GOOD

MORNING
DENTAL CARIES
PART-1
CONTENTS
• Part-1
• Definitions
• History
• Epidemiology
• Theories of etiology
• Part-2
• Classification
• Clinical aspects
• Radiological aspects
• Histopatholgy
• References
DENTAL CARIES
The word “caries” is derived from the
Latin word meaning “ROT” or
DECAY”
DENTAL CARIES
“ Progressive, irreversible disease of microbial
origin occurring in the dental hard tissues which
are exposed to the oral environment leading to
demineralization of inorganic substances and
dissolution of organic substances of the tooth, all
of which lead to cavity formation.”
Acc to Shafer’s
 Acc to Studervent :

 Dental caries is a infectious microbiological disease

of the teeth that results in localized dissolution &
destruction of the calcified tissue.
FACTORS AFFECTING CARIES
PREVALENCE

Race :

Black, Chinese, East Indians <

American Whites

English have poor teeth than

Russians, Chinese.
 Age :

Age differences:

Children > Adults

 Gender :

Permanent teeth of Girls > Boys

 Familial :

More caries –

Siblings of caries active

individuals.

Parents with increased caries.

Monozygotic twins.
 Socio – Economic Status :

High caries incidence in middle & lower socio -

ecenomic status.
 THE EARLY THEORIES

 THE LEGEND OF WORMS:

In earliest reference Homer in 5000 B.C., proposed
that tooth caries is caused by worms.

 ENDOGENOUS THEORIES:

The Humoral theory was advocated by Greek

physicians in that they thought dental caries is
produced by internal action of acids and corroding
humors.
 Vital Theory :

 Hippocrates, Celsus, Galen, and Avicenna

proposed the vital theory

 Tooth decay originated as bone gangrene from

within the tooth itself.
 CHEMICAL THEORY:

 Parmly in 1820 he observed that dental decay

affected externally and not internally.

 It was proposed that an unidentified “Chymal

agent” was responsible for tooth decay.
 Support for chemical theory came in 1835 when
Robertson proposed
 Dental decay was caused by acid formed by
fermentation of food particles around the teeth.
 PARASITIC THEORY:

 This is the first theory for caries related with

microorganisms was proposed by Erdl in 1843.

 He observed the filamentous organism in the

membrane removed from tooth .
After that 1847 FICNUS from DRESDEN proposed
dental caries attributed to denticolae .

Denticolae-
The generic term he proposed for decay related to
microorganisms.
 In addition CLARK 1871&1879, TOMES 1873,
MAGITOT 1878 concluded that bacteria were
essential to caries, for an exogenous source of the acid
 Then in 1880, UNDERWOOD & MILLES proposed
septic theory that acid capable of causing
decalcification was actually produced by bacteria
feeding on the organic fibrils of dentin.

 He also reported sections of decay dentin having

micrococci are oval and rod shaped forms.
Chief theories
Acidogenic theory Miller & Underwood in
1881.
Proteolysis theory
Proteolysis chelation theory
Sucrose chelation theory
 ACIDOGENIC THEORY, HYPOTHESIS

 Dental decay is a chemico parasitic process consisting

of 2 stages
 the decalcification of enamel which results in total
destruction
 the decalcification of dentin, as a preliminary stage
followed by dissolution of the softened residue
 The acid which affects this decalcification is
derived from the fermentation of starches and
sugar lodged in the retaining centers of the teeth.
 This is the accepted theory
ACIDOGENIC THEORY

 Role of carbohydrates

 Role of microorganisms

 Role of acids

 Role of dental plaque

ROLE OF CARBOHYDRATES (CHO)

 Presence of readily fermentable carbohydrates

(CHO) causes loss of caries resistance of the
tooth

 Cariogenic CHO

are dietary in origin

Cariogenicity of a dietary CHO varies with following
factors
 Frequency of ingestion
 Physical form (detergent foods, liquids, sticky food)
 Chemical composition (Polymers/ Monomers)

 Sticky, solid CHO which are more caries producing

than liquid CHO
 Detergent CHO food are less damaging than those of
soft retentive foods

 Easily cleared CHO from saliva is less conductive of

caries than those slowly cleared or sticky food
 Polysaccharides are less easily fermented by
plaque bacteria than mono & disaccharides
ROLE OF MICROORGANISMS

 Gies & Kligler(1915) high numbers of oral

microorganisms in persons with caries
 Clarke(1924) Streptococcus mutans invariably
isolated from carious lesions
 Bunting, Nickerson & Hard Lactobacillus
acidophilus is almost universally absent in the mouth
of caries immune persons
 Cariogenic species
S mutans
L acidophilus

Actinomyces
 Oral streptococci, Most common species are in
oralcavity include S.mutans, S. sanguis, S. mitior, S.
salivarius and S. miller

Most commonly associated with caries is S. mutans

 Keys(1960) Dental caries infectious process

 Keys and Fitzgerald: caries free hamsters inoculated

with caries active streptococci developed

DentalCaries
 Caries free species: non cariogenic microflora

 Fitzgerald : Gnotobiotic rats fed on cariogenic diet did

not develop caries till inoculated with oral

streptococci  S mutans
S mutans

 Pandemic in geographical distribution

 Prevalent in societies with high sucrose consumption
 England, US, Scandinavian countries
 S. mutans is gram positive cocci forming short to
medium chains
 S. mutans having characteristically synthetisize
insoluble polysaccharides from sucrose

 Itis homo fermentative and is more aciduric than

other oral steptococci cariogenic strains.

 S. mutans does not colonize in the infants mouth

prior to the tooth eruption.

 Likewise, it disappears from the mouth after

extraction of all teeth.
 S. mutans divided in five groups based on nucleic
acid and hybridization – In that most commonly
associated with plaque i.e. S. mutans and S.
sobrinus.
 LACTOBACILLI

 Lactobacilli are gram positive, non spore forming

rods that grow best under micro aerophilic
conditions

 In lactobacilli many species exist, oral cavity these

contribute to 1% oral flora
 L. acidophilus are most common
 Most important is the fact that they are both
acidogenic & aciduric and multiply itself in low
pH of plaque & carious lesion
ORAL ACTINOMYCES

 Gram positive, filamentous organisms

 Species- A. naeslundii, A. viscosus
 Associated with dental plaque.
 Prominent- root surface caries.
ROLE OF ACIDS
 The exact mechanism of carbohydrate degradation
to form acids in the oral cavity by bacterial action
is not known.

 Probably by enzymatic breakdown of sugar

 Acids formed - chiefly lactic and butyric acids
 Acid has to be localized upon the tooth surface
for a length of time
 Holding agent: dental plaque
 ROLE OF DENTAL PLAQUE
 Williams(1879)

 Structure of vital significance in contributing to initiation of

carious lesion

 G V Black(1899): very important in the caries process

 Plaque consists of salivary component as mucin &

desquamated epithelial cells & micro organisms in tooth
surface & these are not easily cleaned, appearing as thin
film.
 Acquired pellicle- component of plaque

 Forms prior/ along with bacterial colonization &

facilitate the formation of plaque
 Pellicle is a Glycoprotein, derived from saliva,
adsorbed on tooth surface
 It is not dependent on bacteria but may serve as a
nutrient for plaque microorganisms
 filamentous microorganisms, which grow in long
interlacing threads and have the property of adhering to
smooth enamel surfaces.
 Smaller bacilli & cocci: entrapped in reticular
meshwork
 Aciduric and Acidogenic streptococci, Lactobacilli are
numerous in this area
 Plaque classification-
 depends on anatomical areas

 Supra & Sub gingival

 Supra- responsible for caries
 marginal& Sub plaque- responsible for initiation of
periodontal disease.
 pH of plaque
7.1 caries free individuals
5.5 individuals with extreme caries activity
 PLAQUE HAS 3 BASIC STRAINS

 Streptococci

mutans, sanguis, mitior, millieri and salivarius

 Actinomyces

viscosus, naeslundi, israelii

 Veilonella

parvula, alcalescens

S mutans chief etiologic agent in human dental

caries
 LIMITATIONS OF MILLER CHEMICO PARASITIC
THEORY

 Did not explain specific site on tooth predilection of

dental caries.

 Did not explain why certain population are caries free.

 The phenomenon of arrested & rampant caries is not

explained.
 The correlation of systemic diseases & dental caries
was not proved.

 Cannot explain caries of impacted tooth.

 Cannot explain subsurface demineralization.

PROTEOLYTIC THEORY, GOTTLEIB (1944)

 Organic portion of tooth plays important role in

carious process
 Caries -proteolytic process
 Enamel

Initial attack on organic portion

Destruction of inorganic portion
Liberation of proteolytic enzymes by oral bacteria
Drawbacks

Hypomineralised areas not more susceptible to

caries
In fact, some studies show that caries can occur
in the absence of proteolytic organisms.
 PROTEOLYTIC – CHELATION THEORY

 Proposed by Schatz et al in 1955

 Microbial degradation of the organic components (hence,

proteolysis) & the dissolution of the minerals of the tooth
by the process of chelation
 Chelate = Chele = claw & refers to compounds
capable of binding to metallic ions as Ca, Fe, Cu, Zn by
20 valence bond which results in highly stable, poorly
dissociated or weakly ionized compounds.
 Chelation is independent of pH

 Common chelators are citrates.

 Others are amino acids, hydroxy & ketoesterase,

polyphosphates, carboxylates, proteins,lipids,
nucleic acids & certain enzymes & vitamins.
 This theory considers Dental caries to be due to
bacterial destruction of teeth, initial attack is on
organic component of enamel

 Enamel contains mucopolysaccharides, lipids &

citrates which are susceptible to bacterial attack & act
as chelator
 The breakdown products have chelating properties &
helps in dissolving minerals of enamel.

 Soluble chelates with mineralized components are

formed & they decalcify the enamel at neutral or
alkaline pH.
 This theory proposes that both organic as well as
inorganic components of tooth are attacked
simultaneously.
 Bacterial attack

Organic portion of enamel

Proteolysis

Substances with chelating properties

Chelates
Combines with Ca & P of enamel

Decalcification of enamel
 Topical application of flouride leads to formation
fluoroapatite which provides strong linkage beetween organic
& inorganic phases of enamel, preventing & reducing their
complexing.

 Not a very well supported theory though it has explained lot

of unexplained processes in Dental caries.
 SUCROSE CHELATION THEORY

• Proposed by Egglers – Lura (1967)

• High conc. Of sucrose in oral cavity

• Formation of Ca saccharides & Ca complexing

can cause dissolution of enamel.

•Removal of Ca & P ions from enamel leading to

Dental caries.
LIMITATIONS OF SUCROSE CHELATION THEORY

• Once sucrose readily gets metabolized to form

acids , there is hardly any scope for formation of
Ca saccharides

• High level of pH is reqd. which is never

achieved in oral cavity
DENTAL CARIES
PART-2
CONTENTS
• Etiology
• Classification
• Clinical aspects
• Histo patholgy
• Immunology of dental caries
• Caries activity test
• Prevention of dental caries
• References
 CURRENT CONCEPTS OF ETIOLOGY

 Dental Caries is a word derived

from Latin word meaning rot or
decay

 Multifactorial

 It is due to interplay of 3 primary

factors
 Keyes suggested that micro-
organisms (plaque), a
substrate (sugar), and a
susceptible tooth surface
were required for caries to
initiate. This is the "Keyes
Triad".

 It has since been realized that

“time” is also needed.
 CONTRIBUTING FACTORS

 Tooth :
- Composition
 Morphology
 Tooth position

 Oral Bacteria (Flora)

Diet factor  Saliva
(Substrate)
- Physical nature  Composition
 Quantity
 Carbo. content
 Viscosity
Vitamin
 Antibacterial
content
properties
 Fluoride  Buffering

capacity
 TOOTH
1. Composition

 Chemical composition

 Surface enamel is more

resistant than underlying
enamel
Causes :
1. More of Fl, Zn Pb & Fe
2. Lower Carbon dioxide (solubility
in acids decreases)
Caries susceptibilty of teeth :

1. Max. & mand. 1st molars = 95 %

2. Max. 2nd premolars = 45 %

3. Max. canine & mand. 1st premolars = 10 %

4. Mand. Central & lateral incisors & mand. Canine = 3

%
2. Morphology
 Enamel hypoplasia
 Deep pit & fissures
MORPHOLOGIC CHARACTERISTICS OF
TOOTH
 Enamel hypoplasia predisposes to dental caries
 Deep, narrow occlusal fissures and buccal, lingual pits
 Advanced Attrition: inclined planes become flatless
caries
 TOOTH POSITION

 Malaligned, out of position, rotated teeth difficult to

clean, accumulate debris
SALIVA
 Critical in controlling caries.

 0.5-1.0 litres per day of saliva is produced by major

and minor salivary glands.

 Composition and Buffering capacity of Saliva is

affected by flow rate

 Varies between person to person

 COMPOSITION
 Depends upon whether the saliva is stimulated or resting saliva

 Resting saliva = Constantly secreted saliva

 Increasedflow = increased conc. of protein, Na+,

Ca2+ , Cl-, HCO3- but decreased Mg2+ and PO42

 Ca & P natural defense against dissolution of teeth

 pH of Saliva
 The pH at which any particular saliva ceases to be saturated
with calcium and phosphate is referred to as the ‘critical
pH’; below this value, the inorganic material of the tooth
may dissolve.
Critical pH = 5.5

 Quantity of saliva
Influence caries incidence

Xerostomia – Rampant caries

Rate of flow

 Viscosity
 Not significant
Other factors are-
Antibacterial properties of saliva

 OTHER SYSTEMIC FACTORS

o Hereditary

o Pregnancy & lactation- Neglected oral care

CLASSIFICATION

1) Based on anatomical site-

 Pit and fissure caries
 Smooth surface caries
 Root caries

2) Based on progression

Acute dental caries
Rampant dental caries
Nursing bottle caries
 Chronic dental caries
ACUTE DENTAL CARIES
 Commonly seen in children
 Fast progression of lesion
 Pulp involvement faster
 Frequent pain
 Light yellow discoloration of dentin
 Rampant caries
 Nursing bottle caries
 Rampant caries
• affects almost all teeth in dentition, even lower anteriors
Sudden onset, rapid and uncontrollable destruction of teeth
by widespread caries.
Affects the surfaces of teeth that are relatively caries free.

This includes proximal and cervical surfaces of

mandibular incisors.
Nursing bottle caries/ Nursing caries/ Baby bottle
syndrome/ bottle mouth syndrome
 Affects infants
 Attributed to prolonged use of Nursing bottle
containing milk, fruit juice, sweetened water
Breast feeding
Sugar/Honey sweetened pacifiers
• 4 max. incisors commonly affected, first molars
& cuspids
• Mandibular incisors not affected (characteristic

feature)Covered or protected by the tongue

CHRONIC DENTAL CARIES
 Affects adults
 Pain
usually absent, as pulp involvement
minimal
 Secondary mineralization seen, protection to
pulp
 Cavity is shallow, moderate lateral spread of
caries at DEJ
PIT & FISSURE CARIES
 Seenmainly on occlusal surfaces, affects even
buccal, lingual surfaces
 Brown/Black discoloration, clinically, catch is
felt with probe
 Bordering enamel is Opaque, bluish white as it is
undermined, occurs through lateral spread of
caries at DEJ
 Pit & Fissure Caries

Bluish Discoloration
SMOOTH SURFACE CARIES

 Proximal surfaces more affected, buccal, lingual

affected too, without involvement of occlusal pits

 Generally preceded by formation of microbial /

dental plaque
Proximal caries
•Begins just below
contact points
•Appears as faint opacity
of enamel
•As caries penetrates
enamel, enamel
surrounding lesion
assumes bluish white
appearance
 Cervical caries
 Occurs on buccal, lingual, labial surfaces
 Begins as a crescent shaped cavity
 Directly related to lack of oral hygiene
PRIMARY / VIRGIN CARIES

 Caries formed on an intact tooth surface

SECONDARY / RECURRENT CARIES

• Caries formed on margins of restorations

• due to

• Inadequate extension of original restoration –

favors debris retention

• Poor adaptation of filling material to cavity –

produces “leaky margin”
Secondary / Recurrent Caries
HISTOPATHOLOGY OF DENTAL CARIES

 Pit & Fissure caries

 Triangular in shape
 Apex towards outer surface of enamel, base towards
DEJ
 Greater area of cavitation
 Smooth surface caries
 Apex towards DEJ, base towards outer surface
 Less cavitation
ENAMEL CARIES

Loss of inter-rod substance, prominent enamel-rods

Appearance of transverse striations of enamel rods due to
segmental demineralization
Dark lines appearing at right angles to enamel rods,
suggestive of segments
Accentuation of incremental striae of Retzius
 H/F of enamel caries
Zone 1 – Translucent zone
Zone 2 – Dark zone
Zone 3 – Body of lesion
Zone 4 – Surface zone
 These zones are from the dentin towards the outer
enamel surface
Schematic presentation of Microscopic Zones of
Enamel caries
 TRANSLUCENT ZONE

 Is deepest & forms advancing front of lesion

 Not seen always, seen in 50% of cases.
 When seen, appear clear due to mounting media
which enters these big pores making them look
clear/bright.
 It is more porous than sound enamel.

 Porevolume is 1%, which is more than normal

enamel (0.1%)

 Zone cant be easily identified clinically / radio

graphically
DARK ZONE / POSITIVE ZONE

 Positive zone as it is always present

 Pore volume – 2-4%. 2 types of pores seen here 
large & small
 Initially only large pores, later change to micro-
pores.
 This change mainly due to demineralization
occurring in deeper areas which release ions &
there is remineralization of superficial areas

 This zone is narrower in rapidly advancing

caries & wider in slowly advancing caries.
BODY OF THE LESION

 Largest zone, between dark & surface zone

 Greater amount of demineralization taking place.
 Pore size – 5-25%
 5% variation is near periphery, 25% at center
 Prominent striae of Retzius due to
demineralization of inorganic minerals
 Contains apatite crystals larger than that found in
normal enamel
 SURFACE ZONE

 Quite intact, appears radio-opaque

 Unaffected despite subsurface de mineralization; may be

due to:

surface remineralization by salivary ions

More amount of fluoride

DENTINAL CARIES

 Once lesion spreads to DEJ, there is lateral spread

of caries

 Surface enamel gets unsupported enamel rods 

enamel #  greater cavitation

 Zones of dentinal caries
Zones start from pulpal side towards dentinal side

1. Zone of Fatty Degeneration of Tomes’ process

2. Zone of Sclerosis

3. Zone of Decalcification without Bacterial Invasion

4. Zone of Decalcification with Bacterial Invasion

5. Zone of Decomposed Dentin / Infected dentin

FATTY DEGENERATION OF TOMES’ PROCESS

 Innermost layer of dentinal caries towards pulp

 Due to deposition of fatty tissue in odontoblastic
processes
 Seen usually in rapidly progressing caries
 No crystals or bacteria in lumen of tubules
 Intertubular dentin  normal
ZONE OF SCLEROSIS/SUB-TRANSPARENT
DENTIN
 Deposition of CaPO4 ions in dentin causing
Sclerosis
 This is an adv. prevents further spread of lesion
 Done by odontoblasts which produce more Ca, P
ions which are deposited in tubules
 2 methods
 Natural/Physiological – peritubular dentin deposition
leading to sclerosis
 Calcification of odontoblastic process
ZONE OF DECALCIFICATION WITHOUT
BACTERIAL INVASION / TRANSPARENT
DENTIN
 Decalcification is by bacterial acid diffusion
 Very narrow zone, softer than normal dentin
 Further loss of minerals from inter tubular dentin
ZONE OF DECALCIFICATION WITH
BACTERIAL INVASION / TURBID
DENTIN
 Initially only few tubules are involved & micro-orgs also
less
 These are acidogenic, pioneer bacteria (initiators), present
long before lesion is clinically detected
 Bacteria multiply within tubules & are seen in advancing
front of lesion
 Walls of tubules are thin & when micro-orgs
penetrate, they cause irregularities/distensions of
walls  ROSARY BEAD appearance

 Later, bacteria have proteolytic activity, areas of

proteolysis appear as spaces containing necrotic
material & bacteria
 These areas  “Liquefaction Foci of Miller”.
 These areas vary in number & are parallel to
dentinal tubules
ZONE OF DECOMPOSED DENTIN / INFECTED
DENTIN

 Outermost zone, large scale destruction of dentin

 Foci of Miller join together

 Areas of dentin decomposition, occur perpendicular to

dentinal tubules  “Transverse Clefts”

SECONDARY / REACTIONARY DENTIN

 Protective mechanism to protect pulp, develops

as a result of localized, non-specific irritation to

odontoblasts

 Hyper mineralized,less number of dentinal

tubules, irregular, torturous course

ROOT CARIES / CEMENTAL CARIES

 Cementum is first to get affected, then dentin

 Happens when root get exposed to oral
environment
 Eg: Gingival recession & Periodontal disease

 Actinomyces primary causative org, S.mutans,

secondary causative organism.
CARIES ACTIVITY TESTS
 Done to evaluate Caries’ immune status in an
individual & to assess effectiveness of
preventive measures used
 Lactobacillus colony count
 S.mutans dip-slide method
 Synder test
 Salivary reductase test
 Rosdick calcium dissolution test
 Methyl red test
LACTOBACILLUS COLONY COUNT
TEST
 Hadley, 1933
 Paraffin stimulated saliva + normal saline + 10ml of
Lactobacillus selective media (Rogosa) media incubated
at 37 deg for 4 days
 Basis – counting number of colonies present, counting done
in Quebec Chamber
 Results: Caries Activity


Little/No
0-1,000
 1,000-5,000 slight
 5,000-10,000 Moderate
 > 10,000
marked
 Disadvantages

 Only lactobacillus counted

 Detection of other bacteria not possible
 Patient education not possible
 Time consuming
 Special equipment required
 Costly
S.MUTANS DIP-SLIDE METHOD

 Stimulated saliva poured onto slide which contains

Mitis-Salivarius Agar (MSA). Wait till it dries & add
Bacitracin (selective indicator for S.mutans), incubate
at 37 deg for 48hrs
 If S.mutans were present, Blue colonies seen
 Basis – counting S.mutans colony forming units
 Disadvantage – only S.mutans counted
 Advantage – less time consuming
 Results
0 = No colonies
 1 = 10,000 – 1,00,000
 2 = 1,00,000 – 10,00,000
 3 = > 10,00,000
SYNDER TEST
 1940
 Basis – rapidity of acid formation by cariogenic
bacteria
 Stimulated saliva + Glucose-Agar media
containing Bromocresol Green (indicator dye)
 Indicator dye changes color from green to
yellow in pH range of 5.4-3.8
 Color change indicative of degree of caries
activity
 Results
Color change from Green to Yellow within 24
hrs, caries susceptibility – very high
Similar color change within 48 hrs, patient said
to have definite caries susceptibility
Color change in 72hrs, limited caries
susceptibility indicated
Color change doesn’t occur in 72 hrs, person is
caries immune
SALIVARY REDUCTASE TEST

 Rapp, 1962
 Measures activity of reductase enzyme in salivary
bacteria thought to be harmful to tooth structure
 Stimulated saliva + Diazoresorcinol indicator dye
which colors saliva blue
 Reductase enzyme liberated by cariogenic bacteria
causes color change from blue to other colors
which indicates the caries conduciveness of the
patient
 RESULTS

 Color change in 15 mins  Caries conduciveness

 No color change  Non-coducive

 Blue to Orchid  Slightly conducive

 Blue to Red  Moderately

 Blue to Red immediately  Highly conducive

 Blue to Colorless  Extremely
METHYL RED TEST
 Methyl Red dye is applied to tooth surface
 It colors plaque depending upon amount of acid
present & shows Caries
 Teeth turns yellow

 Advantages
 Simple, Cost effective, Helps in patient education
 Disadvantage
 Not accurate
PREVENTION OF DENTAL CARIES

 Mechanical
 Tooth brushes, dental floss, prophylactic Odontotomy
 Nutritional
 Stickycarbohydrates to be avoided
  fibrous diet,  proteins

 Chemical
 Fluoride application in water, milk, tabs, mouthwashes,
toothpastes
 More effective during developmental stages
REFERENCES
 R RAJENDRN, B SIVAPATHASUNDHARAM,
Shafer’s Taxtbook of OralPathology, 6th edition,
ELSEVIER 2009.

 ERNEST NEWBRUN, A text book of Cariology, 3rd

edition. 2:p29-36.Quintessence Publishing Co, Inc 1989.