Cariology Midterm Part 2 Flashcards - Quizlet

Cariology Midterm Part 2
Terms in this set (88)
Large variations exist in the microflora found in pits

Pits & Fissures: Bacteria and fissures, suggesting that each site can be
considered a separate ecologic system
The caries lesion is the product of disequilibrium

What is the caries lesion a
between the demineralization and remineralization
product of?
processes
What are the three distinctly A. Pits and Fissures
different clinical sites for caries B. Smooth Enamel Surfaces
initiation? C. Root Surfaces
What kind of bacteria are Numerous gram-positive cocci, especially S. sanguis

frequently found in the pits and
fissures of newly erupted
teeth?
What kind of bacteria is found large numbers of MS

in carious pits and fissures?
The long, narrow fissure prevents adequate biofilm

removal
Physical Properties of Pits and

Considerable morphologic variation exists in these
Fissures & Bacteria
structures. Some pits and fissures end blindly,
others open near the dentin, and others penetrate
entirely through the enamel.
Pit-and-fissure caries expands as it penetrates into
the enamel
The entry site may appear much smaller than the

actual lesion, making clinical diagnosis difficult.
Caries lesions of pits and fissures develop from
attack on their walls.
Progression of the dissolution of the walls of a pit-

Why is it difficult to diagnose and-fissure lesion is similar in principle to that of the
caries? smooth- surface lesion because a wide area of
surface attack extends inward, paralleling the
enamel rods. A lesion originating in a pit or fissure
affects a greater area of the DEJ than does a
comparable smooth-surface lesion. In cross-
section, the gross appearance of a pit-and-fissure
lesion is an inverted "V" with a narrow entrance and
a progressively wider area of involvement closer to
the DEJ.
The initial lesions develop on the lateral walls of the

fissure. Demineralization follows the direction of the
enamel rods, spreading laterally as it approaches
First stage of caries in Pits & the dentinoenamel junction (DEJ).
Fissures

Soon after the initial enamel lesion occurs, a
reaction can be seen in the dentin and pulp.
Forceful probing of the lesion at this stage can

result in damage to the weakened porous enamel
and accelerate the progression of the lesion.
Clinical detection at this stage should be based on

Second stage of caries in Pits &
observation of discoloration and opacification of
Fissures
the enamel adjacent to the fissure. These changes
can be observed by careful cleaning and drying of
the fissure.
Initial cavitation of the opposing walls of the fissure

cannot be seen on the occlusal surface.
Opacification can be seen that is similar to the

previous stage.
Third stage of caries in Pits & Remineralization of the enamel because of trace
Fissures amounts of fluoride in the saliva may make
progression of pit-and-fissure lesions more difficult
to detect.

Extensive cavitation of the dentin and undermining
of the covering enamel darken the occlusal surface
Fourth stage in Pits & Fissures
present a less favorable site for cariogenic biofilm

attachment
Cariogenic biofilm usually develops only on the

smooth surfaces that are near the gingiva or are
Smooth Enamel Surfaces under proximal contacts.
The proximal surfaces are particularly susceptible

to caries because of the extra shelter provided to
resident cariogenic biofilm owing to the proximal
contact area immediately occlusal to it

Lesions starting on smooth enamel surfaces have a
broad area of origin and a conical, or pointed,
extension toward the DEJ.
The path of ingress of the lesion is roughly parallel

to the long axis of the enamel rods in the region. A
cross-section of the enamel portion of a smooth-
Smooth Enamel Surface Caries surface lesion shows a V-shape, with a wide area of
origin and the apex of the V directed toward the
DEJ. After caries penetrates the DEJ, softening of
dentin spreads rapidly laterally and pulpally.
is rougher than enamel
• Readily allows cariogenic biofilm formation in the

absence of
good oral hygiene
Root Surface Caries • Cementum covering the root surface is extremely

thin and provides little resistance to caries attack.
• Critical pH for dentin is higher than for enamel, so

demineralization is likely to start even before the pH
reaches the critical level for enamel (pH = 5.5)
Critical pH for dentin is higher than for enamel, so

Why is demineralization likely
demineralization is likely to start even before the pH
in exposed dentin?
reaches the critical level for enamel (pH = 5.5).

Root caries lesions have less well-defined margins,
tend to be U-shaped in cross-section, and progress
Root Caries
more rapidly because of the lack of protection from
an enamel covering
Recently, prevalence of root caries has increased

significantly because of the increasing number of
Why are root caries more
older persons who retain more teeth, experience
prevalent now?
gingival recession, and usually have cariogenic
biofilm on the exposed root surfaces.
The time for progression from non-cavitated caries

What is the progression time
to clinical caries (cavitation) on smooth surfaces is
for cavitation on smooth
estimated to be 18 months ± 6 months. Peak rates for
surfaces?
the incidence of new lesions occur
When is the peak rate for the 3 years after the eruption of the tooth
incidence of new lesions
occur?
What cavitates more quickly, Occlusal pit-and-fissure lesions develop in less time
pit/fissures or smooth than smooth-surface caries.
surfaces?
Poor oral hygiene and frequent exposures to

sucrose- containing or acidic food can produce
White spot lesions
noncavitated ("white spot") lesions (first clinical
evidence of demineralization) in 3 weeks.
What is the first clinical white spot lesions

evidence of demineralization?

Radiation-induced xerostomia (dry mouth) can lead
Xerostomia to clinical caries development in 3 months from the
onset of the radiation
Caries development in healthy individuals is usually

Caries development in
slow compared with the rate possible in
compromised pt's
compromised persons.
Surface (a) appears to be intact.
Body of lesion (b) shows enhancement of striae of

Retzius.

Dark zone (c) surrounds body of lesion, whereas

Enamel Caries Histology
translucent zone (d) is evident over entire
advancing front of lesion.
Non-cavitated enamel caries White spot lesion

lesion
Caveated Enamel Lesion Active Caries
Remineralized Enamel Lesion Inactive Caries
• Developmental white spot.
Hypo calcified Enamel • Same wet or dry.
• Do not restore unless for esthetics.

Demineralized but not cavitated.
• Disappear when wet.
• Chalky, white when desiccated.
• Hard external surface.
• Do not restore.
• Proximal lesions in enamel.
• When a proximal lesion is clearly visible

radiographically, the lesion may have advanced
White Spot Lesion Overview significantly, and histologic alteration of the
underlying dentin probably already has occurred,
whether the lesion is cavitated or not.
• Noncavitated enamel lesions retain most of the

original crystalline framework of the enamel rods,
and the etched crystallites serve as nucleating
agents for remineralization.
Noncavitated caries of enamel can remineralize.
What is a key indicator of a Disappear when wet

white spot lesion?
(Active Caries)
Surface is disturbed or missing.
• Soft, chalky surface discernible with an explorer
How to detect a Cavitated

• Cavitated enamel lesions lose most of the original
Enamel Lesion
crystalline framework of the enamel rods.
Can not remineralize, must be restored
The supersaturation of saliva with calcium and

What is the driving force of
phosphate ions serves as the driving force for the
remineralization?
remineralization process.

greatly enhances the precipitation of calcium and
Presence of trace amounts of
phosphate, resulting in the remineralized enamel
fluoride ions during
becoming more resistant to subsequent caries
remineralization greatly
attack because of the incorporation of more acid-
enhance?
resistant fluorapatite.
observed clinically as intact, but discolored, usually

brown or black, spots. The change in color is
presumably caused by trapped organic debris and
metallic ions within the enamel.
These discolored, remineralized, arrested caries

What of remineralized lesions areas are intact and are more resistant to
look like? subsequent caries attack than the adjacent
unaffected enamel. They should not be restored
unless they are esthetically objectionable.

Enamel interacts with its fluid environment in
periods of undersaturation and supersaturation.
Undersaturation periods dissolve most soluble

mineral at the site of cariogenic attack, whereas
periods of supersaturation deposit most insoluble
minerals if their ionic components are present in
immediate fluid environment.
As a result, under favorable conditions of

Remineralization Cycles remineralization, each cycle could lead toward
higher enamel resistance to a subsequent
challenge.
Enamel Caries Summary
(know this chart--> several

exam questions)
Progression of caries in dentin is different from

Dentin Caries progression in the overlying enamel because of the
structural differences of dentin.

Dentin contains much less mineral and possesses
microscopic tubules that provide a pathway for the
ingress of bacteria and egress of minerals.
•Because of these characteristics, dentinal caries is

Dentin characteristics V-shaped in cross- section with a wide base at the
DEJ and the apex directed pulpally.
•Caries produces a variety of responses in dentin,

including pain, sensitivity, demineralization, and
remineralization.
The DEJ
What area has the least
resistance to caries attack? allows rapid lateral spreading when caries

penetrate the enamel
Caries advances more rapidly in dentin than in

Why do caries advance more enamel because dentin provides much less
rapidly in Dentin? resistance to acid attack owing to less mineralized
content.
- epithelial origin
- Ameloblasts extinct after deposition
Enamel Development

- mesenchymal origin
- Odontoblasts remain in pulp

Dentin/Pulp Complex
Development
1-2% protein
4-8% water
90-95% inorganic (HA) --> mineralized

What is the composition of
enamel?
50 vol% HA --> (75% weight)
25% vol Collagen--> (20% weight)
What is the composition of

25 vol% water includes tubules --> (5% weight)
Dentin?

(A) As dentin grows, odontoblasts become
increasingly compressed in the shrinking pulp
chamber, and the number of associated tubules
becomes more concentrated per unit area.
The more recently formed dentin near the pulp (a)

has large tubules with little or no peritubular dentin
and calcified intertubular dentin filled with collagen
fibers. Older dentin, closer to the external surface
(b), is characterized by smaller, more widely
separated tubules and a greater mineral content in
intertubular dentin.
Dentin Dev. The older dentin tubules are lined by a uniform

layer of mineral termed peritubular dentin. These
changes occur gradually from the inner surface to
the external surface of the dentin. Horizontal lines
indicate predentin; diagonal lines indicate
increasing density of minerals; darker horizontal
lines indicate densely mineralized dentin and
increased thickness of peritubular dentin. The
transition in mineral content is gradual.

Carious dentin undergoes several changes. The
most superficial infected zone of carious dentin (3)
is characterized by bacteria filling the tubules and
granular material in the intertubular space.
The granular material contains very little mineral and

lacks characteristic cross-banding of collagen. As
bacteria invade dentinal tubules, if carbohydrates
are available, they can produce enough lactic acid
to remove peritubular dentin. This doubles or triples
the outer diameter of the tubules in infected dentin
zone.
Pulpal to (below) the infected dentin is a zone

Caries dev. in Dentin
where the dentin appears transparent in mounted
whole specimens. This zone (2) is affected (not
infected) carious dentin and is characterized by loss
of mineral in the intertubular and peritubular dentin.
Many crystals can be detected in the lumen of the
tubules in this zone. The crystals in the tubule lumen
render the refractive index of the lumen similar to
that of the intertubular dentin, making the zone
transparent. Normal dentin (1) is found pulpal to
(below) transparent dentin.

(1) reaction to a long-term, low-level acid
demineralization associated with a slowly advancing
lesion
Three levels of reaction in

pulp-dentin complex caries

(2) reaction to a moderate-intensity attack
reaction

(3) reaction to severe, rapidly advancing caries

characterized by very high acid levels
• Repair demineralized dentin by remineralization.
• Early stages of caries or mild caries attacks

produce long-term, low-level acid demineralization
of dentin.
• Direct exposure of the pulp tissue to

microorganisms is not a prerequisite for an
Reaction to a long-term, low-
inflammatory response. Even when the lesion is
level acid demineralization
limited to enamel, the pulp can be shown to
associated with a slowly
respond with inflammatory cells.
advancing lesion
• Hypermineralized areas may be seen on
radiographs as zones of increased radiopacity
ahead of the advancing, infected portion of the
lesion. (Called sclerotic dentin, shiny, dark, and
hard)
• This repair occurs only if the tooth pulp is vital.

More intense caries activity results in bacterial
invasion of dentin by a wide variety of pathogenic
materials or irritants, including high acid levels,
hydrolytic enzymes, bacteria, and bacterial cellular
debris.
• Can cause the degeneration and death of

odontoblasts and a mild inflammation of the pulp.
• Cause formation (from undifferentiated

mesenchymal cells) of replacement odontoblasts
(secondary odontoblasts).
• These cells produce reparative dentin (reactionary

dentin) on the affected portion of the pulp chamber
wall
Reaction to a moderate- • The structure of reparative dentin varies from well-

intensity attack organized tubular dentin (less often) to very
irregular atubular dentin (more often
• An effective barrier to diffusion of material through

the tubules and is an important step in the repair of
dentin. Severe stimuli also can result in the
formation within the pulp chamber of unattached
dentin, termed pulp stones, in addition to reparative
dentin.
• The success of dentinal reparative responses

depends on the severity of the caries attack and the
ability of the pulp to respond. The pulpal blood
supply may be the most important limiting factor to
the pulpal responses.
What may be the most the plural blood supply

important limiting factor to
pulpal responses?

High levels of acid production overpowers dentinal
defenses and results in:
• Infection,
Reaction to severe rapidly

• Abscess, and
advancing caries
• Death of the pulp, usually due to impaired blood
supply.
Caries advancement in dentin proceeds through

three changes:
(1) Weak organic acids demineralize dentin
Zones of Dentin Caries (2) The organic material of dentin, particularly

collagen, degenerates and dissolves
(3) The loss of structural integrity is followed by

invasion of bacteria
• Zone 1: Normal Dentin
What are the zones of dentin

• Zone 2: Affected Dentin
caries?

• Zone 3: Infected Dentin
The deepest area is normal dentin, which has

tubules with odontoblastic processes that are
smooth, and no crystals are present in the lumens.
The intertubular dentin has normal cross-banded

Zone 1: Normal Dentin
collagen and normal dense apatite crystals. No
bacteria are present in the tubules. Stimulation of
dentin (e.g., by osmotic gradient [from applied
sucrose or salt], a bur, a dragging instrument, or
desiccation from heat or air) produces a sharp pain.

Also called inner carious dentin
• A zone of demineralization of intertubular dentin

and of initial formation of fine crystals in the tubule
lumen at the advancing front.
• Damage to the odontoblastic process is evident.
• Softer than normal dentin and shows loss of

mineral from intertubular dentin and many large
crystals in the lumen of the dentinal tubules.
• Stimulation of affected dentin produces pain.
• Collagen cross-linking remains intact in this zone.
Zone 2: Affected Dentin • The intact collagen can serve as a template for
remineralization of intertubular dentin, and this
region remains capable of self-repair, provided that
the pulp remains vital.
• The affected dentin zone can also be subclassified

in three sub-zones:
(1) subtransparent dentin
(2) transparent dentin
(3) and turbid dentin.
carious layer, the layer that the clinician would

encounter first when opening a lesion
• The zone of bacterial invasion and is marked by

widening and distortion of the dentinal tubules,
which are filled with bacteria.
Zone 3: Infected Dentin • Little mineral is present, and the collagen in this
zone is irreversibly denatured.
• The dentin in this zone does not self-repair.
• This zone cannot be remineralized, and its removal

is essential to sound, successful restorative
procedures and the prevention of spreading the
infection.

During caries excavation, the goal is to remove only
infected dentin, while affected dentin is
remineralizable and can be maintained. For
orientation of layers on tooth.
Zones of dentin
The occlusal enamel appears intact, with a small

opening in the occlusal fissure.
Enamel is darkened where it is undermined by

demineralization. The surface of enamel is
unaffected. The lesion is filled with a bacterial plug
containing high numbers of mutans streptococci
(MS) and lactobacilli. Dentin is infected below the
Appearance of Dentin Zones
plug. Deeper dentin is not infected but is
extensively demineralized. Reparative dentin is
being formed below the lesion.

Increasing demineralization of thebody of the
enamel lesion results in the weakening and eventual
collapse of the surface enamel.
The resulting cavitation provides an even more

protective and retentive habitat for the cariogenic
biofilm, accelerating the progression of the lesion.
Advanced Caries Lesion
TheDEJ provides less resistance to the carious

process than either enamel or dentin.
• The resultant lateral spread of the lesion at the DEJ

produces the characteristic second cone of caries
activity in dentin.
Tooth Centered is surgical intervention to eliminate

Tooth Centered Care
cavitated lesions.
use a medical model to control the disease process.
*Caries Risk Assessment to establish Risk Level
*Individual Risk Indicators
Patient Centered Care

*Individual Risk Factors
*Protective factors
*Non-surgical therapeutics and dental surgical

interventions.
Gather Data on current and recent dental history
*Interview patient to determine risk factors
*Conduct tests to determine status of saliva, bio-
Caries Risk Assessment load, and any other pertinent data.
*Establish a risk level for each patient that indicates

their level of risk to develop new lesions.
*Establish a caries treatment plan or protocol.

Go over the caries risk **************************************************
assessment forms!
are not directly involved in the disease process but

are important because they affect the expression
and management of the caries disease.
The socioeconomic status and educational status of

Social, Economic and
the patient have implications on the necessary
Education Status
compliance and behavioral changes that can
decrease risk for caries in patients.
These are predictive at the population level but are

generally inaccurate at the individual level.
Sugar intake in the form of fermentable

carbohydrates and increased frequency of intake
are conditions that increase risk for caries.
*The use of candies and lozenges frequently during

the day or night increases the risk.
*Acidic beverages, including sport drinks, fruit

juices, and soft drinks, all contribute to increasing
Dietary Analysis
risk by providing energy to the acidogenic and
aciduric bacteria and by influencing the pH of the
biofilm to support cariogenic bacteria.
*Frequency of snacking and the frequency of

consuming these foods and beverages all support
an increase in biologic caries risk factors by
modifying the biofilm to support a lower pH
environment.

Salivary flow rate, buffering capacity, and pH all can
be measured by different tests and means.
The predictive value for these tests for caries is not

Salivary Analysis supported by the highest evidence in all
circumstances.
Patients with good saliva flow and adequate

buffering can still have caries.
In cases of dry mouth, or xerostomia, a salivary

analysis is a predictive risk factor for root caries in
Dry Mouth/xerostomia
older patients with recession and for increased
caries in general in other populations.
inhibition of bacteria, diluting and eliminating

bacteria and their substrates, buffering bacterial
Saliva's role in protection
acids, and offering a reparative environment with
against caries
necessary calcium and phosphate minerals after
bacteria-induced demineralization.
These patients are more susceptible to dietary

changes that are associated with lower pH foods
Why are patients with dry and beverages or foods and beverages containing
mouth at higher risk for caries? fermentable carbohydrates, since the protective
factors of saliva are diminished in patients with
xerostomia.

Determines risk indicators more than risk
factors.Many of the indicators are directly related to
the current caries activity .
*Indicators and current caries activity drive the

decision making process for the type of
intervention.
*Visible cavitated caries lesions,white spots on

teeth, and brown spots on teeth are all indicators
Dental Exam for caries risk.
*Visible plaque or biofilm can be considered a risk

factor for caries development.
Other examination findings that would influence

increased risk for caries are exposed root surfaces,
deep pits or grooves, fixed, removable prosthesis,
or orthodontic appliances used, poor quality
existing restorations with open contacts, open
margins, or overhangs.

Use of supplemental tests to analyze the bacterial
component of the biofilm can help determine the
patient's risk level.
However, the evidence is weaker with some

potential for bias by the examiners for these tests
being predictive of future caries. For example, the
presence of S. mutans or lactobacilli in saliva or
plaque as a sole predictor for caries in primary
teeth was shown to have low sensitivity but high
Bacterial Biofilm Analysis specificity. Other means of bacterial testing still
being evaluated is the measurement of adenosine
triphosphate (ATP) activity of the biofilm bacteria as
a surrogate measure of caries activity.
Although these bacterial tests can be useful for

communication with the patient and can provide
insight into the type of bacteria present and the
type of biofilm environment present, predictive
evidence for caries from these tests need to be
further studied and improved.
presence of active caries in the primary caregiver in

the past year
*feeding on demand past 1 year of age
What are the age-specific risk
factors for children under 6? * bedtime bottle or sippy cup with anything other
than water
*no supervised brushing; and severe enamel

hypoplasia.

In a modern practice model, the restoration of a
caries lesion should no longer be considered a cure
for dental caries.
Modern Practice Model Rather, the practitioner must identify patients who
have active caries lesions and patients at high risk
for caries and institute appropriate preventive and
treatment measures.
Preventive treatment methods are designed to limit

tooth demineralization caused by cariogenic
bacteria, preventing cavitated lesions.
(1) limiting pathogen growth and altering

metabolism
Strategies for prevention
(2) increasing the resistance of the tooth surface to

demineralization
(3) increasing biofilm pH. A caries prevention and

management program is a complex process
involving multiple interrelated factors
reduce the numbers of cariogenic bacteria and to

create an environment conducive to
remineralization.
What is the primary goal of

caries prevention?
Prevention should start with a consideration of the
overall resistance of the patient to infection by the
cariogenic bacteria.

*General Health
*Diet
*Oral Hygiene
*Fluoride Exposure
*Immunization (Caries)
What are the factors that * Function of Saliva
influence caries risk? *Antimicrobial Agents
*Calcium and Phosphate Compounds
*Probiotics
*Sealants
*Restorations
Fluoride Exposure
Antimicrobial Agents
refers to an operative procedure in which multiple

What does "Caries Control"
teeth with acute threatening caries are treated
mean
quickly

(1) removing the infected tooth structure
(2) medicating the pulp, if necessary
(3) restoring the defect(s) with a temporary material.

What are the steps of caries

With this technique, most of the infecting organisms
control restoration?
and their protecting sites are removed, limiting
further acute spread of caries throughout the
mouth. The caries-control procedure must be
accompanied by other preventive measures.
Caries Control Restoration

Overview

Teeth that have large caries lesions but no overt
pulpal or periapical pathology should be managed
conservatively.
*It is generally not advisable to initiate definitive

root canal therapy for asymptomatic teeth with a
healthy pulp and healthy periapical area.
* Growing clinical and scientific evidence indicates

that large carious lesions with healthy pulpal and
Partial Caries Excavation and
periapical tissues should be managed via partial
Indirect Pulp Capping
caries excavation and indirect pulp capping.
*Aggressive complete caries removal that invades

the pulp space and forces a decision of definitive
root canal treatment or extraction in the context of
caries control is to be avoided.
*Partial caries excavation followed by indirect pulp

capping via placement of a sedative restoration has
significant benefits.
What should you follow once a an aggressive preventive protocol.
patient has been determined
to be high risk for ROOT This protocol is based upon four primary strategies
caries? for the prevention of root caries.

1) try to improve salivary flow rates and increase the
buffering capacity
2) try to reduce the numbers of cariogenic bacteria

(S. mutans) in the oral cavity.
What are the four primary
strategies for the prevention of 3)reduce the quantity and numbers of exposures of
root caries? ingested refined carbohydrates.
4) attempt to remineralize noncavitated lesions and

prevent new lesions from developing.
* use of powered toothbrushes. It is critical that

patients susceptible to root caries practice
meticulous oral hygiene. However, many of these
patients have physical and visual deficiencies, and
this makes it difficult for them to adequately cleanse
the mouth. For these patients, a powered
What should you recommend
toothbrush may be advantageous
to patients with high risk for

root caries?
*Restore all root caries lesions with a fluoride-
releasing material. Resin-modified glass ionomer
materials are preferred for definitive restorations
primarily because they bond effectively to both
enamel and dentin and they act as reservoirs for
fluoride which can be re-released into the oral
Why are resin-modified glass because they bond effectively to both enamel and
ionomer materials preferred dentin and they act as reservoirs for fluoride which
for definitive restorations? can be re-released into the oral

Risk Indicator: more likely to have more decay
(best indicator that you are going to get new decay

is if you have decay today!)
Risk Indicator vs. Risk Factor
Risk Factor: drinking sugary drinks etc.

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Cariology Midterm Part 2

Terms in this set (88)

Large variations exist in the microflora found in pits

The caries lesion is the product of disequilibrium

What are the three distinctly A. Pits and Fissures

different clinical sites for caries B. Smooth Enamel Surfaces

initiation? C. Root Surfaces

What kind of bacteria are Numerous gram-positive cocci, especially S. sanguis

What kind of bacteria is found large numbers of MS

The long, narrow fissure prevents adequate biofilm

Physical Properties of Pits and

The entry site may appear much smaller than the

Progression of the dissolution of the walls of a pit-

The initial lesions develop on the lateral walls of the