Dental caries

Dr. Iman Jirjees Ahmed

 What is
dental caries?
 Disintegration
Latin word of hard tissue as
“Dry rot” a result of
bacterial action.

Dental caries is infectious

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

Disintegration
of
E, D & C
-tooth-
 Etiology
of Host
Dental Caries.

Time Diet

Dental caries

Biofilm

Dental caries is
Tooth-Biofilm-Carbohydrate interaction
(Keyes-Jordan diagram)
Not all person wit teeth,
biofilm & consuming
carbohydrates will have
caries over time!!!!
Pathophysiology

?
of
dental caries.
 Thick plaque
visible to the eye.

Soft, tenacious film, Biofilm

not adherent of food
debris.
Composition
Structure
Plaque (pH) Tooth surface

Mature plaque

Stephan curve
Plaque (pH) Tooth surface

Tooth

Stephan curve
Tooth
 Demineralization-Remineralization
take place several times a day over the life of the tooth.
 Caries Balance
Not all
person will
have caries
over time
Poor Oral
hygiene
Fermentable
CHO

Frequent sucrose exposure

maintain pH depression at he tooth surface
resulting in demineralization.
 Benefits of saliva are missing when
patients have salivary hypo-function

Radiation to Medication:
the head Antidepressants
and Diuretics
neck Antihypertensive

Xerostomia

Higher risk for caries.

 The flushing effect of
salivary flow is remove
Bacterial clearance micro. & dilute and
buffer biofilm acids.

Buffers Direct
antibacterial
Concentration of Saliva activity
bicarbonate ion; Natural anti caries agent
reduce the potential for 1-1.5L/day
acid formation. Salivary proteins
(lysozyme,
lactoperoxidase,
Remineralization lactoferrin and
agglutinins)
Saliva supersaturated with
calcium and phosphate ions.
 Protective factors

 Good oral hygiene.

 Healthy diet.
Pathological factors  Normal saliva
flow/function.
 Poor oral hygiene.  Antibacterial (fluoride,
 Frequent eating/drinking CHX, xylitol).
fermentable CHO.
 Sub normal saliva
flow/function.
 Acid producing bacteria.
No Caries

Caries
Caries imbalance
 Pathological factors

 Poor oral hygiene.

 Frequent eating/drinking
fermentable CHO. Protective factors
 Sub normal saliva
flow/function.  Good oral hygiene.
 Acid producing bacteria.  Healthy diet.
 Normal saliva
flow/function.
 Antibacterial (fluoride,
CHX, xylitol).

Caries

No Caries
Remineraliaztio
n
 Dental caries is dynamic process
Understanding the balance between
demineralization & re-mineralization
is

key to caries management?

 Smooth enamel surfaces

Clinical sites
for caries
initiation?
Pits and fissures Root surfaces

Smooth enamel surfaces

 Shallow
groove

Open into an
End blindly irregular
Complete
chamber
penetration of E.
 Primary
grooves/fossae

Smooth "valley/saucer" landmarks

Complete coalescence
of developmental
lobes

Cleansed by the rubbing action of food

during mastication
 Smooth enamel surfaces

Protected from the

effects of
Mastication
Tongue movement
Salivary flow
 Root surfaces

Roughness Plaque formation

Thin Little resistance

cementum to caries

Dentin
si on critical pH 6. 2-6.7
e s
ec
lr
i va Proximal Unaffected by flossing
i ng fluting
G Proximal root caries

Plaque formation
 Root surfaces
Neglected in hygiene
procedure
Gum recession
Caries originating on the root is
alarming because:

 Rapid progression.
 Asymptomatic.
 Closer to the pulp.
 More difficult to restore.

Not rubbed by
Biofilm
bolus of food
Primary
caries.
 Secondary
caries
(recurrent).

20
F F Caries

ge
2

a
0

ak
ole
Caries

i cr
M
 But
Recurrent Caries
or
Residual Caries?

Residual caries can be difficult to differentiate from

secondary caries and it appears similar to secondary
caries in radiograph.
Non acceptable
Residual caries
Accidental F
B

F
B
Acceptable
Residual caries
Intentional
 Progression
Of
caries lesions.
 What is clinical
characteristics of
enamel and dentin
caries?
 Enamel
Incipient lesions
White lesions
Smooth surface

Occlusal surfaces Buccal and lingual surfaces Proximal surface

 Demineralized
enamel not extend
to DEJ

Intact outer White lesion!!

surface

Dentin Subsurface
porosity

Enamel
Enamel lose
Caries limited to enamel translucency
(at a pH 5, the surface
remains intact and the
subsurface mineral is lost)
White lesion
 Incipient lesion

Dentin Dentin

Enamel Enamel

Hydrated enamel Dry enamel

Translucent Opaque
 Hydrated Desiccated
Altered enamel Surface texture
(Wet) (Dry)
Incipient caries
Translucent Opaque Smooth
(Non cavitated caries)

Hypocalcified enamel Opaque Opaque Smooth

Hypo-calcified enamel is affected

less by drying and wetting;
not represent clinical problem.
 Incipient lesions
White lesions

Enamel caries in Enamel smooth surface lesion

Pit & fissure with broad area of origin.
has small sites of
origin.
Pit and-fissure lesion (inverted V
shape):
 Demineralization follows the
direction of the enamel rods.
 Develop on the lateral walls of the
fissure.

Smooth surfaces lesion is V shape:

 The path of ingress of the lesion is
parallel to the long axis of the
enamel rods in the region.
 Intact outer surface
Subsurface porosity

Using probe carefully

Gentle pressure,
blanch a finger nail without causing pain or damage.
 Outer enamel
Not extend to DEJ surface is intact

Protect
crystal Non cavitated lesion
framework
Dentin
p

Remineralization
Enamel

Restoration
Dentin

Enamel
Cavitation
 t ed Ina
s c
re
Ar sion Remineralized les tive
i on
le lesion
Remineralized
lesion

Brown Opaque
Black white
Incipient lesion
Intact
outer
Organic debris surface
Arrested lesion. & metallic ion
within E.

More resistance
to caries

No
restoration
 Enamel is capable of acting as a molecular sieve
by allowing free movement of small molecules
Why incipient caries
and blocking the passage of larger molecules of enamel produce a
and ions. pulpal response before
penetration of
 The movement of ions through carious enamel bacteria?
can result in acid dissolution of the underlying
dentin before actual cavitation of enamel
surface.

 This acid attack at the external ends of the

dentinal tubules initiate pulpal response by
unknown mechanisms
 Rough Active caries
pH= 3 or 4 outer
surface

Probe

Incipient 18 months ± 6 months Cavitation

caries Smooth surface Active caries

Remineralization of cavitated
enamel lead to development
of arrested
cavitated lesion

Restoration
Cavitated inactive (arrested)
enamel caries lesion.
 The time for progression from non-cavitated caries to clinical caries (cavitation)
on pit and fissures is less than smooth surfaces caries.
 Peak rates for the incidence of new lesions occur 3 years after the eruption of the
tooth.
 Poor oral hygiene and frequent exposures to sucrose-containing or acidic food can
produce white spot in 3 weeks.
 Radiation-induced xerostomia (dry mouth) can lead to clinical caries development
in 3 months from the onset of the radiation.

White
Cavitation
lesion
 Clinical significance of enamel lesion
Non restorative,
Normal
Enamel structure therapeutic treatment Restorative
and
(remineralization, treatment
altered
antimicrobial,
enamel
pH control)

Normal
Normal Not indicated Not indicated
enamel

Hypocalcified Abnormal but not

Not indicated Only for esthetic
enamel weakened
Non cavitated
(incipient) Porous weakened Yes Not indicated
caries

Cavitated,
Active caries Yes Yes
very weak

Inactive caries Remineralized,

Not indicated Only for esthetic
(Arrested) strong
 Dentin caries
V-shaped lesion with a
wide base at DEJ and
advance more rapidly
than in enamel?
 DEJ has the least resistance to caries
attack, allows rapid lateral spreading of
Composition of E. and D. by volume percent caries.
Discoloration of the tooth surface could be seen before development of cavitation.
In such case it will extend to dentin.

Clinically
 Caries
produce
variety of
responses
in dentin.
 Pain
&
sensitivity

Operative procedures (cutting/air-drying)

induce fluid movements in dentinal
tubules distort odontoblasts & afferent
nerves, leading to a sensation of pain.
 Normal dentin

Collagen
fibers
&
minerals
Tubule

Carious dentin

Zones of carious Normal dentin Affected dentin Infected dentin

dentin
 Infected dentin Affected dentin
Soft necrotic tissue (wet, mushy) Softer than normal dentin,
followed by dry leathery dentin discolored but does not flake
flakes away with instrument. easily.
Demineralized but not invade by
Contaminated with bacteria.
bacteria.
Collagen irreversibly denatured. Collagen cross link remains.
Stained by caries detecting dye
Does not stain.
(1% acid red in propylene glycol).
Acts as template for
Cannot remineralize.
remineralization.
Require removal. Does not require removal.
During caries excavation, the goal is to remove only infected dentin,
while affected dentin can be preserved.

The relationship of dentin hardness, crystal

deposition, condition of the odontoblastic
process, and zones of dentin caries.
 Clinically to
distinguish
between
infected and
affected dentin

Observe the degree of discoloration Test the area for

(extrinsic staining) hardness. If
penetrated by a
sharp explorer
should be removed.
 In acute rapidly Less time for
progressing caries, the extrinsic
difference between the pigmentation
zones becomes less
distinct.

The discoloration is slight and gradually changeable

and the bacterial front is well behind the discoloration
front. The hardness (softness) felt by the hand through
an instrument may be an inexact guide.
 In chronic slowly
progressing caries, the
zones are most clearly
distinguished.

Infected dentin is discolored and because the bacterial front is

close to the dicoloration front

It is a natural barrier that blocks the penetration

of toxins and acids.
Sclerotic dentin shiny and darker
in color but feels hard to the
explorer tip (By contrast, normal,
freshly cut dentin lacks a shiny,
reflective surface and allows
some penetration from a sharp
explorer tip); such dentin occur in
slowly advancing lesion and may
be seen under an old restoration.
Comparison of acute and chronic caries regarding closeness, hardness and depth
factors of the softening, discoloration and bacterial invasion.
Management
Of
dental caries
Drill and fill Dealing with end stage of
the disease

Removal of caries
lesions Incipient caries

Not treat the underlying

cause of the disease

Tooth Restoration

Recurrent caries
 The loss of mineral is not a continuous process.

 Alternating periods of mineral loss with intervening periods of

remineralization.

 The critical event for the tooth is cavitation of the surface

destruction and irreversible loss of tooth structure.
 Caries
management by
risk assessment
(CAMBRA)
Patient at High risk
for caries
development
 Risk factors for caries

Risk factor Risk increasing observations

Age Childhood, adolescence, senescence.
Gender Women at slight greater risk.
Economic and
Lower status
educational status
Debilitation, decrease ability to give self-
General health
care.
Medication Medications that reduce salivary flow
Fluoride exposure No fluoride in public water supply.
High intake of refined carbohydrates;
Dietary habits
tobacco and alcohol use.
Clinical examination findings associated
with increased caries risk
 Clinical examination findings associated with increased caries risk

Clinical appearance Appears sick, obese or malnourished

Mental or physical disability comply with dietary and oral hygiene
Mucosal membranes
Active carious lesions
Plaque
Gingiva
Existing restorations
Patients who are unable or unwilling to
instruction.
Dry, red, glossy mucosa suggested
decreased salivary flow.
Cavitation and softening of enamel and
dentin; circumferential chalky opacity at
gingival margins.
High plaque scores.
Puffy, swollen and inflamed bleeds easily.
Large numbers indicate past high caries
rate.
Poor quality (with open contacts, open
margins, or overhangs) indicates increased
habitat for cariogenic organisms.
 Cavitation in pits and fissures

Cavitation in proximal surfaces

Rampant (acute) caries, a rapidly invading infectious process usually
involving several teeth; dietary inadequacy, a complete absence of oral
hygiene practice, or systemic illness. .
 Multiple cavitation

Circumferential chalky opacity at gingival margins.

Softening of enamel and dentin.
High plaque scores.
Gingiva, swollen and inflamed
bleeds easily.

Exposed root surfaces Dry red glossy mucosa

 Poor quality (with open contacts, open margins, or overhangs)
indicates increased habitat for cariogenic organisms.

Orthodontic appliance
Large numbers indicate past high caries
rate. In the past 3 years
Low risk Moderate risk High risk
Preventive
treatment
Method of caries management by medical model
 Limit cariogenic substrate

Decrease frequency of
sucrose or acidic food,
Frequent sucrose intake Using sugar free food.
Poor quality diet.

Acid
 Disorganize plaque biofilm

Electric tooth brushing

Daily removal of plaque biofilm

High plaque scores
Puffy red gingiva
High bleed gum

Professional plaque removal Oral irrigation device

every 2 weeks
 Fluoride exposure

 Increases the resistance of tooth structure to

demineralization.
 Has antibacterial effect on cariogenic
bacteria.
 Incipient (non cavitated) caries.

Professional application Self application

Fluoride exposure
 Stimulate saliva flow
 Dry mouth with little saliva.
 Red mucosa.
 Medication reduce salivary flow.

Medication stimulate salivary flow

Chewing sugar free gum.

Eat non cariogenic foods
that require lots of chewing.
Pilocarpin HCl
5mg tid up to 90 days Cevimeline HCl
30mg tid up to
6weeks
 Antimicrobial agent

Eliminate cariogenic bacteria from biofilm (MS, lactobacilli)

CHX CHX Xylitol

mouth wash varnish Natural five-carbon sugar
0.12% At office obtained from birch trees,
Home applied Root surface caries keeps the sucrose
Remineralization, molecule from binding
Decrease MS with MS.
 Probiotics

 Probiotics; One of the modern concept for reducing

dental caries.

 The fundamental concept is to inoculate the oral cavity

with bacteria that will compete with cariogenic bacteria
and eventually replace them.

 The effect of probiotics strains on MS levels in saliva

and/or dental plaque, using different vehicle (ice-cream,
chewing-gum, water, yogurt and tablets) showing MS
concentrations decrease significantly.
 Anti caries vaccine
Cost
Not effective
Safety has not been than fluoride
shown; cross reaction therapy
with human heart
tissue

 For many years, investigators have

been trying to develop an effective
anti-caries vaccine.

 Some concerns remain, which may

affect its widespread use.
 Pit and fissure Sealants

Dental sealants are used primarily

to protect child’s newly formed
teeth.
 Do adults need sealants on teeth? 
Sealants have three preventive effects:

1. Mechanically fill pits and fissures with an acid-

resistant resin.
2. Prevent trap of plaque and bacteria.
3. Sealants render the pits and fissures easier to clean
by tooth brushing and mastication.

Sealant applied to the central fossa

of a maxillary second molar
because of the appearance of
chalky enamel and softening in the
central fossa.
 Smooth surface resin sealants
New option for minimal invasive treatment of white spots. Use of extremely low-viscosity resin sealants to
infiltrate into the white spot caries lesion and arrest the developing caries.

15% hydrochloric acid for 2-5 minutes The tooth is rinsed with water and dried with
alcohol for 2min

TEGMA resin is applied onto the tooth for 2-5 minutes to infiltrate, cured for 30 sec.
Amorphous Calcium phosphate compounds

Soluble calcium phosphate

compound that releases
calcium and phosphate ions
to convert to apatite and
remineralize the enamel
when it comes in contact
with saliva.
 Whit spots Ecthing 2 minutes

ACP paste application, 5 minutes One month after application

 Restorations

 The status of a patient existing restorations have effect on the out come of preventive
measures and caries treatment.

Correct all
defective
restoratio
n (plaque
retention)

Old rough restorations

Restore all cavitated
(plaque retentive) lesions to eliminate
Smoothed or replaced. nidus of MS &
lactobacilli
 Restorations

The placement of a restoration into a cavitated carious tooth does not

cure the carious process.
 Caries control restorations

The treatment objective for caries control is to remove the decay from all of the
advanced carious lesions, place appropriate pulpal medication and restore the tooth
with GIC or amalgam (temporary restorative materials).

Unsupported enamel
 Active cavitated lesions Extensive carious lesion in molar tooth
in numerous teeth with questionable pulp
prognosis/inadequate available time.

Lesions have
progressed at least half
the distance from the
DEJ to the pulp.
 Caries control restoration

Preventive procedure

Removing large Stop the Large numbers

numbers of advance of and sites of cariogenic bacteria
cariogenic lesions
organisms.

Prevent the spread of pathogenic

bacteria to other tooth surfaces
 Technique

Anesthesia High speed hand piece

Isolation

Caries removal with spoon

excavator Good control and High speed hand-piece
Pulp exposure require less skill at full speed is
Great skill & sharp instruments
contraindicated
The traditional caries removal technique involves the removal of all
soft and leathery dentin until hard, sound dentin is reached before
placing a final restoration. This technique is often used without the
risk of exposing the pulp
In deep cavity, caries lesions radiographically extend more
than 70-75% into dentin

Deep caries
lesion

Complete removal
of soft/leathery
dentin

Pulp exposure
 In deep excavation with pulp exposure, a decision must be made
whether to proceed with root canal therapy or do a direct pulp
capping.

Hemorrhage
is
profuse.
Normal pulp
No
hemorrhage
or exudates.

Mechanical pulp exposure Carious pulp exposure

Operator error
Occur in area of normal dentin
No bacterial contamination
DPC
Infected dentin extending
into the pulp and infection
of the pulp already has
occurred.
RCT
 Favorable prognosis for the pulp after direct pulp capping may be expected if

The tooth is asymptomatic (no spontaneous pain, normal response to thermal testing,
and vital) before the operative procedure.
The exposure is <0.5mm in diameter.
The hemorrhage from exposure site is easily controlled.
The exposure occurred in a clean, uncontaminated field (such as that provided by
rubber dam isolation).

Calcium hydroxide promotes reparative dentin bridges over any area of

frank pulpal exposure. Such repair usually occurs in 6 - 8 weeks and
may be evident radiographically in 10- 12 weeks.
 When Is
Treatment of
the Vital Pulp
Preferable to
Root Canal
Treatment?
 The traditional complete caries removal procedure may be detrimental
to the pulpo-dentinal complex and does not take into consideration the
biological natural response of the tooth to the caries stimuli.

Cavitated caries lesions radiographically

extend more than 70-75% into dentin

Deep caries In a tooth with a deep caries

lesion lesion, no history of
spontaneous pain, normal
responses to thermal stimuli,
and a vital pulp

Indirect pulp capping

Incomplete caries removal

based on the understanding of

the biological response of the Stepwise caries removal
tooth to caries stimulus and the
Prevent pulp exposure
protective response of the tooth
Maintain pulp vitality
to bacterial invasion.
 Indirect pulp capping
Slowly progressing Dark brown dentinal color Dry leather

 In slowly progression lesion, the dentin has

been exposed to a remineralization process in
the presence of minerals from saliva and
fluoride and to the protective changes in
dentin and pulp to occur (tubule sclerosis).
 Complete caries excavation peripherally to a
sound, caries-free DEJ.
 Leaving a thin residual layer (0.5mm–1.0mm)
of leathery affected dentin over the pulpal
floor or axial wall.
 Place liner and final restoration that provide a
good seal over the remaining bacteria which
result in arrest the lesion progression by
isolating the bacteria from the substrate and
decreasing acid production.
 Stepwise caries removal
Rapidly progressing Yellow light color Soft, wet

A radiograph suggests that Medication with

there is a high risk of pulpal Removing the Ca(OH)2 and TF (GIC
exposure during preparation very soft, necrotic or RMGIC).
and infected
dentin and leaving
the soft,
discolored yellow
or dark leathery
dentin
Next visit, 2-3 months later, Place a new lining (will stimulate further
remove the dressing and tertiary dentine formation) and base
last layer of caries.
 Root caries management

Risk factors for root caries include the following:

Gingival recession.
Poor oral hygiene .
Cariogenic diet.
Presence of multiple restorations or multiple missing
teeth.
Existing caries.
Xerogenic medications.
Compromised salivary flow rates.
 Restore all root caries lesions
with RMGIC

Bond to enamel and dentin They act as reservoirs for fluoride which
can be re-released into the oral cavity.

Preventive protocol for root surface caries

Improve salivary Remineralize

Reduce the quantity
flow rates and non-cavitated
Reduce the and numbers of
increase the lesions and
numbers of exposures of
buffering capacity prevent new
cariogenic bacteria ingested refined
lesions from
(S. mutans) in the carbohydrates
developing.
oral cavity
Thank you