries 1970’s view?

A
  • Bacterial disease

- Dependent on presence of sugars and carbohydrates

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6
Q

What is the Dental Caries 1990’s view?

A
  • Involves these 4 factors: Microbe, Host& Teeth, Substrate & Time.
  • Bacterial disease
  • Dependent on presence of sugars and carbohydrates
  • Modified by salivary flow & composition
  • Modified by fluoride
  • Dental caries is a complex multi-factorial disease process
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7
Q

What are other factors that can affect Today’s complete view?

A
  • Education
  • Social Class
  • Income
  • Knowledge
  • Attitude
  • Behavior
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8
Q

Describe Dental Enamel

A

1) Highly mineralized acellular tissue
- Consists of calcium phosphate crystals
- 99% dry weight
- Crystals resemble the mineral hydroxyapatite

2) Solubility of hydroxyapatite affected by pH

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9
Q

What 2 types of lesions can exposure of Enamel to Acids lead to?

A

1) Carious lesions

2) Erosion

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10
Q

What are Caries?

A
  • Can remineralize
  • Chemical dissolution of the dental hard tissues by acidic bacterial products from degradation of low molecular wt sugars
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11
Q

What is Erosion?

A
  • CANNOT remineralize

- Dissolution of the dental hard tissues caused by acids of any other origin or mechanical wear

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12
Q

What is Remineralization?

A

1) Partially demineralized apatite crystals can grow to their original size (especially in the presence of fluoride)
2) Formation of entirely new crystals is rare
3) If goal is to remineralize removal of intact surface layer is NOT advisable

Note: Can’t develop new crystals from scratch

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13
Q

Dental caries is a disease that….?

-In absence of treatment what occurs?

A
  • Chronic disease that progresses very slowly in most individuals
  • In the absence of “treatment” will progress until the tooth is destroyed
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14
Q

What are the Enamel Reactions During Eruption?

A

1) Erupting tooth
-Enamel is FULLY mineralized
-Outermost surface layer is porous and low in fluoride
Note: Immature enamel is more prone to decay, overtime it becomes resistant to decay.

2) If fluoride is present in the oral fluids
-Gradual increase in fluoride in surface enamel
-“Secondary maturation”
Note: Adding fluoride to water systems, that adds an additional benefit.

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15
Q

For an Experimental caries model in completely UNDISTURBED plaque, what happens visually & histologically from week 1, 2 & 4?

A

After 1 week-
Visual: none
Histological: slight increase in enamel porosity

After 2 weeks
Visual: Whitish changes with air-drying
Histological: Subsurface lesion starts to form

After 4 weeks
Visual: White spot lesion with chalky surface
Histological: Enlarged inter-crystalline spaces

Note: Caries lesion starts below surface–>we can still remineralize

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16
Q

What happens when plaque is REMOVED after 1 and 2 weeks?

A

After 1 week:
Visual: Chalky appearance diminishes

After 2 weeks:
Visual: Surface has a shiny appearance of normal enamel

Note: This occurs because it becomes remineralized from saliva which contains the proteins. There is a balance of remineralization and mineralization going on.

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17
Q

Lesions can be classified as ?

A

1) Non-cavitated; demineralization with surface enamel STILL INTACT
2) Cavitated; demineralization with a BREAK in the surface enamel ( need to use a tool to restore)

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18
Q

Which Caries Classification D1-D4 is Cavitated vs Non-cavitated?

A

D1-D3 Non-cavitated

D3-D4 cavitated

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19
Q

What is D0 Caries?

A
  • Lesion detectable only w/ additional diagnostic aids & Sub-clinical lesions in a dynamic state of progression/regression
  • Sub-clinical lesions in a dynamic state of progression/regression (white spot lesions after 2 wks)
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20
Q

What are D1 Caries?

A

Clinically detectable enamel lesion w/ INTACT surface

caries reaches outer-half of enamel

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21
Q

What are D2 Caries?

A

Clinically detectable cavitation LIMITED to ENAMEL

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22
Q

What are D3 Caries?

A

Clinically detectable lesion in dentin (Caries on outer half of the dentin)

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23
Q

What are D4 Caries?

A

Lesion into pulp

Caries on inner half of dentin

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24
Q

What is the relationship between the Host and Teeth?

A

It has been estimated that the human body is composed of approximately 1014 cells, of which only 10% are mammalian. The remainder are the organisms that comprise resident microflora of the host.

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25
Q

What is the Resident microflora

Necessary for

A
  • Normal development of the host
  • Assist with nutrient absorption

-Contribute to host defense by acting as a barrier to
colonization by transient bugs

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26
Q

What is the challenge to the dental clinician regarding microflora?

A

-The challenge to the dental clinician is to use treatment strategies that target the causative organisms without disrupting the beneficial properties of the resident oral microflora.

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27
Q

What is the Bacterial nature of caries?

A

-1950s and 1960s

  • Rodent studies:
  • Germ free – no caries
  • Transmissible from animal to animal
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28
Q

What is the Acquisition of Mutans streptococci?

A

1) Majority of children colonized between 18-36 months
- “window of infectivity”

2) Can be as early as 3 months
- possibly even sooner

-~ 70% of children get Strep mutans from MOM
Transmission associated w/ maternal salivary levels of bacteria

-Referred to as “vertical transmission”

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29
Q

What is Vertical transmission?

A

1) Typically mother

2) Primary caregiver

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30
Q

What is Horizontal transmission ?

A

1) Siblings

2) Others

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31
Q

Individuals can have ______________ of Strep mutans in their oral flora

A

Multiple strands

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32
Q

What was the Swedish study of Strep mutans transmission?

A
  • 55% from mothers
  • Vertical transmission
  • None from fathers
  • 45% from someone other than parent
  • Horizontal transmission from mother

Spouses did not share strains of MS

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33
Q

What was the Japanese study of Strep mutans transmission?

A

-All children attended preschool daily
-33% from mother
-8% from father
58% from someone other than parent
-Other children at preschool

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34
Q

What is the Impact of delayed transmission?

A

1) Delaying acquisition of MS reduces caries experience in both the primary and permanent dentition

2) Delay transmission by reducing maternal bacterial load
- Reducing MATERIAL BACTERIAL LOAD reduces children’s also.

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35
Q

What is the % w/ Caries at age 4 years of age?

A

Mutans at 2 Yrs of Age = 89%

NO Mutans at 2 yrs of Age= 35%

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36
Q

What is the Mean DFS at 4 yes of age?

A

Mutans at 2 Yrs of Age = 5.0%

NO Mutans at 2 yrs of Age= 0.3

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37
Q

What are the Risk factors for early transmission?

A
  • High maternal levels of MS > 105 CFU/mL
  • Sweetened fluids taken to bed
  • Frequent sugar exposure and snacking
  • Sharing foods with adults
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38
Q

What does DMF stand for?

A 
DMFT= Measures caries history
D= Decayed
M= Missing
F= Filled
T =Teeth

Teeth (DMFT) or surfaces (DMFS)
**Capital letters DMFT/S “permanent teeth”

**Lower case dmft/s “primary teeth”

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39
Q

Most studies measure what classification of caries & least?

A

-Most studies measure D2-D4 caries

-A few studies measure D1-D4 caries
Very DIFFICULT to standardize examiners at D1 level

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40
Q

What are the Reasons for decline in caries?

A

1) Increased exposure to fluoride
-Fluoride toothpaste
Fluoridated water

2) Improved preventive behaviors/services
- Better oral hygiene (brushing with F toothpaste)
- Dental sealants

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41
Q

What is the Distribution of Caries by Surface?
Most?
Least?

A 
#1= Occlusal  55%
#2= Buccal/Lingual (pits)  34%
#3= Smooth surface (inter-proximal)
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42
Q

What are the Oral health disparities in sub-groups?

A
  • High caries rates in sub-groups
  • Low income children
  • Racial and ethnic minorities
  • Caries incidence is increasing in Native American populations
  • Children with special health care needs
  • 20% of children experience 80% of decay
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43
Q

What is the Severity of Caries in Children?

A

No Caries 56%> 24% Low Caries> High Caries 20%

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44
Q

What is the Impact of decreased edentulism?

A

1) More teeth at risk of caries
2) Increasing caries rates in adults

3) The new “at-risk” population
- Xerostomia – new carious lesions
- Previous restorative work – larger restorations

4) Caries, not periodontal disease, is the primary cause of tooth loss in adults

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45
Q

Describe Dental fluorosis?

A
  • Increasing prevalence corresponding with decline in caries
  • MOSTLY “very mild” and “mild”
  • Prevalence in towns with 1.0 ppm F
  • 1930s: about 10%
  • Today:30-80% (depends on study)
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46
Q

Since Fluorosis is Dose response what does Prevalence and severity depend upon?

A

1) Amount and/or concentration of fluoride
2) Duration of fluoride exposure
3) Stage of tooth development (age)
4) Individual variation of susceptibility (weight)
5) Current fluoridation levels in water are 1.0 ppm
6) 2011 USA commission looking to reduce levels

Note: too much fluoride can cause brittle bones..

47
Q

What is the Epidemiology of dental caries disease progression for PERMANENT and PRIMARY teeth?

A

Permanent teeth:

1) Progression is a slow process in most individuals
- There are exceptions
- Low salivary flow
- Systemic disease
2) ~4 years for lesion to progress through enamel of permanent teeth

Primary teeth:

1) Progression is faster
2) Enamel thinner
3) Teeth are less mineralized

48
Q

What are the Risk Factor for Caries you CAN’T CHANGE?

A

1) Race/ethnicity
Prevelance of caries by race in 2-4 year olds
White < Black < Hispanic < Native

2) Socioeconomic status
- Individuals below federal poverty level have higher incidence of caries
- Regardless of race
- Low income groups have higher decay rate and a higher rate of untreated caries

3) Previous history of caries
Children with caries in primary teeth are 3 times more likely to have caries in their permanent teeth

4) Inherited risks
-Minnesota Study of Twins Reared Apart
Monozygotic (identical) twins have similar caries patterns but dizygotic twins don’t
-Genetic modification may be due to
-Structure of dental enamel
-Immunologic response to cariogenic bacteria
-Salivary gland function and/or composition of saliva
-Sugar metabolism

5) Salivary composition

49
Q

What are the Risk Factor for Caries you CAN’T CHANGE?

A

1) Race/ethnicity
Prevelance of caries by race in 2-4 year olds
White < Black < Hispanic < Native

2) Socioeconomic status
- Individuals below federal poverty level have higher incidence of caries
- Regardless of race
- Low income groups have higher decay rate and a higher rate of untreated caries

3) Previous history of caries
Children with caries in primary teeth are 3 times more likely to have caries in their permanent teeth

4) Inherited risks
-Minnesota Study of Twins Reared Apart
Monozygotic (identical) twins have similar caries patterns but dizygotic twins don’t
-Genetic modification may be due to
-Structure of dental enamel
-Immunologic response to cariogenic bacteria
-Salivary gland function and/or composition of saliva
-Sugar metabolism

5) Salivary composition

50
Q

How does Diet affect Dental Caries?

A

Diet:

  • Fermentable carbohydrates
  • Calcium
  • General nutrition

Soda:

  • Acidic nature of soda demineralizes teeth
  • Soda consumption in the US has increased

Sugar & Dental Caries:
1) Sugar intake drops oral pH

2) Impact dependent on presence of fluoride
DMFS decreases as sucrose intake decreases

3) Sugar consumption in the US has increased, especially high fructose corn syrup

*Frequent quote …
“The cariogenicity of sugary food is related to its stickiness”

  • The facts …
  • The amount & frequency of high sugar drinks is associated w/ increased rates of caries
  • High sugar drinks are not sticky
51
Q

Regarding Diet, Drop in pH leads to ?

A

1) Demineralization

2) Altered plaque ecology that favors acid uric bacteria such as streptococci

52
Q

Regarding Diet, what are the Issues to consider?

A

1) Amount consumed
2) Form of sugar
3) Frequency of exposure

53
Q

What is the General opinion for sugar of many dentists?

A
  • The total amount of sugar consumed is not important.
  • Focus education toward the reduction in the frequency of sugar consumption

***It’s not how much sugar you eat, its how often you eat it that is important

54
Q

What is the difference between Frequency or total amount?

A
  • Difficult to distinguish between the two, they are highly correlated
  • Both are important for caries
  • TOTAL AMOUNT is most important for the prevention of obesity and other conditions
55
Q

What are the Recommendations for sugar intake?

A 
1) Total amount: Limit intake of free (added) 
sugars to ..
-40 grams/day in non-fluoridated areas
-55 grams/day in fluoridated areas
-6-10% of energy intake

2) Frequency:Limit sugar intake to 4x/day

  • Preferably at meals
  • Limiting frequency will limit total amount
56
Q

How does sugar consumption affect Infants?

A

1) Sugar impacts a child’s oral flora
- Discourages colonization by noncariogenic bacteria
- Encourages colonization by acid uric bacteria
a) Mutans streptococci
b) Lactobacilli

2) Infants and toddlers with high sugar intake have
- Earlier colonization by S. Mutans
- Higher caries rates

57
Q

Oral hygiene and caries:

  • Is there evidence that removal by brushing or flossing decreases caries explain.
  • Daily oral hygiene helps control what?
A

There is no evidence that removal of plaque by brushing (with a non-F toothpaste) or flossing decreases the incidence of caries
Daily oral hygiene does help to control gingival disease and is necessary for the application of fluoride toothpaste

58
Q

What is the # 1 Factor w/ caries?

A
  • Salivary [ ] of S Mutans

- Establishment of a care is risk profile

59
Q

Why is there no evidence?

A

1) Plaque indices designed for studies of periodontal disease not caries
2) Plaque indices don’t measure microbes

3) Plaque removal is important
Effective plaque removal

60
Q

What is the best way to remove plaque?

A

1) Brushing
- The winner by a landslide
- No significant difference between manual and “motorized” toothbrushes*

2) Flossing
- Introduce floss only when brushing is mastered
- We don’t know the best frequency
- Probably every few days to once a week

61
Q

What is Caries diagnosis?

A

1) Detection
2) Observe and describe patient and oral tissues
3) Select appropriate form of intervention
4) Prerequisites for detection
5) Treatment (Clean teeth)

62
Q

What are the prerequisites for Detection?

A

1) Clean Teeth
2) Dry teeth
3) Sharp eyes & magnification
4) Lighting

63
Q

Sharp eyes and magnification:

What is the visual acuity of dentists?

A
  • Visual acuity of dentists > 45 years
  • 60% of dentists failed close vision test at 24cm
  • 40% failed at 33cm
64
Q

Why Early diagnosis?

A

1) Changes in management of disease requires change in how we diagnose
- Detection of cavitated lesions is no longer an appropriate diagnosis of dental caries

2) If detected before cavitation, caries is reversible
- We need systems that allow us to diagnose before cavitation

65
Q

What is the Problems in diagnosis?

A
  • Instruments currently available for the diagnosis of carious lesions do not detect lesions early and quantitatively
  • We can not detect caries until it is 1/3-1/2 way through enamel
66
Q

What is Conventional diagnosis?

A

1) One generation ago, caries diagnosis was relatively simple
- Semi-annual visits
- Check all surfaces for signs of cavitation
- Immediate restoration
- Irreversible damage to tooth not

67
Q

What is the Conventional Diagnostic Tools?

A

1) Visual inspection
- Transillumination

2) Probing w/ a sharp explorer
3) Radiographs

68
Q

What occurs when Probing with a sharp explorer?

A

-Passing the explorer into pits
Noting whether or not there is any softening or if instrument catches or enters at any point

  • Black, 1924
  • Not entirely accurate
  • Can result in false positive or false negativ
69
Q

What is the Blunt Statement #1 for sharp explorer

A
  • Teaching the use of the explorer may be potentially damaging
  • 1984, Dr. Kidd, United Medical & Dental Schools, London
70
Q

What can probing with a sharp explorer do?

A

1) Cause damage to newly erupted teeth
2) Cause cavitation at superficial lesion
3) Transmit bacteria to uninfected fissures

Note: 60% of fissures that were probed had tissue loss

71
Q

How does the explorer accelerate caries?

A

1) Lab study found- sound & demineralized fissures
- All demineralized fissures became activated
- Created microscopic “entrances” for bacteria
- increased rate of lesion growth

72
Q

When probing, all surfaces of a tooth are CLEANED of debris & plaque, the teeth are DRIED using air syringe & EXAMINED visually. If there are suspicious areas THEN an explorer is used with what pressure to check for the surface texture?

A

Enough light pressure to blanch a finger nai

73
Q

What is the concern with x-rays?

A
  • Caries prevalence has declined
  • Awareness of the consequences of ionizing radiation has increased
  • Radiographs are an invasive procedure that should be used with caution
  • In populations with a low prevalence of caries, the routine use of ionizing radiation as a means of diagnosing caries in becoming less desirable as the potential benefit is being outweighed by the potential risk of its use (Stookey, 1999)
74
Q

Accuracy of Radiographs?

A
  • Interpretation between dentists varies when viewing same radiographs
  • Multiple diagnostic tools should be used to avoid missed diagnosis
  • Quality is important
  • Horizontal over lap can result in false or exaggerated radiolucency

-Contrast can effect appearance of radiolucency
ADA Guidelines

Note: Occlusal decay is MORE inaccurate b/c it can not be seen in x-rays

75
Q

What are the Newer Diagnostic Technologies?

A

1) Digital imaging fiber optics trans-illumination (DIFOTI)
2) Lager Fluorescence (LF)
3) Quantitative light fluorescence (QLF)
4) Infra Red Light Imaging

76
Q

What is Digital imaging fiber optic trans-illumination (DIFOTI)?

A

1) Superior sensitivity compared to x-rays
- Occlusal caries (3 times as sensitive)
- Approximal caries (twice as sensitive)
- Other smooth surface caries (10 times)

2) DIFOTI can detect incipient or recurring caries before they are visible on x-rays

  • -Non ionizing radiation
  • Decary scatters & absorbs more light than healthy tissue
  • -Can indicate early decay before x-rays.
77
Q

What is Laser fluorescence (LF)?

A
  • DIAGNODent
  • A laser diode provides pulsed light directed onto tooth.
  • When the light meets a change in tooth substance, it stimulates fluorescent light of a different wavelength
  • Translated through the hand piece into an acoustic signal
  • Wavelength is then evaluated by an appropriate electronic system in the control unit
  • More sensitive but LESS specific in diagnosing dentinal caries
  • Identifies more true caries
  • Identifies more false positives

***Should not be relied on as a clinician’s primary diagnostic method

78
Q

What is Quantitative light –induced fluorescence (QLF)?

A
  • Tooth is illuminated with blue-green light
  • Fluorescence of enamel is observed
  • Demineralized areas appear dark
  • Inspektor Pro
79
Q

What are the QLF measures?

A

-Fluorescence loss
-Lesion area
-Lesion depth
-Detects enamel lesion 5-8 mm in depth
-Quantitative light –induced fluorescence (QLF)
-Tooth is illuminated with blue-green light
Fluorescence of enamel is observed
-Demineralized areas appear dark
Inspektor Pro
-Radiographs detect at about 500 mm

80
Q

Infra red light imaging?

A
  • Can visualize bacteria, caries, and cracks

- Not yet commercially available

81
Q

What is the preferred Treatment?

A
  • Select appropriate form of intervention
  • Remineralization past theory
  • Fluoride is incorporated into the enamel mineral during formation to make the enamel more resistant to acid attack.
  • “Fluoride makes the tooth stronger”
  • Systemic action (little effect)
  • Remineralization current theory
  • Topical application more effective than systemic action
82
Q

Cariostatic mechanism of fluoride?

A
  • Fluoride enhances remineralization
  • Fluoride concentrates in dental plaque
  • Fluoride is released from plaque when pH is lowered
  • Fluoride is taken up more readily by demineralized enamel than by sound enamel
  • Plaque fluoride inhibits bacterial glycolysis
  • Primary cariostatic effect is” TOPICAL”
  • “FREQUENT” exposure to “LOW CONCENTRATIONS”
  • Exposure about every 4 hours
  • Water fluoridation and toothpaste
  • Fluoride prevents smooth surface caries
  • Fluoride arrests enamel and dentine caries
83
Q

What are the Fluoride Delivery Vechicles?

A

1) Community water fluoridation
2) Self applied fluorides
- Toothpaste, OTC mouth rinse, Rx fluoride
- Weekly school rinse programs
3) Professional applied fluorides
- Gels, foams, varnish

84
Q

Community water fluoridation advantages/disadvantages?

A

-Reduces caries by 15-20 percent

Advantage of fluoridation:
-Does not require individual effort

Disadvantage of fluoridation:
Children DO NOT DRINK WATER
Requires cooperative water operator

85
Q

Self applied fluorides?

A

-The main reason for the decline in caries
-Brush at least 2 times per day with fluoridated toothpaste
-Dry brushing does not prevent caries
-Prevents about 24% of caries
Dose
-Age 1-2 slight smear
-Age 3-5 half of pea size
-Age 6> pea size

86
Q

Supplements for Self-Applied Fluorides?

A

-Good for high-risk compliant patients
Regardless of age
Including teens, adults and elders

  • Use lozenges to prolong contact
  • LOZI-FLUR (www.dreirpharmaceuticals.com)
  • Not appropriate for low-risk patients
87
Q

Professionally applied fluorides?

A

1) Gels, foams, varnish:
Professional rinses not approved by ADA

2) Mechanism of action:
- Arrestment of incipient lesions
- Increased resistance to further demineralization

3) Fluoride ingestion:
-Gels and foams: up to 35 mg of F
Varnish: up to 5 mg of F

4) Do not use gels/foams in children 5 years and younger

5) Frequency of application:
At least 2 times per year
4-6 times per year for very high risk patients

88
Q

What are the Indications for use for Professionally applied fluorides?

A

1) Patients at high risk of caries on smooth surfaces
2) Patients at high risk of caries on root surfaces

3) Special patient groups such as
- Orthodontic patients
- Patients undergoing head and neck radiation
- Patients with decreased salivary flow

4) NOT recommended for patients at low caries risk

89
Q

Application specifics?

A
  • Applying gel with floss can help with contact areas
  • Do not apply fluoride varnish to teeth that are being prepared for composite restorations, it can effect bonding
  • Prophy not required before professional fluoride application
  • Polishing does not remove enamel fluoride
  • When contact time is reduced to 1 minute, enamel fluoride uptake is significantly less
  • No clinical data to support the 1 minute application of any product
90
Q

Fluoride and root caries?

A
  • Fluoride prevents root caries
  • Fluoride arrests root caries
  • Daily self-application of 5,000 ppm NaF gel plus fluoride toothpaste for 12 months
  • arrested 91% of incipient root lesions
  • arrested 57% of actual root lesions
91
Q

Recommendations for high risk patients?

A
  • Fluoride therapy alone may not be effective in arresting caries progression & remineralizing enamel.
  • Use additional therapies to control the infection.
92
Q

What are additional caries therapies?

A
  • Combine with appropriate fluoride
  • Goal is to alter oral environment and reduce levels of mutans streptococci
  • Prior to using these therapies
  • Restore existing carious lesions
  • Apply pit & fissure sealants
93
Q

What are Chemo-Therpaeutics?

A

1) Fluorides-remineralization
2) Baking Soda-pH Buffers
3) Chlorhexidine- Anti-microbials
4) Xylitol- non fermentable sugars

94
Q

Benefits of Baking Soda?

A

1) Increases salivary pH, neutralizes salivary pH
2) Suppresses mutans streptococci
3) Improves taste in those with xerostomia related taste dysfunction

  • Used as a rinse
  • Dissolve 1 teaspoon in tumbler of water
  • Rinse vigorously and spit
95
Q

Chlorhexidine

A
  • For those who will self medicate
  • 14 day regimen suppresses mutans streptococci for 12-26 wks
  • CHX vehicles
  • Mouthrinse – available in US
  • Varnish – clinical trials only
  • Gel – clinical trials only
  • Meta-analysis of CHX clinical studies average caries inhibitory effect was 46%
  • Chlorhexidine and fluoride treatment complement each other
96
Q

CHX varnish

A
  • Cervitec and Prevora (Not available in US)
  • 3-4 month applications reduce root caries
  • More effective then CHX rinses in reducing mutans streptococci
97
Q

CHX varnish product development ?

A

-10% CHX Varnish (Prevora)

  • CHX Technologies, Toronto, Canada
  • Approved in Canada and Ireland
  • Clinical trials for FDA approval in process
  • Moms and infants

-1% CHX Gel (no name yet) University of Iowa

98
Q

How is CHX varnish applied?

A
  • 2 stages – medication then varnish
  • Painted on teeth
  • Once per week for 4 weeks then every 6 months
  • Bitter taste
  • Burns if it touches gums
99
Q

What is Xylitol?

A

-A five carbon sugar alcohol
As sweet as sucrose

  • Prevents mutans streptococci from metabolizing other sugars
  • Inhibits enamel demineralization
  • Inhibits bacterial adhesion
100
Q

Proposed action of xylitol?

A
  • Non-fermentability by plaque organisms
  • Reduction in plaque quantity
  • Selective reduction of mutans streptococci
  • Induction of mutans streptococcus strains with reduced virulence
  • Increased concentration of ammonia in plaque
  • Accumulation of xylitol-5-phosphate in some plaque streptococci
  • Participation in a futile metabolic cycle in some plaque organisms
  • Reduced adhesion of plaque flora
  • Reduced transmission of mutans streptococci
  • Changes in quantity and quality of saliva
  • Aids remineralization
101
Q

Xylitol dose?

A
  • Recommended for patients who chew gum
  • Reduces decay and reverse si ncipient lesions
  • Chew 3-5 times/day, 5 minutes each time
  • Xylitol gum chewing should start at least 1 year before permanent teeth erupt
102
Q

What are the Benefits of Xylitol?

A
  • Teeth erupted during 2nd year 93% reduction in caries risk
  • Teeth erupted after chewing stopped 88% reduction in caries risk
103
Q

Difference between CHX & Xylitol Gum users?

A

Gum users had:

1) Increased salivary flow
2) Reduced denture debris

CHX gum users had:
1) Lower levels of oral bacteria mutans streptococci, lactobacilli, and yeast

2) 91% reduction in denture stomatitis
- 62% reduction in xylitol only group
- No reduction in control group

104
Q

Xylitol users had osmotic diarrhea at what amount?

A

Osmotic diarrhea at:

  • 100 grams/day in adults
  • 45 grams/day in children

Dose for dental caries prevention:
-6-10 grams per day

105
Q

What are the other benefits w/ Xylitol and other health issues?

A

1) Ear infections
40% reduction in incidence of ear infections in children that chewed 8.4 g of xylitol/day

2) Osteoporosis
Xylitol added to the diet of rats increased their bone mineral content and accelerated bone recalcificati

106
Q

What are dental Dental sealants ?

A
  • An important dental caries prevention technology
  • Should be used in combination with fluoride
  • Safe & effective
  • Prevent pit and fissure caries
  • Arrest caries progression
107
Q

What are the consideration for Sealants use?

A
  • Morphologic characteristics
  • Risk for pit and fissure caries extends into adult life
  • Some patients with pit and fissure caries are candidates for sealants
  • “therapeutic sealants”
108
Q

The surgical management of noncavitated carious lesions should be __________________

A

The treatment of LAST RESORT

109
Q

Why wait to restore?

A
  • Caries progression is slow in permanent teeth
  • Preserving sound tooth structure is beneficial
  • Restorations compromise tooth integrity and possibly vitality through a cycle of restoration and re-restoration
110
Q

Benefits of remineralization versus surgical intervention?

A
  • Prevents loss of tooth structure
  • Reduces exposure to anesthetic agents
  • Reduces pain and inconvenience
  • Preserves esthetics
111
Q

How successful are fillings?

A
  • 70% of fillings are replacements of existing fillings

- Replacements get bigger and lead to more replacements

112
Q

Cycle of re-restoration?

A
  • Re-restoration results in teeth receiving progressively larger restorations
  • 70% of replaced posterior restorations increase the number of restored surfaces
113
Q

When are lesions cavitated?

A
  • Radiolucency in outer half of enamel
    0. 0% of permanent teeth were cavitated
    2. 0% of primary teeth were cavitated
  • Radiolucency in inner half of enamel
    10. 5% of permanent teeth were cavitated
    2. 9% of primary teeth are cavitated
  • Radiolucency in outer half of dentin
    40. 9% of permanent teeth were cavitated
    28. 4% of primary teeth were cavitated

-Radiolucency in inner half of dentin
100% of permanent teeth were cavitated
95.5% of primary teeth were cavitated

114
Q

Restore active caries only when what?

A

1) Must determine if the caries process is
- Progressing
- Arrested
- Shifting toward remineralization

2) Early lesions must be recorded and monitored
- Filling teeth does not treat the disease of dental caries
- Filling teeth simply restores the effects of the disease

Operative (week 1) (6 decks)

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