DENTAL CARIES

(Part-2)
Dr Preeti Sharma, MDS
Associate Professor
Dept of Oral & Maxillofacial Pathology & Oral Microbiology,
Subharti Dental College & Hospital
Swami Vivekanand Subharti University
Meerut, UP

Clinical aspects of Dental Caries

Clinical
Classification
– Location
Pit and fissure caries
Smooth surface caries
Root caries

• Linear enamel caries

• Cervical caries

Clinical
Classification
• Rapidity of the process or severity
and rate of progression
– Acute dental caries
•Rampant dental caries
•Nursing bottle caries
•Radiation caries

– Chronic dental caries

Clinical Classification
According to the nature of attack
•New lesion: Primary caries
•Margins of restoration: Secondary
(recurrent) caries
•Arrested caries

Based on Chronology
• Infancy caries (rampant caries)
• Adolescent caries
 Pit & Fissure Caries
• On occusal surface of molars &
premolars
• B & L surfaces of molars
• Lingual surfaces of max incisors

Pit & Fissure Caries

• Pits & fissures with steep walls and
narrow bases more prone for
caries. - enamel in depth is thin.
- difficult to clean

Pit & Fissure Caries

• Brown or black
• ‘catch’ with a fine explorer point.
• Enamel bordering the pit or fissure
may appear bluish white.

Pit & Fissure Caries

• Lateral spread at DEJ.
• The enamel directly bordering the pit or
fissure may appear opaque bluish white as it
becomes undermined.
• This undermining occurs through lateral
spread of the caries at DE junction.
• Penetration may be extensive into the dentin
without fracturing the overhanging enamel.

• The lateral spread at DE junction as

well as penetration into the dentin
along the dentinal tubules may be
extensive without fracturing away
the overhanging enamel.Thus, there
may be a large carious lesion with
only a tiny point of opening.

• This undermined enamel may

suddenly give way under the
stress of mastication, or the
dentist may suddenly open into a
large cavity when excavating the
pit or fissure.
 pit and fissure
caries

Smooth surface caries

• On the proximal surfaces of teeth
• On the gingival third of B & L
surfaces
• Usually begins just below the
contact point

• Generally preceded by the formation

of a microbial or dental plaque. This
ensures the retention of carbohydrate
and micro-organisms on the tooth
surface in an area not habitually
cleansed,
and
the
subsequent
formation of acid to initiate the caries
process.

Smooth surface caries

• Early : faint white roughened
opacity of enamel with intact
enamel surface.
• Later: open, shallow cavity

Root caries

Cervical caries

Smooth surface
caries

Linear enamel caries

• An atypical form of dental caries
that has been observed in the
Primary dentition of children, in
Latin American and Asian countries.
• Labial surface of anterior max teeth,
in the region of neonatal line
 • A variant of the linear enamel
form of caries in the primary teeth
of children in the Far East has
been named Odontoclasia.

Cervical caries
• Crescent shaped
• On B, Li or La surfaces of any tooth
• Extends from the area opposite the
gingival
crest
occlusally
to
the
convexity of the tooth surface marking
the self-cleansing portion of the surface.
• Extends laterally to involve proximal
surfaces

• Frequently related to lack of oral

hygiene.
• There is least excuse for cervical
caries, since it can be prevented in
nearly every instance by proper
oral hygiene practice.

Root caries
• Usually in old age with significant
gingival recession & exposed root
surfaces
• ‘caries of cementum’
• On B & Li surfaces of root

Acute Dental Caries

• Runs a rapid clinical course
• Results in early pulp involvement
• Most freq in children & young
adults - dentinal tubules are large
- d.t. are open
- there is no sclerosis
• Rapid process, so no time for
reparative dentin deposition
 Acute Dental Caries
• Small opening of the carious lesion.
• Rapid spread of the process at the DE
junction and diffuse involvement of the
dentin produce a large internal
excavation.
• Dentin is stained Light yellow.
• Pain is more apt to be a feature of acute
caries.

Rampant Caries
• Sudden, rapid, uncontrollable
destruction of teeth.
• Affects surfaces of teeth that are
relatively caries-free
- proximal & cervical surfaces of
mand incisors.

Rampant Caries
• A caries increment of 10 or more new carious
lesions over a period of about a year is
characteristic of rampant caries.
• Primary dentition of young children
• Permanent dentition of teenagers involved.
• Dietary factors affecting oral substrate and
oral flora and physiological factors affecting
saliva.

Nursing bottle caries

Also called:
• Nursing caries
• Baby bottle syndrome
• Bottle mouth syndrome
Form of rampant caries affecting the
deciduous dentition.

Nursing bottle caries

Attributed to the habitual use of :
• Nursing bottle containing milk or
milk formula, fruit juice or
sweetened juice
• Breast feeding
• Sugar or honey-sweetened pacifiers
 Nursing bottle caries
• Presents as wide spread carious
destruction of deci teeth, mostly
max C.I. & L.I., followed
by 1st molars, then cuspids
• Only root stumps may be left

Nursing bottle caries

• Manifests clinically as widespread
carious destruction of teeth, most
commonly the four maxillary incisors,
followed by the first molars and then
the cuspids.
• absence of involvement of mand
incisors distinguishes it from rampant
caries

• The mandibular incisors usually

escape because they are covered
and protected by the tongue.

Adolescent caries
• Acute caries attack in 11-18 yrs of age
• Usually seen in teeth which are
immune to caries
• Small carious opening with extensive
undermining of the enamel
• Rapid progression. Little time for
reparative dentin formation.

Chronic Dental Caries

•
•
•
•
•
•
•

Progresses slowly
Most common in adults
Entrance to the lesion is larger
Pulp involvement is late
Deep brown
Shallow cavity
Little undermining of enamel

• Slow progress of the lesion allows

sufficient time for both sclerosis of
the dentinal tubules and
deposition of secondary dentin in
response to the adverse irritation.
• Pain is not a common feature.

Recurrent Caries
• Occurs in immediate vicinity of a
restoration
• Due to ‘leaky’ margins.
• Due to inadequate extension of the
original restoration, which favors
retention of debris, or to poor adaptation
of the filling material to the cavity, which
produces leaky margins.

Arrested caries
•
•
•
•

Static or stationary
No tendency for further progression
Both deci & perm teeth can be affected
Almost exclusively on occlusal surface

Arrested caries
• Large open cavity
• Burnished superficial dentin :
brown, polished & hard
(eburnation of dentin).
• Sclerosis of dentinal tubules & sec.
dentin formation

• Occurs almost exclusively in caries of

occlusal surfaces and is characterized
by a large open cavity in which there
is lack of food retention.
• Sometimes on the proximal surfaces
when adjacent approximating tooth
has been extracted.

Radiation Caries
• In pts undergoing radiation
therapy in head & neck region
• Due to xerostomia, inc salivary
viscosity & low pH of saliva

• Characteristic caries like lesion

completely encircling the neck of the
tooth.
• Sometimes as brown to black
discoloration of the crown. The occlusal
surface of posterior teeth and incisal
edges of anterior teeth wear away.

• Third type of lesion begins as a

spot depression which spreads
from incisal or occlusal edges on
labial or buccal and lingual
surfaces.

Radiation caries

Histopathology of Dental Caries

• Caries of enamel
– Smooth surface caries
– Pit and fissure caries

• Caries of dentin
– Early dentinal changes
– Advanced dentinal changes
– Secondary dentin involvement

• Root caries

Caries of Enamel

Smooth surface caries

• Preceded by formation of dental plaque
• Earliest manifestation of caries: area of
decalcification, which appears as smooth
chalky white area
• Enamel over this white spot is hard & shiny
• loss of interprismatic substance with
increased prominence of rods
• Roughening of ends of enamel rods

Caries of Enamel

Smooth surface caries

• Appearance of transverse striations of

the enamel rods
• Accentuation of Striae of Retzius:
optical phenomenon due to loss of
minerals which causes organic
structures appear more prominent

Caries of Enamel

Smooth surface caries

• Accentuation of perikymata

Early caries

Caries of Enamel

Smooth surface caries

– Triangular/ Cone shaped lesion
• Apex towards DEJ
• Base towards surface of tooth

Surface/ Enamel

Dentino-Enamel Junction

• Loss of continuity of surface

• Rough surface

Smooth Surface Caries

 Zones of enamel caries
beginning from inner advancing
front of the lesion
• Zone
• Zone
• Zone
• Zone

1:
2:
3:
4:

Translucent Zone
The Dark Zone
Body of the Lesion
Surface Zone

Caries of Enamel

Smooth surface caries

• Zone 1: Translucent Zone
- at advancing front of enamel lesion
First recognizable zone of alteration.
Seen in long GS in clearing (quinoline-RI1.62.)
–
–
–
–
–

Structureless
Not always present
Slightly more porous than sound enamel
Pore volume of 1%
Fluoride content more than sound enamel

• Zone 2: The Dark Zone

– Adjacent and superficial to translucent
zone
– Called as ‘Positive zone’ as it is always
present.
– Shows positive birefringence ( in contrast
to sound enamel)
– Appears dark brown
– Pore volume of 2 – 4%

• Presence of small pores; large

molecules of quinoline are unable
to penetrate.
• Micropore system- gets filled with
air and become dark.
• Medium like water may penetrate.

• Zone 3: Body of the Lesion

– Lies between surface layer and dark zone
– Area of greatest demineralisation
– Pore volume of 5% at periphery to 25% in
the centre
– Quinoline imbibition- body appears
transparent.
– Prominent striae of Retzius

• Water imbibition- positive

birefringence compared to sound
enamel.

• Zone 4: Surface Zone

– Appears relatively unaffected
– Partial demineralization of 1-10%.
– Pore volume is less than 5% of the
spaces.
Negative birefringence- water
imbibitions.

• Positive birefringence- porous

subsurface.

Zones of enamel
caries

Translucent zone
Dark zone
Body of Lesion
Surface zone
Accentuated Striae of Retzius

Zones of enamel caries

Caries of Enamel

Pit and Fissure caries

• Food stagnation & bacterial decomposition
in base of pits and fissures
• Carious lesion more often starts at the walls
of fissures rather tan at the base
• Enamel thin at base, so frequent dentin
involvement

Pit and Fissure caries

Caries of Enamel

Pit and Fissure caries

• Triangular/ Cone shaped lesion
• Base towards DEJ
• Apex towards tooth surface
Enamel Surface

Dentino-Enamel Junction

Histopathology of Dental Caries contd.

Pit and Fissure caries

• Greater no. of dentinal tubules
involved at DEJ
• Pit and fissure caries especially of
occlusal surfaces produces greater
cavitation than proximal smooth
surface caries
• More undermined enamel

Histopathology of Dental Caries contd.

Caries of Dentin
• Begins with the natural spread of carious
process along DEJ
• Rapid involvement of large no. of dentinal
tubules
• Tract for microorganisms to reach pulp

Caries of Dentin

Caries of Dentin
Early Dentinal Changes
Transparent dentin/ Dentinal Sclerosis
- reaction of vital dentin & pulp
- Calcification of d.t. occurs to seal off the infection
- Minimal in rapidly progressing caries
- Prominent in slow chronic caries
- Called so:
* Appears transparent under transmitted light
* Dark – reflected light

Caries of Dentin
Early Dentinal Changes
• Fatty degeneration of Tomes’ dentinal
fibers
– Deposition of fat globules in dentinal
tubules
– May contribute to impermeability of d.t.
– May be predisposing factor for sclerosis

Caries of Dentin

Caries of Dentin
Early Dentinal Changes

• Decalcification of dentin
• ‘Pioneer bacteria’ :
microorganisms penetrating
dentinal tubules before there is
any clinical evidence of caries
• Walls of d.t. get distended due to
packing with m.o.

• Almost pure forms of bacteria in

each d.t. seen
• As m.o. penetrate farther into
dentin – separated from
carbohydrate source – proteolytic
m.o. predominate in deep caries

Histopathology of Dental Caries contd.

Advanced Dentinal Changes

• Decalcified dentinal tubules become
confluent, but organic structure is
maintained
• Thickening & swelling of Sheath of Neumann
at irregular intervals
• Increase the diameter of d.t. – due to
packing by m.o.

• ‘Millers liquefaction foci’

- formed by coalescence & breakdown of a
few d.t.
– Focus: ovoid area of destruction parallel to
course of tubules. Filled with necrotic
debris which causes expansion of tubule
– Produces compression and distortion of
adjacent dentinal tubules - course of d.t.
bent around liquefaction focus

Miller’s liquefaction foci

Histopathology of Dental Caries contd.

Advanced Dentinal Changes

• Decalcification & confluence of d.t. rapid in
areas of interglobular dentin.Ultimate
destruction of remaining organic matrix
• Proteolytic destruction of organic matrix of
decalcified dentin

Advanced Dentinal Changes

• Destruction occurs at focal areas which
coalesce to form a necrotic mass of
leathery consistency
• Clefts at 90° to dentinal tubules: due to
caries extension along lateral branches
of dentinal tubules or along matrix
fibres which run in this direction
 Dentinal Caries
• Triangular shaped lesion
– Base towards DEJ, Apex towards Pulp
Dentino-Enamel Junction

Pulp

Zones of Dentinal Caries

(Beginning pulpally, at the advancing edge of the
lesion)
• Zone 1: Zone of fatty degeneration of Tomes’ fibers
• Zone 2: Zone of dentinal sclerosis characterized by
deposition of calcium salts in dentinal tubules
• Zone 3: Zone of decalcification of dentin, a narrow
zone, preceding bacterial invasion
• Zone 4: Zone of bacterial invasion of decalcified but
intact dentin
• Zone 5: Zone of decomposed dentin

Zones of Dentinal
Caries

1. ZONE OF FATTY DEGENERATION

2. ZONE OF DENTINAL SCLEROSIS
3. ZONE OF DEMINERALIZATION
4. ZONE OF BACTERIAL INVASION

Secondary dentin
involvement
• Similar to involvement of primary dentin,
except:
- Slower
- D.t. are fewer
- D.t. more irregular in course, thus
delaying penetration of m.o.
• Occasionally, caries may spread laterally at
the junction of primary & secondary dentin,
producing a separation of the two layers

Double cone lesion of Caries

Pit and fissure caries

Smooth surface caries

Enamel

Dentine

Diagnosis of Dental
caries

Radiologic diagnosis
• Imp. for interproximal caries as they are
not easily detected clinically.
- Small triangular radiolucent area of
enamel and later dentin approx. at level
of contact point
• X ray is not of much value in detecting
occlusal caries or small lesions on the
buccal and lingual pits.
• Proximity of caries to pulp can be
assessed.

Radiologic diagnosis of
dental caries

INFRARED LASER FLUORESCENCE

• This instrument is used for detection &
quantification of Dental Caries
• Material responsible for fluorescence is
bacterial metabolities- porphyrins
• Makes use of laser light source, fibre optic cable
& fibre optic probe.

Digital Imaging Fiber Optic

Transillumination
• This is used to identify lesion on
interproximal surfaces of posterior teeth
• By transillumination technology we
capture a visual image and transfer it to
a computer for analysis

Methods of Caries
Control

Methods of Caries Control

• Immunologic measures
• Nutritional measures
• Chemical measures
• Physical measures

Chemical methods
Substances which alter tooth surface/
structure
•
•
•
•

Fluorine
Bis-biguanides: chlorohexidine & alexidine
Silver Nitrate
Zinc Chloride and Potassium Ferrocyanide

• Fluorine
– Fluoridation of water supplies – 1 ppm
– Fluoride supplements – fluoride tablets,
drops or lozenges : taken daily from birth to
about 14 yrs of age
– Topical application of Fluoride sodium
fluoride, stannous fluoride
– Fluoride dentifrices
– Fluoride mouthwashes or rinses

Mechanism of action of
ingested fluoride
• Prevents carbohydrate degradation
- Inactivates the co-enzyme portion of enolase system
- Inhibits conversion of 2-phosphoglyceric acid to
(enol) phosphopyruvic acid
• Alters structure of developing tooth through systemic
absorption of the element – incoroparation of fluorine
in crystal lattice of enamel, forming fluorapatite, which
is less acid soluble.

Chemical methods
• Substances which interfere with CHO
degradation through Enzymatic
Alteration
– Vitamin K
– Sarcoside

• Substances which interfere with

bacterial growth and metabolism
–
–
–
–
–

Urea and Ammonium compounds

Chrolophyll
Nitrofurans
Penicillin
Other Antibiotics: Erythromycin, Tetracycline

Nutritional measures
• Restriction of refined carbohydrate
intake
• Phosphated diets

Mechanical measures
•
•
•
•
•
•
•
•

Dental prophylaxis
Tooth brushing
Mouth rinsing
Dental floss
Oral irrigators
Detergent foods
Chewing gum
Pit and fissure sealants

Immunologic methods
Caries vaccine
• Saliva contains immunoglobulins (1-3%)
• IgA, IgG and IgM
• Cellular components of immune system:
lymphocytes, macrophages and
neutrophils (gingival sulcus)
• Control of cariogenic bacteria by these
molecules plays an important role in
maintaining oral health

methods
Mode of action of Antibodies
1. Salivary Igs act as specific agglutinins
interacting with bacterial surface
receptors and inhibiting colonization
and subsequent caries formation
–

Inactivate surface glucosyl transferases

which reduce the synthesis of extracellular
glucansreduced plaque formation

2. The Antibodies also increase

opsonization leading to phagocytosis by
lymphocytes and PMNs

Caries Vaccine
• By means of immunization with a
homologous Lactobacillus vaccine,
in 1944 Williams was partially
successful in reducing the number
of lactobacilli in human saliva.

• Considering the properties of

S.mutans, which are associated
with its cariogenicity. An antibody
approach to caries control could
be accomplished by a number of
mechanisms:

• Interfering with adherence,

colonization & dissemination of the
organisms in the oral cavity.
• Reducing its ‘stickiness’ by altering
its polysaccharide metabolism.
• Altering the ability of the
microorganisms to produce acid.

• Although an antibody can reach

the oral environment via saliva or
gingival crevicular fluid, much
more research will be necessary
before a caries vaccine becomes
available to the general public.

Risks of using caries

vaccine
• Sera of some patients with
rheumatic fever who show
serological cross-reactivity b/w
heart tissue antigens and certain
antigens from hemolytic
streptococci.

Caries activity tests

• Caries activity test- measures the

degree to which the local
environmental challenge favors
the probability of carious lesions.
• Caries activity- increment of active
lesions(new or recurrent lesions)
over a slated period of time.

• Caries susceptibility- inherent

tendency of the host, the target
tissue, i.e. the tooth to be afflicted
by the caries.

Potential uses
• Determine the need for caries
control measures.
• Indicate patient co-operation.
• Assist in timing recall appointments.
• Guide the desirability of placing
extensive restorations.

• Help in determination of prognosis.

• Guide orthodontist when undertaking
appliance therapy.
• Aid in selection of patients for
studies on caries.
• Help in screening for potential
cariostatic agents.

• Aid in motivating patient to

practice good oral hygiene habits.

REQUIREMENTS
• Caries activity tests should be:
• 1) simple
• 2) rapid
• 3) relatively cheap to perform.
• 4) correlating closely with the caries
experience of the individual.
• 5) reproducible.

Caries activity tests

1) Biochemical properties of saliva
•Salivary reductase test.
2) acidogenic potential of salivary
constituents
•Snyder’s test
•Swab test
•Dip-slide test

• Enamel dissolution (Fosdick’s

test).
• pH test.
3) Bacterial counts of saliva/plaque
Lactobacillus count test
Streptococcus mutans count test

Lactobacillus Colony
test
• Measures the number of aciduric
bacteria in a patient’s saliva by
counting the number of colonies
which appear on tomato peptone
agar plates, a selective medium
with pH 5.0, after inoculation of
the patient’s saliva and incubation.

• Rogosa’s medium- highly selective

for growth of Lactobacillus.
• Colonies grown on media upon
incubation reflect the number of
aciduric flora in the patient’s
saliva.

Relactobacilli count in
relation to caries
activity

Colorimetric Snyder
test
• Developed by Snyder in 1951.
• Based on the rate of acid produced
when a sample of stimulated saliva
is inoculated into a glucose and agar
containing medium of pH 4.7-5.0.
• Medium has bromocresol green as a
color indicator.

• Changes from blue-green at pH 4.75.0 to yellow at pH 4.0, indirectly

checking the presence of acidogenic
and aciduric microorganisms.
• Snyder test is simple and correlates
well with Lactobacillus colony count.

Observations in
Snyder’s test

Swab test
• Swabbing the buccal surfaces of teeth
with a cotton applicator, which is
subsequently inoculated in the
medium.
• pH following a 48-hour incubation is
read on a pH meter or the color change
is read by use of color comparator.

• pH of 4.1 and below denotes

marked caries activity.
• 4.2-4.4- considered active.
• 4.5-4.6- slightly active.
• pH of 4.6 and above is considered
as caries inactive.

Salivary S.mutans level

test
• Incubation of a sample obtained
using tongue blades or a wooden
spatula on Mitis salivarius
agar(MSA), a selective
streptococcal medium with
increased concentration of
sucrose(20%).

• Agar plates are incubated at

37degree C for 48 hours.
• Levels of S.mutans greater than
100000 are indicative of an
acceptable cariogenic challenge.

• Colonization does not occur until

the level of S.mutans reaches 4.5
x 104/ml for smooth surface and
103 /ml of occlusal fissures.

S.Mutans Dip-slide
method
• This test classifies salivary samples
according to estimates of S.mutans
growing on modified MSA.
• Stimulated saliva collected and poured
over the agar coated slide.
• After the slides are dry, bacitracin disks
are placed in the middle of the inoculated
agar, about 1cm from each other.

• Slide is then incubated in a tube

containing a CO2 tablet for 48 hrs.
• Zone of inhibition formed around
each bacitracin disk.
• If present, S.mutans appears as
small blue colonies growing within
the zone of inhibition.

• Colony density is compared with a

model chart and classified as
0(negligible), 1(less than
100,000), 2( (100,000-1000,000),
3 ( more than 1000,000) S.mutans
CFU/ml of saliva.

Buffer capacity test

• Evaluates the quantity of acid
required to lower the pH of saliva
or the amount of acid or base
necessary to bring color indicators
to their endpoint.
• pH meter or color indicators used
to measure the buffer capacity.

• Patients with increased proneness

to carious lesions have a lower
buffering capacity in their saliva
than saliva of those who are
relatively free.

Enamel solubility test

• The Fosdick calcium dissolution
test measures a milligram of
powdered enamel dissolved in 4
hrs by acid formed when the
patient’s saliva is mixed with
glucose and powdered enamel.

Salivary reductase test

• Measures the rate at which the
indicator molecule diazoresorcinol,
changes from blue to red to colorless
or whitish on reduction by the mixed
salivary flora.
• Activity of the reductase enzyme
present in salivary bacteria is
measured.

Interpretation of
salivary reductase test

Frequently asked
questions
• Define dental caries. Describe the
etiological theories of dental caries.
• Clinical classification of dental
caries.
• Histopathology of dental caries.
• Histopathology of enamel caries.

• Histopathology of dentinal caries.

• Dental caries vaccine.
• Caries activity tests.

References
• Shafer’s Textbook of Pathology.
Eighth edition.