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MICROBIOLOGY OF
DENTAL CARIES
INTRODUCTION
 INFECTION:
 DISEASE:
 ASYMPTOMATIC
 COLONIZAION:
CARRIAGE:
( NORMAL FLORA)
BACETRAIL PATHOGENESIS
 What
is virulence?
The ability of a bacterium to cause infection.
 Virulence
factors: Two types:
 Those that promote bacterial colonization and invasion
of the host tissue
 Those that cause damage of the host tissue.
Research in the past four decades have accumulated
information which led to identification of possible
pathogens of human dental caries.
Q. How a cause and effect relationship is established
between bacterium and the disease?
A. Koch’s Postulate (1800s).
KOCH’S POSTULATES
 The
bacterium should be found in people with the
disease
 The bacterium should be isolated from the lesions
of infected person
 Pure culture, inoculated into a susceptible
individuals or animals should produce the disease
 Same bacterium should be re-isolated from
intentionally infected animals or humans.
LIMITATIONS OF KOCH’S
POSTULATES
Virulence is within the bacterium and is independent of
the host
 Isolation and growth of bacterium is necessary: Yet, some
pathogens not yet cultured
 Nos. 2 & 4: assume that all members of the same species
are virulent
 No. 3: Ethics with human subjects, Yet some pathogens
from humans can not cause the same effect in animals.

WHAT IS THE ALTERNATIVE?
MOLECULAR POSTULTES
1. Gene should be found in the bacterial strain.
2. Disturbing the virulent gene should reduce its virulence.
3. Bacterial virulent gene should be expressed in the
animal or human at sometime during the infectious
process
4. Abs to gene product should be protective or should elicit
protective immunity (cell-mediated).
Q. Why Did it Take Long Time for
Caries Microbiology?
 Complex
ecology of the oral cavity.
– 400 species are indigenous oral flora.
 History:
 300
 Miller (1880): Little knowledge about which bacteria.
 Clarke (1924): First who associate bacteria with dental caries
First to isolate MS from human dental caries
o First to produce caries in extracted teeth.
o
 Orland (1955): Used animals to induce dental caries using
MS.
DENTAL CARIES
MICROBIOLOGY RESEARCH
 1960s
: germ-free animals
 1960s and 70s: importance of glucan (glucanase):
 Clinical
trials using glucan hydrolyase rinses
 Glucan is plaque enhancer
 Problem with isolation: Number, media ….etc.
 Specific plaque theory
 MS
identified as an associated bacteria with caries.
MUTANS STRPETOCOCCI (MS)

TYPES: (Coykendall, 1989)
S. anginosus : important in purulent infections
 S. bovis : found in patients with colon cancer
 S. mitis : similar to sanguis but doesn’t ferment any sugar
 S. mutans : seven species
 S. salivarius : in saliva, rare in infections
 S. sanguis : causes endocarditis
 S. vestbularis : new species from oral cavity.

STREPTOCOCCUS MUTANS
Species
S mutans
Serotype
c, e, f
S rattus
S cricetus
S sobrinus
S ferus
S macacae
S downei
b
a
d, g
c
c
h
Arg Raf
Mel H2O2 Aero
Baci
Source
-
+
+
-
+
-
Human
+
-
+
+
+
-
+
+
-
+
-
+
+
-
+
+
+
+
Rats
Rats
Human
Rats
Monkey
Monkey
SUMMARY
WHY S. mutans SUCCEED?
 Three
factors:
 Ability to adhere to other bacteria and tooth surface
 Ability to rapidly metabolize nutrients (CHO)
 Ability to tolerate acidic environment.
ADHERENCE OF S. mutans
 Saliva:
 Lysozyme
 IgA: (IgA protease), (IgA deficiency)
 Bacterial




proteins:
Ag I/II family: Adhere to saliva proteins
Adhesin
Fimbrial adhesion: Adhere to saliva pellicle
glucan binding (GBP)
CHO METABOLISM BY S.mutans
 CHO
must be transported across the membrane
(Sugars must be phosphorylated):
 Multiple
Sugar Metabolism (MSM) System:
 Transport
 Sugar
via the Phosphoenolpyruvate (PEP):
Phosphotransferase System (PTS):
CHO Metabolism
PEP + CHO
 S.mutans
PTS
Pyruvate +P-CHO
enolase: Fluoride inhibits it.
 S.mutans store polysaccharides .. Why?
S. mutans ACID TOLERANCE
 Through
cell membrane, extrusion of protons:
 Membrane ATPase hydrolyze ATP molecules
 Hydrolysis of one ATP, results in extrusion of three
protons
 This results in elevation of cytoplasmic pH.
 When pH decreases, ATPase activity increases 4-folds.
COLONIZATION OF S. mutans
 Based
on ability of S. mutans to synthesize
insoluble glucan.
 S. mutans have 3 genes:
 gtfB encodes GTF-I enzyme: insoluble glucan
 gtfC encodes GTF-SI enzyme: insoluble glucan
 gtfD encodes GTF-S enzyme: soluble glucan
RESEARCH USING GTFs
 Purified
S.mutans GTFs were used for caries
immunization in rodents.
(Smith et al., 1979).
 Implantation of S. mutans defective in IS glucan
synthesis into rats resulted in reduced smooth
surface caries induction.
(Munro et al., 1991).
Strain
Gtase
Adherence%
MT8148
I,SI/S
72.8  2.6
B29
/SI/S
16.3  1.0
B29
I/SI/S
46.9  5.9
B58
I/ /S
9.6  1.0
B58
I/SI/S
69.9  1.8
B32
/ /S
1.4  0.4
(Fujiwara et al., 1996)
SUMMARY
ACQUISITION OF S. mutans
 Sterile
 S.
mouth at birth
sanguis and S. mutans colonize teeth
 Number of
 Sucrose
 Caries
 Teeth
bacteria increases in the presence of:
ACQUISITION OF S. mutans
MS
26
Birth
5 Year
First Tooth
6.8 +/- 1.4 mo.
19
33
N=38
Caufield et al., J Dent Res. 72:37-45, 1993.
ACQUISITION OF S. mutans
 Important
facts:
 Difficult to change S. mutans strain(s)
 High number of S.mutans strains and isolates.
 One (or more) strain (isolates) is/are present in the
mouth.
GENETIC VARIATIONS
OF S.mutans
TRANSMISSION OF
CARIOGENIC FLORA
 Mothers
to children:
 DNA technique
 Method of transmission
 Spouses:
 Different bacteria studied
 Replacement Therapy
IF WE UNDERSTAND THE DENTAL CARIES
MICROBIOLOGY WELL..
WE WILL TREAT PATIENTS
DIFFERENTLY !!!!
HOW?????????????????????????????