Immunology of dental caries

1. IMMUNOLOGY OF DENTAL CARIES
DR. CHARANJEET SINGH
ASSOCIATE PROFESSOR
DEPT. OF PEDODONTICS AND PREVENTIVE DENTISTRY
RAMA DENTAL COLLEGE AND HOSPITAL
RAMA UNIVERSITY

2. Contents
• Introduction
• Dental caries- a biofilm-induced disease
• Acquisition and development of the oral flora in humans
• Plaque hypothesises
• Normal oral flora
• Organisms cariogenic in humans: accepted odontopathic bacteria
• The virulence factors of cariogenic bacteria
• Microbial nutrients in the oral cavity
• Microbial competition for nutrients
• Microbiology of caries
• Enamel
• Dentin
• Root
• Caries vaccine
• Conclusion

3. INTRODUCTION
• In utero the human fetal oral cavity is sterile, but the
colonization of bacteria begins at birth.
• Streptococcus salivarius is the first dominant colonizer and may
make up 98% of the total oral flora.
• S. mutans as well as other bacteria that compose the normal oral
flora provide valuable services to the human host.
• The oral flora contributes to host nutrition through the synthesis
of vitamins, and they contribute to immunity by inducing low
levels of circulating and secretory antibodies that have the
potential to react with other pathogens.
• In addition, the oral flora exerts microbial antagonism against
foreign species through the production of inhibitory substances.

4. DENTAL CARIES- A BIOFILM-INDUCED
DISEASE
• The resident flora in the oral cavity will inevitably form biofilms
on teeth.
• A biofilm may be defined as a population or community of
bacteria living in organized structures at an interface between a
solid and liquid.
• The oral cavity generally presents two types of surfaces for
colonization by bacteria:
o Soft tissues
o hard tooth enamel and exposed root surfaces.

5. ACQUISITION AND DEVELOPMENT OF THE
ORAL FLORA IN HUMANS
• Bacteria begin to colonize an infant’s oral cavity during birth
and succession of bacteria in the mouth continues throughout
life.
• Tooth eruption has a major impact on the composition of the
oral flora.
• Cauualho et. al in 1989 reported that the teeth most prone to
caries are those that have recently erupted and are those which
do not get in occlusion.
• S.R.Brailsford conducted a study in 2005 on the microflora of
the erupting 1st permanent molar. (Caries Res. 2005;39:78-84)

6. Conclusion:
• Fully erupted teeth yielded greater number of mutans
streptococcci as compared to greater number of Actinomyces
israelii in partially erupted.
• In partially erupted teeth significant association was seen
between white spot lesions and increased number of
Streptococci salivarius. The presence of Actinomyces
naesulundii was associated with health.
• Streptococci mutans was isolated in significantly greater
numbers and proportions from fully erupted molars with white
spots.

7. Caufield P.W et. al (J Dent Res 1993; 72(6): 37-45 )
• Studied the initial acquisition
of mutans streptococci by
infants from their mothers
(vertical transmission)
• They concluded that the most
critical time for the initial
aquisition of mutans
streptococci in children is
between the age of 19 and 31
months. This period is
designated as ‘the window of
infectivity’

8. PLAQUE HYPOTHESISES
• Specific plaque hypothesis:
Mutans streptococci are important in caries initiation
• Non-specific plaque hypothesis:
Heterogeneous groups of bacteria are involved in caries initiation
• Ecological plaque hypothesis:
Cariogenic flora found in natural plaque are weakly competitive and
comprise only a minority of the total community.
Increase in fermentable carbohydrates results in prolonged low pH,
promoting the growth of acid-tolerant bacteria and initiating
demineralization.

9. NORMAL ORAL FLORA
 BACTERIA
 VIRUS
 FUNGI
 PROTOZOA
 MYCOPLASMA
9
Natural microflora exists in harmonious relationship with
the host

10. BACTERIA
Gram positive
cocci
Gram positive
Rods and
filaments
Gram negative
cocci
Gram negative
rods
1. Streptococcus
2. Enterococcus
1. Actinomyces
2. Eubacterium
3. Lactobacillus etc.
1. Neisseria
2. Veillonella
1. Haemophilus
2. Actinobacillus
3. Porphyromonas
etc.
10

11. ORGANISMS CARIOGENIC IN HUMANS: ACCEPTED
ODONTOPATHIC BACTERIA
Mutans streptococci
• Streptococcus mutans
• Streptococcus sobrinus
Lactobacilli
• Lactobacillus casei
• Lactobacillus fermentum
• Lactobacillus plantarum
• Lactobacillus acidophilus
Other Possible odontopathic bacteria
• Streptococcus mitis
• Actinomyces viscosus serovar 2

12. THE VIRULENCE FACTORS OF CARIOGENIC BACTERIA
1. Acid production (Acidogenicity)
• Lower the pH to below 5.5(Critical pH); which results in dissolution of calcium
phosphate (hydroxyapatite) of the tooth enamel.
• Inhibit the growth of beneficial bacteria, promote the growth of aciduric bacteria.
• Further lower the pH to promote progression of the carious lesion.
2. Acid tolerance (Aciduricity)
• Allows the cariogenic bacteria to thrive under acidic,conditions while other beneficial
bacteria are inhibited. This results in dominance of the plaque by cariogenic bacteria.
3. Glucan formation
• Glucan mediated biofilms are more resistant to mechanical removal.
• Bacteria in these biofilms are more resistant to antimicrobial treatments
• Allows the cariogenic bacteria to stick onto the teeth and form a biofilm

13. MICROBIAL NUTRIENTS IN THE ORAL CAVITY
• Bacteria in the oral cavity reside in a ‘feast’ or ‘famine’
environment. Saliva is the main basic source of
nutrition for the oral bacteria; however, the
concentration of readily available nutrients in salivary
secretions is very low.
• The consumption of food results in a transitory burst of
nutrients to the oral microflora. Sudden exposure of
oral bacteria to the high nutrient levels in food can
cause cell death.
• Dietary sugar is the most obvious threat since there
may be a 10000-fold increase in sugar concentration
upon food in take.

14. MICROBIAL
COMPETITION FOR
NUTRIENTS
• Those populations best
adapted to compete for the
low levels of nutrients
available in the oral cavity
will be the most successful.
• Growth rate of the micro-
organisms increase with
increase in the concentration
of growth-limiting nutrient as
defined by the saturation
constant (Ks).

15. Pit and fissure caries-
• They are the most common carious
lesions found in humans.
• Fissures provide mechanical
retention for the bacteria.
• S. Mutans, S. Salivarius, S.
Sanguis, L. Acidophilus, L. Casei,
Actinomyces Israelii etc. are most
significant in developing fissure
lesions.
Smooth surface caries-
• Only a limited number of
microorganisms are able to
colonize smooth surfaces in large
enough numbers to be able to cause
decay.
• Streptococcus mutans is very
significant in this respect.
MICROBIOLOGY OF ENAMEL CARIES

16. DENTINAL CARIES
• Because the environment in deep dentinal lesions is different from
that at other locations the flora here is also different
• The predominant microbe- lactobacillus
• pH of carious dentin can be low and the members of the dentin
bacterial community tend to be more aciduric than those of
supragingival plaque.

17. ROOT CARIES
In cross-sectional studies of plaque overlying carious root surfaces, S.
Mutans alone or in combination with Lactobacilli, have been isolated
most frequently. (Billings et al., 1985; Brown et al., 1986; Fure et al.,
1987; Keltjens et al., 1987; Bowden et al., 1990; van Houte et al., 1990)
• Root surfaces are thought to be more vulnerable to caries as
compared to enamel surfaces.
• Critical pH for root surface caries is lower than 6.7. Amdal Scheie
et. al (J. Dent. Res 1996:75:1901-1908)

19. Vaccines
• A vaccine is “ An immuno-biological substance designed
to produce specific protection against a given disease.”
• Stimulates the production of a protective antibody and
other immune mechanisms.
• Prepared from live modified organisms, inactivated or
killed organisms, extracted cellular fractions, toxoids, or a
combination.

20. Active immunity Passive immunity
Produced actively by the immune
system.
Induced by infections or contact
with immunogenes.
Long lasting and effective
protection.
Immunity is effective only after a
lag period.
Immunological memory present,
therefore subsequent challenge is
more effective.
Received passively by the host,
hosts immune system does not
participate.
Conferred by administration of
readymade antibodies.
Protection short lived and less
effective
No immunological memory.
Subsequent administration of
antibody is less effective due to
immune elimination.

21. Some of the possible ways antibodies might control
bacterial growth are listed below:
The salivary immunoglobulin ---- act as a specific agglutinin
interacting with the bacterial surface receptors ---- inhibits
colonization and subsequent caries formation
The salivary glands produce secretory IgA antibodies--- may
prevent S. mutans from adhering to the enamel surface or
they may prevent formation of dextran by inhibiting the
activity of glucosyltransferase (GTF).
The gingival crevicular mechanism involves all the humoral
and cellular components of the systemic immune system,
which may exert its function at the tooth surface.

22. Routes of Immunization
• Common mucosal immune system
• Oral route
• Intranasal route
• Tonsillar route
• Minor salivary gland
• Rectal
• Systemic (subcutaneous)
• Active gingivo-salivary
• Passive dental immunization

23. Risks of Using Caries Vaccine
• Most serious is that sera of some patients with rheumatic fever who show
serological cross-reactivity between heart tissue antigens and certain antigens from
hemolytic Streptococci.
• Because of the potential of Streptococcal whole cells to induce heart reactive
antibodies, the development of a sub-unit vaccine for controlling dental caries has
been the focus of intense research interest.

24. Conclusion
• Despite increase aids in management of dental caries many of the
population is under the risk of extensive tooth decay.
• Although several methods such as topical or systemic use of fluorides,
fissure sealants, and dietary control have been developed to prevent
dental caries, the efficacy of these methods is not enough to eradicate
dental caries in humans
• Caries vaccine has the potential of making a highly valuable
contribution to control the disease