Our Lady of Fatima University

COLLEGE OF DENTISTRY

Dental caries

Sharon Alvarez, DMD, Ph.D.

Dental Caries
Definition:

An infectious microbiologic disease of the

teeth that results in the localized
dissolution of the calcified tissues
Dental caries
 Multifactorial, transmissible, infectious oral disease
caused primarily by the complex interaction of
cariogenic oral flora, biofilm, with fermentable
carbohydrates on the tooth surface over time
One of the two most prevalent oral
diseases affecting humans.
….It is also one of the most common
reasons of tooth loss in general
population!
EPIDEMIOLOGY OF CARIES
 POPULATION – CONSIST
 DENTAL CARIES HAS BEEN
STUDIED EXTENSIVELY OF ALL INDIVIDUALS
DURING LAST 50 YEARS IN LOCATED IN PRESCRIBED
NORTH AMERICA AND AREA.
EUROPE.  PREVALENCE- THE
NUMBER OF
 THES STUDIES ARE VERY INDIVIDUALS IN
USEFUL IN DETERMINATION POPULATION HAVING A
OF THE EXTENT OF THE DISEASE AT SPECIFIC
NEED FOR, EFFECTIVENESS, POINT IN TIME.
DENTAL TREATMENT.  INCIDENCE- THE # OF
INDIVIDUALS
DEVELOPING NEW CASES
IN A POPULATION OVER A
SPECIFIC PERIOD OF
TIME.
1. CHEMICAL (acid) THEORY
In 17 th and 18 th century,there emerged a
concept that teeth are destroyed by acids
formed in the oral cavity by
fermentation of food particles around
the teeth
2. PARASITIC THEORY
Microorganisms were associated with
the carious process
1. ACIDOGENIC THEORY
W.D Miller was the first well known scientist and
investigator of dental caries and published his
results in 1882.
“dental decay is a chemoparasitic process.
It is a two stage process there is
decalcification of the enamel which also
results in the destruction of the dentin.
In the second stage there is dissolution
of the softened residue of the enamel
and dentin.”
3. PROTEOLYTIC THEORY
Heider, Bodecker (1878)and Abbott (1879) contributed
considerably to this theory.

There has been evidence that the organic

portion of the tooth plays an important role
in the development of dental caries . The are
some enamel structure which are made of the
organic material such enamel lamelle and
enamel rods These structure prove to be the
path ways for the advancing microorganisms.
3. PROTEOLYTIC THEORY
enamel contains 0.56 % of organic matter of
which 0.18% is keratin and 0.17 % is a soluble
protein . Microorganisms produce
proteolytic enzymes,which destroy the
organic matrix of enamel, loosening the
apatite crystals….so they are eventually lost
and tissue collapses
5. PROTEOLYSIS-CHELATION THEORY
t is a process in which there is complexion
of the metal ions to form complex
substance through coordinate covalent
bond which results in poorly dissociated
/or weakly ionized compound
5. PROTEOLYSIS-CHELATION THEORY
The bacterial attack on the surface of the
enamel results in the breakdown of the
protein ,chiefly keratin and results in the
formation of soluble chelates with
calcium which decalcify enamel even at
neutral PH.. Mucopolysaccarides may
also act as secondary chelators. 
The Classical Keyes-Jordan Diagram
The caries balance:
Pathological factors
• Acid producing bacteria
• Subnormal saliva flow
• Frequent eating and drinking
of fermentable carbs
• Poor oral hygiene

Protective factors
• Saliva flow and components
• Remineralization (F, Ca,
PO4)
• Antibacterials
• Good oral hygiene
 Medical history factors that are associated with increased
caries risk
History factor Risk increasing observation
Age Childhood
Gender Women are at slightly greater risk
Fluoride exposure No fluoride in water supply
Smoking Risk increases with amount
Alcohol smoked
General health Risk increases with amount
consumed
Medication Chronic illnesses, delibitation
decrease
ability to give self-care
Medications that reduce salivary
flow
 Medical history factors that are associated with increased
caries risk
Clinical Risk increasing findings
examination
General appearance Appears sick, obese, or malnourished
Mental or physical Unable or unwilling to comply with
disability dietary and OHI
Mucosal membranes Dry, red and glossy mucosa suggests
decreased salivary flow
Active carious Cavitation and softening of enamel
lesions and dentin, circumferential chalky
opacity at gingival margins
High plaque scores
Plaque Puffy, swollen, inflamed, bleeds easily
Gingiva Indicate past high caries rate; poor
Existing restorations quality indicates increased habitat for
cariogenic organisms
 0 1 2 3
Clinical examination for caries:
Sound tooth
Pitssurface
and Fissures Distinct visual
DESC No caries change in Loc. Enamel
Visual change in
change, enamel, seen breakdown
RIPTI hypoplasia
anamel after
wihen wet, with no dentin
drying
ON Wear, erosion white, or shadow
Non-caries colored
phenomena
Sealant Sealant or
/ minimally
Resto Sealant optional Sealant optional Sealant optional invasive
(LOW- restoration
RISK) needed
Sealant Sealant or
/ minimally
Sealant Sealant
Resto Sealant optional invasive
recomnended recomnended
(MOD- restoration
RISK) needed
Sealant Sealant or
/ minimally
Sealant Sealant Sealant
invasive
 0 4 5 6
Clinical examination for caries:
Pits and Fissures

Extensive distin
dark shadow from Distict cavity, visible
cavity with dent
dentin, with or dentin, frank
DESCRIPTION cavity is deep an
without localized cavitation (<1/2 of
wide involving m
enamel breakdown tooth surface)
than ½ of the to

Sealant/
Minimally invasive Minimally invasive Minimally invasi
Resto restoration restoration restoration
(LOW-RISK)

Sealant/ Minimally invasive Minimally invasive Minimally invasi

Resto restoration restoration restoration
(MOD-RISK)
Clinical Significance of Enamel Lesions
NON-
RESTORATIVE,
THERAPEUTIC
PLAQUE ENAMEL TREATMENT RESTORATIVE
BIOFILM SURFACE ( Antimicrobials, TREATMENT
Remineraliza-
tion, pH Control )

Normal
Normal Normal Not indicated Not indicated

Abnormal, but Only for

Hypocalcified Normal Not indicated
not weakened esthetics
Noncavitated Cariogeni Porous,
Yes Not indicated
caries c weakened
Cariogeni Cavitated, very
Active caries Yes Yes
c weak

Remineralized, Only for

Inactive caries Normal Not indicated
strong esthetics
1. The causative agent
Caries is caused by bacteria as proven by the
following:
 Teeth free from bacterial infection,
either in germ-free animals or
unerupted teeth do not develop caries
 Antibiotics are effective in reducing
caries in animals and humans
Caries is caused by bacteria as proven by the
following:
 Oral bacteria can demineralize enamel
in vitro and produce lesions similar to
naturally occurring caries
 Specific bacteria can be isolated and
identified from plaque over carious
lesions
Dental Plaque
Definition:

A gelatinous mass (soft, translucent and

tenaciously adhering) of bacteria adhering
to the tooth surface.
Bacterial Plaque

filamentous
microorganisms

Gram (+) Gram (–)

Factors Needed for Caries Initiation
 Flora – Bacteria
- Plaque
 Diet
 Susceptible Surface
 Time
Streptococcus mutans Serotypes Associated
with Caries
 Streptococcus mutans
 Streptococcus sobrinus humans
 Streptococcus rattus - rats
 Streptococcus cricetus - hamsters
 Streptococcus ferus – wild rats
 Streptococcus macacae
 Streptococcus downei primates
 mutans streptococci or MS is the collective term for all
the serotypes

MS and Lactobacilli can produce great amounts of acids

(acidogenic), are tolerant of acidic environments
(aciduric), are vigorously stimulated by sucrose, and
appear to be the primary organism associated with
caries in man.
 MS – enamel caries
 MS and Lactobacilli species – dentin caries
 Actinomycetes species (e.g. Actinomycetes viscosus) –
root caries
Cariogenic Attributes of S mutans
 Acidogenic – able to produce lactic acid from sucrose
 Aciduric – can live in pH as low as 4.2
 Has ability to adhere to pellicle and contribute to plaque
formation. The survival of organisms in the oral
environment depends on their ability to adhere to a
surface.
 Able to form large amounts of extracellular, sticky and
insoluble glucan plaque matrix
Threshold dose
 The total number of bacteria inoculated into the
mouth
 MS has high threshold dose to compete with S.
sanguis.
 For MS to spread to other tooth surfaces, it must be
present in sufficient numbers in the saliva to
overcome the colonization resistance afforded by the
normal oral flora
Therefore it should be noted that an active
carious lesion can serve as a reservoir of
MS and lactobacilli, providing the large
threshold dose necessary to establish
infections on other tooth surfaces.
Pellicle
 A relatively cell-free layer of precipitated salivary
protein material

Functions:
- Protects enamel
 Reduces friction between teeth
 Provides matrix for remineralization
Development of the Bacterial Plaque
1. Pellicle (1 µm thick) covers all oral surfaces within
30 minutes to 1 hour after brushing
2. It becomes colonized by bacteria within 12-24
hours.
3. High sucrose diet or frequent ingestion of sucrose
- favors colonization of acidogenic bacteria and
exclusion of non-cariogenic bacteria (e.g., S.
sanguis, S. mitis)
4. Special receptors make it easy for acidogenic
bacteria to adhere and extracellular matrix
facilitates cohesion
Development of the Bacterial Plaque

5. Metabolism of sucrose results in acid production –

lactic acid from sucrose.
6. Plaque pH below 5.5 – period of demineralization
7. Plaque pH above 5.5 – period of remineralization
The gelatinous nature of the plaque limits outward
diffusion of metabolic products and thus serve to
prolong the retention of acids.
Basis for Bacteriologic testing of saliva to determine the caries.
STIMULATED SALIVA Interpretation of results
Sample colony forming
units for mi of saliva

Lactobacilli >10 5 HIGH RISK – high counts

suggest there already exxixt
cariogenic plaque and good
potential to infect other sites
by overcoming colonizaation
resistance

Mutans Streptococci <10 Lower counts suggest

5 insufficients # to overcome
colonization resistance and
therefore reduced risk of
infection
  Orderly sequence of replacement communities, each
communities modify the local environment of that site

 Two types of succession:

Plaque Growth

a. Primary succession
b. Secondary succession
 Two types of succession:
a. Primary succession--In general ecology occur as the process of
development of a biological community where with non previously
existed
--In oral cavity it is the process of normal change in the oral flora occuring
over the lifetime of an individual.
Plaque Growth

b. Secondary succession

Newborns:
 Mouth is sterile at birth
 Rapidly colonized by skin bacteria and S. salivarius
 Transient organisms may be noted
 Major changes in the species composition of the oral cavity occur
with the eruption of teeth because
 Two types of succession:
a. Primary succession
b. Secondary succession
Plaque Growth

 process of plaque regrowth after the tooth surface is

cleaned
 similar plaque will reform on the teeth after
prophylaxis if there is no other change in the oral
environmental conditions.
 Adults:
 general composition of a well-established oral flora
remains relatively stable if there are no major
changes in the health of the host
Plaque Growth

 Loss of all teeth in elderly patients results in the loss

of organisms specialized for tooth attachment and,
consequently, the oral flora reverts to a composition
similar to that of a newborn
 Adults:
 general composition of a well-established oral flora
remains relatively stable if there are no major
changes in the health of the host
Plaque Growth

 Loss of all teeth in elderly patients results in the loss

of organisms specialized for tooth attachment and,
consequently, the oral flora reverts to a composition
similar to that of a newborn
Non-specific plaque hypothesis
 assumes that all plaque is pathogenic
specific plaque hypothesis
 recognizes plaque as pathogenic only when signs of
associated disease are present.
Dental caries
at tooth level:

demineraliza
tion

remineraliza
tion
2. time
 8

pH 6

4
0 0 10 20 30 40 50 60

Minutes after glucose rinse

Caries Free Slight Caries Activity Extreme Caries Activity
 Effect of frequency of ingestion of sugary
foods on caries activity

pH Three meals per day

5.5
8 AM Noon 8 PM

5.5
Between meals sugar
3. Susceptible tooth
Common clinical sites of caries initiation
 Base of pits and fissures
 Smooth enamel surfaces that shelter plaque
- areas cervical to the contact areas
- distal surface of most posterior tooth
- areas cervical to the heights of
contour on the facial and lingual
 Root surfaces
Common clinical sites of caries initiation
 Base of pits and fissures

High prevalence of all dental caries.

Provides excellent mechanical shelter for organism.
Common clinical sites of caries initiation
 Smooth enamel surfaces that shelter plaque
areas cervical to the contact areas
- distal surface of most posterior tooth
- areas cervical to the heights of
contour on the facial and lingual
These are the areas also protected physically and
are relatively free from the effects of mastication of
food, tongue movement and salivary flow.
Common clinical sites of caries initiation
 Root surfaces
 Proximal root surfac near cervical line is often unaffected by
the action of hygienic procedure susch as flossing reuently
harbor caries-producing plaque.
CARIES ORIGINATING FROM THE ROOTS IS
ALARMING BECAUSE
 1. Has a comparatively rapid progression
 2.It is often asymptomatic
 3.Closer to the pulp
 4.It is more difficult to restore.
Common clinical sites of caries initiation
 Base of pits and fissures
 Smooth enamel surfaces that shelter plaque
- areas cervical to the contact areas
- distal surface of most posterior tooth
- areas cervical to the heights of
contour on the facial and lingual
 Root surfaces
 The Oral Mucosa is populated by organism with receptors
specialized for attachment to the surface of epithelium.

 Streptococcus Salivarius- plaque at the dorsum of the tongue.

 S. Sanguis and S.Mitis- dominated the teeth normally have
plaque community.
 First clinical sign of caries induced
demineralization is the white spot
lesion

White spot lesion

vs.
Enamel hypocalcification
 Zones of Incipient Enamel caries
1. Surface Zone – intact hypermineralized zone.
Pore volume (PV) is < 5%

2. Body of the lesion – porous and soft.

PV is 5 - 25%

3. Dark Zone – due to deposition of ions in

previously empty pores, PV is 2-4%

4. Translucent Zone – due to perfusion of quinoline, PV

is 1% or 10X of sound enamel
Zones of Incipient Enamel Caries

Surface Zone

Body of the Lesion

Dark Zone

Translucent Zone

Ground section viewed with

transmitted polarized light
with a Red 1 filter
Microradiograph of Incipient Enamel
Caries
HISTOPATHOLOGY OF CARIES
 ENAMEL CARIES

 The mineralization process is apparently some what discontinuous and is

characterized by alternating phases of high and low activity.
 Thus enamel, is capable of acting as a molecular sieve like by allowing free
movement of small molecules and blocking the passage of larger molecular
and ions.

 The movement of ions through carious enamel can result in acid dissolution of
the underlying dentin before actual cavitations of the enamel surface.
CLINICAL CHARACTERISTIC OF ENAMEL CARIES
 1. Incipient smooth surface lesion
 This lesion are usually observed on the facial and lingual surface of the tooth.

 White spots are chalky white, opaque areas that are reversed only when the
tooth surface is dessicated (dried)

 These areas of enamel lose their translucency because of the extensive

subsurface porosity caused by demineralization.
Clinical Characteristics of Enamel and Altered Enamel

SURFACE SURFACE
HYDRATED DESSICATED
TEXTURE HARDNESS

Normal
Transluscent Transluscent Smooth Hard

Hypocalcified Opaque Opaque Smooth Hard

Noncavitated
Transluscent Opaque Smooth Softened
caries

Active caries Opaque Opaque Cavitated Very soft

Opaque, Opaque,
Inactive caries Roughened hard
dark dark
 Pit & Fissure Enamel Caries

Compare thickness of
enamel below base of pit
Advanced Pit & Fissure Caries
Dentinal caries
DENTINAL CARIES
 3 levels of dentinal reaction to caries can be recognized

 1. reaction to a moderte intensity attack

 2. Reaction to a long term , low level acid remineralizaton associated with a
slowly advancing lesion.
 3. reaction to severe rapidly advancing caries characteristics by high acid
levels.
ZONES OF DENTINAL CARIES
 3 changes,
 1. Weak organic acid demineralized dentin.
 2.Organic material of dentin particularly collagen is degenerated and
dissolution.
 3.loss of structural integrity is followed by invasion of bacteria.
Zones of Dentinal Caries
1. Infected zone
2. Turbid zone
3. Transparent dentin
4. Subtransparent dentin
5. Normal dentin
Infected Zone

Turbid Zone

Transparent dentin
Subtransparent
dentin
Normal dentin
ZONES OF DENTINAL CARIES
 ZONE 1 NORMAL DENTIN
 Has a tubule with odontoblastics rocesses that are smooth and no crystals in
the line.
 There are no bacteria in the tubules
ZONES OF DENTINAL CARIES
 ZONE 2 SUB TRANSPARENT DENTIN
 Zone of demineralized (by acid from caries) of the intertubular dentin and
initial formation of very fine crystals in the tubules and lumen at the
advancing prone.
 Damage to the odontoblastic process is ended, however no bacteria are founf
in this zone.
ZONES OF DENTINAL CARIES
 ZONE 3 TRANSPARENT DENTIN
 Zone of carious dentin that is softer than normal dentin.
 Shows further loss of mineral from intertubular dentin and many large crystals
in the lower of dentinal tubules
ZONES OF DENTINAL CARIES
 ZONE 4 TURBID DENTIN
 Zones of bacterial invasion marked by widening and distortion of dentinal
tubules w/c filled with bacteria.
 Dentin in this zone will not self repair.
ZONES OF DENTINAL CARIES
 ZONE 5 INFECTED DENTIN
 Outermost zone of infected dentin
 Decomposed dentin that is teeming with bacteria.
 No recognizable structure to dentin, seems to be absent of collagen and
mineral.
NECROTIC DENTIN
 It recognized clinically, as a wet, mushy, easily removable mass.
 This is structure less/ granular in histologic appearance and contain masses of
bacteria.
 Sensitivity Presence of Capacity to
to stimuli bacteria remineralize
Zone 1, IZ
- + -
Zone 2, TZ
- + -
Zone 3, TrD
+ - +
Zone 4, STrD
+ - +
Zone 5, ND
+ - +
 Infected and Affected Dentin
 Infected dentin = Zones 1 and 2
- significantly discolored
- can be removed by
excavators
- stained with caries detector
- needs to be removed
unless judged to be within
0.5 mm of pulp
 Infected and Affected Dentin
 Affected dentin = Zones 3 and 4
- not significantly
discolored
- feels hard already
- capable of remineralization
CARIES TERMINOLOGY
 Acute (Rampant) Caries- Soft, light- colored lesion
 Chronic (Slowly progressing) Caries- Fairly hard or
leathery texture and highly discolored
 Arrested Caries- Hard, shiny, smooth surface with
brown-black discoloration
CARIES TERMINOLOGY
 Active lesion
In enamel, it has a dull, white, opaque
appearance. In dentin, a soft, yellowish or light to
dark brown discolorations of the demineralized
tissues prevail.
 Arrested lesion
Varied appearance, ranging from a shiny, white,
opaque or discolored spot in the enamel to a hard,
dark dentinal surface exposed to the oral
environment
 If mineralization occurs after cavitations , the remaining exposed
surface becomes harder and softer and often becomes dark
brown/ black in color –termed as ARRESTED CARIES
CARIES TERMINOLOGY

 Type of caries according to extent

 Incipient or reversible
 Cavitated or irreversible
Progression of carious lesion
 The time for progression from incipient caries to clinical caries on smooth
surface is estimated to be 18 mos.
 Peak rates for the incidence of new lesion occurs 3 years after the erruption of
the tooth.
 Both for oral hygiene and frequent exposure to sucrose containing food can
produce incipients (white spot lesion)– first clinical evidence of
demineralization as little as 3 weeks.
CARIES TERMINOLOGY
 Primary caries lesions
Lesions found in intact tooth surfaces
 Secondary caries lesions (Recurrent caries)

Lesions found adjacent to restorations

 Remaining caries lesions

Caries lesion left behind in the preparation or at the enamel margin of a

preparation when a restoration is placed
CLINICAL CHARACTERISTIC OF ENAMEL CARIES
 2. Arrested Caries ( mineralized
lesion)

 Clinically observed as intact, but

discolored usually brown or black
spots.

 The change in color is presumambly

due to trapped organic debris and
mettalic ions with the enamel.
 CARIES TERMINOLOGY
 Slowly progressing lesions

- commonly without clinical symptoms

- hard, dry, and dark brown
- very similar clinical appearance as
arrested caries lesions
 Rapidly progressing lesions
- Often painful or hypersensitive
- soft, wet and light yellow
- demineralization penetrates deep into
dentin
 CARIES TERMINOLOGY
 Slowly progressing lesions
- commonly without clinical
symptoms
- hard, dry, and dark brown
- very similar clinical appearance as
arrested caries lesions
 Rapidly progressing lesions
- Often painful or hypersensitive
- soft, wet and light yellow
- demineralization penetrates deep
into
dentin
CARIES TERMINOLOGY
 Rapidly progressing lesions
- Often painful or hypersensitive
- soft, wet and light yellow
- demineralization penetrates deep into
dentin
CARIES TERMINOLOGY
 Slowly progressing lesions
- commonly without clinical symptoms
- hard, dry, and dark brown
- very similar clinical appearance as
arrested caries lesions
 Rapidly progressing lesions
- Often painful or hypersensitive
- soft, wet and light yellow
- demineralization penetrates deep into
dentin
 To diagnose SPL from RPL, consider the following
surface characteristics of the lesion:
- degree of cavitation
- discoloration
- consistency and wetness of the
involved dentin
- subjective symptoms such as pain and
hypersensitivity
Early Enamel Caries
Dentin Sclerosis in Slowly
Progressing Caries
Reactionary Dentin Formation Induced by
Caries in Dentin
 DENTINAL CARIES
 The dej has the least
resistance to caries
attach and allows
rapid lateral spreading
once caries has
penetrated the enamel.
 Demineralization
Cellular proliferationofindentin
the ODstarts
layer
Deposition of reactionary dentin
Hypermineralization of Dentin

P Dentin Enamel
u
l
p
Methods of Caries Prevention
1. LIMIT SUBSTRATE
 Substantially reduce sucrose from diet
 Eliminate sucrose from between meal snacks
Rationale: Reduce number, duration and intensity
of acid attacks.
Reduce selection pressure for MS

Goal of diet counseling is to identify source of sucrose

in the diet and reduce the intake of these foods
Methods of Caries Prevention
2. Modify Microflora
 Bactericidal mouth rinses (chlorhexidine)
 Topical fluoride treatments
 Antibiotic treatment (vancomycin, tetracycline,
polymyxin B)

Rationale: Eliminate MS from mouth

Methods of Caries Prevention
Plaque Disruption / Removal
 Brushing
 Flossing
 Other oral hygiene aids (water piks, interdental
brushes)

Rationale: Decrease plaque mass

Promote buffering
Prevents plaque succession
Methods of Caries Prevention
Modify Tooth Surfaces
 Systemic Fluoride
 Topical Fluoride application
 Enameloplasty
 PRR: Preventive Resin Restoration
 Prophylactic Odontotomy

Rationale: Decrease plaque retention and increase

resistance to demineralization
 Fluoride Treatment  This presence result in enamel
becoming more acid resistant (
 Excessive fluoride exposure (10 PPM/ more)
results in fluorosis, brownish discoloration of
enamel term MOTTLED ENAMEL.
 The optimal fluoride levels for public supplies is
about 1 part per million PPM at 0.01 PPM and
below the preventive effect is loss and caries rate
is higher.

 1st- presence of fluoride ion greatly enhances the

precipitation into tooth structure of
FLUOROAPATITE from calcium and phosphate
ions present in salive.
 2nd- incipient, non cavitated carious lesion are
remineralized by the same process.

 3rd- fluoride has antimicrobial activity.

Methods of Caries Prevention
Stimulate Salivary Flow
 Sugarless chewing gums (Xylitol)

Protective functions of saliva

- Bacterial clearance
- Direct bacterial activity
- Buffers
- Remineralization
Importance of Saliva in the maintenance of normal
flora
 1. Bacterial Clearance
 2.Direct Antibacterial Activity
 3.Buffer
 4.Demineralization
Methods of Caries Prevention
Restore Tooth Surfaces
 Restore all cavitated lesions
 Seal pit and fissures of high caries risk teeth
 Correct all defects (marginal crevices, cervical
overhangs

Rationale: Eliminate sites of infection and

deny habitat for reinfection