2. DENTAL CARIES
--Progressive bacterial damage to
teeth exposed to saliva.
--one of the most major causes of
all diseases and major cause of
tooth loss.
--ultimate effect-to breakdown
enamel and dentin and open a
path for bacteria to reach pulp.
Consequences-inflammation of
pulp and periapical tissues.
3. AETIOLOGY
• Four major factors involved in etiology:-
• Cariogenic bacteria
• Bacterial plaque
• Susceptible tooth surface
• Fermentable bacterial substrate (sugar)
4.
5. Bacteriology of Dental
Caries
• Major organisms
responsible for
caries are:-
• Strep mutans
• Lactobacilli
• Other strains of
streptocooci
•
6. Cariogenic prop of strep
mutans
• Produces lactic acid from sucrose
• Can live at ph as low as 4.2
• Forms large amounts of
extracellular,sticky,insoluble glucan
plaque matrix.
• Adheres to pellicle and contributes
to plaque formation.
7. BACTERIAL PLAQUE
• Adherent deposit on the teeth.
• BIOFILM-consists of viscous
phase formed from bacteria and
extracellular polysaccharide
matrices.
• In stagnation areas,plaque
bacteria can form acid from
sugars over long periods to
attcack tooth surfaces.
• Production of high acid
concentration contributes to low
ph.
8. SUCROSE
• Colonisation by cariogenic bacteria is highly
dependant on sucrose content of diet.
• In absence of sucrose-S mutans cannot be made
to colonise the mouth.
• Severe reduction in dietary sucrose-causes S
mutans to decline in number or disappear from
the plaque.
• Frequent feeds of small quantities are more
cariogenic.
9. CARIES SPREAD TO
ENAMEL
• Acids formed by bacterial fermentation from
dietary sugars leads to a pH fall in the plaque
which dissolve tooth enamel, initiating the
development of carious lesions.
• The progression of demineralization in enamel
continues to the point where dissolution of
hydroxyapatite exeeds remineralization.
• Bacteria cant invade enamel until
demineralization provides them pathways
to enter.
10. CARIES SPREAD TO
DENTIN
• Non bacterial pre-
cavitation,acid softening
of the matrix.
• Migration of bacteria
along the tubules.
• Distortion of tubules
• Breakdown of intervening
matrix forming
liquefaction foci.
• Progressive disintegration
of remaining matrix
11. PULPAL RESPONSE
• Pulpal tissue subjacent to deep caries
lesions often shows the presence of
chronic inflammation, including
lymphocytes, macrophages and plasma
cells.
• Formation of tertiary dentin is
usually visible on the pulpal aspect
and the increase in dentin thickness.
12.
13. CLINICAL
Symptoms and Signs
Caries initially involves only the
enamel and produces no
symptoms. A cavity that invades
the dentin causes pain, first when
hot, cold, or sweet foods or
beverages contact the involved
tooth, and later with chewing or
percussion. Pain can be intense
and persistent when the pulp is
severely involved
14. CLINICAL
• Direct inspection
• Sometimes use of x-rays or special testing instruments
• Routine, frequent (q 6 to 12 mo) clinical evaluation identifies
early caries at a time when minimal intervention prevents its
progression. A thin probe, sometimes special dyes, and
transillumination by fiberoptic lights are used, frequently
supplemented by new devices that detect caries by changes
in electrical conductivity or laser reflectivity. However, x-
rays are still important for detecting caries, determining
the depth of involvement, and identifying caries under
existing restorations
SIGNIFICANSE
16. Consequences of Dental Caries
•Possible facial cellulitis
requiring hospitalization
•Impaired language
development
•Reduced self-esteem
•Possible systemic illness for
children with special health
care needs
19. Spread from maxillary
teeth
• may cause purulent sinusitis,
• meningitis,
• brain abscess,
• orbital cellulitis,
• and cavernous sinus thrombosis.
20. Spread from mandibular teeth
may cause
• Spread from mandibular teeth may
cause
• Ludwig's angina,
• parapharyngeal abscess,
• mediastinitis, pericarditis,
• empyema, and jugular
thrombophlebitis.
