Dental Caries

This Presentation has been made from the Book Summit's Fundamentals of Operative Dentistry for my Final Year BDS Studies.

1. DENTAL CARIES
Management: Diagnosis & Treatment Strategies
SARANG SURESH HOTCHANDANI 1

2. WHAT IS DENTAL CARIES?
•Dental caries is a multifactorial, transmissible, infectious oral disease caused
primarily by complex interaction of cariogenic oral flora (biofilm)with fermentable
dietary carbohydrateson the tooth surfaceover time.
•However, not all persons with teeth, biofilm, & consuming carbohydrates will have
caries over time because of presence of several modifying risk & protective factors.
•It is product of disequilibrium b/w remineralization & demineralization
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3. KEYES-JORDAN DIAGRAM
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7. WHAT IS DENTAL CARIES? (CONT’D)
•Dental caries results from dynamic
process of demineralization &
remineralization.
•Critical pH
•Enamel; 5.5
•Dentine; 6.2
•This dynamic process is affected by
many factors;
•Number & type microbial flora
•Diet
•Oral hygiene
•Genetics
•Anatomy of tooth
•Use of fluorides
•Chemotherapeutic agents
•Salivary flow
•Buffering capacity
•Resistance of tooth
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8. •Predominate pathologic environment Demineralization.
•Demineralization is characterized by localized dissolution
and destruction of calcified dental tissues resulting in
“Cavity” formation.
•Dentine demineralization exposes organic protein matrix, which
is denatured and degraded by host’s matrix metalloproteinases
(MMP) and bacterial proteases.
•Cavitation in tooth is Sign of underlying disease and it
is caused by imbalance between protective and
pathologic factors.
•Read Box 2.1 in Art & Science of Operative Dentistry.
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10. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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11. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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12. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
•Soft, tenacious film accumulating on
the surface of teeth.
•Composition (bio), Structure (film)
•Composition
•Bacteria
•Bacterial by products
•Extracellular matrix
•Water
•It is not food debris or haphazard
collection of microbes.
•Formation of Plaque;
•Formation of acquired pellicle over
perikymata ridges of enamel in 30min-
2hr
•Attachment of plaque bacteria to pellicle
•Cocci 12-24 hrs.
•Filamentous 1-3 days
•Growth of microbes
Surface of non-cavitedenamel lesion have “Punched out appearance in Electron Microscope
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13. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
•Plaque anaerobically metabolize
carbohydrates.
•Plaque pH independent of Quantity
carbohydrates but it Depends on Frequency
of carbohydrate intake
•In active caries lesion, mineral loss is
not continuous but alternating period of
demineralization & remineralization.
•Different areas of oral cavity or even
different teeth and different surfaces of
same teeth contains the different
community of microbes in the dental
plaque of that area not the same.
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14. MICROBES OF DENTAL PLAQUE
•Normal non-carious teeth
•Streptococcus sanguis
•Streptococcus mitis
•Enamel caries
•Streptococcus mutans
•Dentine caries
•S. Mutans
•Lactobacilli
•Root caries (filamentous & spiral)
•Actinomyces
•S. Mutans = Initiation of
Caries
•Lactobacilli = Progression
of Caries
•High sugar intake
increases the
concentration of mutans
streptococci & lactobacilli
while restriction of sugar
intake decrease them.
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15. ROLE OF DENTAL PLAQUE OR BIOFILM IN
CARIES PROCESS.
•Biofilm is controlled by
professional tooth
cleanings.
•Pellicle form within 2
hours.
•pellicle is formed by
precipitation of saliva.
•Functions of Pellicle
•Protect the enamel
•Reduce friction b/w
teeth
•Provide matrix for
remineralization.
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16. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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17. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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18. ROLE OF TEETH IN DENTAL CARIES.
•The tooth is ideal surface for attachment of
plaque because it lacks the shedding
mechanism like other areas of body.
•Enamel in primary teeth is
•less mineralized,
•optically more active, have
•greater porosity &
•less resistant to caries.
•Dentine is more vulnerable to caries than
enamel because of structural differences and
greater number of impurities in its crystal.
•Sites of tooth where caries
frequently occur;
•Pits & fissure
•Smooth enamel surface
•Gingival to proximal contacts
•Gingival 3
rd
of facial &
lingual/palatal surfaces
•Root surface
•Subgingival areas
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19. PIT & FISSURES (FIG; 2-12, 2-15 TO 2-19)
•Most common surface for development
of caries.
•Dominated by; S. sanguis other
streptococci.
•Initial lesion develop on lateral walls of
fissure.
•They have small site of originon
occlusal surface with wide base.
•Shape of pit & fissure lesion is inverted
V.
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20. SMOOTH ENAMEL SURFACE
•Proximal enamel surface gingival
to the contact area are 2
nd
most
common susceptible area to
caries.
•These surfaces are free from
effects of mastication, tongue
movement & salivary flow.
•Smooth surface lesion is V-
shaped with wide origin &
narrow base.
•Apex of V directed towards
pulp. (figure 2-21 in art &
science)
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21. ROOT SURFACE CARIES
•Mostly occur in gingival
recession.
•More common in old age persons
because;
•Decreased salivary flow
•Poor oral hygiene
•Lack of motivation
•Lowered digital dexterity
•Gingival recession
•Root caries is more damaging than
other surface caries because;
•It has rapid progression because it
starts directly from dentine and dentine
is less resistant than enamel.
•It is often asymptomatic
•It is closer to pulp.
•More difficult to restore.
•U shaped in cross section
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22. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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23. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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24. ROLE OF ORAL HYGIENE IN CARIES
•Careful mechanical cleaning of teeth disrupts the biofilm and leaves clean enamel
surface.
•Cleaning process does not destroy the oral bacteriabut merely removes them from tooth
surface to prevent growth of biofilm.
•Some obligate anaerobes may be killed by exposure to oxygen during tooth cleaning.
•Biofilm species are not destroyed but they are continue to be present but most of them
are unable to initiate colonization on clean tooth surface.
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25. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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26. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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27. SALIVA; NATURAL ANTI -CARIES AGENT.
•Decreased salivary production or
salivary flow will lead to Rampant caries
& xerostomia
•Salivary is decreased in following
condition;
•Medications
•Illness
•Radiation to head & neck
•Salivary glands become fibrotic
•Autoimmune disease
•Protective mechanisms of
saliva which maintain normal
flora of oral cavity and tooth
surface integrity include;
•Bacterial clearance
•Direct antibacterial activity
•Remineralization.
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29. ROLE OF SALIVA IN CARIES
•Lubricates oral tissues
•Bathes teeth & biofilm
•Flushes micro-organisms
which are not adherent to oral cavity.
•Flushing effect is most effective during
mastication or oral stimulation due to large
volume of saliva.
•Slowest on labial aspects of Max. incisors &
buccal aspects of mandibular molars.
•Adult produce1 –1.5 liters of saliva
per day.
•Very little saliva is produced during
sleep.
•Saliva possess direct antibacterial
activity from its components, but normal
oral flora has developed resistance to
most of these antibacterial mechanisms.
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30. ROLE OF SALIVA IN CARIES.
•Antibacterial proteins in saliva play important
role in defense of soft tissues while they have
little effect on caries.
•Similar levels of antibacterial proteins are
found in caries active and caries free persons.
•So, it is clear that caries susceptibility does
not depend on composition of salivain
healthy persons.
•While caries susceptibility depends on
quantity of saliva.
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32. ROLE OF SALIVA IN CARIES
•Saliva also possess buffering
capacity.
•Buffering capacity of saliva depends
on;
•Concentration of bicarbonate ions
(Primary)
•Volume of saliva
•Buffering capacity is measured by
titration techniques.
•Molecules of saliva which increase the pH of
biofilm;
•Urea
•Sialin
•Hydrolysis of these compounds produce ammonia
which increase the pH of biofilm.
•Saliva help in remineralization of teeth.
•Saliva contains Statherian, a proline rich peptide
that stabilizes the calcium and phosphate and
prevents excessive deposition of these ions on
teeth.
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33. ROLE OF SALIVA IN CARIES
•Flow rate & buffering capacity are most importantprotective
mechanisms of saliva.
•Normal stimulated flow rate = 1.0 ml/minute
•Stimulated flow rate below 0.7 ml/minute is a high risk for caries
•Areas which are inaccessible to salivary flow or flushing are;
•Interproximal areas
•Fissures
•Cavity
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35. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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36. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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37. DIET & CARIES
•High frequency exposure is most important factor in development of caries.
•Frequent ingestion increases growth of highly acidogenic bacteria.
•When ingestion of carbohydrates is restricted, biofilm is made but it does not lead to caries
because acid is not produced.
•Dietary Sucrose is important in development of caries.
•Acidic food also lead to caries because the ultimate metabolic product of cariogenic
diet is acid which cause demineralization.
•So we should advise the patient to avoid frequent use of sweet and acidic products, not
just sucrose.
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38. DIET & CARIES.
•Principles of dietary advice for caries prevention.
•The pH drops for 30 for approx. 30 minutes.
•However if the salivary flow is low pH drop may be longer.
•Long pH depression occur in those areas of oral cavity where salivary flow is restricted as mentioned in
previous slide.
•Frequency of sugar intake is more important than quantity of sucrose.
•Stickiness of food is important factor in its cariogenecity.
•During retention time, carbohydrates are hydrolyzed to simple sugar providing more substrate to bacteria.
•Example; chocolate, caramel, potato chips.
•Caries preventive effect is small with sugar restriction as compared to fluoride use.
•Means fluoride use better reduces prevalence of caries as compared to sugar restriction.
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39. •So, Snack in
MODERATION , limited
to 3 OR 4 SNACKS A DAY.
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42. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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43. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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44. ROLE OF TIME IN DENTAL CARIES.
•Caries is chronic disease.
•Substrate/ dietary sugars require sufficient time for
demineralization.
•Same, time is required for remineralization process.
•Because caries does not develop in overnight but take time.
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45. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride
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46. ECOLOGIC BASIS OF DENTAL CARIES
Biofilm/ Plaque
Teeth
Oral Hygiene
Saliva
Diet
Time
Fluoride SARANG SURESH HOTCHANDANI 46

47. ROLE OF FLUORIDE IN DENTAL CARIES.
•A lack of fluoride constitutes caries risk.
•Fluoride administration is more effective in reducing caries than lowering use of
carbohydrates.
•Post-eruptive use of fluoride is more effective against caries than pre-eruptive
use of fluoride.
•Fluoride protects enamel more effectivelywhen it is present in ambient solution
during acid challenge than when it is incorporated into the enamel crystals.
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48. ROLE OF FLUORIDE IN DENTAL CARIES.
•Fluoride inhibits remineralizationby;
•Reprecipitation of dissolved calcium & phosphateand prevent
them from being leached out of enamel.
•Fluoride hamper penetration of acid into enamel.
•By narrowing the pores in enamel surface which help in
diffusion of acids.
•Fluoride facilitate remineralization.
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49. ROLE OF FLUORIDE IN DENTAL CARIES.
•Retention of fluoride is site specific.
•Mostly found on maxillary labial surfaces of incisors & buccal surfaces of lower
mandibular molars after rinsing with fluoride solution.
•Fluoride from tablets remain highly concentrated at the site of tablet dissolution.
•There is very little or no transport of fluoride b/w the right & left sides of mouth or
maxillary & mandibular arches.
•Coz of this localized caries lesion in the mouth may be related to insufficient spread of
fluoride when person used fluoride paste.
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53. SOCIAL & DEMOGRAPHIC FACTORS
•In western world, dental caries is more prevalent in;
•Lower socioeconomic
•Less affluent areas
•Some ethnic minorities
•Root caries is more prevalent in older persons of low socio economic status.
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54. RATE OF CARIES LESION PROGRESSION
•Now a days, caries lesion progress more slowly than they did several decades ago, due to
increased use of fluoride.
•Rate of caries progression is not same for each site or each tooth.
•Not all initial fissure lesion will develop to involve the dentine but number of them may
become arrested.
•The progression rate of caries is independent of the DMFSof individuals.
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55. RATE OF CARIES LESION PROGRESSION
(CONT’D)
•Rate of caries progression on proximal surface is low than pit & fissure lesion.
•Distal surfaces of 1
st
molars are.
•Caries lesion on smooth surfaces progress more slowly than on proximal surfaces or pits
and fissures.
•If there is not cavity and caries has not reached dentine, preventive measure can be used
to stop the caries process.
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56. PULP-DENTINE COMPLEX RESPONSES TO
CARIES
•3 levels of dentinal reaction to caries occur.
•Reaction to long term, low-level acid demineralization
associated with slowly advancing lesion.
•Reaction to a moderate-intensity attack
•Reaction to sever, rapidly advancing caries characterized
by very high acid levels.
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57. MANAGEMENT OF DENTAL CARIES
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58. DETECTION & DIAGNOSIS OF CARIES
•Caries Detection; it is an objective method of
determining whether or not clinical signs of
caries are present at one point in time through;
•Clinical examination, caries diagnostic aids, etc.
•Caries Diagnosis; it is assessment of dynamics
and determinants of caries process.
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59. CARIES DETECTION METHODS
Visual
Examination
Radiographic
Examination
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60. CARIES DETECTION METHODS
Visual
Examination
Radiographic
Examination
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61. VISUAL EXAMINATION OF DENTAL CARIES
•The first clinical sign of caries: a chalky and matte
whitish surface.
•this white spot is a porous surface that can easily be
stained into brown or black discoloration by
chromogens from foods; thus, a caries lesion
can be seen either as a white or as a
brown/black spot lesion.
•MOST COMMON METHOD OF CARIES EXAMINATION.
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62. PREREQUISITES FOR VISUAL
EXAMINATION OF DENTAL CARIES
•CLEAN TOOTH;
•Plaque must be removed from teeth
•DRY TOOTH;
•Teeth should be dried with air –water
syringe before examination.
•A white spot lesion is porous surface, in
which pores are filled with saliva when
teeth are wet.
•MAGNIFICATION & LIGHTENING
•For good visual examination appropriate
magnification & lightening are necessary.
•Drying the tooth surface during
examination has diagnostic as well as
prognostic value;
•Diagnostic Value of Drying;
•If white spot lesion is visible on wet tooth; it
indicate that demineralization is
extended into dentine.
•No chances of reversal, lesion only can be
arrested
•If white spot lesion is visible after drying of
tooth; it indicate that demineralization is
in enamel and is NOT extended into
dentine.
•Better chances of reversal of lesion
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63. CLINICAL CHARACTERISTICS OF THE
CARIES LESION.
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64. •The cavitation of tooth surface produces a synergetic
acceleration of the growth of cariogenic biofilm and
expansion of demineralization and cavity.
•When enamel caries reached DEJ, rapid lateral expansion
occurs.
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65. CLINICAL SITES FOR CARIES INITIATION
•Characteristics of caries lesion depends upon the nature of the surface on which it
develops;
•Developmental pits and fissures (most susceptible)
•Smooth enamel surface
•Root surface
•Each of the above surface have different surface topography, environment, biofilm
population, treatment, prevention etc.
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66. PROGRESSION OF CARIES LESIONS
•The time for progression from non-cavited caries to cavitation on smooth surface is
18 months ±6months
•Peak rate of incidence of new lesion occur 3 year after eruption of the tooth.
•Poor oral hygiene and frequent sucrose intake produces white spot in 3 days.
•Radiation induced xerostomia can lead to caries in 3 months from the onset of
radiation.
•Caries rate is slow in healthy as compared to compromised individuals
•Caries progression is delayed by fluoride use.
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67. ENAMEL CARIES
•Non cavited enamel caries lesion;
•White spot, chalky white, opaque area revealed
after desiccation.
•Loss of translucency in them is due to
subsurface porosity caused by
demineralization.
•Softened chalky enamel that can be chipped
away with explorer is sign of active caries.
•Non cavited enamel lesion on radiograph
appear as faint radiolucency that is limited to
superficial enamel
•If, the radiolucency is clear, then the caries
have been advanced and histologic changes of
caries in dentine will be present.
•Non cavited enamel lesion can be re-
mineralized.
•Because they retain the original crystalline
framework of enamel rods which are etched
from the acid of bacteria.
•These etched crystallites serve as nucleating
agent for remineralization where calcium and
phosphate from saliva bind resulting re-
mineralization.
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69. •Fluoride enhances this precipitation of ions from saliva and increase resistance to
caries attack by incorporating Fluorapatite.
•Active or arrested caries on radiograph look similar in appearance that’s why we can
diagnose the caries on the basis of radiograph only.
•The change in color of arrested caries is because of trapped organic debris and
metallic ions within enamel.
•Arrested caries lesion is more resistant than the normal unaffected enamel
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71. DENTINE CARIES
•Progression of caries in dentine is different from that of enamel because of structural
differences of dentine.
•Dentinal caries is V shaped in cross section because DEJ allows rapid lateral spread when
caries from enamel reaches at DEJ before going to dentine.
•Wide BASE at DEJ and apex towards PULP.
•Caries progress more in dentine than enamel because dentine contain less mineral
content resulting decrease in resistance to acid attach/ demineralization.
•Pain in caries occurs due to stimulation of pulp by the movement of fluid through dentinal
tubules that have been opened to the oral environment.
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72. CLINICAL VISUAL CARIES SCORING
SYSTEM
ICDAS (International Caries Detection and Assessment System)is a two-stage, two-digit coding system
comprised of a code for the restoration and sealant status of the tooth surface, followed by a code for the caries
severity.
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First digit (restoration and sealant codes)Second digit (caries severity codes)
0= No sealant or restoration 0 =sound tooth surface
1 = partial sealant 1 = First visual change (opacity or discoloration) in enamel
hardly visible on the wet surface but distinctly visible after air
Drying
2 = full sealant 2 = Distinct visual change (opacity or discoloration) in enamel,
visible without air drying
3 = Tooth-colored restoration 3 = Enamel breakdown, no dentin visible
4 = Amalgam restoration 4 = Dentin shadow (not Cavitated into dentin)
5 = Stainless steel crown 5 = Distinct cavity with visible dentin
6 = Porcelain, gold, PFM crown or veneer6 = Extensive distinct cavity with visible dentin
7 = Defective restoration
8 = Temporary restoration

73. CORRELATION OF THE ICDAS CARIES SEVERITY CODES WITH
THE HISTOLOGIC DEPTH OF THE LESIONS INTO THE TOOTH
TISSUE ON THE OCCLUSAL SURFACE
Caries Severity Code Histologic Depth
0 No Enamel Demineralization
1 Enamel demineralization limited to outer halfof enamel
layer
2 Demineralization involving enamel & outer 3
rd
of dentine
3–4 Demineralization involving the middle 3
rd
of dentine
5 –6 Demineralization involving the pulpal 3
rd
of dentine
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74. INTERNATIONAL CARIES CLASSIFICATION SYSTEM
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740 (green)–sound tooth surface; 1 (yellow)–distinct, visual noncavitated change
in enamel; 2 (orange)–localized enamel breakdown; 3 (red)—distinct cavity
with visible dentin.

75. VISUAL EXAMINATION OF
PIT & FISSURE CARIES LESIONS
•Shadowing or grayish discolorationof the adjacent translucent
enamel along the pits and fissures may indicate possible
undermining of enamel by hidden caries.
•Opaque, matte texture of enameladjacent to the stained pits and
fissures may indicate the presence of active cariesunderneath
them.
Illustration of the visual detection of lesions on the walls of stained
pits/fissures. (a) A stained fissure (red circle) under visual
examination. (b ) Looking perpendicularly through the translucent
adjacent healthy enamel along the fissure (white arrows), lesions on
the walls of the fissure are seen as discoloration extending (ie,
underneath the translucent enamel) beyond the confines of the
fissure with a “bottle-brush” appearance(red arrows).
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76. THE EXPLORER TIP CAN EASILY DAMAGE
WHITE SPOT LESIONS
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77. VISUAL EXAMINATION OF CARIES LESION
ON PROXIMAL SURFACES
•Extensive active proximal lesions of posterior teeth can be revealed by shadowing or grayish
discoloration of the undermined occlusal enamel ridge.
•when there is contact between proximal surfaces, the radiograph is the most accurate method for
detecting demineralization of proximal caries lesions.
•For detection of proximal lesions in anterior teeth, the fiber-optic trans illumination technique is
particularly appropriate and convenient.
•a fine light, coned down to a 0.5-mm diameter, is transmitted through a contact area.
•A lesion appears as a dark shadow.
•use of an orthodontic separator has been advocated in some cases to allow the dentist to see
more clearly and to gently feel for a break in the enamel surface.
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78. VISUAL EXAMINATION OF CARIES LESIONS
ON BUCCAL, LINGUAL & ROOT SURFACE
•Active caries lesions in smooth, free enamel surfaces are
typically located close to the gingival margin and have
chalky matte, whitish/ yellowish surfaces.
•A caries lesion on a root surface is seen as a clearly
demarcated, light brown, dark brown, or black discolored
area on the root surface or at the cemento-enamel junction.
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79. CARIES DETECTION METHODS
Visual
Examination
Radiographic
Examination
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80. CARIES DETECTION METHODS
Visual
Examination
Radiographic
Examination
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81. •Bitewing radiograph is essential for proximal caries.
•However, it cannot distinguish b/w cavited or non cavited lesions.
•Radiographic evaluation of occlusal surfaces has been found to be of minimal diagnostic value
for detecting enamel caries and superficial dentinal caries because of the large amounts of
surrounding sound enamel.
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•E1—less than halfway
through proximal
enamel;
•E2—more than halfway
through proximal
enamel, not penetrating
past the Dentino enamel
junction;
•D1—slightly past the
DEJ;
•D2—less that halfway
through dentin toward
the pulp;
•D3—halfway or more
through dentin.

82. CARIES
DIAGNOSIS
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83. ASSESSING CARIES ACTIVITY
Characteristics of active and arrested lesions in enamel and roots
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CONDITION TOOTH TISSUE ACTIVE ARRESTED
Appearance ENAMEL Lesion is chalky (lacks luster) when air
dried and is whitish or yellowish
Lesion has shiny surface when air
dried and may be whitish,
brownish, or blackish.
ROOT Clearly demarcated and may be
discolored yellowish/light brown Note:
Color change is not a reliable indicator
SAMEAS ACTIVE LESION
TEXTURE ENAMEL Feels rough with explorer Feels hard and more smooth with
explorer
ROOT Lesion has soft or leathery base on
gentle probing using blunt or CPITN
probe
Lesion has hard and shiny base
using blunt or CPITN probe.
TRANSLUCENCY ENAMEL Opaque Semi transparent
ROOT Not available Not available
LOCATION ENAMEL Plaque stagnation areas Location is plaque free
ROOT Anywhere Anywhere

84. ASSESSING CARIES ACTIVITY
Characteristics of active and arrested lesions in enamel and roots
SARANG SURESH HOTCHANDANI 84
CONDITION TOOTH TISSUE ACTIVE ARRESTED
CAVITATION ENAMEL From localized surface defect (micro
cavity) in enamel only to distinct cavity
with soft or leathery base on gentle
Probing.
From localized surface defect
(micro cavity) in enamel only to
distinct cavity with hard base on
probing with gentle pressure;
surface of cavity may be shiny
ROOT Cavitated if there is loss of surface
integrity or if the depth is ≥ 0.5 mm
measured using the ball of the CPITN
probe;
Noncavitated if no loss of surface
integrity or if the depth is < 0.5 mm
SAMEAS ACTIVE LESION

85. SARANG SURESH HOTCHANDANI
85
Active Caries Lesion Arrested Caries Lesion Matte, white, active cervical caries lesion
Cavited, Active Cervical Caries Lesions

86. ASSESSING CARIES RISK
•CARIES RISK; it is probability of an
individual developing caries lesion.
•Common Causes of DRY MOUTH
•Medications;
•antidepressants, antipsychotics,
tranquilizers, antihypertensives, and
diuretics
•Sjögren syndrome;
•affects the salivary and lacrimal glands,
leading to a dry mouth and dry eyes;
•rheumatoid arthritis may indicate the
presence of this disorder
•Eating disorders,
•induce hypo salivation;
•this, combined with a poor diet,
can lead to extensive caries
•Radiation therapy in the region of the
salivary glands for a head and neck
malignancy, which often induces
xerostomia
SARANG SURESH HOTCHANDANI
86

87. SARANG SURESH HOTCHANDANI 87

88. AMERICAN DENTAL ASSOCIATION (ADA)
RECOMMENDED GUIDE TO IDENTIFYING AN
OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 88
CARIESRISK
CATEGORY
YOUNGER THAN 6 YEARS 6 YEARS OR OLDER
Low Risk NowhitespotorCavitatedprimaryor
secondarycarieslesionsduringthelast3
yearsandnofactorsthatmayincrease
cariesrisk.
NowhitespotorCavitatedprimaryor
secondarycarieslesionsduringthelast3
yearsandnofactorsthatmayincrease
cariesrisk.
Moderate Risk NowhitespotorCavitatedprimaryor
secondarycarieslesionsduringthelast3
yearsbutpresenceofatleastonefactor
thatmayincreasecariesrisk
OneortwowhitespotsorCavitatedprimary
orsecondarycarieslesionsinthelast3
years
OR
NowhitespotorCavitatedprimaryor
secondarycarieslesionsinthelast3years
butpresenceofatleastonefactorthatmay
increasecariesrisk

89. AMERICAN DENTAL ASSOCIATION (ADA)
RECOMMENDED GUIDE TO IDENTIFYING AN
OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 89
CARIESRISK
CATEGORY
YOUNGER THAN 6 YEARS 6 YEARS OR OLDER
HighCaries Risk•Any white spot or Cavitated primary or
secondary caries lesions during the
last 3 years.
•Presence of multiple factors that may
increase caries risk
•Low socioeconomic status, especially in
children too young for their risk to be
based on caries history
•Suboptimal fluoride exposure
•Xerostomia
•Three or more white spots or Cavitated
primary or secondary caries lesions in
the last 3 years.
•Presence of multiple factors that may
increase caries risk
•Suboptimal fluoride exposure
•Xerostomia.

90. SPECIFIC CARIES RISK FACTORS THAT MAY
GUIDE THE OVERALL CARIES RISK STATUS
SARANG SURESH HOTCHANDANI 90

91. RISK BASED
CARIES
MANAGEMENT
SARANG SURESH HOTCHANDANI 91

92. ALGORITHM FOR CARIES MANAGEMENT IN
FISSURED SURFACES OF PERMANENT TEETH.
SARANG SURESH HOTCHANDANI 92

93. ALGORITHM FOR MANAGEMENT OF INITIAL
CARIES LESIONS IN NON -PROXIMAL CORONAL
SMOOTH SURFACES OF PERMANENT TEETH.
SARANG SURESH HOTCHANDANI 93

94. ALGORITHM FOR DIAGNOSIS AND MANAGEMENT OF CARIES
LESIONS IN ROOT SURFACES OF PERMANENT TEETH.
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94

95. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A HIGH CARIES-RISK
PATIENT, BASED ON PTPM
SARANG SURESH HOTCHANDANI 95

96. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A HIGH CARIES-RISK
PATIENT, BASED ON PTPM
SARANG SURESH HOTCHANDANI 96

97. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A MODERATE-
CARIES-RISKPATIENT,
SARANG SURESH HOTCHANDANI 97
Step 1: Plaque
control
•Provide
prophylactic
treatment
followedby
fluoride
application
•Seepatient
regularlyto
reinforce
oralhygiene
Step 2:
Treatment of
existing caries
lesions
•Treat
noncavitated
lesions as
needed
•Restore
cavitated
lesions and seal
surrounding
pits and fissures
as needed
Step 3:
Protection of
surfaces at
risk
•Seal all
deep pits
and fissures
•Apply
fluoride
varnish to
exposed
roots
Step 4: Maintenance care for prevention
•Review oral hygiene and dietary habits and advise
patient to:
•Reduce the number of between-meal sweet snacks
•Substitute snacks rich in protein
•Advise patient to brush twice daily with over-thecounter
fluoride toothpaste
•Advise patient to floss once daily
•Provide home treatment and/or other adjunctive
therapy:
•Use over-the-counter fluoride rinse daily
•Chew or suck xylitol-containing gum or candies three
times daily
•Recall patient every 3 to 6 months to:
•Reevaluate current caries risk
•Receive fluoride varnish treatment of all teeth
•Obtain bitewing radiographs every 12 to 18 months to
check for cavities

98. GENERAL GUIDELINES FOR CARIES
MANAGEMENT FOR A LOW CARIES-RISK PATIENT
SARANG SURESH HOTCHANDANI 98
Step 1: Plaque control
Step 2: Maintenance care for
prevention
•Review oral hygiene habits
•Advise patient to brush twice
daily with over-the-counter
fluoride toothpaste
•Recall patient every 12 to 24
months to reevaluate current
caries risk
•Obtain bitewing radiographs
every 24 months to check for cari

99. PREVENTIVE & NON –
INVASIVE TREATMENT
OPTIONS
SARANG SURESH HOTCHANDANI 99

100. BASIC PREVENTIVE STEPS FOR
MODERATE/HIGH -RISK PATIENTS
SARANG SURESH HOTCHANDANI 100
Patient Motivation
•Emphasis on
Behavioral Change
Diet Counselling
•Reduce carbohydrate
intake & frequency
Toothbrushing
•Twice daily with
fluoride toothpaste
Flossing
•Daily, Few Times a
week
Sugar Free Gum
•Two pieces for ≥ 5
minutes three times a
day (after each meal
preferred)
Sealant

101. ADJUNCT TOPICAL THERAPIES FOR
MODERATE/HIGH -RISK PATIENTS
SARANG SURESH HOTCHANDANI 101
HOME
FLUORIDE
OPTIONS
•Prescription fluoride
(5,000 ppm) toothpaste
•Apply via tray daily for
patients with radiation-
induced hypo salivation
•Fluoride Rinse
•Twice daily/daily/weekly
depending on need

102. ADJUNCT TOPICAL THERAPIES FOR
MODERATE/HIGH -RISK PATIENTS
SARANG SURESH HOTCHANDANI 102
•Fluoride gel/foams
•1.23% APFor neutral 2% NaF
•4 minutes, two to four times per year
•For root caries, four times over 2 to 4
weeks
•Fluoride varnishes
•Apply to lesions and other surfaces at
risk two to four times per year
depending on risk
IN OFFICE FLUORIDE OPTIONS

103. SARANG SURESH HOTCHANDANI 103

104. SOME POINTS
•If interdental spaces are closed = advice dental floss
•If interdental spaces are open = advice interproximal brush
•Want to prevent caries only = floss once daily
•want to prevent caries & gingivitis = floss twice daily
•Stannous fluoride = inhibit plaque formation
•Triclosan= disrupt cell wall of plaque bacteria
SARANG SURESH HOTCHANDANI 104

105. HOME USE FLUORIDE GEL -1.1 % NAF.
•recommended for high-risk adults and children 6 years and
older
•applied once daily over the tooth surfaces using a finger,
toothbrush, or individually fitted trays, preferably
immediately before bed.
•The gel should be left in contact with the teeth surfaces for 5
minutes, after which the individual should spit and not rinse.
SARANG SURESH HOTCHANDANI 105

106. Acidic topical fluoride solutions, such as APF
solutions and other acidified fluoride
preparations, degrade glass-ionomer materials,
porcelain crowns, and veneers and should be
avoided in these patients
SARANG SURESH HOTCHANDANI 106

107. DIETARY MANAGEMENT FOR CARIES
PREVENTION
•Eat a diet that is low in sucrose and retentive fermentable carbohydrates.
•Reduce the frequency of eating or drinking fermentable carbohydrates.
•Combine cooked and processed foods with non acidogenic foods.
•Do not eat cariogenic snacks.
•Include foods of firm or hard texture.
•Choose fats in diet wisely to reduce risk of chronic disease while still benefiting from fat
coating on tooth surfaces, which reduces the adherence of plaque.
•Chew sugarless gum (preferably with xylitol) for 15 to 20 minutes after eating to increase
salivary benefits.
•Combine and sequence foods to encourage chewing and saliva production.
•Only eat sweets with non cariogenic sweeteners
SARANG SURESH HOTCHANDANI
107

108. PIT & FISSURE SEALANTS
Resin based
Composites
Glass Ionomer
Cement
Release fluoride
Light cured
GIC in varnish
form
Used on where
moisture control is
difficult just like
partially erupted
molar
SARANG SURESH HOTCHANDANI 108

109. NONINVASIVE OPTIONS FOR
TREATMENT OF EXISTING LESIONS
SARANG SURESH HOTCHANDANI 109

110. TREATMENT OF NONCAVITATED LESIONS
SARANG SURESH HOTCHANDANI 110

111. LESION ARREST
(REMINERALIZATION THERAPY)
SARANG SURESH HOTCHANDANI 111
Improved Oral
hygiene and
application of
topical fluorides
every 3 months
until caries activity
is under control
The choice of treatment for active noncavitated lesions on proximal
coronal surfaces depends on the CARIES RISK STATUS OF THE
PATIENT as well as the DEPTH OF THE LESION.

112. OCCLUSAL &
PROXIMAL
SEALANT
•Done in ICDAS Score 1 & 2
•Perform Acid Etching for
Resin Composite Sealant.
•Perform Conditioning for
GIC Sealant.
•Sealants are more effective
during the period of tooth
eruption, but can be applied
on older persons.
SARANG SURESH HOTCHANDANI 112

113. ADVANTAGES OF SEALANTS
•No irreversible intervention necessary.
•Active dentine or enamel lesion do not progress
further.
•Possible developments of new lesions in other sites
of fissure is prevented.
SARANG SURESH HOTCHANDANI 113

114. LESION
INFILTRATION
•It is a new technique & alternative to sealant.
•Used for treating lesions extending into inner enamel or outer 3
rd
of dentine. –
ICDAS 1 & 2.
•It occludes lesion pores with low –viscosity light
curing resins in order to create diffusion barrier
& arrest caries progression.
SARANG SURESH HOTCHANDANI 114

115. STEPS IN LESION INFILTRATION
SARANG SURESH HOTCHANDANI 115
Etch
•HCL
Dry
•Ethanol & Air
Drying
Apply the
INFILTRATE for 3
minutes & Light
Cure
2
nd
Coat of
Infiltrate for 1
minute only &
Light Cure it.

116. OPERATIVE & MINIMALLY INVASIVE
TREATMENT OPTIONS
SARANG SURESH HOTCHANDANI 116

117. INDICATIONS OF RESTORATIVE
TREATMENT
•The Cavitated tooth is sensitive to hot, cold, sweetness, etc.
•Occlusal and proximal lesions extend deep into dentin (and cannot be
reached by the toothbrush).
•The pulp is endangered.
•Previous attempts to arrest the lesion have failed, and there is evidence
that the lesion is progressing (such evidence usually requires an
observation period of months or years).
•The patient’s ability to provide effective home care is impaired.
•Drifting is likely to occur through loss of proximal contact.
•The tooth has an unaesthetic appearance
SARANG SURESH HOTCHANDANI
117

118. PREVENTIVE RESIN RESTORATION &
PREVENTIVE AMALGAM RESTORATION
•In this, Restoration of the carious surface occur
accompanied with sealing of surrounding pits
and fissures with sealant.
•Advantages
•Conserve surrounding sound tooth structure.
•Protects margins of restoration
•Prevent secondary caries
SARANG SURESH HOTCHANDANI 118

119. INTERIM THERAPEUTIC RESTORATION
(ITR)
It involves removal of caries using hand
instrument or low-speed rotary instruments,
with caution not to expose the pulp, followed by
restoration of the tooth with an adhesive
restorative material, such as conventional or
resin-modified glass ionomer cement.
SARANG SURESH HOTCHANDANI 119

120. INDICATIONS OF ITR
•When Caries control is necessary before placement of definitive
restoration.
•Multiple caries lesions.
•Children experiencing early childhood caries.
•Rampant caries
•High caries risk patients
•Uncooperative patients
•During stepwise excavation technique.
SARANG SURESH HOTCHANDANI 120

121. ADVANTAGES OF ITR
•Reduce level of cariogenic bacteria in the oral
cavity.
•Make tooth surfaces more cleansable prior to
placing definitive restoration.
SARANG SURESH HOTCHANDANI 121

122. RECALL & REASSESSMENT VISITS
SARANG SURESH HOTCHANDANI 122

123. THE END
Written by;
SARANG SURESH
HOTCHANDANI
Final Year BDS, Roll#21
Bibi Aseefa Dental College,
SMBBMU, LARKANA
Email:
[email protected]
Slideshare:
http://www.slideshare.net/sarangsureshhotchandani
Twitter:
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SARANG SURESH HOTCHANDANI 123