marka

1. Microbiology of dental
caries
Oday altaani

2.  Definition: chronic endogenous infection caused by
the normal oral commensal flora.
 the initial process of enamel demineralization is
usually followed by remineralization
 Caries is defined as localized destruction of the tissues
of the tooth by bacterial fermentation of dietary
carbohydrates.

3. Epidemiology
Dental caries (with periodontal disease) is one
of the most common human diseases
Caries of enamel surfaces is particularly
common up to the age of 20 years, after which
it tends to stabilize.
in later life, root surface caries becomes
increasingly prevalent, due to gingival
recession

4. Classification

5. Classification
Dental caries can be classified with respect to the
site of the lesion:
i. pit or fissure caries (seen in molars, premolars
and the lingual surface of maxillary incisors)
ii. smooth-surface caries (seen mainly on
approximal tooth surfaces just below the
contact point)
iii. root surface caries (seen on cementum or
dentine when the root is exposed to the oral
environment)
iv. recurrent caries (associated with an existing
restoration).

6. Clinical presentation

7. Clinical presentation
The primary lesion of caries is a well-demarcated,
chalky white lesion in which the surface
continuity of enamel has not been breached. This
‘white-spot’ lesion can heal or remineralize
(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

8. Diagnosis
Diagnosis is usually by a combination of:
i. Direct observation.
ii. Probing.
iii. Radiographs.
iv. Experimental methods. laser fluorescence for
diagnosis of buccal and lingual caries and electrical
impedance (resistance) to detect occlusal caries.
v. Microbiological tests

9. Aetiology

10. Aetiology
The major factors involved in the aetiology of
caries are:
i. host factors (tooth, saliva)
ii. diet (mainly the intake of fermentable
carbohydrates)
iii. plaque microorganisms (i.e. supragingival plaque).

11. Host factors
Tooth structure
some areas of the same tooth are much more
susceptible to carious attack than others,
possibly because of differences in mineral
content (especially fluoride).

12. Host factors
Flow rate and composition of saliva
The mechanical washing action of saliva.
high buffering capacity.
it is supersaturated with calcium and
phosphorus ions.
Delivery vehicle for fluoride.

13. Diet
direct relationship.
The most cariogenic sugar is sucrose
Sucrose is highly soluble and diffuses easily into
dental plaque, producing extracellular
polysaccharides and acids.
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.

14. Diet
The frequency of sugar intake rather than the
total amount of sugar consumed appears to
be of decisive importance.
Stickiness and concentration.
Period
…Polyol carbohydrates, ‘sugar alcohols’ (e.g.
xylitol)

15. Microbiology
Microorganisms in the form of dental plaque
are a prerequisite for the development of
dental caries.
mutans streptococci have been recognized as
the major group of organisms involved in
caries.

16. Microbiology
Specific plaque hypothesis one or more
specific groups of bacteria are principally
involved in caries.
Nonspecific plaque hypothesis the disease is
caused by a heterogeneous mixture of non-
specific bacteria.
…Lactobacillus spp. and Actinomyces spp.

17. The role of mutans streptococci
Streptococcus mutans’ is a loosely applied group
name for a collection of seven different species
(S.mutans, S. sobrinus, S. criceti, S. ferus, S. ratti,
S. macacae and S. downei) and eight serotypes
(a–h).
S. mutans serotypes c, e, f and S. sobrinus
serotypes d, g are the species most commonly
found in humans, with serotype C strains being
the most prevalent, followed by d and e.

18. 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.
 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.

19. The role of mutans streptococci
 ability to initiate and maintain microbial growth and to
continue acid production at low pH values.
 rapid metabolism of sugars to lactic and other organic
acids.
 ability to attain the critical pH for enamel
demineralization more rapidly than other common
plaque bacteria.
 ability to produce intracellular polysaccharides (IPSs) as
glycogen, which may act as a food store for use when
dietary carbohydrates are low.
 immunization of animals with specific S. mutans
serotypes significantly reduces the incidence of caries.

20. The role of mutans streptococci
Note: Caries may therefore be an infectious disease
in a minority, with a highly pathogenic strain being
transmitted from one individual to another.

21. The role of lactobacilli
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.
their ability to grow in low-pH environments
(below pH 5) and to produce lactic acid.
their ability to synthesize both extracellular and
IPSs from sucrose.

22. The role of lactobacilli
lactobacilli are rarely isolated from plaque before
the development of caries, and they are often
absent from incipient lesions.
it is believed that:
• they are involved more in the progression of the
deep enamel lesion (rather than the initiation)
• they are the pioneer organisms in the advancing
front of the carious process, especially in dentine.

23. The role of Actinomyces spp.
Actinomyces spp. are associated with the
development of root surface caries (softened
without obvious cavitation).
Actinomyces spp. (especially A. viscosus)
predominate in the majority of plaque
samples taken from root surface lesions

24. The role of Veillonella
Veillonella is a Gram-negative anaerobic
coccus that is present in significant numbers in
most supragingival plaque samples.
require lactate for growth.
Unable to metabolize normal dietary
carbohydrates.
Beneficial effect on dental caries.

25. Plaque metabolism and dental caries
The main source of nutrition for oral bacteria
is saliva.
 Oral bacteria have developed a number of regulatory
mechanisms, which act at three levels:
i. transport of sugar into the organisms.
ii. the glycolytic pathway.
iii. conversion of pyruvate into metabolic end
products.

26. Plaque metabolism and dental caries
dietary sucrose is broken down by bacterial
extracellular enzymes such as glucosyl and
fructosyl transferases, with the release of glucose
and fructose.
Glucans are mostly used as a major bacterial food
source.
the insoluble fructans contribute to the plaque
matrix while facilitating the adhesion and
aggregation of plaque bacteria and serving as a
ready, extracellular food source.

27. Plaque metabolism and dental caries
During glycolysis, glucose is degraded
immediately by bacteria via the Embden–
Meyerhof pathway, with the production of
two pyruvate molecules:
Under low sugar conditions, pyruvate is
converted into ethanol, acetate and formate
(mainly by mutans streptococci).
In sugar excess, pyruvate is converted into
lactate molecules.

28. Plaque metabolism and dental caries
The mutans group streptococci, being the
most acidogenic and aciduric (acid-tolerant),
are the worst offenders and reduce the plaque
pH to low levels, creating hostile conditions
for other plaque bacteria.

29. Ecological plaque hypothesis

30. Management of dental caries
The modern philosophy in caries management
highlights:
i. early detection.
ii. the importance of accurate diagnosis.
iii. minimal cavity preparation techniques.
iv. active prevention.

31. Patient evaluation
 In patients with a low incidence of caries, a case history
and clinical and radiographic examination are probably
adequate for treatment planning.
 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.

32. Microbiological tests in caries
assessment
Saliva samples can be used to establish the
numbers of S.mutans and Lactobacillus spp. in
the oral cavity, as follows:
i. A paraffin wax-stimulated sample of mixed
saliva is collected.
ii. In the laboratory, the saliva is appropriately
diluted and cultured on selective media.
mitis salivarius bacitracin agar for S. Mutans.
Rogosa SL agar for Lactobacillus spp.

33. high caries activity: >106/ml S. mutans and/or
>100 000/ml Lactobacillus spp.
low caries activity: <100 000/ml S. mutans
and <10 000/ml Lactobacillus spp.

34. Microbiological tests in caries
assessment
 The disease of multifactorial aetiology. Other factors,
such as diet, buffering capacity, fluoride content of
enamel and degree of oral hygiene, should also be
considered.
 The main uses of microbiology tests in caries
assessment are:
 to identify patients who have unusually high numbers
of potential pathogens.
 to monitor the efficacy of caries prevention techniques,
such as dietary and oral hygiene advice and the use of
antimicrobial agents such as chlorhexidine.

35. Microbiology of root surface caries
 The soft cemental surfaces thus exposed are highly
susceptible to microbial colonization by virtue of their
irregular and rough surfaces.
 high prevalence of Actinomyces naeslundii,
Actinomyces odontolyticus and Rothia dentocariosa
from human root surface caries.
 Lactobacilli, S. mutans together with pleomorphic
Gram-positive rods, are also frequent in the deeper
dentinal parts of the lesion.
…polymicrobial aetiology for caries initiation and
progression on root surfaces.

36. Prevention of dental caries
The major approaches to prevention of caries
are:
i. sugar substitutes.
ii. Fluorides.
iii. Sealants.
iv. reducing cariogenic flora.
v. Probiotics: replacement of cariogenic bacteria
by organisms with low or no cariogenic
potential.

37. Sugar substitutes
Artificial sweeteners cannot be absorbed and
metabolized to produce acids by the vast majority
of plaque bacteria.
Two types of sugar substitute are available:
I. nutritive sweeteners with a calorific value, e.g.
the sugar alcohols, sorbitol and xylitol, and
lycasin.
II. non-nutritive sweeteners, e.g. saccharin and
aspartame.

38. Fluoridation
Can 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.

39. Fluoridation
 Fluoride ions exert their anticariogenic effect by:
I. substitution of the hydroxyl groups in hydroxyapatite and
formation of fluoroapatite, which is less soluble in acid during
amelogenesis.
II. promotion of remineralization of early carious lesions in enamel
and dentine.
III. modulation of plaque metabolism by:
 interference with bacterial membrane permeability.
 reduced glycolysis.
 inactivation of key metabolic enzymes by acidifying the cell interior.
 inhibition of the synthesis of IPSs, especially glycogen.

40. Fissure sealants
Sealants prevent caries in pits and fissures by
eliminating stagnation areas and blocking
potential routes of infection.
Early lesions.

41. Control of cariogenic plaque flora
Control may be achieved by mechanical
cleansing, antimicrobial therapy,
immunization and replacement therapy.
Mechanical cleansing techniques…
it is unlikely that mechanical cleansing even
with flossing, interdental brushes and wood
sticks will affect pit and fissure caries.

42. Control of cariogenic plaque flora
 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 Gram negative
bacteria.
 It is able to bind tenaciously to oral surfaces and is slowly
released into the saliva.
 It interferes with the adherence of plaque-forming
bacteria, thus reducing the rate of plaque accumulation.
 mutans streptococci are exquisitely sensitive to
chlorhexidine and are therefore preferentially destroyed.
 tooth staining and unpleasant taste…short-term therapy.

43. Active immunization against dental caries
cell wall-associated antigens (antigen I/II) or
glucosyl transferases (extracellular enzymes) from
mutans streptococci.
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.

44. The antibodies that develop after
immunization with most antigens of S. mutans
tend to cross-react with heart tissue, and the
possibility that heart damage could result has
made human vaccine trials very difficult.

45. Passive immunization
 when the natural levels of oral mutans streptococci
are suppressed by chlorhexidine, topical application
of monoclonal antibodies against antigen I/II of
mutans streptococci prevents recolonization by the
organisms.
 Transgenic plants could be used to produce dimeric
antibodies with specificity to antigen I/II of
streptococci that are stable in the mouth and persist
for longer periods.

46. Replacement therapy
 The term probiotic therapy or probiotics is now used
for approaches where the offending pathogen is
replaced artificially by innocuous commensals that are
allowed to obtain a permanent foothold in the locale.
 genetically engineered, low-virulence mutants of
mutans streptococci that are deficient in glucosyl
transferase or deficient in lactate dehydrogenase
activity can be ‘seeded’ into the oral environment.
…These organisms can replace their more virulent
counterparts and prevent their re-emergence.