The History of caries

Over the years tooth decay has been

attributed to many factors.
The Syrians believed it was caused by
„tooth worms”; in the 18th and 19th
century it was thought to grow from
within the tooth.
 DEFINITION

Dental caries is an infectious microbiologic
disease of teeth that results in localized
dissolution and destruction of the calcified
tissues..
tissues

Dental caries is a chronic, infectiou

infectiouss disease
initiated through a series of complex chemical
and microbial reactions associated with the
dental biofilm that results in the destruction
(decalcification, proteolysis) of the tooth
tissue..
tissue
 CARIES

It develops often insidiously over a long period of time

progressing from the surface of the tooth to the interior.
 Dental Plaque

A tenacious structure formed on tooth surfaces

which contain large numbers of closely packed
microorganisms surrounded by salivary
components and extracellular material of
bacterial origin

Cannot be removed by a stream of water or

Cannot
rinsing
 Dental Plaque
Dental plaque – part of the defence
system of the host – protects enamel
from the colonization by exogenous
bacteria (pathogenic)
Properties of the bacteria associated
with the biofilm can differ from
planctonic cells
 Dental Plaque

Plaque is not homogenous

Consists of:

- pellicle
- bacteria
- bacterial products
- salivary constituents
 Composition:
 one third = bacteria
 two thirds = extracellular matrix
(secreted by bacterial cells; holds
microcolony together):
 inorganic: calcium, phosphorus,
fluoride
 organic:
 bacterial by-
by-products: acids, enzymes,
toxins
 saliva: proteins, sugars,
sugars, lipids
 dietary carbohydrates
carbohydrates
 leukocytes
 epithelial cells
 extracellular polysaccharides: dextran
 Dental Plaque (SEM)

This scanning electron micrograph of caries-producing plaque illustrates the coccal

microorganisms usually found there. [Courtesy of Drs. Krutchkoff and Wei]
 Appearance::
Appearance
 fresh plaque:
 transparent
 stains pink

 mature plaque:
 heavier;fur
heavier;fur--like
 Gray
Gray,, white,
white, yellow
 stains red; clings to instrument
 Location::
Location
 common areas of mouth
 individual teeth:
 heaviest - cervical third
 lightest - incisal third
 supragingival vs. subgingival
 can cover whole tooth (neglect)
 forms on restorations, appliances

Wherever there is
plaque on the teeth
there is potential
caries formation, as
well as the
formation of
periodontal disease.
Here we see that
plaque unstained
can cover the tooth
completely.

If we use a disclosing
solution, which is usually a
food coloring agent and
have the individual rinse,
we notice that the amount
of plaque covering the
tooth is quite extensive.
Wherever there is mature
plaque, it will absorb the
disclosing solution.
 Plaque

Examination of the
individual's mouth showed
that he had a relatively
clean mouth. There was
some gingival
inflammation, but nothing
too extreme just early
signs of gingivitis. The
important issue here is
that the teeth were well
aligned, appeared to be
quite clean and there
were no apparent caries.
 Plaque

Before the individual began
participation in the project, a
thorough prophylaxis removed all the
areas of plaque formation, and
flossing intraproximally removed any
residual plaque formation.
 Plaque

When the individual returned the
following day after 24 hours the
teeth were once again disclosed.
disclosed. The
appearance now demonstrated an
increased plaque formation on the
teeth..
teeth
 Plaque

This appearance of plaque formation presented
48 hours after non-
non-brushing or mechanical
removal of the plaque. Notice how the teeth are
almost completely covered with plaque. The
reason that the incisor edges of the maxillary
incisor teeth appear to be plaque free was
because the individual rubbed his teeth with a
towel, as he expressed the teeth felt furry and he
was too uncomfortable.
 Plaque

Notice the posterior teeth are almost
completely covered. So, the lesson to be
learned here is that the mechanical removal
of plaque is essential to maintain a sound
oral health. And remember that wherever
plaque formation occurs dental caries also
might occur.
 Stages of formation:
1. acquired pellicle forms
2. colonization:
 initial colonization (adherence) of bacteria
to pellicle
 multiplication
3. development of extracellular matrix
(slime layer)
 secreted by bacteria
 anchors bacteria to tooth
 provides protection from host response
4. growth and maturation
 plaque ages; new colonizers adhere to
previously attached cells; bacteria cluster
together
 colony blooms into mushroom shape
 channels exist that allow fluid movement
 Plaque Bacteria
 days 1-
1-2:
 Streptococci

 some rods

 days 2-
2-4:
 rod increase

 fusiform bacilli and filamentous

m/o appear

 days 4-
4-7:
 rods increase; filamentous increase

 spirochetes and vibrios appear

 plaque thickens
 Plaque Bacteria
 days 7-
7-14:
 spirochetes and vibrios increase
 white blood cells increase
 anaerobic conditions
 signs of inflammation in gingiva

 days 14-
14-21+:
 older plaque
 vibrios and spirochetes prevalent
 Factors influencing plaque
formation:

 types of bacteria
 role of saliva
 diet (although food not required)
 presence of other deposits
 oral hygiene habits
 poor dentistry
 malignment
 Acquired Pellicle

An organic film on tooth enamel surfaces formed by

selective adsorption to apatitic surfaces of specific
glycoproteins of salivary origin.

Acellular, structureless

Comprised of:
- aminoacids
derived from saliva
- carbohydrates
Enamel Pellicle (EM)

Enamel pellicle (arrow) is the uniform thick

deposition of salivary protein between a
thin layer of immature bacterial plaques
and enamel. [Courtesy of Drs. Krutchkoff
and Wei]
 Acquired Pellicle

Protective functions:
1) restrict diffusion of acids
2) antibacterial factors-
factors-sIgA,
Lysozyme, C3
3) helps to counteract acid pH
4) F-
F-, Ca, P bound in pellicle layer
5) may reduce bacterial attachment
 Acquired Pellicle

Damaging functions:
1) initial step in dental plaque
formation
2) selective bacterial adhesion
3) can promote staining of dental
surfaces
 Microbial aetiology of caries

Gnotobiotic animal studies showed that caries
could be induced by specific bacteria, especially
members of the mutans streptococci-
streptococci-group
(eg. Streptococcus mutans and Strep.
sobrinus), when fed a cariogenic (high
sucrose) diet.

the potential for transmission from animal to

animal

protection could be achieved by antimicrobial

agents and vaccination and by passive
immunisation (when antibodies from another
source are applied to teeth).
 Flora of the Mouth

Gram (-
(-)
-Prevotella melaninogenica
-Fusobacterium nucleatum
-Veillonella spp.
Gram (+)
-Lactobacillus
-Actinobacillus, Actinomyces
Others
 Flora of the Mouth

Pioneer species-
species- Earliest colonizers

-S. salivarius
-S. mitis
-S. oralis
-S. sanguis
-S. mutans
 Flora of the Carious Lesion

Smooth surface: S. mutans-

mutans-very significant
S. sanguis

Pits and fissures: -mutans Streptococci
Streptococci--very
significant
-S. salivarius
-Lactobacillus spp. very
significant

Flora of the root surface: Actinomyces spp.
Streptococcus spp

Pits and fissures are the most caries prone
 Bacteria in Carious Lesions
(Summary)

mutans Streptococci can be isolated more often in
higher numbers from a range of carious lesions

advanced lesions generally yield a more diverse
microflora including acidogenic and proteolytic
species working together

mutans Streptococci are not always present
when there is caries

There is a role for other bacteria
Pathogenic Properties of Cariogenic
Bacteria

Produce Extracellular Polysaccharides (EPS) and

Intracellular Polysaccharides (IPS)
-EPS
EPS--glucans, fructans--
fructans--contribute
contribute to plaque
matrix
-IPS-
IPS-glycogen like storage compounds, can be
used for energy production and converted to
acid when free sugars are not available

Ability to maintain sugar metabolism in a low pH
Pathogenicity of cariogenic bacteria

Rapid transport of dietary sugars: the
sugar phosphotransferase uptake
system is a high affinity process. Mutans
streptococci possess more than one sugar
transport system.

Rapid rates of glycolysis (acidogenicity):

can result in a terminal pH of below 4.5 in
only a few minutes.
Pathogenicity of cariogenic bacteria

Tolerance of, and growth at, low pH
(aciduricity): the growth of many of the
bacteria found on sound enamel (eg.
Sanguis) is inhibited at pH <5.5,
Strep. Sanguis)
whereas this is optimal for cariogenic
species.

— Intracellular polysaccharide
synthesis (IPS): can be used during
starvation conditions and catabolised to
acid when dietary sugars are not available
Pathogenicity of cariogenic bacteria

A striking feature of the main
cariogenic bacteria (mutans
streptococci and lactobacilli) is their
combined acidogenicity and
aciduricity; mutans streptococci but
not lactobacilli produce EPS.
Pathogenicity of cariogenic bacteria
• — Extracellular polysaccharide synthesis
(EPS): these polymers help make up the plaque
matrix.
• Glucosyltransferases (GTF's) convert sucrose
to soluble and insoluble glucans, that help
consolidate bacterial attachment; Strep. mutans
also produces a specific highly insoluble polymer
(mutan).

• Fructosyltransferases (FTF's) convert sucrose

to fructans; these polymers are labile and can
be used by plaque bacteria as an energy source.
 Substrate

Contributions of Diet
-Sugar
-Simple sugars diffuse acid into plaque
-Bacteria produce acid from sugar
-Brief sugar exposure leads to rapid decrease in
plaque pH
-Repeated sugar consumption leads to demineralization
of tooth
 control:
Plaque control:
 professionally
 patient’s role
 the longer plaque biofilm remains undisturbed, the
greater the pathologic potential
 research
 significance to disease (caries; periodontal)
 biofilm structure protects bacteria, making removal
difficult
 physical removal of plaque biofilm is necessary, and
most effective for controlling disease