Prevention of Dental

caries 1
Dental caries is the main cause of tooth loss in people of all ages. For
most of the 20th century caries was seen as a disease of economically
developed countries, with low prevalence in the developing
countries. by the late 20th century this pattern was changing. Why?
To study prevention of dental caries we must start with the etiology of
dental caries.

Definition of dental caries

localized destruction of tooth tissue caused by microorganisms. It is
the cumulative result of de- and remineralization processes.

`
 Dental caries is a multifactorial disease, as it is due to the
interaction of various factors:

1. Diet
2. Host’s susceptibility
3. Microorganisms

Over a certain length of

time
Dental plaque
 Plaque is a biofilm-a community of microorganisms attached
to a surface. The organisms are organized into a three
dimensional structure enclosed in a matrix of extracellular
material.
 Sequential stages of plaque formation:

-formation of pellicle: an a cellular proteinaceous film derived

from saliva which forms in a naked tooth surface.
-Within 0-4 hours single bacterial cells colonized the
pellicle( streptococci, Acitnomyces species and gram-postive
bacteria). Only about 2%of the initial streptococci are MS.
 - 4-24 hours the attached bacteria grow, leading to the
formation of micro colonies.
 Microbial succession in 1-14 days streptococcus dominated
plaque changes to Actinomyces dominated plaque the
bacterial species become more diverse and the micro colonies
continue to grow.
 -in 2 weeks the plaque is mature but there are considerable site
to site variations in its composition. This variations may
explain why lesions progress in some sites but not others in
the same mouth.
 Which plaque bacteria cause caries?

There are 3 possibilities

1-The non specific plaque hypothesis proposed that all
plaque micro flora were involved in caries process. For
prevention all plaque should be disturbed.
2-The specific plaque hypothesis proposed that only a
few organisms in the plaque flora were actively
involved in the disease. Preventive measures targeting
specific bacteria.
3- the ecological plaque hypothesis proposed that dental
caries will result from a shift in the balance of these
resident micro flora driven by a change in the local
environment.
Both mechanical cleaning and restriction of sugar intake
are important in controlling caries progression.
Pathogenic properties of cariogenic bacteria:

1- acidogenic bacteria: produce acids from sugars.

2- produce extracellular polysaccharides (dextran) and

intracellular polysaccharides (can be used for energy
production and converted to acids when sugars are not
available).

3- aciduric: can thrive at low pH.

Where does caries occur?

In sites on the tooth surface where encourage plaque

retention
 Enamel in pits and fissures.
 Proximal enamel just cervical to the contact point
 The enamel of the cervical margin of the tooth just

coronal to the gingival margin.

 Expose root surface after gingival recession.
 The margin of deficient restoration.
 Tooth surfaces adjacent to dentures and bridges which

make cleaning more difficult.

Dental caries process
 Dental caries process is a natural process.
 500 different types of bacteria can be isolated from dental
plaque most of them live in harmony as a commensals .

 Very small number of them are capable of fermenting

carbohydrate and produce acids as a waste. Causing plaque pH
to fall to blew 5 within 1-3 minutes, repeated fall in pH →
demineralization, however the acid produced is neutralized by
saliva so pH increases → remineralization.
Bacteria plus food Demineralization
makes the saliva
very acidic within
3 minutes

Saliva is normal
25-30 minutes
Remineralization after eating

Cyclic Process of Decay

Caries is driven by the frequency of eating
deminremin balance
Critical pH: the pH blew which enamel mineral start to
dissolve 5.5
Steven curve
Histological features of enamel caries
 Initial lesion formed under undisturbed biofilm (cementing
band onto tooth)
1- after one week no changes in the enamel were seen
clinically even after air drying at ultra structural level there
were signs of direct dissolution of the outer enamel surface
(enlargement of the inter crystalline space).
2- after 2 weeks the enamel changes were visible clinically
after air drying (white spot)
3- after 4 weeks these changes could be seen without air drying
ultra structurally there was complete dissolution of the thin
perikymata overlapping forming matt surface lesion or white
spot lesion. (due to increased porosity of the enamel)
Appearance of the white spot lesion in
polarized light
 The first change seen histologically is the loss of inter-rod
substance of enamel with increased prominence of the rods.
 -this is followed by the loss of mucopolysaccharides in the
organic substance.
 -presence of transverse striations of the enamel rods,

 The white spot lesion has 4 histological zones

 1- surface zone
 2- body of the lesion
 3- dark zone
 4-translucent zone
Zone 1: Translucent zone,
-lies at the advancing front of the lesion,
-slightly more porous than sound enamel,
-it is not always present
Zone 2: Dark zone,
-this zone is usually present and referred
to as positive zone
Zone 3: Body of the lesion,
-found between the surface and the dark zone,
-it is the area of greatest demineralization,
Zone 4: Surface zone,
-relatively unaffected area,
-greater resistance probably due to greater degree of mineralization and
greater F concentration.
CARIES OF ENAMEL
Smooth surface Caries:
As the lesion goes deeper, the caries forms a triangular pattern or
cone shaped lesion with the apex towards DEJ and base towards
the tooth surface, it flows the direction of enamel prism.
Occlusally once a cavity forms it is narrower at the top than at the
base
Dentine reactions
Dentine react to the carious process before cavity
formation, it defines it self by

 1-tubular sclerosis ( deposition of minerals within the

dentinal tubules)
 2- formation of tertiary dentine (at the pulp dentine

border)
Cavitations- an important moment clinically

breakdown of the outer enamel surface is important

because now it may be difficult to clean the biofilm out
of the cavity →ecological shift towards anaerobic and
acid producing bacteria now demineralization can
spread laterally along DEJ, undermining sound enamel
Breakdown of outer enamel surface can be created by
1- mechanical injuries during mastication
2- micro-traumas during interdental wear
3- careless probing
The link between Mutans streptococci and caries
 Cross-sectional study revealed increased proportion
of MS at sites of initial caries lesions.
 longitudinal study revealed high number of MS at a

tooth site correlate with subsequent caries.

 and animal experiments conclude that MS cause

caries in animal in the presence of sugar.

 Virulence properties: Ms are acidogenic, aciduric and

produce extracellular and intracellular poly

saccharides.
 Other species with similar properties may also be

cariogenic.
 MS(a group consist of eight serotypes)
 MS are associated with the onset of caries.
 Lactobacilli are associated with the active

progression of cavitated lesion.

 Although newborn baby’s mouth is sterile, it soon

acquires microbes.
Classification of dental caries

 Carious lesions can be classified in different ways according

to
1- anatomical site
2- activity
3- etiology
1- anatomical site
pits and fissures, smooth surfaces, enamel caries root caries,
Black’s classification according to tooth surface involve.
2- activity
Active carious lesion (progressive), inactive carious lesion
(arrested)
This concept of activity is very important as it impinges directly
on management because active lesions require active
management.
3- etiology:
Rampant caries: multiple active carious lesions involving
surfaces of teeth that are usually caries free, It may be seen in
the permanent dentition of teenagers and is usually due to
poor oral hygiene and frequent cariogenic snacks between
meals.
is also seen in mouths where there is a sudden marked reduction
in salivary flow.
 Rampant caries
 Baby bottle caries: or "Bottle Rot" is a pattern of
decay found in young children in deciduous teeth.
Pit and fissures caries
 Properties of arrested caries
Arrested white spotted lesion
 has shiny surface; may be brown in color is more

resistant to attack by acid than sound enamel.

 Arrested caries in dentine: 

  discolored (yellow, brown or black)
 Hard or leathery in consistency due to presence of

tertiary and sclerotic dentine and rest of dentine

appears polished
Arrested caries
Active caries
Saliva and dental health
1- saliva help swallowing and digestion and required for optimal
function of taste buds.
2- maintain the integrity of the teeth, tongue, and mucous
membranes of the oral and oropharyngeal regions.
Its protective actions include:
Physical cleaning: its flow help to clear the mouth of food and

bacterial debris so it is retard plaque formation.

Saliva provide minerals (Ca ,Ph) which are taken up by the

incompletely formed enamel surface soon after eruption and

enhance remineralization particularly when fluoride is present.
 Buffering capacity: saliva contain bicarbonate,
phosphate and protein → regulate pH of the oral
cavity.
 anti bacterial and antiviral action: it contain specific

antibodies (IgA, lysozyme, and lactoferrin).

 Daly salivary flow 1-1.5 L
 Salivary flaw either stimulated or unstimulated.

Normal stimulated salivary flaw rate is 1-2 ml/minute.

Unstimulated 0.3-0.5 ml/min.
Diagnosis of dental caries

There are many ways for dental caries diagnosis:

 Clinical means or visual tactile means using ( vision

and explorer) use of explorer may damage the enamel

matrix of noncavitated lesions.
This method need good light and tooth should be dry.
Hidden caries: not seen clinically, dentinal caries found
radio- graphically beneath sound occlusal surface.
 Radiograph
 Caries detecting dyes
 Newer methods of caries diagnosis such as fiberoptic

transillumination and electrical caries detector. These

diagnostic aids permit noncavitated lesion to be
detected.
Criteria for diagnosis caries through the full
range of lesion development (D1-D3 scale)
 Sound surface: no treated or untreated caries.
 D1. initial caries: no clinically detectable loss of

substance. For pits and fissure there may be

significant staining or discoloration or rough spots in
the enamel that do not catch the explorer.
 D2. enamel caries: loss of tooth substance but no

softened floor or wall or undermined enamel. Cavity

not penetrate dentine.
 D3. caries of dentine: detectable softened floor,
undermined enamel, or softened wall.
 D4. pulpal involvement: deep cavity with probable

pulpal involvement.
 D1-D3 scale is of extreme value in research studies

on dental caries for it permits identification of lesion

progression as well as initiation, it is complicated so
dichotomous scale is used.
 Root caries: the lesion located at the cemento-enamel
junction or wholly on the root surface.
 Although most lesion occur on exposed root

approximately 15% of root lesions have been found

in surfaces without gingival recession.
Measuring dental caries
1- Counting of carious teeth.
2- DMF index: is attributed to Klein and Palmer in
1930