DENTAL CARIES
NORMAL TOOTH
TYPES OF TOOTH LOSS
TYPES OF TOOTH LOSS
Loss of tooth substance in
different ways:
TYPES OF TOOTH LOSS
Loss of tooth substance in
different ways:
• Microbial tooth loss
(dental caries)
TYPES OF TOOTH LOSS
Loss of tooth substance in
different ways:
• Non microbial tooth
loss
(attrition, abrasion and
erosion)
Definition
It is a disease of microbial origin in which the
dietary carbohydrates are fermented by the
bacteria forming an acid which causes the
demineralization of the inorganic part and
disintegration of the organic part of the tooth
Epidemiology
Dental caries & periodontal disease are the
most common chronic disease in the world.
Presence has increased in modern times on a
world wide epidemiology measured with the
DMF bases prevalence.
Dental caries is increased in less developed
countries and decreased in developed
countries
Epidemiology
Slightly more in females than in males.
Increased prevalence with bad oral hygiene.
Increased with medically compromised
patients.
Increased with acute & chronic illnesses.
(medications that decrease salivary flow).
Epidemiology
Increased with young patients & elderly.
Patients with sucrose rich diet intake.
Smokers & alcohol consumers.
Minimal exposure to fluoride.
Etiology
Etiology
Etiology
1.Role of bacteria
Plaque Is a gelatinous
mass of bacteria
adhering to the tooth
surface.
It is an adhesive layer
which deposits on the
surface of the tooth and
has colonies of bacteria
Etiology
1.Role of bacteria
Plaque tends to adhere
to the surface of the
teeth and in this way
the bacteria can have
there cariogenic effect
on the tooth
Etiology
Etiology
1.Role of bacteria
Cariogenic bacteria
1. Bacteria involved :
• Streptococci e.g mutans, sobrinus
• Lactobacilli e.g acidophilus
2. Possibly associated bacteria :
• Steptococci e.g mitis
• Actinomyces e.g viscosus
Etiology
1.Role of bacteria
Sreptococcus mutans are the main
cariogenic organisms because:
i. Adhere to enamel
ii. Transport sugars and convert
them to acid (acidogenic)
iii. Produces bacterocin substances
that kill other competing bacteria.
Etiology
1.Role of bacteria
Sreptococcus mutans are the main
cariogenic organisms because:
Iii Produce extracellular and
intracellular polysaccharides which
contribute to the plaque matrix;
intracellular polysaccharides can be
used for energy production and
converted to acid when sugars are not
available
Etiology
Role of saliva:
• Saliva plays a major role in protecting the
teeth against acid challenge.
Etiology
Role of saliva:
• The main protective factors of saliva are:
1. The Ca and PO4 ions usually the saliva is
supersaturated when the enamel appetite is
at neutral pH.
Etiology
Role of saliva:
• The main protective factors of saliva are:
2. Pellicle this layer forms naturally over the tooth
surface from saliva helps in high level of protection
against acid by
• Barrier of diffusion of acid into the tooth
• Barrier to movement of dissolution products out of
the tooth.
• Inhibits mineralization of appetite to form calculus
Etiology
Role of saliva:
• The main protective factors of saliva are:
3. Bicarbonate buffering.
4. Presence of fluoride ions (although low 0.03
p.p.m) but will still contribute to the overall
protection & repair of the tooth mineral
Etiology
Role of saliva:
• The main protective factors of saliva are:
5. Salivary flow & oral clearance rate influence
removal of food debris and microorganisms.
Etiology
Role of carbohydrates:
• Fermentable carbohydrates are on of the most
important cause of dental caries.
• Increase in the intake of refined carbohydrates
are directly proportional in causing dental
caries (frequency of intake is more important
than the quantity)
Etiology
Role of carbohydrates:
• Increased frequency
leads to increased
periods of pH reduction
which causes an
immediate drop of 2-4
points (Stephen curve)
and demineralisation.
Etiology
Role of carbohydrates:
• Recovery to normal
resting pH takes from
20 min for the normal
patient to several hrs
for those with high
susceptibility to caries.
Etiology
Role of carbohydrates:
• The degree of fall depends
on :
1. Salivary flow rate
2. The plaque thickness
3. The number and mix of
plaque bacteria
4. The type of carbohydrates
i.e. sticky food have low
clearance rate
The Progression of Carious
Lesion
The Progression of Carious Lesion
Caries into the enamel
Advancing coronal lesion
Caries into the dentine
The Progression of Carious Lesion
• Early enamel lesion
• Appears when the pH
falls at the level of tooth
& remineralization fails.
The Progression of Carious Lesion
• Early enamel lesion
This lesion is characterized
by:
1. Loss of translucency
white chalky
appearance especially
when dehydrated.
The Progression of Carious Lesion
• Early enamel lesion
This lesion is characterized
by:
2 Fragile surface layer
susceptible from
damage from probing.
The Progression of Carious Lesion
• Early enamel lesion
This lesion is characterized
by:
3. Increased porosity esp.
in subsurface so can
uptake stain
The Progression of Carious Lesion
• Early enamel lesion
This lesion is characterized
by:
4. Reduced density in
subsurface that maybe
detectable
radiographically or with
transillumination.
The Progression of Carious Lesion
• Early enamel lesion
• A potential for re-mineralization with an
increased resistance to further acid damage.
The Progression of Carious Lesion
• Early enamel lesion
The reversed lesion will either:
Regain normal translucency
Or
The chalky white
appearance may
remain and take up stain
The Progression of Carious Lesion
• The advancing coronal
lesion
• If the deminerilization-
reminerilsation imbalance
continues the incipient
lesion collapses through
dissolution of the apetite
or fracture of the
weakened crystal
resulting in cavitation
The Progression of Carious Lesion
• The advancing coronal
lesion lesion
• Plaque can now be
retained within the depth
of the cavity and the re-
minerilization stage
becomes more difficult
Dentine Caries
• Caries advances faster in the dentine due to
i. Decreased mineral content
ii. Tubules give a pathway
• In deep dentinal caries due to infection near
the pulp
• In mild caries due to movement of fluid in
dentinal tubules that have been opened
Dentine Caries
Dentine Caries
Dentine response to slow
advancing
When dentin is damaged,
odontoblastic processes die
or retract leaving empty
dentinal tubules. Areas with
empty dentinal tubules are
called dead tracts and appear
as dark areas in ground
sections of tooth.
Dentine Caries
Dentine Caries
Dentine response to slow
advancing
With time, these dead tracts
can become completely filled
in mineral. This region is
called blind tracts and
appears white in sections of
ground tooth
Dentine Caries
Dentine Caries
Dentine response to slow
advancing
The dentin in blind tracts is
called sclerotic dentin. The
adaptive advantage of blind
tracts is the sealing off of the
dentinal tubules to prevent
bacteria from entering the
pulp cavity.
Dentine Caries
Dentine Caries
Dentine response to slow
advancing
Clinical feature: shiny
darkly colored hard to
probe
Dentine Caries4
Dentine Caries
Dentine response to severe irritation
• Results in infection abscess and death of the
pulp
Dentine Caries
Dentine Caries
Dentine response to severe irritation
Rampant caries
• Sudden rapid destruction of many teeth,
frequently involving surfaces of teeth that are
ordinarily relatively caries-free.
Dentine Caries
Dentine Caries
Dentine response to severe irritation
Rampant caries
• Most commonly observed in the primary dentition
of infants who continually suck a bottle with sugar.
Dentine Caries
Dentine Caries
Dentine response to
severe irritation
Rampant caries
• May also be seen in the
permanent dentition of
teenagers and is usually
due to frequent
cariogenic snacks and
sweet drinks between
meals.
Dentine Caries
Dentine Caries
Dentine response to severe irritation
Rampant caries
• Mouths where there is a sudden marked
reduction in salivary flow (xerostomia) i.e
radiation for cancer pts & Sjögren’s syndrome,
an autoimmune condition which may involve
the salivary glands.
Dentine Caries
Dentine Caries
• Zones of dentinal caries
Zone 1 :The deepest area
normal dentin
no bacteria
Dentine Caries
Dentine Caries
• Zones of dentinal caries
Zone 2: Sub transparent
Dentin.
which is a zone of
demineralization
no bacteria
is capable of
remineralisation
Dentine Caries
Dentine Caries
• Zones of dentinal caries
Zone 3 Transparent dentine
soft
decreased mineral content
no bacteria
self repair
Dentine Caries
Dentine Caries
• Zones of dentinal caries
Zone 4 Turbid zone
zone of bacterial
invasion
not mineralized
dry, leathery dentine
will not self repair
Dentine Caries
Dentine Caries
• Zones of dentinal caries
Zone 5 Infected dentine
with bacteria
soft.
no recognizable structure
to the dentin and collagen
mineral seem to be
absent.
Classification of Tooth Prep.
• As presented by Black, based on the frequency
of caries on certain aspects of the tooth this
was divided into 5 classes, a 6th class was
added later on.
Class I
• Pits and fissures of
occlusal surfaces of
molars and premolrs
• Occlusal 2/3 of facial and
lingual walls of post
teeth.
• Lingual aspects of
maxillary incisors
Class II
Proximal surface of
posterior teeth.
Class III
Proximal surface of
anterior teeth not
involving the incisial
edge
Class IV
Proximal surface of
anterior teeth involving
the incisial edge
Class V
Gingival 1/3 of all
teeth
Class VI
- Tip of the cusp of posterior teeth
- Incisal edge alone of anterior teeth
Clinical Sites for Caries Initiation
Clinical Sites for Caries Initiation
Pits & fissures
Smooth surface
enamel
Root surface
Restoration margins
Clinical Sites for Caries Initiation
Pits & fissures
Either: Non cavitated Caries likely
Caries unlikely
Or
Cavitated
Occlusal caries in molars showing stained fissures.
Clinical Sites for Caries Initiation
Pits & fissures
Non cavitated
• Deep grooves maybe
present
• Superficial staining
Cavitated
• Chalkiness of enamel
• Brown grey
discolouration
Clinical Sites for Caries Initiation
Pits & fissures
Non cavitated
• Deep grooves maybe
present
• Superficial staining
Cavitated
• Chalkiness of enamel
• Brown grey
discolouration
Clinical Sites for Caries Initiation
Pits & fissures
• Prevalence
Account for much of the caries in the school
aged children
Clinical Sites for Caries Initiation
Pits & fissures
• Diagnosis
1.Clinical appearance
2.Radiographs: Non cavitated no radiolucency
beneath occlusal enamel. Cavitated
radiolucency.
3. Probing careful use so not to cause cavitation.
Cavitated mechanical binding. Non cavitated
softening at the base of the pit & fissure.
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• Observed in facial and
lingual surfaces of the
teeth.
Clinical Sites for Caries Initiation
Pits & fissures
• Histological feature
Triangular with its base at the dentinoenamel
junction so it is deceptive in examination
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• Approximal enamel
smooth surfaces just
cervical to the contact
area
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• Approximal enamel
smooth surfaces just
cervical to the contact
area
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• Approximal enamel
smooth surfaces just
cervical to the contact
area
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• The enamel at the
cervical margin of the
tooth at the gingival
margin In patients with
gingival recession, the
area of plaque
stagnation is on the
exposed root
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
• The enamel at the
cervical margin of the
tooth at the gingival
margin In patients with
gingival recession, the
area of plaque
stagnation is on the
exposed root
Clinical Sites for Caries Initiation
Clinical Sites for Caries Initiation
Clinical Sites for Caries Initiation
Smooth enamel surface
Location
Restoration margin
Clinical Sites for Caries Initiation
Smooth enamel surface
• Clinical feature
- Appear chalky white more advanced lesions
develop cavitation
- Marginal ridge discoloured in cavitated and
normal in non cavitated
Clinical Sites for Caries Initiation
Clinical Sites for Caries Initiation
• Smooth enamel surface
• Prevalence
Increased beneath the contact point in patients
with recession of the papilla extra sheltered ,
so increased plaque accumulation.
Diagnosis
1. Simple visual
examination
Diagnosis
1. Simple visual
examination
Diagnosis
2. Probing
• Inserting a blunt probe carefully with appropriate
load.
• Too much presure or ecxesive load may cause Non
cavitated intact surfaces to break down.
Diagnosis
3. Radiographs non
cavitated maybe
radiolucent cavitated
radiolucent
Diagnosis
• Smooth enamel surface
• Diagnosis
• Bitewing radiographs are of paramount
importance in diagnosing approximal caries in
both enamel and dentine
Diagnosis
4. Transillumination
opaque area seen
Diagnosis
• Differential Diagnosis for
smooth surface caries:-
- From enamel hypocalcification
you have to examine the tooth
dry if the clinical white structure
disappears this means it is
caries.
- Arrested lesion slightly
discolored hard spots in older
patients after extracting
neighboring teeth.
Diagnosis
• Smooth enamel surface
• Differential Diagnosis
- Arrested lesion slightly
discolored hard spots
after extracting
neighboring teeth.
Diagnosis
• Smooth enamel surface
• Differential Diagnosis
- Arrested lesion slightly
discolored hard spots in
after extracting
neighboring teeth.
Histopathology
• Smooth enamel surface
• Histopathology
Triangular with the apex towards the pulp
Histopathology
Enamel Caries
Consists of four zones from inwards outwards
1. Translucent zone
2. Dark zone
3. Body of the lesion
4. Surface zone
Caries diagnosis
1. History
2. Clinical examination
3. Nutritional analysis
4. Salivary analysis
5. Radiographic assessment
Nutritional analysis
Caries prevention
1. Assessing general health
2. Fluoride exposure
3. Antimicrobial agents
4. Diet changes
5. Oral hygiene (tooth brushing,
flossing, xylitol gums)
6. Pits & fissure sealants
7. Restorations
Caries prevention
Caries prevention
Caries prevention
Caries prevention
Caries prevention
Caries prevention
Caries prevention
Caries prevention
Caries prevention
