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OSU Cariology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is dentistry

A

evaluation, diagnosis, prevention and or treatment of diseases/disorders of the oral cavity.

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2
Q

Purpose of Incisors

A
  • Cut/shear food

- phonetics, function, and aesthetics

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3
Q

Purpose of Canines

A
  • seize, pierce, tear, cut food
  • longest roots. and strategic position in arch
  • key to occlusion (protection)
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4
Q

Purpose of Premolars

A
  • grind and tear

- fine chewing

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5
Q

Purpose of Molars

A

(large, multi-rooted strong)

-crushing, grinding, and chewing

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6
Q

Characteristics of Enamel

A

hard, translucent white, shell structure, striated appearance due to enamel rods that run from DEJ to surface

  • very hard, brittle in parallel direction to rods
  • low tensile strength in perpindicular direction to rods
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7
Q

Characteristics of Dentin

A

-softer than enamel, yellowish
-higher tensile strength due to collagen
isotropic properties
-stops propagation of cracks in enamel
-striated appearance with tubules that extend from pulp chamber to DEJ
-tubules are related to the odontoblasts
-not unifromly mineralized

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8
Q

% Volume composition of enamel

A

1-2% protein
4-8% water
90-95% hydroxyapitite

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9
Q

Origin of Enamel

A

epithelial origin

made from ameloblasts

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10
Q

Origin of Dentin/pulp complex

A

mesenchymal origin

made from odontoblasts and these odontoblasts remain in pulp

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11
Q

Describe the characteristics of enamel rods

A
  • 4-8 um
  • Interlocking prisms with a head region (5um wide) and a tail region (5um long)
  • Rods are surrounded by an organic sheath
  • Rods are made of millions of crystallites
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12
Q

What are the crystallites within enamel rods made of? Describe their key features

A

Hydroxyapitite

  • needle-like
  • irregular in shape, but arranged in a regular pattern within an enamel rod
    - body is parallel to rod direction
    - tail is up to 65 degrees from prism or rod direction
  • make up the surrounding organic matrix
  • 200-400 Angstroms wide and 1600 Angstroms long
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13
Q

What is gnarled enamel

A

Occurs at cervical and incisal/occlusal areas and it is harder to cleave

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14
Q

What is interprismatic

A

An elaboration of dental enamel prisms that are separated by interprismatic substance and is softer than regular enamel prism and

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15
Q

% volume composition of Dentin

A

50% HA
25% collagen
25% water includes tubules

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16
Q

% weight composition of dentin

A

75% HA
20% collagen
5% water includes tubules

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17
Q

Purpose of dentin tubules

A

-allow fluid movement and ion transport to allow for remineralization, apposition of peritubular dentin and pain perception

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18
Q

what are odontoblastic processes

A

cytoplasmic extensions of the cell body (Tomes Fibers) from the dentin tubules

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19
Q

Tubules in superficial dentin are ______ and more ____ compared to deeper dentin

A

smaller and more sparsely distributed

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20
Q

Tubules in superficial and deep root dentin are ____ and _____ than those in comparable depths of coronal dentin

A

smaller

less numerous

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21
Q

Peritubular dentin is more mineralized than ___

A

intertubular dentin

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22
Q

Prinicpal organic component to dentin is ____. What is its purpose?

A

collagen (long rope-like protein)

adds toughness to dentin

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23
Q

How do the HA crystals within dentin differ from the HA crystals within enamel

A

smaller and 200-1000 Angstroms long with a 30 Angstrom diameter

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24
Q

What is predentin

A

unmineralized zone of dentin immediately adjacent to cell bodies of odontoblasts

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25
Q

Types of dentin

A 
primary
secondary
predentin
reparative dentin
sclerotic dentin
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26
Q

when does primary dentin exist

A

Forms up to 3 years after tooth eruption

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27
Q

What is secondary dentin

A

the directional change of dentin and decrease in deposition without any obvious stimulus

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28
Q

How does dentin differ from enamel

A
  • less mineral content
  • small tubules run throughout dentin (more fluid and ion transport)
  • Dentin has ability to repair or regnerate (physical chemical response and cellular response)
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29
Q

Four functions of dental pulp

A
  • Formative or developmental (production of primary and secondary dentin by odontoblasts)
  • nutritive (supplies nutrients and moisture to dentin through the blood vascular supply to odontoblasts)
  • sensory or protectives (nerve fibers for pain, ONLY PAIN response - no differentiation)
  • defensive or reparative (Inflammatory reaction to severe irritation)
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30
Q

Characteristics of cementum

A
  • light yellow, slightly lighter than dentin
  • lost as periodontum is lost
  • removed by scaling, polishing, and abrasion
  • slightly softer than dentin
  • permeable to a variety of materials
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31
Q

Composition of cementum

A

5-10% mineral content
45-50% Inorganic (HA)
50-55% organic matter and water by weight (Collagen and protein polysaccharides)
HIGHEST FLUORIDE CONTENT OF ALL MINERALIZED TISSUES

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32
Q

How is cementum formed

A
  • formed continually throughout life: acellular and cellular
  • formed by cemtoblasts which develop from undifferentiated mesenchymal cells in the connectivetissue of the dental follicle
  • can undergo self repair
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33
Q

What is dental caries

A

multifactorial transmissable, infectious oral disease caused by bacteria (biofilm)

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34
Q

things necessary to create a caries potential

A 
bacteria
carbohydrates
tooth structure (host)
time
(all are needed to yield active caries)
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35
Q

What is the modified view of caries

A

dental caries is the result of interaction between cariogenic oral flora (biofilm) with fermentable dietary carbs on the tooth’s surface over time, but several modifying and protective factors influence the dental caries process

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36
Q

Actual caries formation depends on

A

variety of lifestyle factors and genetic factors including primary and secondary factors

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37
Q

primary modifying affecting caries development

A 
Tooth anatomy
Saliva (pH and production)
Biofilm pH
Use of fluoride
Diet specifics
Oral hygiene
Immune system
Genetic factors
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38
Q

secondary modifying factors affecting caries development

A 
Socioeconomic status 
Education
Life-style
environment 
Age
Ethnic group
occupation
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39
Q

What is the view on caries at the tooth level

A
  • caries activity is characterized by localized demineralization and loss of tooth structure
  • bacteria in biofilm metabolize and produce organic acid as by-products which lowers the pH of the biofilm to below critical level.
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40
Q

A low pH in tooth structure causes what

A

calcium and phosphate to be driven from the tooth to the biofilm to reach an equilibrium that results in a netloss of minerals from the teeth. (reversing equilibrium can be done to an extent)

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41
Q

What is the caries balance

A

balance between demineralization and remineralization in terms of pathogenic vs protective factors

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42
Q

What are pathological factors

A 
(Demineralization) 
acid producing bacteria
sub-normal saliva flow 
Consumption of fermentable carbohydrates
Poor oral hygiene
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43
Q

What are protective factors

A

(remineralization)
Saliva (buffers pH) flow and components
Remineralization (fluoride, calcium, phosphate)
Anti-bacterials (fluoride, chlorhexidine, xylitol)
Good oral hygiene

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44
Q

Critical pH’s of biofilm

A
  1. 5 enamel (hydroxyapatite)
  2. 2 dentin
  3. 5 enamel w/ fluoride mineralization (hydroxyfluorapatite)
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45
Q

What is the key to caries management

A

understanding the balance between demineralization and remineralization

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46
Q

four parts to primary etiology of caries in a patient and describe each

A
  • Symptoms: demineralization lesions in teeth
  • Treatment, symptomatic: restoration of cavitated lesions.
  • Treatment, therapeutic: reverse pH equilibrium; ie, biofilm control, elevating biofilm pH, enhancing remineralization–>curing the disease.
  • Post treatment assessment, therapeutic: re-evaluation of etiologic conditions and primary and secondary risk factors; and continuous management based on findings.
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47
Q

▪Caries lesion. Tooth demineralization as a result of the caries process. Other texts may use the term carious lesion. Laypeople may use the term cavity. ▪Smooth-surface caries. A caries lesion on a smooth tooth surface.▪Pit-and-fissure caries. A caries lesion on a pit-and-fissure area.▪Occlusal caries. A caries lesion on an occlusal surface.▪Proximal caries. A caries lesion on a proximal surface.▪Enamel caries. A caries lesion in enamel, typically indicating that the lesion has not penetrated into dentin. (Note that many lesions detected clinically as enamel caries may very well have extended into dentin histologically.) ▪Dentin caries. A caries lesion into dentin.▪Coronal caries. A caries lesion in any surface of the anatomic tooth crown.▪Root caries. A caries lesion in the root surface.▪Primary caries. A caries lesion not adjacent to an existing restoration or crown.▪Secondary caries. A caries lesion adjacent to an existing restoration, crown, or sealant. Other term used is caries adjacent to restorations and sealants (CARS). Also referred to as recurrent caries, implying that a primary caries lesion was restored but that the lesion reoccurred.▪Residual caries. Refers to carious tissue that was not completely excavated prior to placing a restoration. Sometimes residual caries can be difficult to differentiate from secondary caries.

A

JUST REREAD THIS….. KEEP MARKING IT AS A 1 IF YOU HAVE TO. MOST OF THEM ARE COMMON SENSE. BUT I DIDN’T WANT O LEAVE ANYTHING OUT FROM SHARPLES SLIDES- SHOOTING FOR THE B ;)

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48
Q

What is a cavitated caries lesion

A

A caries lesion that results in the breaking of the integrity of the tooth, or a cavitation.

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49
Q

What is a non-cavitated caries lesion

A

caries lesion that has not been cavitated. In enamel caries, non-cavitated lesions are also referred to as “white spot” lesions.

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50
Q

What is an active caries lesion

A

A caries lesion that is considered to be biologically act

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51
Q

What is an inactive caries lesion

A

A caries lesion that is considered to be biologically inactive at the time of examination, that is, in which tooth demineralization caused by caries may have happened in the past but has stopped and is currently stalled. Also referred to as arrested caries, meaning that the caries process has been arrested but that the clinical signs of the lesion itself are still present

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52
Q

What are rampant caries

A

Term used to describe the presence of extensive and multiple cavitated and active caries lesions in the same person. Typically used in association with “baby bottle caries,” “radiation therapy caries,” or “meth-mouth caries.” These terms refer to the etiology of the condition.

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53
Q

What is dental plaque

A

soft, tenacious film accumulating on the surface of teeth. (biofilm)
composed of bacteria, their byproducts, extracellular matrix, and water

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54
Q

What is non-pathogenic bacterial plaque and its characteristics

A
  • It is when an acquired pellicle (natural biofilm) forms
  • Forms in 30-60 mins
  • Composition: salivary proteins, cell free.
  • Role of the pellicle is to Protect tooth via antibodies (IgA, IgG, lysozymes)
  • Reduces friction during remineralization
  • Both acidic and basic proteins that absorb calcium and phosphate ions.
  • Plaques become thick enough to readily take up a stain in aid to visual oral hygiene
55
Q

If bilfilm gets too thick, it will produce what

A

an anaerobic environment adjacent to the tooth surface

56
Q

Tooth habits favorable for harboring pathogenic biofilm

A

Pits and fissures
Smooth enamel surfaces on the gingival third near the proximal surfaces and facial and lingual surfaces.
Root surfaces, particularly near the cervical line.
Subgingival areas.

57
Q

Predominant bacterial species in mucosa and its environmental conditions within plaque

A

S. mitis
S. sanguis
S. salivarius

-aerobic, pH 7, oxidation-reduction potential postitive

58
Q

Predominant bacterial species in tongue and its environmental conditions within plaque

A

S. salivarius
S. mutans
S. sanguis

-aerobic, pH 7, oxidation-reduction potential postitive

59
Q

Predominant bacterial species in Teeth (non-carious) and its environmental conditions within plaque

A

S. Sanguis

-aerobic, pH 5.5, oxidation-reduction potential negative

60
Q

Predominant bacterial species in gingival crevice and its environmental conditions within plaque

A

Frutobacterium
Spirocheata
Actomyces
Veillonella

-anaerobic, pH variable, oxidation-reduction potential very negative

61
Q

Predominant bacterial species in enamel caries and its environmental conditions within plaque

A

S. Mutans

-anaerobic, pH < 5.5, oxidation-reduction potential negative

62
Q

Predominant bacterial species in dentin caries and its environmental conditions within plaque

A

S. Mutans

-anaerobic, pH < 5.5, oxidation-reduction potential negative

63
Q

Predominant bacterial species in root caries and its environmental conditions within plaque

A

Actinomyces

-anaerobic, pH < 5.5, oxidation-reduction potential negative

64
Q

What are the tooth habitats for cariogenic biofilm

A
  • Not protected by surface shedding mechanisms
  • Covered w/ pellicle of precipitated salivary components.
  • Ideal surface for the attachment of many oral streptococci
65
Q

The proximal root surface near the CEJ is often not brushed or flossed because it has concave anatomic structure known as

A

fluting and occasional roughness at the termination of enamel.

66
Q

Caries formation at a roots surface is more serious because

A

More rapid progression
Often asymptomatic
Closer to the pulp
More difficult to restore

67
Q

What is the role of oral hygiene when it comes to caries formation

A
  • Brushing and flossing is an ecological detriment of caries onset and formation.
  • Leaves a clean enamel surface and disrupts the biofilm
  • Brushing removed bacteria from tooth structure and it is then swallowed–but sufficient numbers remain on teeth to recolonize.
68
Q

What is the function of saliva and a few clinical correlations dealing with saliva

A
  • Natural anticaries agent
  • Some medications reduce saliva production
  • After radiation, saliva glands become fibrotic and produce little to no saliva (xerostomia)
69
Q

What are examples of salivary tooth mechanisms that maintain the normal flora in the mouth

A

bacterial clearance
direct antibacterial activity
buffers
remineralization

70
Q

What is bacterial clearance

A
  • Secretions from various saliva glands mix to form whole or mixed saliva.
  • Saliva production varies greatly over time
  • Lubricated oral tissue and bathes teeth and biofilm
  • Adults produce 1-1.5L of saliva a day–very little while asleep.
  • The flushing effect of this salivary flow is, by itself, adequate to remove virtually all microorganisms not adherent to an oral structure.
71
Q

Siliva contains a ___ property

A

direct antimicrobial property, but the normal resident oral flora apparently has developed resistance to most of its protective mechanisms

72
Q

What is buffer capacity of saliva and what is it determined by

A

-Determined by the concentration of bicarbonate ion
-The molecules within saliva that contribute to increasing the pH of biofilm (urea and sialin) by production of ammonia
(salivary testing should be done on patients with high caries activity – 5 mL per minute is normal)

73
Q

Saliva and biofilm are supersaturated with _____. How are these things controlled, so that the teeth do not become encrusted with minerals?

A

calcium and phosphate ions

saliva contains statherin to stabalize them (remineralization)

74
Q

Most important factor in producing cariogenic biofilm, and ultimately caries

A

high frequency exposure to fermentable carbs such as sucrose

75
Q

Exposure to ____ leads to the formation of caries

A

acidity (dried fruits, fruit drinks, sport drinks, other acidic foods/drinks)

76
Q

Once a tooth surface becomes cavitated, what happens

A

a more retentive surface becomes available to the biofilm because there is an increase in surface area. This rapidly increases the growth of the biofilm community

77
Q

What happens when caries lesions pass the DEJ

A

rapid lateral expansion occurs because dentin (highly acidic, anaerobic) is the ideal niche for bacteria

78
Q

Three distinct clinical sites for caries initiation

A

Pits and Fissures
Smooth Enamel Surfaces
Root Surfaces

79
Q

Bacteria that are found in pits and fissures

A

Large gram positive cocci (S. Sanguis in newly erupted teeth and S. Mutans in Adult teeth)

80
Q

Describe the progression of pit and fissure caries

A
  • Enamel becomes porous–> discoloration of the fissure
  • Accelerates decay movement into the dentin
  • bacteria expands into the dentin in an upside down triangular shape
  • Cavitation on the walls of the fissure cannot be seen
  • Remineralization of the enamel can make decay impossible to see underneath
  • Extensive cavitation can eventually darken enamel after underlying dentin is toasted
81
Q

What are the difficulties in diagnosing pit and fissure caries

A
  • Entry site may appear smaller than than actual lesion
  • develop from attack on their walls
  • Lots of surface area in a fissure compared to smooth surface enamel
  • Inverted V of decay
  • Enamel shows little decay, while dentin may be entirely compromised
82
Q

Why do smooth enamel surfaces present a less favorable site for cariogenic biofilm

A

Typically the areas do not have shelter. Caries usually develop near gingiva or under proximal contacts

83
Q

Describe the progression of smooth enamel caries

A

-Carie path = parallel to the enamel rods
-V shape is taken by the decay to break through enamel and reach the DEJ
-After DEJ, softening dentin spreads rapidly (Laterally and Pulpally)
(18 to 24 months for caries to fully invade into dentin in the proximal contact spaces, which is why we take xrays every two years)

84
Q

Characteristics of root surfaces and why they can readily allow cariogenic biofilm formation

A
  • Root surface is rougher than enamel allowing cariogenic biofilm to attach more easily
  • Cementum covering root is extremely thin and provides little resistance
  • More surface area on the roots for U shaped cross secions of caries due to lack of enamel covering
  • Old people have gingival recession which meansthey typically have cariogenic biofilm on exposed root surfaces
85
Q

Describe the progression of caries from noncavitated to cavitated

A

18 months +/- 6 (smooth surface enamel)

  • occlusal Pits and fissures slightly less time
  • White spots can appear in 3 weeks
  • Compromised patient–> rampant caries
  • Peak rates for incidence of caries occurs 3 years after eruption
  • xerostomia can lead to clinical caries development in 3 months
86
Q

What is enamel caries histopathology

A

Histo slides that show white spot progression and the remineralization of the enamel after a white spot
-artificial calcification can remineralize the tooth

87
Q

Four types of enamel caries

A

hypocalcified enamel
white spot lesion(noncavitated)
cavitated enamel lesion
remineralized enamel lesion

88
Q

Characteristics of hypocalcified enamel

A
  • developmental white spot that cannot remineralize
  • same wet or dry
  • not restored unless for esthetics
89
Q

Characteristics of white spot lesions

A
  • Demineralized but not cavitated
  • disappears when wet
  • chalky white when dry
  • Hard external surface-Not restored because they can remineralize
  • Retain most of their crystalline framework to serve as nucleating agents for remineralization
90
Q

Characteristics of cavitated enamel lesions

A
  • surface is distrubed or missing = active caries
  • soft, chalky surface
  • proximal lesions areinto dentin
  • lose most of their crystalline framework of enamel rods
  • CANNOT REMINERALIZE, and must be restored
  • When radiographically visible = dentin alteration has already occurred
91
Q

Characteristics of Remineralized Enamel lesions

A

(inactive caries)

  • Fluoride calcium and phosphate have remineralized over the previously decayed surface
  • Remineralization takes 3-6 months (6-8 weeks to see first changes)
  • Observed as Brown or black arrested lesions (color is by trapped organic debris)
  • More resistant to caries than the adjacent unaffected teeth
  • Every remineralization event makes tooth a little more resistant to decay= more hydroxyflouroapetite
  • Not restored unless esthetic
92
Q

Dentin contains ____ to provide a pathway for the ingress of bacteria and egress of minerals

A

less minerals and possesses microscopic tubules

93
Q

____ has the least resistance to caries attack and allows rapid lateral spreading when caries has penetrated the enamel

A

DEJ

94
Q

Rssponses of caries in dentin

A
  • pain, sensitivity, remineralization and demineralization

- decay runs down the tubules

95
Q

Two types of odontoblast tubules

A
  • Pulpal dentin (newer)

- External dentin (older)

96
Q

Describe the odontoblastic pulpal dentin tubules

A
  • More dense (tubules) at pupal wall = rapid decay
  • larger tubules= rapid decay
  • little peritubular dentin/ calcified intertubular dentin
97
Q

Describe the odontoblastic external dentin tubules

A
  • Smaller tubules and less dense
  • Greater mineral content
  • Larger peritubular dentin and calcified intertubular dentin
98
Q

Carious dentin lacks ____ causing what

A

minerals and cross-banding of collagen, which causes peritubular dentin to be removed once bacteria enters and the widening of external dentin tubules

99
Q

Three levels of dentinal reaction to caries that can be recognized are:

A
  • Long-term, low level acid demineralization associated with slowly advancing lesion
  • moderate intensity attack
  • severe, rapidly advancing caries characterized by very high acid levels
100
Q

Describe the reaction to slowly advancing caries lesion

A
  • long term, Low level Demineralization, low level acid
  • Pulp tissue can become inflamed if enamel or dentin is exposed to microorganisms, but inflammation is less likley
  • Hypermineralization can occur at advancing infected line = Sclerotic dentin
101
Q

What is sclerotic dentin

A

shiny, dark, hard hypermineralized dentin

102
Q

Describe the reaction to a moderate intensity attack caries lesion

A
  • High acid levels, Hydrolytic enzymes, bacteria, bacterial cellular debris
  • Degeneration or death of odontoblast- mild inflammation
  • Secondary odontoblasts= produce reparative dentin
  • Severe stimuli can create pulp stones in pulp chamber
103
Q

Describe the reaction to rapidly advancing caries lesion

A
  • High levels of acidic production, infection, Abscess

- Pulp death–> impaired blood supply

104
Q

Advancement of caries in dentin occurs through what three changes

A

Weak organic acid demineralizes dentin
Collagen Dissolves
Structural loss–> bacterial invasion

105
Q

3 zones of dentin caries

A

normal dentin
affected dentin
infected dentin

106
Q

What is zone 1 of dentin caries

A

(NORMAL DENTIN)

  • tubules with smooth odontoblastic processes
  • normal cross-banded collagen and dense apatite crystals
  • Deepest, normal odontoblasts
  • No bacteria
  • Normal Collagen
  • stimulation (with bur) induces sharp pain
107
Q

What is zone 2 of dentin caries

A

(AFFECTED DENTIN)

  • Demineralization and odontoblast process
  • Softer and shows loss of mineral from intertubular dentin and large crystals in lumen = pain
  • Collagen banding decreased, but repair still possible as long as pulp remains vital
108
Q

zone 2 of dentin caries can be classified into what 3 subzones

A
  • Subtransparent Dentin
  • Transparent Dentin
  • Turbid Dentin
109
Q

What is zone 3 of dentin caries

A

(INFECTED DENTIN or CARIOUS DENTIN)

  • Zone of bacterial invasion marked by widening of tubules, which are filled with bactera
  • Little mineralization
  • Collagen band unrepairable
  • removable is essential
110
Q

What is tooth centered intervention

A

surgical intervention to eliminate cavitated lesions

111
Q

What is patient centered intervention

A

use of a medical model to control the disease process

112
Q

purpose of caries risk assessment and the steps to a caries risk assessment

A

purpose: to establish a risk level
- Gather current and recent data
- interview patient
- conduct test (saliva, bioload)
- establish risk level for potential new lesions
- establish a treatment plan

113
Q

Types of forms for caries risk assessment

A

ADA Form
UNC Form
Cari-Free Form
Osu Form

114
Q

How to get to caries risk assessment in axium

A

Forms -> add form -> AAMDHX

115
Q

Parts to Axium caries risk assessment

A

-High risk indicators at top that are ten points each
-Other risk factors after high risk indicators that are 1 point each
(Low risk = 0, Moderate risk = 1-9, High risk = >10)

116
Q

What are axium low risk minimal recommendations

A
  • Bitewings every 24-36 months (ADA)
  • periodic recall exams every 6-12 months
  • OTC fluoride containing toothpaste twice daily
117
Q

What are axium moderate risk recommendations

A
  • Bitewings every 18-24 months (ADA)
  • periodic recall exams every 4-6 months
  • OTC fluoride containing toothpaste twice daily
  • NaF rinse daily
118
Q

What are axium high risk minimal recommendations

A
  • Bitewings every 6-18 months (ADA)
  • periodic recall exams every 3-4 months
  • Xylitol gum (two tabs of gum or candy)
  • Rx: 1.1% NaF toothpaste twice daily
  • Chlorohexidene gluconate rinse
  • NaF varnish at every visit
119
Q

Social status and economic status are not directly involved in the disease process but are important because

A
  • they affect the expression and management of the caries disease. (access to health care/ able to afford health care)
  • these are predictive at the population level but are generally inaccurate at individual level.
120
Q

How do sport drinks, fruit juices and soft drinks contribute to increasing caries risk

A
  • By providing energy to the acidogenic and aciduric bacteria to influence pH of the biofilm. (MORE ATP = LOWER pH)
  • Frequency of snacking and consumption of sugary foods increases caries risk factors as well, by modifying biofilm to support a lower pH
121
Q

What is a salivary analysis

A
  • analysis of Flow rate, buffering capacity, and pH
  • Not supported in all case analysis
  • patients with good saliva flow/buffering can still have caries
  • Dry mouth= high risk
122
Q

Purpose of Dental Exam and its indicators

A

-Determine risk indicators more than risk factors.
-Determine process of intervention
-Indicators: visible white spots and brown spots.
Visible plaque and biofilm is also kind of an indicator.
-Other indicators: exposed root surfaces, deep pits and grooves, fixed, removable prosthesis, or orthodontic appliances used, poor quality existing restorations with open contacts, open margins, or overhangs

123
Q

Purpose of biofilm analysis

A
  • indicate risk level

- has potential for bias

124
Q

Presence of S. Mutans or lactobacilli in saliva or plaque as a sole predictor for caries in primary teeth has been shown to have ____ during biofilm analysis

A

low sensitivity but high specificity

125
Q

Risk considerations for children under six years old

A
  • Presence of active caries in primary caregiver
  • Feeding on demand past 1 year of age
  • Bedtime bottle–anything other than water
  • Unsupervised brushing
  • Severe enamel hypoplasia
126
Q

Describe caries management and potocols/ strategies for prevention

A
  • restoration of a caries lesion should no longer be considered a cure
  • practitioner must determine patients who have active caries and those at high risk for caries
127
Q

Purpose of preventivie treatment methods and the methods included

A

starts with a consideration of overall resistance of the patient to infection by cariogenic bacteria nad is designed to limit tooth demineralization caused by cariogenic bacteria
-limiting pathogen growth and altering metabolism
-increasing the resistance of the tooth surface to
demineralization
-increasing biofilm
pH

128
Q

Factors influencing caries risk

A
  • General Health
  • Diet
  • Oral Hygiene
  • Fluoride Exposure
  • Immunization (Caries)
  • Function of Saliva
  • Antimicrobial Agents
  • Calcium and Phosphate Compounds
  • Probiotics
  • Sealants
  • Restorations
129
Q

Concentration of fluoride in water

A

1 ppm

130
Q

Growing clinical and scientific evidence indicates that large carious lesions with healthy pulpal and periapical tissues should be managed via

A

partial caries excavation and indirect pulp capping

131
Q

Partial caries excavation followed by indirect pulp capping via

A

placement of a sedative restoration has significant benefits

132
Q

Strategies to prevent caries

A

-FIRST strategy is to try to improve salivary flow rates and increase the
buffering capacity.
-SECOND strategy is to try to reduce the numbers of cariogenic bacteria (S.
mutans) in the oral cavity.
-THIRD strategy is to reduce the quantity and numbers of exposures of
ingested refined carbohydrates.
-FOURTH strategy is to attempt to remineralize noncavitated lesions and prevent new
lesions from developing.
(RECOMMEND USE OF powered toothbrushes)

133
Q

DO NOT FORGET TO LOOK AT THE PACKET

A

WOOOOOOO :)

OSU Cariology (1 decks)

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