Dental Caries DR - Hanna

DR HANNA ABDUL MAJEED
DENTAL CARIES
Presented by
Dr.Hanna Abdul Majeed
Assist Prof/HOD (opt)
Islam Dental College

Outlines of Lecture:
 Defination(def,epidemiology,hypothesis concerning etiology of cariesecological basis of
caries)
 Etiology(plaque,plaque communities and habitat,development of plaque
 Pathophysiology of caries
 Classification & clinical characteristics of caries
 Progression of caries
 Histopathology(histology of enamel,clinical characteristics of enamel caries,zones of
incipient lesion,histology of dentin,clinical&histologic characteristics of dentinal caries,acid
levels & reparative responses,zones of dentinal caries)
 Caries diagnosis(assessment tools,caries diagnosis for pits & fissure,smooth surface,root
surface caries,caries activity tests)
 Caries risk assessment
 Prevention(general health,flouride exposure,immunization,salivary fuctioning,antimicrobial
agents,diet,oral hygiene,xylitol gums.pits &fissure sealants,restorations)
 Caries treatment(caries control restorations,restorative care)

DEFINITION

DENTAL CARIES
DEFINITION
Dental caries is a multifactorial microbial disease of the calcified tissues of
the teeth, characterized by demineralization of the inorganic portion and
destruction of the organic substance of the tooth, which often leads to
cavitation.

EPIDIMIOLOGY

Caries Susceptibility Jaw
Quadrants
Bilateral distribution between the right and left quadrant of both maxillary and mandibular
arches.
Maxillary teeth more susceptible than mandibular arch  relate to gravity and saliva, with
its buffering action, would tends to drain from upper teeth and collect around lower teeth .
Individual teeth: 1st primary and permanent molar

Tooth surfaces: Interproximal surfaces (Pri. Molars) & Occlusal surfaces (Per. Molars)
Gender distribution: equal in both (early eruption in female)
Ages: 4-8yrs ; 11-18yrs ; 55-65yrs --- THREE PEAK AGES
¤ 1 to 2 years ( baby bottle caries)
¤ 5 to 7 years ( primary caries)
¤ 11 to14 years Key risk age group in young adults and adults(secondary caries/ root
caries)

Caries Susceptibility Of Individual
Teeth
Upper and lower first molar  95%
Upper and lower second molar  75%
Upper second bicuspid  45%
Upper first bicuspid  35%
Lower second bicuspid  35%
Upper central and lateral incisor  30%
Upper cuspids and lower first bicuspid  10%
Lower central and lateral incisor  3%
Lower cuspids  3%
Teeth farthest back in the mouth are more frequently carious
Caries susceptibility of individual tooth surface
occlusal > mesial > buccal > lingual

HYPOTHESIS
CONCERNING ETIOLOGY OF CARIES

HYPOTHESIS
?
SPECIFIC PLAQUE HYPOTHESIS
NON-SPECIFIC PLAQUE
HYPOTHESIS
1960 – Keyes “rediscovered” S. mutans
W.D. Miller –
considered all bacteria in mouth He demonstrated that:
were specific microorganisms were responsible
potentially cariogenic – hence, for caries
non-specific plaque caries was transmissible
theory
Later, the responsible bacteria were found to
Acid production by bacteria comprise seven distinct species – only mutans
considered and sobrinus are associated with caries in
responsible for breakdown of tooth humans

ECOLOGICAL BASIS

ECOLOGY “is interaction btw organisms &their environment”
ECOLOGICAL NICHE: “human oral cavity”
(Development & growth of plaque is a normal phenomenon)
Plaque community under goes succession of changes during periods of unrestricted
growth change the overall metabolism & characteristics of plaque
Unrestricted plaque growth produces local environment that promote selectively the
accumulation of pathogenic bacterial species
High frequency sucrose exposure is the most imp. factor in producing a cariogenic
plaque
Sucrose metabolic product is acid and this acid leads to CARIES
ECOLOGICAL DETERMINANTS : Factors determining characterstics of plaque are:- host
resistance, extent & nature of shelter for bacteria, host diet, oral hygiene, status of
dentition & composition of oral flora

Theories
OF DENTAL CARIES

S.mutans, Lactobacilli species
attack the pit and fissures,
S.mutans,S.salivarius,S.sanguis,S.miti A.naeslundi and A.viscosus prefer
or,S.milleri, root surfaces.
L.acidophilus, Peptostreptococcus
The Lactobacilli species and
intermedius, A.naeslundi, A.naeslundi attack to deep
A.viscosus dentinal lesions.

DENTAL PLAQUE

COMPOSITION OF DENTAL PLAQUE “Plaque defined as a soft,
unmineralized, bacterial
Water – 80%
deposit or biofilm which
Solids – 20% forms on teeth and dental
prostheses that are not
Dry weight of plaque composed of: adequately cleaned”
 Bacterial & Salivary proteins – 50%
 Carbohydrates & Lipids - 25% Resists cleansing by physiological
---
 Inorganic ions, mainly Ca++ & Po4 -10% oral forces like salivary
washing and tongue
CLASSIFICATION OF DENTAL PLAQUE
movements but is
Supragingival plaque – essential role in causing caries removable by tooth
brushing.
subgingival plaque – role in periodontal diseases.
MECHANISM OF FORMATION :
Plaque formation proceeds through following stages
DENTAL PLAQUE
1. Deposition of a cell free layer, ACQUIRED PELLICLE which is derived from salivary
glycoproteins. This layer acts as nutrient for plaque bacteria.
2. Colonization of pellicle by Gram positive bacteria like S.sanguis and S.mutans within 24 hours.
3. Maturation of plaque by further colonization with filamentous and other bacteria. Also there
is build up of plaque substance by polysaccharides produced by plaque bacteria.

ETIOLOGY
(multifactorial)

Intro..
Dental caries – a multifactorial disease – interplay of 3 primary factors plus
time also.
1. The host ( teeth, saliva etc.)
2. Micro flora
3. Substrate (diet)
 Mere presence of bacteria and a suitable substrate on a tooth

surface at a given time is not enough to cause caries.
 Must have a tooth, plaque bacteria, fermentable carbohydrate,
saliva, and enough time in order for a carious lesion to develop
 Caries results when all of the factors that contribute to caries
overlap.
 Several factors influencing each component ( see the diagram)
affect the rate and severity of the caries.

THE CLASSIC
VENNE
DIAGRAM OF
CARIES.

A – Saliva protection
B – Adequate remineralization capacity
C – Good oral hygiene
D – Ideal Diet
E – Good tooth resistance
F – Dental Management

1)
HOS
T

SALIVA
CLASSIFICATION INGREDIENT FUNCTION
OF COMPONENT
Inorganic Water (99%)
Inorganic, organic Carbonate, Buffers acid

phosphate, protein
Organic Amylase, lipase, Antibacterial

protease,
pyrophosphatase,
lysozyme
Organic Mucins Lubricant, calcium binding
Organic IgA Antibacterial

pH of Saliva Quantity of Saliva Viscosity of Saliva Anti- mocrobial
properties of Saliva
700-800 ml per day viscous saliva is
The “critical” pH at associated with high Lactoferrin(bind Fe
which the inorganic caries rate required for
material of tooth microbial growth)
begins to dissolve is Lactoperoxidases(H2
about 5.5, since O2 mediated killing of
above this pH, saliva microbes)
is supersaturated Lysozyme(+ve
with Ca and Po4 ions. enzyme bind –ve
peptidoglycan in
Acid production microbial cell wall)
during caries occurs IgA(prevent
at a localized site on adherence&colonizati
tooth, which in initial on)
stages at least, is
covered by dental Proline rich proteins
plaque. This plaque (Mucus,
prevents a free Glycoprotein)form
exchange of ions. pseudomembranous
layer on oral
surfaces&oral flora
Aromatic rich protein
(cause remineraliztn)
2) MICRO
BES

Microbial Flora

HELLO! Me
S.mutans
CARIOGENIC PROPERTIES
◦ ability to produce acid (acidogenicity)
◦ ability to withstand acid conditions (aciduricity)
◦ ability to adhere to teeth
METABOLISM YIELDS:
 acids, primarily lactic, from a variety of sugars
 extracellular polyglucose, called glucan, which creates irreversible
attachment (from sucrose metabolism only)
SM is responsible for initiation of caries
SM is a necessary, but not solely sufficient, factor for dental caries

3) DIET

soft and lacking in roughage. As a result, food sticks tenaciously to teeth and is not
cleansed mechanically.
CARBOHYDRATE CONTENT OF DIET: -
most important factors in caries process.
LIPID CONTENT OF DIET: -
medium chain fatty acids & their salts antibacterial effects at low pH. Mechanism of
action not understood.
CALCIUM & PHOSHORUS CONTENT:-
no relation between dietary calcium and phosphorus and dental caries.
FLUORIDE CONTENT: -
topical and water fluoridation has been known to be effective in caries control, dietary
fluorine may have no role as it is unavailable metabolically.
VITAMIN CONTENT OF DIET: -
Of all vitamins, only Vit D and Vit K appear to have some role in the caries process. Vit D
may have an indirect effect on caries process. Its deficiency can cause enamel
hypoplasia which can make the tooth more susceptible to caries. Vit K has enzyme
inhibiting action in carbohydrate degradation cycle. Can be utilized as an
anticariogenic agent.

4) Systemic
Factors

1. HEREDITY: -
 Racial tendency for high or low caries may be explained by heredity.
However, local factors like change in dietary habits can change this
tendency.
 Possible that caries tendency may be inherited through tooth form &
structure.
2. PREGNANCY & LACTATION: -
Commonly observed that during pregnancy, women tend to neglect
their oral health owing to all her attention being diverted to that of
care for the newborn.
Thus increased caries incidence during pregnancy & lactation is more
a problem of neglect !
Prepared by Dr Sundeep S Bhagwath

Stephen Curve

• A high-risk individual, when given a glucose
rinse , will experience a dramatic drop in the
plaque pH well below the critical pH of 5.5.
• The ThepHrecovery
of dentaltoplaque
neutralinpH
response to glucose
in the high risk has been studied using the
classic
individual
 The area will be slow&no
under time
the pH-time for (AUC)representing the time spend at pH lower
curve
than the critical pH.
remineralization to occur
Stephan curve
The AUC for a high risk individual will be very large.
• If that daily trend continues, the person will
have
AUC dental
The diagram decay.
isillustrates
a better measure of total
the plaque caries risk.
pH response curves that have been obtained from
patients with different risks for caries.

 For a moderate risk individual (yellow),
the initial pH drop may only be a little For a caries-resistant person (green),the
lower than the critical pH, and the AUC initial pH drop of that person’s plaque may
will be much less. not even reach the critical pH, and the
 and the AUCs below the critical pH might recovery will be very quick.
result in a net loss of mineral.
 At this stage, remineralization strategies This allow remineralization to occur
might work.

Pathophysiology
of Dental Caries

Release of calcium
and phosphate ions
Carboxylic acids ;
Amino –Acids; Citrates
; Lactates

1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been stopped.
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.

CLASSIFICATION

Based on Anatomical Site

Based on Progression

NURSING CARIES
Nursing caries can also be called as:
1. Nursing bottle caries
2. Nursing bottle syndrome
3. Milk bottle syndrome
4. Baby bottle tooth decay
5. Early childhood caries

 The new name given for early childhood caries is
“maternally derived streptococcus mutans disease
(MDSMD)”
DR.CAROLINE MOHAMED 41
• type of acute carious lesion,
• which occurs among those children who
• take milk or fruit juices by nursing bottle, for a considerably longer
duration of time, preferably during sleep.
• As the child takes larger amount of easily fermentable sugars along with the
milk, the sugar facilitates the cariogenic bacteria to produce caries at a rapid
pace by fermenting those sugars. Nursing bottle caries commonly occurs in the
upper anterior teeth (as these are constantly coming in contact with the
sweetened milk); while the lower teeth are not usually affected as they
remain under the cover of the tongue.
PROGRESSION OF THE
LESION
CLASSIFICATION
RAMPANT CARIES
Caries in a patient with impaired salivary function as result of radiation
therapy
Rampant caries, many tooth involved at same time with acute caries
feature often accompanied by systematic disorder, such as Sjogren
syndrome or saliva reduction after radiation

Compare & Contrast

NURSING CARIES RAMPANT CARIES
NURSING CARIES RAMPANT CARIES
RADIATION CARIES
Radiotherapy is frequently associated with xerostomia due to
decreased salivary secretion
This and other causes of decreased salivation may lead to a rampant
form of caries, indicating the significance of saliva in preventing
caries.

Based on virginity

Based on Extent of Caries

Based on Severity

Based on Involved Tissue
1. Initial caries- demineralization
2. Superficial caries- enamel
3. Moderate caries- dentin caries
4. Deep caries – dentin close to the pulp
5. Deep complicated caries – pulp involvement

Based on Pathway of
Spread
FORWARD CARIES BACKWARD CARIES
ased on Number of Surface
Simple A caries involving only one tooth surface
Compound A caries involving two surfaces of tooth
Complex A caries that involves more than two surfaces of

a tooth
Based on Surfaces restored
BUCCAL/LABIAL
DISTAL OCCLUSAL MESIAL
PALATAL/LINGUAL
Black’s Classification
Class V
Class I
Class II
Class VI
Class III Class IV

WHO CLASSIFICATION
In this classification the shape and depth of the caries
lesion scored on a four point scale
D1. clinically detectable enamel lesions with intact

(noncavitated) surfaces
D2. Clinically detectable cavities limited to enamel
D3. Clinically detectable cavities in dentin
D4. Lesions extending into the pulp
Histopathology Of Dental
Caries

1)
ENAMEL CARIES
SMOOTH SURFACE

Base : towards Surface
Apex : towards Dentine
ZONE
S
1. Translucent Zone
2. Dark Zone
3. Body of Lesion
4. Surface Zone

The zones seen before complete disintegration of enamel are:
Zone 1: Translucent zone,
-lies at the advancing front of the lesion,
-slightly more porous than sound enamel,
-it is not always present
-slightly more porous than sound
enamel having a pore volume of 1% compared
to 0.1% of sound enamel.
Zone 2: Dark zone,
-this zone is usually present and referred
to as positive zone
-formed due to demineralization.
-Pore volume is 2 – 4%.
Increased porosity is due to Drgreater degree of demineralization .
Hanna Abdul Majeed
,Zone 3: Body of the lesion
,found between the surface and the dark zone-
,it is the area of greatest demineralization-
having a pore volume of 5% near the periphery -
,.to about 25% in the center of body of lesion -
Dr Hanna Abdul Majeed

Zone 4: Surface zone
,relatively unaffected area-
Interestingly, this zone not only remains intact during the early-
stages of attack by caries, but also REMAINS MORE HEAVILY
.MINERALIZED
.Pore volume of only 1%-
Ions for remineralization come either from those within plaque-
or from reprecipitation of calcium and phosphate ions diffusing
.outwards as deeper layers are demineralized
Eventually, this zone is demineralized by the time caries-
.penetrates dentin
Dr Hanna Abdul Majeed

CAVITY FORMATION &
BACTERIAL INVASION
The enamel crystallites are progressively dissolved until the disintegration

becomes visible macroscopically.
Now the pathways are large enough for the bacteria to physically enter the
enamel, destroy organic matrix by proteolysis and then proceed to DEJ and
dentinal tubules.

ENAMEL CARIES
PITS AND FISSURES

2)
DENTINE CARIES

Base: towards enamel
Apex: towards pulp ZONE
S
Zone of Decomposed Dentine
Zone of Bacterial invasion

Zone of Decalcification
Zone of Bacterial invasion
Zone of Fatty Degradation

of Tome’s Process

ZONES OF DENTINAL CARIES
Observing from the pulpal side at the advancing edge of carious lesion
following different zones can be seen –
ZONE 1 – Zone of fatty degeneration of Tomes’ fibers -due to degeneration of
the odontoblastic process. This occurs before sclerotic dentin is formed and makes the
tubules impermeable
ZONE 2 – Zone of dentinal sclerosis -deposition of Ca salts in the tubules

ZONE 3 – Zone of decalcification
ZONE 4 – Zone of bacterial invasion
ZONE 5 – Zone of decomposed dentin due to acids and enzymes

3)
ROOT CARIES

• Root caries as defined by HAZEN, is a soft, progressive lesion that is found
anywhere on the root surface that has lost its connective tissue attachment
and is exposed to the environment.
• the root surface must be exposed to the oral environment before caries can
develop here.
• Plaque and micro-organisms are essential for the cause and progression of the
lesion, mostly Actinomyces
• micro-organisms invade the cementum either along the Sharpey’s fibers or
between the bundles of fibers.
• spread laterally, since cementum is formed in concentric layers.
• after decalcification of cementum, destruction of matrix occurs similar to
dentin with ultimate softening and destruction of this tissue.
• invasion of micro-organisms into the dentinal tubules, finally leading to pulp
involvement.
• the rate is slower due to fewer dentinal tubules than crown area

ARRESTED CARIES
Dark brown pigmented carious lesion , insensitive to painful stimuli in which
caries progression is halted
HISTOPATHOLOGICAL ZONES
ZONE 1: Surface layer- Brown in colour and of leathery consistency.
ZONE 2: Pigmented zone- Hard, dark brown in colour, forming main bulk with
presence of coalesced bacteria bodies
ZONE 3: Sclerotic layer- Hard, white zone having highly calcified tubules with
absence of bacteria.

SECONDARY CARIES
IN ENAMEL: A triangular outer lesion is seen which continues with the dentinal
lesion along the dentinal wall. Both lesions are walled by dark zone.
IN DENTIN: Appearance can be-
1.Superficial demineralization of cavity walls
2.Subsurface demineralization without visible changes of wall surface
3. Subsurface demineralization with increased mineralization of surface layer
4.Alternating zones of demineralization and remineralization.

Next Lecture
DIAGNOSIS &
PREVENTION

INVESTIGATIONS

Radiographs

Amalgam over hanged filling #24
PERI-APICAL Proximal Caries #24 and #25
Dilacerated root #24
Round radiolucencies
Pits and Fissure caries Small grey area at DEJ associated with #11 and
#21
Carious #26; Radiolucency

seen in the crown of #27
involving pulp horns (black
point)
Radiolucency also visible
at mesial and distal root
tips ; also see crown of #28
in developing stage
Root Caries #31; #32; #33

Periapical Radiolucency associated with #32
BITEWING Best for Proximal Caries

PANOREX RADIOGRAPH

RECURRENT CARIES
 Occurs immediately next to restorations
 Results from microleakage or residual caries
OTHER RADIOGRAPHIC SHADOWS
 Radiolucent Cervical Burn out:
- Evident at the neck of tooth well
demarcated above by enamel cap& below by
alveolar bone level
- It is triangular in shape being less
apparent at the center of tooth
-good alveolar bone height will enhance
cervical burn-out
DON’T CONFUSED IT
WITH CARIES
Analysis

Nutrition
al Salivary
Frequent exposure to sucrose It provide important information abt
increases the likelihood of plaque appropriateness of secretion rates &
development by more cariogenic MS buffering capacity & numbers of MS &
organisms. lactobacilli.
Sucrose intake & frequent sucrose Bacterial counts may be helpful in
exposure is related to caries activity. assessing populations they may not be
accurate for an individual patient
The direct cause of carious activity is
acidity Knowing what constituents high
values for the numbers of colony
The decrease in pH associated with
forming units may be helpful
significant acidity may be due to either information,in identifying high risk
sucrose metabolism or other acidic patients.
foodstuffs,both of which may result in
caries.
Caries Activity Test
1. Lactobacillus Colony test: Stimulated saliva collected & diluted with
distilled water. Incubatedon Rogasa’s SL agar
2. Calorimetric Snyder test: Measures the ability of micro organisms to
form organic acids in carbohydrate. 0.2 ml of patient’s saliva is pipetted
into melted medium at 50C. Incubated for 72 hrs. medium contains
bromocresol green which changes color from green to yellow in the
range of pH5.4 – 3.8
3. Swab test: Swab is taken from the teeth & incubated in medium pH
change after 48 hrs is read on a pH meter
4. Buffer test : Tests the buffering capacity of bicarbonate ion in saliva
5. Alban test : Patient to expectorate saliva in test tube containing Alban
test medium. Incubated at 37C upto 4 days . Colour cange is noted after
72 hours

Caries Susceptibility Test
Enamel solubility test:
When glucose is added to saliva containing powdered enamel, organic acids are
formed. This will decalcify enamel leading to an increase in soluble Ca ions
Amount of Ca obtained gives a direct measure of caries susceptibility
Salivary reductase test:
Measures the activity of reductase enzyme in salivary bacteria
Kit commercially available- Treatex
Salivary sample mixed with Diazoresorcinol dye
DIAGNOSIS

Caries diagnosis implies deciding whether a lesion is active, progressing
rapidly or slowly or whether is already arrested.
Identify pts with lesions that require

 Restorative treatment,
Non-restorative treatment
Pts who are at high risk for developing carious lesions
Assessment (Step wise!!)

First Step…

Clinical examination findings
associated with increased caries risk
CLINICAL EXAMINATION RISK INCREASING FINDING
General appearance Sick,obese,malnourished
Mental/physical disability Pts unable to comply with dietry/oral hygiene instructions
Mucous membranes Dry,red,glossy mucosa showing decreased salivary flo

Cavitation & softening of enamel & dentin,chalky opacity
Active carious lesions at gingival margins
Plaque High plaque score
Gingiva Puffy,swollen,inflamed,bleed easily
Existing restorations Large number---past high caries rate
Factors associated with increase Caries risk
HISTORY FACTORS OBSERVATIONS
NON-ORAL
Age Childhood, adolescence, senescence

Gender More in females
SES Lower status (getting variation)
Fluoride exposure No water fluoridation
Tobacoo & Alcohol More with amount of consumption
Dietary habits Refined carbohydrates

General health Chronic illness and debilitation and decrease ability to self care ; family
history
Medication Reduce salivary flow
ORAL
Tooth anatomy & Development of fissures and low Fl content
composition
Oral flora High MS
Previous dental Rx Hx of extensive restorations
Restoration Defective restorations
Oral hygiene Poor oral hygiene
HIGH RISK LOW RISK
Social History
Socially deprived Middle class
High caries in siblings Low caries in sibling
Low knowledge of caries High dental aspirations
Medical History
Medically compromised No such problem
Xerostomia
Long-term cariogenic
medicine
Dietary habits
Sugar intake: frequent Infrequent

HIGH RISK LOW RISK
Use of fluoride
Non-fluoridated area Fluoridated area
No fluoride supplements Fluoride supplements used
Plaque control
Poor oral hygiene maintenance Good oral hygiene maintenance
Saliva
Low flow rate& buffering capacity Normal flow rate& buffering

 S.mutans & lactobacillus counts capacity
 S.mutans & lactobacillus counts

Clinical Risk of Assessment for Caries
:Patient is at high risk for the development of new cavitated lesions if
1. High MS count. (Bacteriologic testing should be done for: )

One or more medical health history
Anti-microbial history
Presence of new incipient caries
Orthodontic treatment
Treatment plan calls for extensive restorative work
2. Any two of the following factors if present:

 two or more active carious lesions
Multiple restorations
Poor dietary habits
Low salivary flow
Categorization of Adults according to caries risk Indicators
Caries risk Risk Indicator

category
Low •No carious lesion in last 3 yr
•Adequately restored surface
•Good oral hygiene
•Regular dental Checkup
•Use of Fl denitrifies
Medium :Presence of two of the following indicators

•Current orthodontic treatment
•RPD
•Exposed root surfaces
•Poor oral hygiene
•Frequent carbohydrate intake
•Inadequate topical fluoride exposure
High Presence of one of the following indicators:

•Any carious lesion in previous 2 yr
•Inadequate salivary flow
•Initial enamel inter-proximal radiolucencies
•Presence of two factors (in medium risk factor)
HIGH RISK LOW RISK
Clinical evidence
New lesions No new lesions
Premature extractions No extraction for caries
Anterior caries restorations Sound anterior teeth
Multiple/repeated No/few restorations
restorations
No fissure sealants Fissure sealed
Multi-band orthodontics No appliances

Clinical
Examination

Conventional Method(Visual)
Is skilled technique
Detection of white spot ; discolouration; frank cavitations
Remember it is unreliable technique as
Sometimes large percentage of caries are to small to be
detected
Discolouration of pits and fissure can be interpreted as caries
Limitation of this methods = Cannot assess level of penetration
of Caries

Conventional Method
(Tactile)
Explorers are widely used for the detection of carious tooth structure
- Right angled probe - no.6 (Probe C)
- Back action probe - no.17 (Probe A)
C
- Shepherd's crook - no. 23 (Probe B)
Dental floss
Keep in mind Explorers can be dangerous!! Why?

Advanced Method

Fibro-optic Trans
illumination Method
Illumination is delivered by
means of fiberoptics from the
light source to the tooth
surface using a fiberoptic
handpiece
The decalcified area will not
let light pass through as much
as it does in a noncarious
surface
appears as a darkened shadow
corresponding to decay

Dye
s
Mechanism : Selectively complex with carious tooth structure which is later
disclosed with the help of fluorescence. It stain collagen associated with less
mineralized organic matrix.
DYES FOR ENAMEL CARIES: DYES FOR DENTIN CARIES:
1) Procion: N2 & (OH) groups
irreversibly complex with caries. Acts 1% acid red 52 in propylene glycol
as a fixative complexes specifically with denatured
2) Calcein: complexes with collagen, hence used to differentiate
calcium & remains bound to infected and affected dentin
the tooth
3) Zyglo ZL-22: fluorescent tracer
dye. not used Iodine penetration method (Pot
4) Brilliant blue: 10% aqueous
iodide) for evaluating enamel
Brilliant Blue. not used permeability

DISADVANTAGES:
1.Dye staining and bacterial penetration are
independent phenomena, hence no actual
quantification
2.They also stain food debris, enamel pellicle,
other organic matter
3.Dye aided carious removal laborious
4.Stains DEJ

Some Clinical Views

Non-cavitated carious lesion
ENAMEL DENTIN
Cavitated Lesion Questionable Lesion

Recurrent Caries
Arrested Caries
Pits and Fissure Caries

Non-Carious Enamel Opacities
Mild Fluorosis
Not Fluorosis Moderate Fluorosis Severe Fluorosis

Treatment

What to do??
Traditional caries management has
consisted of detection of caries lesion
followed by immediate restoration. In
other words, caries was managed
primarily by restorative dentistry.
However, when the dentist takes the bur

in hand, an irreversible process begins.
Because this is the start of a restoration
cycle in which the restoration will be
replaced several times.

Before restoration a group of certain questions has to
be asked
?
•Is the caries present
•If so how far does it extend
•Is the restoration required or could the process be
arrested by preventive treatment
The modern dentistry and with the introduction of

adhesive dentistry, the dentists are allowed to make
smaller preparations. Which have led to preservation
of hard dental tissues. This allowed elimination of G.V
Black’s principles.
GOALS
The treatment goal in caries management should be:
• To prevent new lesions from forming
• To detect lesions sufficiently early in process that they
can be treated and arrested by non operative means.
If these attempts have failed, restorations will be required

to restore the integrity of the tooth surface
• The activity of caries should be determined and causative
factors should be evaluated
• Caries risk should be assessed before treatment is
considered
• Treatment should include preventive regimens to arrest
the caries process
IN Conclusion
The 1st step in caries management start with detection of the caries lesion
whether it is active or arrested
Detection is done by:

1. Clinical exam (visual, tactile)
2. Radiographs
If the examination reveals arrested caries
NO treatment is required
If the patient is found to have active caries and the
dentist immediately and skillfully restore the teeth is the
patient still at risk????
THE ANSWER IS YES unless the biological environment that

caused the caries to occur has been changed.
Caries risk factors has to be determined and the patient
should be made aware of his or her caries risk status to
encourage them to become involved in his or her own
preventive care
If the lesion is active
The general approach to active caries should be preventive treatment
• Reduce sugar consumption/ reduce frequent consumption by
confining sugar to meal time. Use sugar substitutes
• Plaque control: brushing twice daily with effective fluoride tooth
paste. Use dental floss
• Application of topical fluoride gels, solutions, and varnishes.
• Stimulate saliva by use of sugar free gums such as Xylitol chewing
gums
If the examination reveals active caries but initial or incipient
The dentist has to think of a way to arrest the the lesion (remineralization)
then restoration is never required
Caries on exposed smooth surfaces:
• Operative intervention is not required prior to cavitation
• Even cavitated lesions can be arrested
• Lesions which are plaque traps or deep should be restored
Caries in pits and fissures :
• Since it is difficult to diagnose in its early stages and fissures are
susceptible sites, the dentist may decide to fissure seal susceptible teeth
as soon after eruption as possible
• The occlusal lesion which shows on a bite-wing radiographs should be
restored. These lesions are larger than they appear on radiographs and
rate of their progression may be rapid.
PIT AND FISSURE SEALANTS
When active fissure caries has been diagnosed or if a high risk has been
established and fissures have susceptible morphologic characteristics, sealants
with a low filled resin is indicated
Preventive resin restoration

If additional preparation is needed to the pits and fissures other than opening of
the fissure, posterior resin composite is placed in that area and remaining
fissures and surface of resin composite restoration is sealed with sealant material
ROOT CARIES
• It is possible to re-harden root caries by preventive measure, although as the
lesion become arrested, a brownish black discoloration cannot be avoided
• Root caries should be restored where it endanger the pulp, where cavitation
is encouraging plaque stagnation, or if sensitivity or appearance are
problems
If restoration
Required

Indication for restorative
treatment
1. The tooth is sensitive to hot, cold or sweet……
2. Occlusal and proximal lesions extend into dentin
3. The pulp is endangered
4. Previous attempts to arrest the lesion have failed and the lesion is
progressing
5. The pt. Ability to provide effective home care is impaired
6. Drifting might occur due to loss of proximal contact
7. Esthetic reasons
AMALGAM
Used in posterior teeth where its
strength, abrasion resistance, and ability
to retain a good polish make it a popular
material
COMPOSITE RESIN
Tooth-colored esthetic restorative material used for anterior teeth where
appearance is most important . Also, some are designed to be used in posterior
teeth where strength and abrasion resistance are of prime importance.
GLASS IONOMER
CEMENT
Are not commonly used when esthetic is a major
consideration.in anterior teeth. It is
recommended for patients with high caries rates
because they release fluoride.
Prevention
Best Treatment of Dental Caries is

GOALS OF
PREVENTION

Levels OF
PREVENTION

Reduce the pathogenic
potential of dental plaque
Brushing
Flossing
Oral irrigators
Mouthwash
Anti-microbials
Chewing gums
Lactic acid produced by MS

is controlled by a gene
mutated Diet
General Health
Declining health signalz---need for increased preventive measures
Radiation/chemotherapy—decrease immunocompetence—
increased risk
Medically compromised pts should be examined for changes in
following: plaque ,salivary flow ,oral mucosa , gingiva teeth
Decreased salivary flow is common during acute & chronic systemic
illness– increase in plaque
Ambulatory pts with chronic illness often take multiple medications
—which decrease salivary flow significantly
Fluoride Application
Systemically, from ingestion of fluorides in water, beverages
Topically from the bathing of enamel by oral fluids such as saliva,
water, topical fluoride solutions
Diet & Diet Counseling
Goals of Diet Counseling:
 Reducing high frequency exposures to sugars
 Avoid frequent consumption of sugar containing drinks
 Restricting sugar containing snacks that are eaten slowly
 Limiting cariogenic foods to mealtimes and promoting non-cariogenic
food for snacking
 Rapidly clearing cariogenic foods from the oral cavity by brushing or by
protective means (Xylitol) (Ref: DCNA, October 2006)
Anti-microbials

Mech of action spectrum Persistance in Side effectsm
mouth
ANTIBIOTICS
vancomycin Block cell wall Narrow short Increases gram –ve
synthesis flora
kanamycin Block protein synthesis Broad Short Can increase caries
activity
actinobolin Block protein synthesis Streptococci Long unknown
BISBIGUANIDES
alexidine Antiseptic,prevent Broad Long ,stains teeth &tongue
bacterial adherence bitter,mucosal
irritationBitter taste
chlorhexidine Antiseptic,prevent Broad Long ,stains teeth &tongue

bacterial adherence bitter,mucosal
irritationBitter taste
HALOGENS
iodine bactericidal Broad Short Metallic taste
fluoride 1-10ppm—reduces broad long Increases enamel

acid production resistance
250ppm— ,fluorosis
bacteriostatic
1000ppm--
bactericidal
Oral Hygiene

Pits & Fissure Sealants
A sealant is a dental resin that is firmly bounded to enamel surface and isolates pit
and fissure from caries producing conditions in oral environment
Types:
1st generation – ultraviolet light activated
2nd generation – chemical activated

3rd generation – visible light activated
4th generation – fluoride containing
INDICATIONS
Criteria seal Donot seal
Tooth age Recently erupted teeth Teeth that hv remained caries
free for>4yr;staining is usually
present in pits&fissures
Tooth type Molars Premolars except when pt is
caries active
Occlusal morphology Deep,retentive,narrow pits & Well-calesced fossae &
fissures grooves;wide,easily cleaned
grooves
Recent caries activity Teeth showing signsof Teeth that hv remained caries-
softening/opacity in pits &fissures free for >4yr ; staining is usually
present in pits &fissures
General caries activity Occlusal /smooth surface lesions Proximal cavitated lesion on
on other teeth;no proximal tooth to be sealed;cavitation of
cavitated lesions on tooth to be occlusal(tooth will require
sealed restoration)
Other preventive Pt receiving appropriate systemic Pts water supply is fluoride
measure or topical fluoride therapy or both deficient;pt is not cooperatingin
& still caries active recommended caries-preventive
prgrm(restoration of pits
&fissures is preffered)
Immunization (Caries
Vaccine)
Vaccine is defined as a “Suspension of
attenuated or killed microorganisms
administered for the prevention,
amelioration or treatment of infected
diseases
The concept of a vaccine can be visualized
primarily with the recognition of MS as the
key organism in caries development
Xylitol Gums
Keeps the sucrose molecule from binding with MS
MS cannot ferment (metabolize) Xylitol
Xylitol reduces MS by altering their metabolic pathways and
enhances Remineralization
Recommended to chew gum after meals/snacking for 5-30 mins
Reduces the acidogenicity of plaque and increases salivary flow
Protects salivary proteins, has a protein-stabilizing effect
Summary

Methods of caries Treatment
Method and Indications Rationale Technique /Material
Modify tooth surface: Increase resistance to Systemic flourides

Indications: demineralization Topical flourides
•Incipient lesions Decrease plaque retention Smooth surfaces
•Surface roughening
Stimulate saliva flow: Increases clearance of Eat noncariogenic foods

Indications: substrate&acids that require lots of chewing
•Dry mouth with little Promote buffering Sugarless chewing gum
saliva Medications to stimulate
•Red mucosa salivary flow
•Medication that reduce
salivary flow
Restore tooth surfaces: Eliminate nidus ofMS & restore all cavitated
Indications: lactobacillus inf lesions
• cavitated lesions Deny habitat for MS Seal pits & fissures
•Pits&fissures at caries risk reinfection Correct all
•Defective restorations defects(proximal overhang)
Methods of caries Treatment
Method and Indications Rationale Technique /Material
Limit Substrate: Reduce number,duration Eliminate sucrose from

Indications: &intensity of acid attacks btwn meal snacks
•Frequent sucrose exposure Reduce selection pressure Substantially reduce or
•Poor diet for MS eliminate sucrose from
meals
Modify Microflora: Intensive antimicrobial Bactericidal

Indications: treatment to eliminate MS mouthwash(chlorhexidiene)
•High MS from mouth Topical Fl treatmnt
•High Lactobacillus Select against reinfection Antibiotic
by MS treatment(vancomycin,tetr
acycline)
Plaque Disruption: Increase resistance to Systemic Fl

Indications: demineralization Topical Fl
•High plaque Scores Decrease plaque retention Smooth surface
•Puffy red gingiva
•High bleeding point score

Dental Caries DR - Hanna

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Dental Caries DR - Hanna

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DR HANNA ABDUL MAJEED

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Individual teeth: 1st primary and permanent molar

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 Mere presence of bacteria and a suitable substrate on a tooth

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Inorganic, organic Carbonate, Buffers acid

Organic Amylase, lipase, Antibacterial

Organic Mucins Lubricant, calcium binding

Organic IgA Antibacterial

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Prepared by Dr Sundeep S Bhagwath

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2. Nursing bottle syndrome

3. Milk bottle syndrome

4. Baby bottle tooth decay

5. Early childhood caries

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Compound A caries involving two surfaces of tooth

Complex A caries that involves more than two surfaces of

DISTAL OCCLUSAL MESIAL

Class III Class IV

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D1. clinically detectable enamel lesions with intact

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