1. MICROBIOLOGY OF DENTAL CARIES
Localized destruction of the tissues of the
tooth by bacterial fermentation of dietary
carbohydrates
A multifactorial, plaque-related chronic
infection of the enamel, cementum or dentine

2. Traces of plaque
and
decaying enamel

3. Enamel
penetrated by bacteria

4. Early enamel
caries seen by polarized light microscopy

5. MICROBIOLOGY OF DENTAL CARIES
Key factors in the development of caries:
Host
Susceptible tooth surface
Saliva
Plaque bacteria
Diet
Fermentable carbohydrates
Flourappatite is much less likely to be degraded

6. Interplay of major etiologic factors in dental caries

8. MICROBIOLOGY OF DENTAL CARIES
Specific plaque hypothesis:
mutans streptococci are important in caries
initiation
Non-specific plaque hypothesis:
Heterogeneous groups of bacteria are involved
in caries initiation

9. MICROBIOLOGY OF DENTAL CARIES
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

10. MICROBIOLOGY OF DENTAL CARIES
Ecological plaque hypothesis:
The balance in the plaque community turns in favor
of mutans streptococci and lactobacilli
There is a dynamic relationship between the bacteria
and the host, and changes in major host factors such
as salivary flow can affect plaque development

11. Ecological plaque hypothesis

12. MICROBIOLOGY OF DENTAL CARIES
Properties of cariogenic flora that correlate with
their pathogenicity:
Ability to rapidly metabolize sugars to acids
(acidogenicity)
Survival and growth under low pH conditions
(aciduricity)
Ability to synthesize extracellular and intracellular
polysaccharides

13. (Glucan) n + n-fructose
glucosyltransferase
n-sucrose
(Glucan) n + n-fructose

14. (Fructan) n + n-glucose
fructosyltransferase
n-sucrose
(Fructan) n + n-glucose

15. “Primary enemy of the teeth” Lennart Nilsson
The Body Victorious
Streptococcus mutans

16. CARIOGENICITY OF STREPTOCCUS MUTANS
Significant correlation between S. mutans counts in
saliva & plaque with the prevalence and incidence
of caries
Prevalence: The number of cases of a disease present
in a specified population at a given time
Incidence: The frequency of occurrence of any
disease over a period of time in relation to the
population in which it occurs
S. mutans can be isolated from precise sites on the
tooth surface before the development of caries

17. CARIOGENICITY OF STREPTOCCUS MUTANS
Correlation between the progression of carious
lesions and S. mutans counts
Produces extracellular polysaccharides from sucrose
which facilitates microbial colonization
Most effective Streptococcus in experimental caries
in animals (rodents & non-human primates)
Ability to initiate and maintain growth and continue
acid production in sites with a low pH

18. Formation of end products of metabolism by
Glucose-6-phosphate Fructose-1,6-diphosphate
Phosphoenolpyruvate Glyceraldehyde
-3-phosphate
Formation of end products of metabolism by
mutans streptococci

19. CARIOGENICITY OF LACTOBACILLUS SPECIES
Present in increased numbers in most carious
cavities affecting enamel & root surfaces
Numbers in saliva correlate with caries activity
Some strains produce caries in gnotobiotic rats
Initiate and maintain growth at low pH (aciduric)

20. CARIOGENICITY OF LACTOBACILLUS SPECIES
Produce lactic acid in conditions below pH 5
(acidogenic)
However:
Affinity for the tooth surface is low
Numbers in dental plaque in early carious lesions
are usually low
Their population size is a poor predictor of the
number of future plaques
Their numbers in saliva increase only after
caries develop

21. CARIOGENICITY OF LACTOBACILLUS SPECIES
Present consensus:
Lactobacilli are not involved in the initiation of
dental caries
They are involved in the progression of the
lesion deep into enamel and dentine
They are pioneer organisms in the advancing
carious process

22. Low pH causes demineralization by reducing
the concentration of the tribasic phosphate (PO43-)
which is needed to form hydroxyapatite
10Ca2+ + 6PO H2O ---> 2H+ + Ca10 (PO4)6(OH)2
hydroxyapatite

23. Low pH tends to reduce the concentration of
DEMINERALIZATION
Low pH tends to reduce the concentration of
tribasic phosphate by adding H+ to phosphate
6PO43- + H > 6HPO42- + H > 6H2PO41-
pK= pK= 4.0

24. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
• Sugar substitutes
• Fluoridation (to increase enamel hardness)
• Fissure sealants
• Control of cariogenic flora
Antimicrobials
Passive immunization?
Replacement therapy?
Vaccines??

25. Fluoride ions
Substitute for the hydroxyl groups in hydroxyapatite (Fluoroapatite less soluble in acid)
Promote remineralization of early carious lesions

26. Interfere with bacterial membrane ion permeability
Fluoride ions
Interfere with bacterial membrane ion permeability
Reduce glycolysis
(inhibition of enolase: phosphoglycerate -> phosphoenolpyruvate)
Inactivate key metabolic enzymes by acidifying bacterial cell interior
Inhibit synthesis of polysaccharides

27. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
Passive immunization
Antibodies against antigen I/II of mutans streptococci inhibit recolonization after chlorhexidine treatment
Monoclonal antibodies produced in transgenic plants prevented recolonization for 4 months

28. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
Sugar substitutes
Xylitol inhibits sugar metabolism of mutans streptococci as well as glycolysis
pH is maintained at 7, vs reduction to 5 by sucrose

29. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
Replacement therapy
Low virulence mutants of mutans streptococci deficient in GTF or lactate dehydrogenase activity
More competitive S. salivarius that can displace S. mutans

30. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
Antimicrobials
Chlorhexidine
Inhibits sugar transport in streptococci
Inhibits amino acid uptake and catabolism in S. sanguis
Inhibits a protease of P. gingivalis
Affects membrane functions, such as ATP synthase and maintenance of ion gradients in streptococci
Know the general mechanism for this.

31. MICROBIOLOGY OF DENTAL CARIES
Strategies to control or prevent caries:
Antimicrobials
Triclosan
Inhibits acid production by streptococci
Inhibits a protease of P. gingivalis
Enhanced by co-polymer or zinc citrate
“Substantive” : binds effectively to oral surfaces, like chlorhexidine

32. MICROBIOLOGY OF DENTAL CARIES
Microbiological tests:
To identify caries risk factors in patients with
extensive or recurrent caries, prior to delivering
dental care (e.g. extensive crown and bridge
treatment)
High salivary counts of mutans streptococci
(> 106/mL) and lactobacilli (> 104/mL) indicate
high risk of disease

33. Culture slide test to detect mutans streptococci in saliva