Microbiology of Dental caries

Dr jim’ale Hassan (BDS)

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 Dental caries is a chronic endogenous infection
caused by the normal oral commensal flora.
The carious lesion is the result of demineralization
of enamel – and later of dentine – by acids
produced by plaque microorganisms as they
metabolize dietary carbohydrates.
Caries is defined as localized destruction of the
tissues of the tooth by bacterial fermentation of
dietary carbohydrates

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 Epidemiology
Dental caries (with periodontal disease) is one of
the most common human diseases and affects the
majority of individuals.
Although caries was not uncommon in the
developing world, the recent affluence in these
regions has resulted in a remarkable increase in
caries due to the ready and cheap availability of
fermentable carbohydrates.

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 In contrast, caries prevalence is falling overall in the
developed world due to the increasing awareness of
cariogenic food sources and the general improvement
in oral hygiene and the dental care delivery systems.

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 Caries of enamel surfaces is particularly common up to
the age of 20 years, after which it tends to stabilize.
However, in later life, root surface caries becomes
increasingly prevalent, due to gingival recession,
exposing the vulnerable cementum to cariogenic
bacteria.

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 Classification
Dental caries can be classified with respect to the site
of the lesion
 pit or fissure caries
 smooth-surface caries
 root surface caries
 recurrent caries

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 Nomenclature of dental caries. D, dentine; E, enamel; P, pulp.

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 Clinical presentation
The primary lesion of caries is a well demarcated,
chalkywhite lesion.
This ‘white-spot’ lesion can heal or remineralize,
and this stage of the disease is therefore reversible
However, as the lesion develops, the surface
becomes roughened and cavitation occurs.
If the lesion is not treated, the cavitation spreads
into dentine and eventually may destroy the dental
pulp, finally leading to the development of a
periapical abscess and purulent infection
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 Diagnosis
Diagnosis is usually by a combination of:
good lighting
clean teeth
a three-in-one syringe
Radiograph
Microbiological tests
Experimental methods

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 Etiology
 host factors (tooth, saliva)
 diet (mainly the intake of
fermentable carbohydrates)
 plaque microorganisms
(i.e. supragingival plaque)
 Time

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 Host factors
 Tooth structure
The structure of enamel, and dentine in root caries
is important some areas of the same tooth are much
more susceptible to carious attack than others,
possibly because of differences in mineral content
(especially fluoride).
 Flow rate and composition of saliva
The mechanical washing action of saliva is a very
effective mechanism in the removal of food debris
and unattached oral microorganisms.
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 Con’t
It has a high buffering capacity, Which tends to
neutralize acids produced by plaque bacteria on
tooth surfaces, and it is supersaturated with
calcium and phosphorus ions, which are important
in the remineralization of white-spot lesions.
Saliva also acts as a delivery vehicle for fluoride.

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  Diet
There is a direct relationship between dental caries
and the intake of carbohydrates.
The most cariogenic sugar is sucrose,
Sucrose is highly soluble and diffuses easily into
dental plaque, acting as a substrate for the
production of extracellular polysaccharides and
acids.

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 Cariogenic streptococci produce water-insoluble
glucan from sucrose, which, in addition to
facilitating initial adhesion of the organisms to the
tooth surface, serve as a nutritional source and a
matrix for further plaque development.
The frequency of sugar intake rather than the total
amount of sugar consumed appears to be of
decisive importance.

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  Microbiology
Microorganisms in the form of dental plaque are a
prerequisite for the development of dental caries.
 The role of mutans streptococci
The evidence for the aetiological role of mutans
streptococci in dental caries includes the following:
 correlations of mutans streptococci counts in saliva
and plaque with the prevalence and incidence of
caries

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  mutans streptococci can often be isolated from the
tooth surface immediately before the development
of caries
 positive correlation between the progression of
carious lesions and ‘S. mutans’ counts
 production of extracellular polysaccharides from
sucrose (which help to cement the plaque)

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  The role of lactobacilli
Lactobacilli were previously believed to be the
causative agents of dental caries.
They were considered to be candidate organisms
for caries because of:
 Their high numbers in most carious lesions
affecting enamel
 the positive correlation between their numbers in
plaque and saliva and caries activity

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 their ability to grow in low-pH environments
(below pH 5) and to produce lactic acid
 the fact that their numbers in dental plaque derived
from healthy sites are usually low.
 their ability to synthesize both extracellular and
IPSs from sucrose

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 Management of dental caries
The conventional approach to the treatment of
dental caries was to remove and replace diseased
tissue with an inert restoration.
This approach made no attempt to cure the disease,
and the patient often returned some months later
requiring further fillings due to new or recurrent
caries.

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 The modern philosophy in caries management
highlights:
 early detection
 the importance of accurate diagnosis
 minimal cavity preparation techniques
 active prevention.

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 Patient evaluation

In patients with a low incidence of caries, a case

history and clinical and radiographic examination
are probably adequate for treatment planning.

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 for patients with rampant or recurrent caries, or
where expensive crown and bridge work is
planned, additional investigations are necessary.
These include:
 assessment of dietary habits
 determination of salivary flow rate and buffering
capacity
 microbiological analysis

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 Microbiology of root surface caries
Approximately 60% of individuals in the aged 60
years or older now have root caries.
This has arisen mainly because of the reduction in
enamel caries and the consequential retention of
teeth later into life, accompanied by gingival
recession.
The soft cemental surfaces thus exposed are highly
susceptible to microbial colonization by virtue of
their irregular and rough surfaces.

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 Con’t
Early studies showed a high prevalence of
Actinomyces naeslundii,
Actinomyces odontolyticus and Rothia
dentocariosa from human root surface caries.
However, more recent data suggest a stronger
association between lactobacilli, mutans
streptococci and root caries.

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 Prevention of dental caries
The major approaches to prevention of caries are:
 sugar substitutes: stopping or reducing between-
meal consumption of carbohydrates, or substituting
noncariogenic artificial sweeteners, e.g. sorbitol,
xylitol or lycasin
 fluorides: making the tooth structure less soluble
to acid attack by using fluorides

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  sealants: to protect susceptible areas of the tooth
(e.g. pits and fissures) that cannot easily be kept
plaque-free by routine oral hygiene measures
 reducing cariogenic flora: so that even in the
presence of sucrose, acid production will be
minimal (e.g. oral hygiene aids, antimicrobial
agents and possibly immunization)

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 Fluoridation
Fluoride can be delivered to the tooth tissue in
many ways. When administered systemically
during childhood, it is incorporated during
amelogenesis
The best delivery vehicle is the domestic water
supply (at a concentration of 1 ppm) tablets,
topical applications of fluoridated gel or
fluoridated toothpaste may be used.

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 Fluoride ions exert their anticariogenic effect by:
1. Substitution of the hydroxyl groups in
hydroxyapatite and formation of fluoroapatite,
which is less soluble in acid during amelogenesis
2. promotion of remineralization of early carious
lesions in enamel and dentine
3. modulation of plaque metabolism

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 Fissure sealants
Sealants prevent caries in pits and fissures by
eliminating stagnation areas and blocking potential
routes of infection.
Early lesions that are well sealed can be effectively
arrested by this technique, whereas more extensive
lesions may extend into pulp, as the trapped
cariogenic bacteria are able to use the carious
dentinal matrix as a source of nutrition.

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 Control of cariogenic plaque flora
Control may be achieved by mechanical cleansing,
antimicrobial therapy, immunization and
replacement therapy.
o Mechanical cleansing techniques
Conventional tooth-brushing with a fluoridated
toothpaste is not very successful in reducing the
caries incidence as it is entirely dependent on the
motivation and skill of the patient.

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 Further, it is unlikely that mechanical cleansing
even with flossing, interdental brushes and wood
sticks will affect pit and fissure caries.

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 o Antimicrobial agents
Chlorhexidine as a 0.2% mouthwash is by far the
most effective antimicrobial in plaque control:
 Chlorhexidine disrupts the cell membrane and the
cell wall permeability of many Gram-positive and
Gramnegative bacteria.

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  It interferes with the adherence of plaque-forming
bacteria, thus reducing the rate of plaque
accumulation.
 Compared with other bacteria involved in plaque
formation, mutans streptococci are exquisitely
sensitive to chlorhexidine and are therefore
preferentially destroyed.

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 Immunization of dental caries
 Active immunization against dental caries
Using either cell wall-associated antigens (antigen
I/II) or glucosyl transferases (extracellular
enzymes) from mutans streptococci is effective in
reducing experimental dental caries in rats and
monkeys.

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  The vaccine may produce its protective effect by:
 inhibition of the microbial colonization of enamel
by secretory immunoglobulin A (IgA)
 interference with bacterial metabolism
 enhancement of phagocytic activity in the gingival
crevice area due to the opsonization of mutans
streptococci with IgA or IgG antibodies.

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