DENTAL CARIES

AND
ITS MANAGEMENT

Presented by –Dr Shruti

 CONTENTS:
 Introduction.
 Definitions.
 Classifications.
 Early theories of caries.
 Current concepts of caries etiology.
 Microbiology of dental caries.
 Nutrition ,diet and dental caries.
 Histopathology of dental caries.
 Diagnosis.
 Caries prevention.
 Management ---------- Early lesion. (minimal invasive techniques
Non-rotary methods of cavity preparation)

Deep caries lesion- vital pulp therapy

(indirect pulp capping , direct pulp capping, pulpotomy
procedures)

Conclusion.
 INTRODUCTION:
 Dental caries and periodontal diseases are
probably the most common
chronic diseases of the world.

 Dental caries is the latin word for “ ROT or ROTTEN”.

 It is common in population throughtout the world and is

the key factor responsible for dental pain and tooth loss .

 It affects persons of both sexes , in all races,all

socioeconomic status and all age groups.

 It’s a highly complex process with spatial and temporal

variations not only in no. and type of determinants
involved but also in their relative influence.
 DEFINITIONS:
 Dental caries is an infectious disease of the teeth that results in
localized destruction and dissolution of the calcified tissues.
(STURDEVANT)

 Dental caries is the microbial disease of the calcified tissues of

the teeth characterized by the demineralization of the inorganic
tissue and destruction of the organic substance of the tooth.
(SHAFER)

 Localized posteruptive pathological process of external origin,

involving softening of hard tooth tissues, and proceeding into
the formation of cavity.
(WHO)
 CLASSIFICATION:

I. Depending on origin as : (SHAFER)

 Incipient \initial \ primary caries
It is the first attack on the tooth surface.

 Recurrent \ secondary caries

A carious lesion that develops at the interface
of the restoration and cavosurface of the enamel.

 Residual caries – It is the type of caries deliberately

left behind during restorative procedures with an aim of
remineralizaton.
.
II. According to their activity: ( Ole Fejerskov)
Active lesions-
considered to be progressive .

Inactive \chronic lesions-

Formed years previously and
stopped further progression
 Depending on rapidity of progress:
(NIKIFOROUK)
 Acute \Rampant caries: multiple active carious lesion
occurring in same patient.
 Chronic caries: variable depth, long standing, tend to be
fewer in number.
 Arrested caries: Static or stationary and does not show any
tendency for further progression.

 Depending on location: (GORDAN NIKIFORUK)

 Pit & fissure caries:
 Smooth surface caries:
 Root surface caries
 GV BLACKS CLASSIFICATION:
 CLASS I:
Caries begins in structural
defects of the teeth i.e pits,
fissures and sometimes
grooves.
Locations-
 occlusal surfaces of

premolars and molars.

 occlusal 2/3rd of the

buccal and lingual surfaces

of molars and premolars.
 lingual surfaces of

anteriors.
 ClassII-G.V. Black Classification
Proximal surface of posterior teeth.
Class III-G.V. Black Classification
Proximal surface of anterior teeth
 Class IV-G.V. Black Classification
Proximal surface and incisal angle of anterior teeth
 Class V-G.V. Black Classification
Cervical area of anterior and posterior tooth
 Class VI-G.V. Black Classification
Occlusal cusps of posterior teeth ,incisal edge of anterior teeth
 According to pathway: (SHAFER)
 Forward decay: Caries starts in enamel and then
involves the dentin .

 Backward decay : Caries process in dentin progresses

much further than it does in enamel.(lateral spread of caries
in DEJ

 Depending on surfaces of tooth involve

(SHAFER)
 Simple caries
 Compound caries
 Complex caries
 Nursing bottle (infancy)

caries

Adolescent
caries

Senile caries
  CLASSIFICATION BY SIZE & SITE
(Graham mount)

SITE MINIMAL MODERATE ENLARGED EXTENSIVE

1 2 3 4
PIT & 1.1 1.2 1.3 1.4
FISSURE 1
CONTACT 2.1 2.2 2.3 2.4
AREA 2
CERVICAL 3.1 3.2 3.3 3.4
AREA 3
 EARLY THEORIES OF CARIES
 
WORMS – According to the ancient Sumerian text, toothache was caused by a
worm that drank the blood of the teeth and fed on the roots of the jaws.
The idea that caries is caused by a worm was almost universal at one time, as
evidenced by the writing of Homer and popular lore of China, India, Finland, and
Scotland .
GUY DE CAHULIAC (1300- 1368), The greatest surgeon of middle ages believed
that worms caused dental decay .As a cure he advocated fumigation with seeds of leek,
onion and hyoscyamus. The Chinese and Egyptians used fumigation in earlier times,
and fumigation devices continued to be used in England as early as the nineteenth
century.
HUMORS –
The ancient Greeks considered that a persons physical and mental
constitution was determined by the relative proportions of the four
elemental fluids of the body - blood, phlegm, black bile, and yellow
bile which corresponds to the four humors –sanguine, phlegmatic,
melancholic and choleric .All diseases, including caries could be
explained by an imbalance of those humors.

 VITAL THEORY. –
The vital theory regarded dental caries as originating within the tooth
itself, analogous to bone gangrene. This theory proposed at the end
of eighteenth century, remained dominant until the middle of the
nineteenth century .A clinically well known type of caries is
characterized by extensive penetrations into the dentin, and even
into the pulp, but with a barely detectable catch or a fissure.  
 CHEMICAL THEORY –

Parmly (1819) rebelled against the vital theory and proposed that an
unidentified “chemical” agent was responsible for caries .He stated that
caries began on the enamel surface in locations where the food putrefied
and acquired sufficient dissolving power to produce the disease chemically.
Support for the chemical theory came from Robertson (1835) and Regnart
(1938) who actually carried out experiments with different dilutions of
organic acids (such as sulphuric and nitric) and found that they corroded
enamel and dentin.

PARASITIC OR SEPTIC THEORY-

In 1843 Erdl described filamentous parasites in the “ surface membrane”

of teeth. Shortly thereafter Ficinus , observed filamentous
microorganisms ,which he called denticulate in material taken from
carious activities .He implied that these bacteria caused decomposition of
the enamel and then the dentin .Neither Erdl nor Ficinus explained how
these organisms destroyed tooth structure.
 
 CHEMO –PARASITIC THEORY-
 This theory is a blend of the above two theories,
because it states that caries is caused by acids produced
by microorganisms of the mouth. it has been customary
to credit this theory to W. D miller (1890),whose writings
and experiments helped to establish this concept on a
firm basis.
The work of Willoughby D. Miller (1853-
1907) at the university of Berlin has a most profound
effect on the understanding of caries etiology and
subsequent caries research .
In a series of experiments Miller demonstrated the following
facts,
 Acid was present within the deeper carious lesions, as shown
by reaction on litmus paper.
 Different kinds of foods (bread, sugar, but not meat) mixed
with saliva and incubated at 37degree centigrade could
decalcify the entire crown of a tooth .
 Several types of mouth bacteria (at least 30 species where
isolated) could produce enough acid to cause dental caries.
 Lactic acid was an identifiable product in carbohydrate –saliva
incubation mixtures .
 Different microorganisms (filamentous ,long and short
bacilli ,and micrococci ) invade carious dentin .
 Miller concluded that no single species of microorganism
caused caries but rather that the process was mediated by an
oral microorganism capable of producing acid and digesting
protein .
PROTEOLYTIC THEORY –According to this theory ,the organic component
is most vulnerable and is attacked by hydrolytic enzymes of
microorganisms ,this precedes the loss of the inorganic phase .

 Gottlieb (1944) maintained that the initial action was due to proteolytic
enzymes attacking the lamellae ,rod sheaths ,tufts and walls of the
dentinal tubules .
 Frisbie (1944) also described caries as a proteolytic process involving
depolymerization and liquefaction of the organic matrix of enamel .The
less soluble inorganic salts could then be freed from their “organic bond”
favoring their solution, by acidogenic bacteria that secondarily penetrate
along widening paths of ingress .
Pincus (1949) contended that proteolytic organisms first attacked the
protein elements ,such as the dental cuticle and then destroyed the prism
sheaths. The loosened prisms would then fall out mechanically .

 He also suggested that sulfatases of gram-negative bacilli hydrolyzed

“mucoitin sulfate” of enamel or chondroitin sulphate of dentin and
produced sulfuric acid . The released sulfuric acid could combine with the
calcium of the mineral phase .
 PROTEOLYSIS –CHELATION THEORY
According to this theory ,decalcification is mediated by a
variety of complexing agents ,such as acid anions ,amines
,amino acids ,peptides polyphosphates ,and carbohydrate
derivatives .oral keratinolytic bacteria are thought to be
involved in the process. Differences in the keratin content of
the enamel in children with high caries and low caries
experience are considered important
 Schatz and Martin challenged the chemo-parasitic theory
advocated the proteolysis – chelation theory and stated that
acid may prevent tooth decay by interfering with growth and
activity of proteolytic bacteria .
 
 CURRENT CONCEPTS OF CARIES ETIOLOGY
Keyes in 1960 proposed a triad of factors :

Tooth

DC
Substrate Flora

NEWBURN in 1978 proposed that dental caries to be multifactorial disease .

Interplay of 4 perpetual factors:
Micro flora: Acidogenic bacteria that colonize the tooth surface.
Host: quantity and quality of saliva, the quality of the tooth, etc.
Diet: intake of fermentable carbohydrates, especially sucrose, but also starch.
Time: Total exposure time to inorganic acids produced by the bacteria of the
dental plaque
VEN DIAGRAM – Ole Fejerskov
Modified keyes diagram
  The host factor
A. Saliva and
B. Tooth

Salivary anti-caries activity

There is general agreement that saliva may be one of the innate
mechanism against dental caries.

A number of potential mechanism appear to be involved.

Increased salivary flow increase carbohydrate clearance from the oral
cavity.

Salivary bicarbonate buffer acids formed during carbohydrate

fermentation in the dental plaque.
 Salivary components could increase enamel resistance to
acid decalcification due to its component fluoride activity.

 Salivary components (eg. Ca, P & F- ions) could promote

subsurface remineralisation of carious lesion.

 Saliva could promote microbial clearance from the oral

cavity, thereby decreasing plaque formation.

 Salivary components might increase acquired pellicle

thickness prior to plaque microbial colonization.
 TOOTH:
Tooth morphology and arch form .

 . Tooth morphology has long been recognized as an important

determinant . For example attempts to induce caries in dogs
have been unsuccessful mainly because of the wide spacing
and the conical shape of the teeth .

 On the basis of clinical observation it is known that the pit and

fissure areas of the posterior teeth are highly susceptible to
caries . Food debris and microorganisms readily impact in the
fissures

 Certain surfaces of the tooth are more prone to decay whereas

other surfaces rarely show decay . For eg. In mandibular first
molar the likelihood of decay in descending order is occlusal ,
buccal , mesial , distal and lingual , whereas in maxillary first
molars the order is occlusal , mesial , palatal , buccal and distal
.
 An intraoral variation exists in susceptibility to caries between
different tooth types . The more susceptible permanent teeth
are the mandibular first molars closely followed by the
maxillary first molars and the mandibular and maxillary second
molars .

 The second premolars , the maxillary incisors and the first

premolars are the next in sequence , whereas the mandibular
incisors and canines are the least likely to develop lesions .
 Irregularities in arch form , crowding , and overlapping of the
teeth also favor the development of carious lesions .
 TOOTH COMPOSITION

 There is good evidence to indicate that enamel surface is

more caries resistant than the sub surface . Microradiographs
of initial carious lesions frequently reveal marked
demineralization of the sub surface enamel beneath an
outermost layer that is only slightly effective .
 Changes of the enamel such as decrease in density and
permeability and an increase in nitrogen and fluoride content, occurs
with age . These alterations are part of the post eruptive “maturation”
process whereby teeth become more resistant to caries with time .

 The concentration of fluorides of the surface layer of enamel

increases as the fluoride concentration of the drinking water increases,
and such enamel is less soluble in acids. Furthermore , the higher the
fluoride concentration of the water supply , the lower the prevalence of
caries .
 Time Factor In Caries Etiology
 Caries is considered to be a chronic disease in man because lesions
develop over a period of month or years.
 The average time from stage of incipient caries to chemical caries is 18
±6months

 The time of consumption of food greatly enhances caries development.

 Carbohydrate sugar rich diet taken between meals is most cariogenic and
may have serious implication in development of caries.

 If the oral hygiene is not maintained the contact of the acidic environment
with the tooth surface has a deleterious effect.
 Concept of critical pH:
 The loss of tooth mineral during caries formation is caused by the
formation of bacterial acids which lower the pH to the point where the
hydroxyapetite mineral of enamel dissolves.
 The concept of critical pH was initially applied to indicate the pH at
which the saliva was no longer saturated with respect to calcium and
phosphate ions thereby permitting hydroxyapetite to dissolve.
 (Ericsson,1949)
 It has been shown experimentally that both saliva and plaque fluid
cease to be saturated at pH values in the range 5-6 with an average
of 5.5
 It is unlikely that demineralization would occur above 5.7 and this value
is considered ‘safe for the teeth’
 MICROBIOLOGY OF DENTAL CARIES
 Three cariogenic bacteria :
1.Mutant streptococci
S mutans,S sobrinus, S sanguinis, S salivaris,
S milleri.
Gram positive, non- motile arranged in
medium and short chains.

2. Lactobacilli
L acidophilis, L casei.
gram positive ,non sporing rods

3. Actinomyces
While not the first to colonise the tooth, studies
has shown that S mutans to be the main
culprit in DC.
 There is abundant support for the so –called specific plaque
hypothesis ,introduced by Loesche(1982,1986) ,which
proposes that some specific species of the plaque flora be
regarded as major pathogens in the etiology of dental caries .
Included in the major pathogens are those bacteria associated
with caries in humans and also able to induce carious lesions in
experimental animals .

 The most important are the mutans streptococci, there are

seven species, of which two s.mutans and s.sobrinus ,are
closely associated with caries in humans .
 The second genus closely associated with caries is
lactobacillus ,commonly isolated from carious dentin .

 Also associated with the etiology of dental caries ,but

considered to be less cariogenic, are actinomyces
odontologica, actinomyces naeslundii, and some other species
of mutant streptococci.
 Cariogenic features of mutans streptococci
1. Binding to and colonization of teeth
2. Accumulation on tooth surfaces and participation in the formation of
dental plaques.
3. Production of acid at a high rate.
4. Tolerance of high concentrations of sugar, high ionic strength, and highly
acidic conditions.
5. Association with dental caries in humans.
6. Causation of dental caries in animals.
7. Transmissible in animals and apparently in man.
8. Reduction or elimination of mutans streptococci will result in reduction or
elimination of dental caries.
CARIES PROCESS
The formation of mutans streptococci on dental plaques appears to be a primary
requisite for the initiation of the caries process.

There appears to be at least 3 phases during carious process:

- Initial attachment.
- Accumulation.
- Acid formation andCavitations.
 NUTRITION, DIET AND DENTAL CARIES

 Ingestion of food may affect oral-dental health care by both systemic and
local mechanisms .

 Nutritional effects are mediated systemically ; dietary effects are mediated

locally in the oral cavity .

 The systemic effects results from the absorption and circulation of

nutrients to all cells and tissues and may be mediated through influences
on development of teeth , the quality and quantity of salivary secretions ,
improved host resistance and improved function .

 Dietary constituents exert their local effects by influencing the

metabolism of oral flora and by modifying salivary fluids and indirectly the
qualitative aspects of salivary secretion .
 NUTRITIONAL INFLUENCES ON DENTAL
TISSUES AND CARIES
Vitamin D
 Metabolism of Vitamin D : Vit. D along with Parathyroid hormones
and calcitonin play primary roles in regulating the concentration of calcium
and inorganic phosphate in the plasma and extra cellular fluids ,by
regulating the movement of these ions in and out of cell and in controlling
mineralization of bones and teeth .

 Enamel Hypoplasia : Enamel Hypoplasia is the most common

abnormality of development and mineralization of human teeth . Recent
evidences have suggested that the etiology of enamel hypoplasia is highly
specific and linked with disorders of calcium and phosphate hemostasis .
 Enamel hypoplasia was found in conditions characterized by hypocalcaemia
but not in those characterized by hypophosphotemia .

( Nikiforuk and Fraser , 1981 ) .

 OTHER MINERALS AND CARIES:
 Vitamins
The only member of the vitamin B complex which has been associated with
caries is pyridoxine ( Vitamin B6) .

 Lipids : Deficiency of essential fatty acids in man is rare and evaluation of

the role of these nutrients on caries rates is not available .Fat consumed
post eruptively in diets of animals , has been co-related with caries
reduction . ( Williams et al , 1982 ).
 Protein :
Shaw, 1970 and Navia, 1979 showed that protein deficiency induced in rats
caused -smaller teeth ,
-a delay in eruption ,
and a greater susceptibility to caries .

CARBOHYDRATE INTOLERANCE AND DENTALCARIES :

Persons with Hereditary fructose intolerance show a strikingly reduced dental caries
experience when compared to a controlled population of the same age.
(Marthelar,1967). 
 Properties of Foods and Cariogenicity
 The physical properties of food may have significance by affecting
food retention
food clearance
solubility and oral hygiene .
 The high fibrous , cellulose content of plant foods exert a mechanical
cleansing action on teeth.

Physical properties of food , particularly those that improve the

cleansing action and reduce the retention of food within the oral cavity
and increase saliva flow , are to be encouraged in everyday diets

 Natural foods such as lemons , apples , fruit juices and carbonated

beverages , are sufficiently acidic as to cause demineralization of enamel that is
in prolonged contact with them .
FOODS LISTED ACCORDING TO CARIES POTENTIAL INDEX
Fluids- Fruit juice 3
Tea+2sugar lumps 4
Solids –White bread 7
Biscuits 18
Milk products- cheese 0
Ice-cream 9 Cheese- Lowest index
Fruits- Apple 5
Toffee -Highest index
Pear 6
Vegetables- potato 7
Honey 18
Candy- Sweets 22
Caramel 27
Toffee 30
 HISTOPATHOLOGY OF DENTAL CARIES
SMOOTH SURFACE CARIES:
Earliest manifestation is appearance of white
chalky area
first change is loss of inter prismatic
substance with increased prominence of rods.
As process advances & involves deeper it
forms triangular shape lesion with base
towards the surface of the tooth.

PIT & FISSURE CARIES:

Here triangular shaped lesion is formed with
the base towards the DEJ.
 CARIES IN ENAMEL:
 ZONE 1: TRANSLUSCENT ZONE
 ZONE 2: DARK ZONE
 ZONE 3: BODY OF LESION
 ZONE 4 : SURFACE ZONE

CARIES IN DENTIN
ZONE 1: NORMAL DENTIN
ZONE 2: SUBTRANSPARENT DENTIN
ZONE 3: TRANSPARENT DENTIN
ZONE 4: TURBID DENTIN
ZONE 5: INFECTED DENTIN
 Zone 1: TRANSLUCENT ZONE
 The deepest zone and represents
the advancing front of the
enamel lesion.
 Has a structure less appearance
when perfused with quinoline
solution and examined with
polarized light .
 Pores or voids form along the
enamel prism (rod) boundaries,
presumably because of the ease
of hydrogen ion penetration
during the carious process.
 When these boundary area voids
are fitted with quinoline solution,
(same R.I as enamel) the features
of the area disappear.
 The pore column of translucent
enamel caries is 1%, 10 times
greater than normal enamel.
 Zone 2: Dark Zone

 The next deepest zone is dark zone

because it does not transmit polarized
light. The light blockage is caused by
the presence of many tiny pores too small
to absorb quinoline.
 These smaller air or vapor filled pores
make the region opaque.
 The total pore volume is 2% to 4% .
 There is some speculation that the dark
zone is not really a stage in the sequence
of the breakdown of enamel, rather the
may be formed by deposition of ions
into an area previously only containing
large pores.
 ZONE 3 : Body of the lesion:

 The body of the lesion is the largest

portion of the incipient lesion. It has
pore volume , varying from 5% at the
periphery to 25% at the center.
 The striae of Retzius are well marked in
the body of the lesion indicating
preferential mineral dissolution along the
areas of relatively higher porosity.
 The first penetration of caries enters the
enamel surface via the striae of Retzius.
The inter prismatic areas and these cross-
striations provide access to the rod
(prism) cores, which are then
preferentially attacked.
 Bacteria may be present in this zone if the
pore size is large enough to permit their
entry.
 Zone 4: Surface Zone :
 It has lower pore volume than the body
of the lesion (less than 5%) and a
radiopacity comparable to unaffected
adjacent enamel.

 It has been hypothesized that hyper

mineralization and increased fluoride
content of the superficial enamel are
responsible for the relative immunity of
the enamel surface. However removal of
the hyper mineralized surface by
polishing fails to prevent the reformation
of a typical well mineralized surface over
the carious lesion. Thus , the intact
surface over incipient caries is a
phenomena of the caries demineralization
process rather than any characteristics of
the superficial enamel.
 ZONE 1:Normal dentine

 Deepest area is normal dentin which has

tubules with odontoblastic process that
are smooth and no crystals in the lumens.

 The inter tubular dentin has normal cross

banded collagen and normal dense apatite
crystals.

 No bacteria in the tubules.

 Stimulation of dentin (eg :by osmotic

gradient, a bur, a dragging instrument or
air blow) produces a sharp pain. 
 ZONE 2:Subtransparent dentine

 zone of demineralization of the inter

tubular dentin and initial formation of
very fine crystals in the tubule lumen
at the advancing front.

 Odonto blastic process damage is

evident.

 No bacteria are found in this zone.

 Stimulation of dentin produces pain.

 Dentin is capable of remineralization

 ZONE 3:Translucent dentine
 This dentin is softer than normal
dentin and shows further loss of
mineral from the inter tubular dentin
and many large crystals in the lumen
of the tubules.

 Stimulation produces pain.

 Intact collagen can serve as a

template for the remineralization of
the inter tubular dentin and thus this
region is capable of self repair ,
provided the pulp remains vital.
 ZONE 4:Turbid dentine

 Zone of bacterial invasion and is

marked by widening and distortion
of the dentinal tubules which are
filled with bacteria.

 There is very little mineral present

and the collagen is irreversibly
denatured.

 Dentin in this zone will not self

repair .This zone cannot be
remineralized and must be
removed before restoration.
 ZONE 5:Infected dentine

 Outer most decomposed dentin that is

teeming with bacteria.

 No recognizable structure to the dentin

and collagen ,and minerals are absent.

 Removal of infected dentin is essential

to sound, successful restorative
procedure as well as prevention of
spreading of infections.
 INFECTED DENTIN AFFECTED DENTIN

 Softened demineralised  Soft demineralised dentin

teeming with bacteria not invaded by bacteria.

 Collagen irreversibly  Collagen cross linking

damaged. remains.

 Cannot be demineralised  Acts as template for

remineralization.
 Soft necrotic tissue, dry
leathery dentin, flakes  Soft than normal dentin
easily discolored but does not
flake.
 Stains with 1% acid red in
propylene glycol  Does not stain
 DIAGNOSIS
 1.visual tactile method:

Combination of light mirror and probe.

In 1924 G.V.Black proposed the use of sharp explorer
This was challenged latter and the use of blunt probe was
suggested.

Visual examination – European method

Visual tactile system- American system
 2.Radiographic method:
Non –invasive method.

Possible to study parts

inaccesible to other methods.

Depth of the lesion can be

evaluated.

Bite wings used for proximal

caries.
Net mineral loss 20%-50% in
order to radiographically visible.
 3. TOOTH SEPARATION:

Visualizing posterior approximal surfaces

Uses orthodontic bands - Slow separation.

ADVANTAGES
Permits differentiation of
contaminated / non contaminated
lesion
Buccolingual extension of caries
Non invasive ,reversible.
Effective inexpensive.
DISADVANTAGES
Requires additional visit
Occasional discomfort
Occasional failure of separation
Potential danger of ingestion
Potential exacerbation of gingival
infection
 4. Fiber optic
transillumination
(FOTI)
 Used since many years in diagnosis
of a proximal lesion in anterior
teeth.
Caries lesion has lower index of
light transmission hence appears as
dark shadow.
In posterior teeth,fibre optic lights
with beam reduced to .5mm in
diameter has been used.
Advantages in posterior crowding,
pregnant women.
 5. Dyes : Makes the lesion easier to visualise by
enhancing contrast.

 EG: silver nitrate, methyl red, alizarin stain –difficulty in

removing dye from altered enamel areas as calcium
reacts with carboxilic and sulphuric acid groups of the
dyes.
 DYES FOR CARIOUS DENTIN DETECTION
 Stain only infected dentin
 .5% basic fuschin in propyline glycol but due to carcinogenic suspicion it
was replaced by acid red. Staining is suggested due to denaturation of
collagen fibers.
 Methylene blue and acid reacting dyes were used but it was found slightly
toxic and non specific respectively.

Dyes for carious enamel detection:

Procion which are used in neurology as vital stains have been used to stain
enamel lesions but staining is irreversible because the dye reacts with hydroxyl
and ammonia groups and acts as fixative.

Calcein is also used to measure infiltration into carious enamel.It binds to

calcium and remains bound.

Zyglo ZL-22 penetrates into micrpores and can be made visible by UV

illumination.
 6. Digital
radiographic
methods :
Digital image is formed
by spatially distributed
set of discrete sensors
and pixel.
Two types of non film
receptors for indirect
imaging.
Digital image receptor
(DIR).
Video camera
 7. Electrical resistance
measurements (ERM):

First proposed by Magitot in

1878.
Difference in electrical
conductance of caries and
sound enamel.
Two instruments were
developed and tested in 1980.
Vanguard electronic caries
detector, caries meter – L.
 Lasers in caries detection
 Recent research by Hibst and Gall (1998) showed that red light (638 nm, 655
nm) induced fluorescence could differentiate between sound and carious tooth
tissue. KaVo DIAGNOdent (KaVo, Germany), based on the above research by
Hibst and Gall, is a recently introduced laser-based instrument, developed for
detection and quantification of dental caries on smooth and occlusal surfaces.

 Carbonate content is lost with specific laser irradiation. Laser irradiation

interacts with the phosphate groups in the dental mineral which absorbs heat
to raise temperature decomposes carbonate and leaving behind a hydorxy
apatite like mineral that is much less soluble than original mineral.
 Ultrasonography:

Utilizes a sonar device in

which a beam of
ultrasound waves is
directed against the tooth
surface and if reflected is
picked by an appropriate
receive.
Zero radiography:

Uses modified zero

graphic copying
techniques to images
produced by
diagnostic x-rays .

It is twice as
sensitive as
conventional D- speed
films.
Reduction of
radiation dose.
 OTHER METHODS:

Endoscopic filtered fluorescence method

Magnetic resonance microimaging (MRM)

 CARIES PREVENTION:
 Practitioners must identify those patients who have active carious lesions and
those at high risks for caries and institute appropriate preventive and treatment
measures.
 I. General health.
 II Fluoride exposure: increases the resistance of tooth structure to
demineralization .
 ROUTE OF ADMINISTRATION:
Systemic and Topical .
METHOD OF DELIVERY:
1. Public water supply.
2. Self application: Low dose high frequency rinses-0.05%
High frequency low dose rinses-0.2%

3. Professional Application:
APFGel (1.23%)
Sodium Fluoride (2%)
Stannous Fluoride (8%)

Mechanism of action: Forms insoluble fluorapetite crystals replacing soluble crystals of

the tooth structure.
Incipient carious lesions are remineralized.
Antibacterial activity.
 IV Salivary functioning: Salivary stimulants
Gums , paraffin waxes ,Saliva substitutes.

V Antimicrobial agents :
Used in high risk patients
Systemic side effects must be considered.
ANTIBIOTICS:
Vancomycin, Kanamycin, Actinobolin.
BISGUANIDES:
Alexidine , Chlorhexidine.
HALOGENS:
Iodine and fluoride

VI Diet:
The quality and frequency has a very detrimental effect on plaque.
Sucrose containing products provides stronger potential for colonization of

SM.
Increase in frequency of ingestion results in prolonged PH drop.
VII ORAL HYGEINE MEASURES:
“Plaque free tooth surfaces do not decay”
Flossing , Tooth brushing , and Rinsing.
 VIII Xylitol gums: is a natural 5-c sugar obtained from birch trees.It
keeps sucrose molecule from binding with MS.
Also, chewing stimulates salivary flow which improves the buffering of
the PH drop that occurs after eating.

IX Pit and fissure sealants:

The junction of enamel surfaces during tooth development forms pits and
fissures. If these surfaces do not coalesce, they may leave small channels of
varying depth ranging from shallow pits to deep fissures extending upto the
DEJ.
 MANAGEMENT:
 Early lesions:
 No restorative material can adequately replace natural tooth structure for a
long term therefore preservation of this is essential.
 The surgical approach proposed by black is modified .

 Firstly patients education is a must.

 Diagnosis and control of active lesions.
 Identification of bacteria.
 Test for salivary flow.
 Dietary control.
 Perform a thorough prophylaxis.

 Prescribe a chlorhexidine mouthwash.

 The development of restorative material that are both
esthetic and adhesive has opened new possibilities in cavity
design .

First eliminate the disease first and eliminate the existing

lesion through remineralization .

When all else fails, surgical intervention is carried out with

minimal intervention procedures.

Main aim is to eliminate cavitation on the tooth surface to

reduce plaque accumulation.
 TREATMENT OF OCCLUSAL CARIES:
 SITE1 Sizes 1 and 2
(Pit and fissures minimal and moderate involment)

Fissures and grooves should be protected by GI or Resin

sealant.

If dentine is involved then surgical intervention with rotating

instrument or air abrasion is done

GI has the advantage of being bioactive thus having an ability

in remineralization. Lamination with a resin composite is
indicated in cases of heavy occlusal load.
 Treatment of Site 2 sizes 1 and2:
(Proximal caries minimal and moderate involment)
 Progress is usually slow.
 In absence of cavitation

– Surface can be treated with Flouride over a reasonable time

thus promoting remineralization.
_ Etch the proximal surface ,following the prescribed fluoride
treatment and seal it with a light curing low-viscosity unfilled
resin.

In the presence of cavitation,

Surgical intervention is essential……
Three possible approaches in minimal intervention
MOUNT AND HUME.
 If the lesion is located more than 2.5mm below the crest of
the proximal marginal ridge the recommended tech s the
“occlusal fossa” or “ Tunnel” approach .

 If the lesion is closer to the marginal ridge then the lesion

should be entered throughthe occlusal aspect forming a box
like or a small “Slot” preparation.

 The third version is possible only when a larger lesion on the

adjacent tooth is restored, a very conservative cavity is
possible.
SLOT TYPE PREPARATION
 Restoration of site1 sizes 3 and 4:
(Pit and fissure extensive involment)

 The previous surgical approach to cavity design required the

removal of the entire softened infected and affected dentine in
the floor of the cavity.
 But now such preparations are undesirable.

 (Massler) indirect pulp capping indicated in which the affected

dentine is left to remineralize sealed with a provisional
restoration.
 A caries detector dye can be used to differentiate between the
infected and affected dentine.
 Restoration of SITE 2 sizes 3 and 4:
(Proximal lesion extensive involment )

 Demineralized dentine can remain in the axial and the

pulpal wall on the assumption that it will remineralize in the
influence of GI.

 In a very extensive cavity , amalgam may be a better choice

if a large part of the occlusal surface is involved :
 The walls are made to diverge rather than converge , cusp
height is reduced to a limited degree .
The buccolingual widthis extended no more than essential.
Non –working cusps requires 0.5mm and working cusps
require 1.5 mm reduction.
Ditches and grooves are preferred over pins.
 NON ROTARY METHODS OF CAVITY
PREPARATION
 Microdentistry versus macrodentistry:
In the past few years the emwerging techniques of operative
dentistry dedicated to minimal invasion and sacrifice have
been explored.
COMPARISION:
Extension for prevention Microdentistry
Rotary drill Air abrasion
Deep angular cavity prep Remove only affected tooth
material
Amalgam filings Adhesive bonded restorations
New recognition of key
anatomic features
Rudimentary understanding of
tooth structure
 AIR ABRASION:
 IN the late 1940 and early 1950 Dr.Robert B .black developed air abrasion
instruments and techniques applicable to the dental philosophy.

The principle of air abrasion is the importing of kinetic energy to



tiny aluminium oxide particles that are projected by a stream of

compressed air or gas and expelled from a small nozzle.

 A setting of 80 psi or less with 27um particle size and a 0.014 inch tip is
comfortable and adequate for starting most procedures.

Air abrasion may be used for small initial carious lesions in Class I, III, IV,
V, VI and some Class II. Also well suited for debridement of occlusal
fissure before sealant placement.

Air abrasion is not suited for extensive caries removal because the soft
surface of caries absorbs the kinetic energy of the abrasive particles.
 OZONE:
 1. Helps in the treatment and prevention of caries

 2. Root canal treatment

 3. Tooth whitening

 4. Elimination of sensitivity of exposed tooth surface

 5. Gum disease

 6. Dental implant treatment

 7. Control of contamination in dental unit water mouth and face

tissue conditioning.
 Ozone on decayed tissue Kills 99% of microflora by
denaturing the acid metabolites of the bacteria.
 Delivering of ozone gas through hand piece into a polymer
cup that is placed around the tooth surface to be treated for
10-40 seconds at a concentration of 2200ppm cleaned lesion
is able to remineralise with more resistance to decay.

 There are four phases to the treatment

 1 Diagnosis
 2. The “Treatment” phase-Application of Ozone
 3. The “Healing” phase- Re-mineralisation
 4. The “Repair” phase-Permanent restoration
 Chemomechanical caries removal
CARISOLV
 Goldman and Kronman 1997
 Consists of a special gel and special designed hand instrument
 gel - sodium hypo chloride, sodium chloride, sodium
hydroxide, 3 amino acids, glutamic, leucine, lysine
 Colouring agent - Erythrocin,
 thickners -methylcellulose.

 Solution buffered to a PH of 11.4

 It has proteolytic effect

 Sodium hypo chlorite acts on the carious infected dentin and

softens it, amino acid intensify the effect of sodium hypo
chloride. It affects only the Denatured collagen and decreases
healthy hard tissue involvement .
 ART or Atraumatic Restorative Treatment
 This approach was developed in
Tanzania in the mid-1980s. ART
received full endorsement by the
World Health Organisation (WHO)
and was included as an essential
component of its Integrated
Package of Basic Oral Care.

 Rural pateints, Nervous patients,

patients with medical or physical
contraindications and unco-
operative children are ideal
candidates for ART.
  The ART approach works on a minimally invasive, maximally
preventive concept. In ART only the soft decayed material is
removed by excavation, the partially demineralised dentine is
left as this has the potential to remineralise.
 The soft decayed material is easily removed by hand. The soft
area, which is excavated, is dead, non-remineralisable,
invaded with bacteria and insensitive.

Hand removal of the decayed tooth material using an excavator

Glass ionomer cement restorative material is packed into the
excavated cavity.
· The gloved finger is used to smear excess filling material over the tooth
surface to seal the tooth surface and other vulnerable pits and fissures
the 'press finger' technique.
· The complete restoration after excess glass ionomer cement has been
carved away.
Hand removal of the decayed tooth material using an
excavator
Glass ionomer cement restorative material is packed into the
excavated cavity.

· The gloved finger is used to smear excess filling material over

the tooth surface to seal the tooth surface and other vulnerable
pits and fissuresthe 'press finger' technique.

· The complete restoration after excess glass ionomer cement

has been carved away.
 Deep carious tooth management:
Tooth with deep lesion

Removal of peripheral carious dentine

Decision to remove internal caries dentine

Pulp exposed Pulp not exposed

Direct pulp capping Indirect pulp capping

Capping is followed by restoration Remineralization is allowed for 3wks

Successful Unsuccessful
No additional treatment required Reentry done through restoration to
Temporary replaced by permanent perform endodontic treatment.
INTRODUCTION- Vital pulp therapy
 PRIMARY OBJECTIVE IN RESTORATION OF VITAL
TOOTH-PREVENTION OF PULPAL INJURY.
 BASIC STEPS IN RESTORATIVE OPERATIVE
PROCEDURE-REMOVAL OF CARIOUS
DENTIN
 USE OF BASES AND LINERS IN DEEP CAVITIES-TO
PROTECT AND PRESERVE THE VITALITY OF
DENTAL PULP AND TO AID IN REPARATIVE
FUNCTION.
 HISTORY
 1756-PHILLIIP PFAFF, GERMAN DENTIST PACKED SMALL PIECE OF GOLD
LEAF OVER EXPOSED VITAL PULP TO PROMOTE HEATING.

 1826-LEONARD KOCHER, PUBLISHED PRINCIPLES OF DENTAL SURGERY

AND DESCRIBED PULP CAPPING PROCEDURES.

 1920-HERMAN,INTRODUCED CALCIUM HYDROXIDE IN ENDODONTIC
TREATMENT.

 1938-TEUSCHER & ZANDER, INTRODUCED Ca(OH)2 AS A PULPOTOMY

AGENT.

 1964-KAISER & FRANK, PRESENTED INDUCTION TECHNIQUE.

 1990-USE OF RESIN BONDING AGENTS ON EXPOSED PULP.

 TRADITIONAL PULP CAPPING AGENTS
 Many have been used as –materials ,medicaments, antiseptics , anti-
inflammatory agents, antibiotics and enzymes.
 Calcium hydroxide has been the standard of all.
 In 1938, Teuscher and Zander complete dentinal bridging with healthy
radicular pulp under calcium hydroxide dressing.
 Calcium from the blood stream comes from the blood stream.

Cox et al demonstrated that healing is not dependent on the stimulatory effect

of the agent but by providing the biological seal from micro-leakage.
Composite, silicate cement, zinc phosphate cement, amalgam were used as
direct pulp capping agents.
Numerous bonding agents and composite have been tested and healing ,
deposition of hard tissue at the exposure site is demonstated.
Mineral tri-oxide aggregate _ is a new biocompatible agent.
-more dentinal bridging.
-shorter period of time.
-less inflammation.
Disadvantage is that it requires 3-4 hrs for setting.
 INDICATIONS
 DIRECT PULP CAPPING  INDIRECT PULP CAPPING
 Small mechanical exposure less  Ideally when pulpal inflammation
than 1mm. has been judged to be minimal
 Traumatic exposure in a dry clean and complete removal of caries
field reported in 24hrs. would cause pulpal exposure.
 Light red bleeding from exposure
site that can be controlled by
cotton pellet.

CONTRA-INDICATIONS
 Spontaneous pain.  Any signs of pulpal or periapical
 Toothmobility. pathology.
 Thickening of periodontal ligament.  Soft leathery dentine covering a
 Intraradicular radiolucency. very large area of cavity in a non-
restorable tooth.
 Excess bleeding and purulent
discharge at exposure site.
 INDIRECT PULP CAPPING

Definition
“A procedure where in a small amount of carious
dentin is retained in deep areas of cavity preparation to
avoid exposure of the pulp and placement of a
medicament to seal the dentin, and encourage pulp
recovery.”

“The application of a suspension of calcium hydroxide

to a thin layer of dentin overlying the pulp, in order to
stimulate secondary dentin formation and protect the
pulp.”
Medical Dictionary Search
Case selection : Reversible pulpitis

Symptoms : Thermal stimulus –

momentary pain

Percussion : Non tender

Vitality : Normal or slightly

exaggerated

Radiography : Absence of –
Periodontal ligament
thickening
Periapical rarefaction
 DEEP CARIOUS LESION

AFTER GROSS EXCAVATION

 CARIOUS DENTINE COVERED
WITH CALCIUM HYDROXIDE

CAVITY FILLED WITH ZINC OXIDE

-EUGENOL
 Traubman studies indicated that the
After six weeks cement was removed rate of regular dentine formation
,calcium hydroxide washed away and was highest during first month and
excavation of carious dentine completed. continued the observation for 1
year.
At the end of 1st year teeth had
390um of new dentine on floor.

Cavity was restored with silver

amalgam
 DIRECT PULP CAPPING
A procedure for covering and protecting an exposed vital
pulp.”
Medical Dictionary Search

Factors determining success of direct pulp capping

Size of exposure : Large exposure – poor prognosis

Traumatic exposure – size does not interfere as long as pulp is healthy.

Hemorrhage : Necessary to arrest bleeding

Continued bleeding indicates irreversible inflammation

Location of exposure : Compared to occlusal or incisal, exposure on the axial wall

had poor prognosis.

Isolation from saliva : Rubber dam isolation is a must to prevent the exposure siye
from salivary contamination.
Dentin chips intrusion: Severe foreign body reaction
worsens inflammation –
“Chipitis”
Marginal seal: coronal seal crucial to prevent microbial leakage
irrespective of pulp capping material. Improper seal worsens
pulpal inflammation.

Age of Tooth: Younger tooth responds better than older

ones- capacity to heal better.

Extrapulpal clot: Presence of extrapulpal clot impairs healing

- Acts as bacterial substrate
- Barrier between capping material and the pulp
Direct pulp capping- Procedure

a. Control of hemorrhage and pre-treatment

b. Pressure application
c. Haemostatic agents
d. Sodium hypochlorite pre-treatment : 2.5%
i. Controls hemorrhage
ii. Provides disinfection
iii. Removes dentin chips from subjacent pulp tissue
iv. Removes fibrin and clot (chemical amputation)
e. Pretreatment with chlorhexidine to disinfect prior to capping
f. Steroid antibiotic paste – Symptomatic tooth for 3-4 days
prior to capping (Stanley)
 PULPOTOMY

Definition: “Surgical removal of inflamed or infected

coronal pulp leaving intact vital tissue in the canals. A
suitable medicament is placed over remaining tissue
attempt to promote healing and retention of vital
tisuues.”

Partial pulpotomy
Introduced by Cvek, differs from Sweet’s pulpotomy in
that, only a portion of the coronal pulp, (Superficial
layers – just sufficient depth to reach the tissue that is
free of inflammation) is removed before placing a
medicament.
Indications:

1. Traumatic exposures where coronal pulp is likely to be inflamed in

young healthy teeth.

2.Mechanical or carious exposure in teeth with incomplete root formation

Procedure:

Pulp amputation

Hemorrhage control

Placement of medicament

Final restoration
PARTIAL
PULPOTOMY
COMPLETE
PULPOTOMY
 Completely remove caries.

Open pulp chamber by completely

removing the roof with 330 high speed
bur.
 Remove pulp from pulp
chamber with a sharp
curette ,discoid spoon
excavator or a large round
low-speed bur or a 330 high
speed bur.

Stop bleeding by
applying a moist cotton pellet
in the pulp chamber for 3
minutes
5- Place a cotton pellet with
formocresol for 5 minutes
in the pulp chamber.

Remove cotton pellet and confirm

pulp fixation, by the “black eye”
appearance of the pulp stumps .

“Black eye”
 Fill the pulp chamber
with ZOE-eugenol

Calcium hydroxide pulpotomy technique recommended for permanent teeth

with immature root development but with healthy pulp tissue in the root canal.
Also indicated with pulp exposure resulting from crown fracture (including root
fracture).
After placement of calcium hydroxide an hard setting cement is used to cover
the cavity for an adequate seal.
If tissue in the pulp canal appear hyperemic after the amputation of the
coronal tissue ENDODONTIC Treatment is the choice.
After a year a successful treatment should have a normal periodontal ligament,
and lamina dura ,and radiographic evidence of calcific bridge.
Conclusion
Ultimate goal of Vital Pulp Therapy is to maintain the vitality and function of
pulp dentin complex.

 Natural defense mechanism of pulp have been fully recognized.

 Healing and recuperation of pulp largely depends on providing an

irritation free environment.

 Varieties of materials are tested for V.P.T. with variable degree of

success – therefore dentin bridge formation does not seem to be
material specific.

 Do not employ procedures and materials, which will over power

pulpal defenses and push the pulp beyond a point of no return.
“Do the right thing at the right time –the right
way for the right patient – to get the best
possible results”
 REFERENCES:
 Understanding dental caries.
Etiology, mechanism and clinical aspect-
Gordon nikiforuk(1985)
 A text book of oral pathology.
4th edition William G shafer.
 The Art and science of operative dentistry.
Strudevant 4th edition.
 Dental caries , disease and management.
oleFejereskov, Edwina kidd.
 Text book of pediatric dentistry- Mc donalds.

 Minimal intervention: Early lesions.

Quintessence Int 2000:31;535-546)
 Minimal intervention:advanced lesions
Quintessence Int 2000;31:621-629)

 Indian dentist research and review.

Vol 4 Issue6 June2005.