DENTAL CARIES

CONTENTS
 INTRODUCTION
 EPIDEMIOLOGY
 DEFINITION
 CLASSIFICATION
 THEORIES OF CARIES
 CURRENT CONCEPTS IN CARIES
ETIOLOGY
 HISTOPATHOLOGY
 CONCLUSION
INTRODUCTION
 EPIDEMIOLOGY
 Pre-historic man have decreased
caries prevalence

 Decreased caries prevalence in

African and Asian communities

 Factors affecting caries prevalence:

1. Race
2. Age
3. Sex
4. Familial

 Current trends in caries incidence:

 DEFINITION
1. “Dental caries is a microbial disease of the
calcified tissues of the teeth, characterized by
demineralization of the inorganic portion and
destruction of the organic substance of the
tooth” [Shaffer]
2. “Localized post eruptive pathologic process of
external origin involving softening of the hard
tissue and proceeding to the formation of a
cavity” [WHO]
3. “An infectious microbiological
disease of the teeth that results in
localized dissolution and destruction
of calcified tissues” [Sturdevant]
 CLASSIFICATION

I. STURDEVANT
Based on - Location
- Extent
- Rate of progression
According to location:
a. Primary caries
b. Caries of pit and fissure origin
c. Caries of enamel smooth surface origin
d. Backward caries
e. Forward caries
f. Residual caries
g. Root surface caries
h. Secondary (recurrent) caries
• According to extent:
a. Incipient (reversible) caries
b. Cavitated (irreversible) caries

• According to rate of progression:

a. Acute (rampant) caries
b. Chronic (slow or arrested) caries
 G.V.Black’s Classification
• Class-I: - caries on the occlusal surfaces of molars
and premolars
- occlusal 2/3 of the buccal and lingual
surfaces of molars
- lingual surfaces of the anterior teeth
• Class-II: - lesions found on the proximal surfaces
of molars and premolars
• Class-III: - lesions found on the proximal surfaces
of anterior teeth, but do not involve the incisal
angle
• Class-IV: - lesions found on the proximal surfaces
of anterior teeth and involving incisal angle
• Class-V: - lesions found on the gingival
third of the facial and lingual surfaces of
anterior and posterior teeth.
• Class-VI: - were not included in Black’s
classification
- proposed by Siomon
- lesions on the incisal edge and
cusp tips of the teeth
 GRAHAM MOUNT’S
CLASSIFICATION
Based on
• Location of caries
• Size of the carious lesion
Cavity Size 1 Size 2 Size 3 Size 4
site (minimal) (moderate (enlarged (extensive
) ) )

Size 1 1.1 1.2 1.3 1.4

Pit and
fissure
Size 2 2.1 2.2 2.3 2.4
Contact
area
Size 3 3.1 3.2 3.3 3.4
Cervical
 PIT AND FISSURE CARIES
 Limited to the – occlusal surfaces of
molars and premolars
- buccal pits of molars
- lingual surfaces of
maxillary anterior teeth
 Poor self cleansing features
 Usually occurs before smooth surface caries
 Clinically - black or brown in
color
- slightly soft consistency
- “catch” the tip of a fine
explorer
 Adjacent enamel appears bluish white
 “Internal Caries”
 Smooth Surface Caries
 Develops on - proximal surfaces of the teeth
- gingival third of the buccal and
lingual surfaces (cervical caries)

 Preceded by the formation of dental plaque.

 Usually initiate just below the contact point.

 Clinically- initially as faint white opacity or yellow

brown pigmented area.

 Adjacent enamel appears bluish white.

 Cervical Caries
Appears as crescent shaped lesion.
May extend proximally.
Almost always an open cavity.
Lack of oral hygiene on the part of
patient.
 Backward Caries
Lateral spread of the lesion along the
DEJ exceeds the caries in the
contiguous enamel, caries extends
into this enamel from the junction.
Forward Caries
Caries cone in enamel is larger or at
least the same size as that in dentin
 Residual Caries
Caries that remains in a completed
cavity preparation
Not acceptable if - present at DEJ
- prepared enamel
wall
 Root Surface Caries
 In old age patients

 Initiates at the surface of a

mineralized dentin and
cementum which have
greater organic content

 Usually have rapid clinical

course
Recurrent (secondary) caries:
 Occurs at the junction of the
restoration and the
cavosurface of the enamel
 May extend beneath the
restoration
 Indicates unusual
susceptibility to caries attack,
poor cavity preparation,
defective restoration.
 Also indicates presence of
microleakage.
 Incipient (reversible) caries:
 First evidence of caries
activity in enamel
 Clinically as white opaque
region
 Subsurface demineralization
has occurred but no cavitation
 May take up extrinsic stains
 May undergo
remineralization- called as
“caries reversibility” or
“consolidation” of early
enamel carious lesion
 Cavitated (irreversible) caries:
 Lesion that has advanced into
dentin with broken surface
 Remineralization is not
possible
 Treatment include cavity
preparation and restoring
with suitable material.
 Linear enamel caries
(odontoclasia):
 Atypical form of dental
caries in primary dentition
 Lesion predominates on the
labial surface of the
maxillary anterior teeth in
the region of neonatal zone
 Lesion is crescent shape
 Increase caries susceptibility
of posterior teeth.
 Odontoclasia:
- variant of linear enamel caries
- results in gross destruction of the
labial surfaces of incisor teeth
- cause may be an inherent
structural defect
 Acute dental caries:
 Rapid clinical course resulting in early
pulp involvement
 Frequently in children and young adults
 Entry of lesion remains small while rapid
spread along the DEJ
 Clinically appears light yellow in colour
 Pain is often present
 Chronic dental caries
Slowly progressive lesion that
involves pulp much later
Common in adults
Large entrance of the lesion
Dentin is stained deep brown
Moderate lateral spread of caries at
DEJ
Pain is not a common clinical finding.
 Rampant caries:
 Sudden and rapid onset
and almost uncontrollable
destruction of teeth
 Involves teeth that are
ordinarily caries free
(mandibular incisors)
 Ten or more new
increments of carious
lesion in one year
 Nursing Bottle (Infancy or
Soother) Caries
 Rapidly progressing caries
affecting primary dentition
usually during first 2 years
of life
 4 maxillary anterior are
affected first
 If unchecked, maxillary
and mandibular molars
may also get involved
 Lower anterior are spared
(characteristic feature)
 Adolescent caries:
 Acute caries attack at 11-18
years of age
 Lesion in teeth and surfaces
that are relatively immune to
caries
 Small opening in enamel
with extensive undermining
 Rapid clinical course
 Little or no secondary dentin
formation
 Arrested caries:
 Caries which becomes static or
stationary and does not show
any tendency for progression
 Almost exclusively occurs on
occlusal surfaces
 Both dentitions are affected
 Lesion appears as large open
cavity with lack of food
retention
 Superficially softened and
decalcified dentin gets
burnished and has brown
stained polished appearance
“Eburnation of dentin”
 Xerostomia induced caries
(radiation caries)
 Complication of radiation therapy
of oral cancer lesion
 Radiation induced xerostomia
produces caries conducive
environment
 Carious lesion develops as early
as 3 months after onset of
xerostomia
 May be caused by other factors
like salivary gland tumors,
autoimmune diseases, prolong
illness
 Senile Caries
Caries activity that spurts up during
the old age.
They are located exclusively on the
root surfaces of the teeth.
Also seen in association with partial
denture clasps.
Causes: gingival recession, decreased
salivary secretion, poor oral hygiene.
 Occult Caries / Hidden Caries
• Not clinically diagnosed, but detected
only on radiograph.
• Seen in persons with low caries index
suggestive of increased fluoride
exposure.
• Also called as fluoride bombs or
fluoride syndrome
1. Simple caries: one surface is
involved

2. Compound caries: two surfaces are

involved

3. Complex caries: three or more

surfaces are involved
ETIOLOGICAL THEORIES
Early theories

Endogenous theories

Exogenous theories
 EARLY THEORIES
1. The Legend of the Worm:
• According to an ancient Sumerian text, tooth
ache was caused by a worm that drank the
blood of the teeth and fed on the roots of the
jaws
• Antony Van Leeuwenhock (1700) the father
of modern microscopy wrote a letter to the
Royal Society of London describing little
worms taken out of a corrupt tooth and said
that they caused the pain in tooth ache.
 ENDOGENOUS THEORY
• Humoral Theory
“dental caries is produced by internal
action of acid and corroding humors”.
• Four elemental fluids of the body-blood,
phlegm, black bile and yellow bile

• Vital Theory
“tooth decay originated, like bone
gangrene, from within the tooth itself”
 EXOGENOUS THEORY
• Chemical (Acid) theory:
“ teeth are destroyed by acids formed in the
oral cavity ”

• Parasitic (Septic) theory:

“ microorganisms are associated with
carious process ”
 Acidogenic Theory
 Proposed by W.B.Miller 1890, most accepted
 “Acids formed due to the fermentation of dietary
carbohydrates by oral bacteria leads to
progressive decalcification of tooth structure with
subsequent disintegration of organic matrix.”
 He isolated micro-organisms from his
experiments & stated that many were involved in
the carious process.
 3 important factors which can influence process
of tooth destruction in process of dental caries:
Dietary carbohydrates, micro-organisms and
acid
• Limitations
– Did not explain sub-surface
demineralization
– Failed to justify rampant caries
– Did not explain caries in impacted
tooth
– Phenomenon of arrested caries is
not explained
– Smooth surface caries is not
accounted in this theory
 Proteolytic Theory
 Proposed by Gottlieb in 1941.
 “formation of dental caries is essentially
proteolytic process. Bacteria present produce
hydrolytic enzymes and cause proteolysis
leading to the dissolution of organic substance.”
 Microorganisms invade the organic substance
first.
 He did admit that, acid formation accompanied
the proteolysis.
 Yellow pigmentation of dental caries is because
of pigment production by proteolytic organism.
 Caries is initiated at slightly alkaline pH.
Limitations:
In vitro studies didn’t prove the
proteolytic process of caries.
Proteolytic bacteria are uncommon in oral
cavity.
Didn’t explain about the role of sucrose,
pH and fluoride in dental caries.
Protein content of enamel is 0.6%. So,
initiation of caries by proteolytic process is
questionable.
Proteolytic-chelation Theory
 Proposed by Schwatz in 1955.
 Stated that two processes are involved in caries –
proteolysis & chelation.
 Chelation is a process involving complexing of
ions into a complexing substance by covalent
bond which results in a highly stable, poorly
dissociated and weekly ionized compound called
chelate.
 Bacterial attack on enamel is initiated by
keratolytic microorganisms.
 Eg: citrates, lactates
 Chelates are always –ve.
Limitations:
 Fails to make a mention of sugar and acid
production.
 Scientists proved that chelates are weak
and can not cause de calcification.
 Schwatz said, carbohydrates does not cause
acid production but it stimulates
proteolysis, which is not true.
 Lactobacillus in dental caries is because of
chelation and said that microorganisms are
not involved in caries.
 Sucrose Chelation Theory
• If there is a very high concentration of
sucrose in mouth of a caries active
individual, there can be formation of
complexes like calcium saccharates,
calcium complexing intermediaries,
etc by action of phosphorylating
enzymes
• These complexes cause release of Ca,
P ions from enamel and result in DC
• Limitations
 Sucrose readily gets metabolized to
form acids, hardly any scope for
formation of calcium saccharates, etc.
 Very high levels of pH required for
formation of Calcium saccharates,
which is no achievable in the oral cavity
 Autoimmune Theory
 Few odontoblast cells at specific sites
within pulp of specific teeth are damaged
by autoimmune mechanism
 Due to this the defense capacity & integrity
of of enamel and dentin in those specific
areas are compromised and act as potential
sites for caries development in future
 Sulfatase Theory
 Proposed by Pincus in 1951.
 Bacterial sulfatases hydrolyses the
mucoitin sulfate of enamel and chondroitin
sulfate of dentin producing sulfuric acid
that in turn causes decalcification.
 Limitation:
Sulfated polysacharide in enamel is
very small and not readily accessible as a
substrate for enzymatic degradation. So,
this is highly unlikely hypothisis for the
degragation of tooth enamel.
 Levine’s theory
 Proposed by Levine in 1977.
 Established chemical relationship between
enamel, plaque and factors which favors the
movement of minerals between them.
 Also called as “SEW – SAW” mechanism.
 Said enamel demineralization and
remineralization is a continuous process.
 Movement of ions between enamel and plaque
occurs in both direction which depend upon
- plaque ph
- calcium and phosphate ions at the interface
- fluoride ion concentration
 CURRENT CONCEPTS IN
CARIES ETIOLOGY

KEYE’S DIAGRAM VENN DIAGRAM

 Etiological Factors:
Secondary
Factors:
Primary Factors: • Saliva
Teeth • Other dietary
Diet factors
Microorganisms • Vitamins &
minerals
• Hereditary
 TEETH
1. Morphology:
• Accentuated pits and fissures
• Enamel hypoplasia
• Mottled enamel
• Bucco-lingual width of carious teeth
2. Position:
• Malpositioned teeth
• Rotated teeth
3. Composition:
• Surface vs subsurface enamel
 DIET
• Carbohydrate is a cariogenic diet
• Cariogenicity is based on
1. Physical nature
2. Chemical nature
3. Mode of intake
4. Clearance rate
5. Frequency of intake
6. Other dietary factors
 PLAQUE AND
MICROORGANISMS
PLAQUE:
• The concept about dental plaque was first
proposed by Williams in 1897
• Consist of
- salivary component- mucin
- desquamated epithelial cells
- microorganisms
- calcium and phosphate
To produce caries, micro organisms
should have following properties:
1. Should be acedogenic.
2. Should be aceduric.
3. Should posses attachment
mechanism.
4. Should have the capacity to store
sucrose.
5. Should be able to synthesize
extracellular glucans.
1. Pioneer / primary bacteria – initiate
caries
• S.mutans (smooth surface caries)
• Lactobacillus acidophilus (pit &
fissure caries)
• Actinomyces (root surface caries)
1. Invaders / secondary bacteria
• Staphylococcus, Veillonellae
 Streptococci mutans:
• Chief etiological agent in dental caries disease
1. it can produce low pH (acidogenic)
2. it can survive in low pH (acidouric)
3. utilize sucrose at a faster rate than other
bacteria
4. can metabolize sucrose to synthesize glucan
and fructan ( attachment mechanism )
5. it can store intracellular glycogen amylopectin
type polysaccharides that act as a reservoir of
substrate and prolongs its metabolic activity
 Other Bacteria
• Lactobacillus acidophilus
– Found in carious dentin & saliva of persons
with high caries activity
– Release lactic acid
• Actinomyces
– Found esp. in root caries
– Acidogenic
– Attachment to tooth by glycoprotein called
Lectin
Acids produced are
a) Lactic acid
b) Acetic acid
c) Butyric acid
d) Propionic acid
e) Traces of formic acid
• Lactic acid is the strongest acid
 Plaque pH:
 Critical pH- 5.5
 Caries active, pH- 5 to 5.5
 Caries immune, pH- 6.8

STEPHEN’S CURVE
 MINOR FACTORS
I. SALIVA:
1. Flow rate
2. Viscosity
3. Buffering capacity
4. Amount of saliva

Components of saliva:
• Bicarbonates
• Anti-bacterial agents
• Ig-A
• Salivary urea and bicarbonates
II. Dietary factor
– Diet containing Phosphates decreases caries
– Proteins & fat also prevents or decreases caries, as
they prevent attachment of carbohydrates to tooth
– Trace elements of Vanadium & Molybdenum
decreases caries
– Selenium increases risk of caries
– Vitamin A & B are important in formation of hard
tissues. Thus if they are deficient, hypoplasia of
teeth is seen, teeth more prone to caries
– Fibrous food help in cleansing of teeth, removal of
lodged food

III. Hereditary factors:

 HISTOPATHOLOGY
Important for:
1. Research purpose
2. To know the changes taking place in
dental caries
 Not important for diagnosis.
Studied under:
 Light microscope
 Electron microscope
 Polarized microscope
 microradiographs
H/F of early enamel caries
– Loss of inter-rod substance
– prominent enamel-rods
– Appearance of transverse striations of
enamel rods due to segmental
demineralization
– Accentuation of incremental striae of
Retzius
H/F of Advanced enamel caries
Classified on the basis of pore volume and
mounting media used
 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
 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
• Pore volume is 1%, which is more than
normal (0.1%)
• Zone cant be easily identified clinically /
radiographically
 Dark zone / positive zone
• Dark zone as mounting media cant penetrate
this 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

demineralization; 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
 As the microorganisms cause destruction to
dentin, initially there is an attempt to stop the
advancement of caries by depositing the
minerals.
 There is a deposition of mineral in intertubular
dentin.
 Zone is called “transparent zone”
 Odontoblasts are also start depositing dentin.
 At the periphery of sclerotic dentin, dead tracts
are present.
 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
• Large crystals within lumen of dentinal
tubules
 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”
• Mechanism of formation of Clefts - not known
– May follow course of incremental lines or
– May result from coalescence of liquefaction of
adjacent tubules
– Also may rise by extensive proteolytic activity
along interconnecting lateral branches of
odontoblastic processes
• Bacteria shift from dentinal tubules to the peri &
inter tubular dentin
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 having irregular & torturous course

 Root Caries / Cemental Caries
Histopathology:
• Outer surface of cementum – hyper mineralized,
thus more caries resistant
• Resistance due to
– Reprecipitation of minerals from within
– Precipitation of minerals from Plaque
• Clefts formed, through which bacteria penetrate
& cause tooth structure destruction
• Penetration occurs along course of Sharpey's
fibers
• Once cementum completely exposed &
destroyed, underlying dentin is involved