hello Khubaib Ahmed Shaikh is back # and this time presenting topic of Enamel Caries i am student of bachelors of dental surgery 3rd prof year.

1. ENAMEL CARIES
Khubaib Ahmed Shaikh
3rd Year BDS Student
CEO: Young Social Reformers.

2. DEFINATION.
• A bacterial disease of the calcified tissue
of the teeth characterized by
demineralization of the inorganic and
destruction of the organic substance of
the tooth.
• Physiochemical as well as biological process
because of interface between tooth and
external environment and interaction of
bacteria and tooth surface respectively.

3. DENTAL CARIES
--Progressive bacterial damage to
teeth.
--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.

4. AETIOLOGY
• Four major factors involved in etiology:-
• Bacterial plaque.
• Susceptible tooth surface.
• Fermentable bacterial substrate (sugar).
• Time.

5. CARRIES
FERMENTABLE
SUGAR
TIME
SUCEPTIBLE
TOOTH
SURFACE
BACTERIA
Diagrammatic
representation
of the
parameters
involved in the
aetiology of
dental caries.

6. Bacteriology of Dental
Caries
Major organisms
responsible for caries
are:-
• Streptococcus mutans.
• Lactobacilli.
• Other strains of
streptococci.

7. Species strongly associated with carries
• Mutans Streptococci specially S.Mutans.
• Lactobacilli.
Species that may be associated
• Non mutans streptococci, e.g. mitis group
• Actinomycetes

8. Enamel Caries
• Early lesion (white spot lesion) in smooth
surface enamel carries is cone shaped, with
the base of the cone on the enamel surface
and the apex pointing towards the
amelodentinal junction.

9. Ionic Exchange In
Enamel Caries.
• Ions see-saw across the plaque-enamel
interface depending on pH.
• Ions in plaque can be rediposited into the
enamel at a neutral pH or lost into the
saliva.
• Enamel carries progresses when the net
rate of loss of ions due to acid attack is
greater than the net rate of gain due to
remineralization.
•

10. Ionic Exchange In
Enamel Caries.
• Fluoride ions encourage
reprecipitation of minerals into
enamel.
• Fluoride ions can replace hydroxyl
ions in hydroxyapatite to form less
acid soluble fluorapatite.

11. • It consists of series of zones, the optical
properties of which reflect differing
degrees of demineralization.
1. Translucent zone
2. Dark zone
3. Body of the lesion
4. Surface zone

13. Translucent Zone
• This is first recognizable histological
change at the advancing edge of the
lesion.
• It is more porous than normal enamel and
contains 1% by volume of spaces, the pore
volume, compared with the 0.1% pore
volume in normal enamel.
• Decrease in magnesium and carbonate
when compared with the normal enamel.

14. • Dissolution of minerals occur mainly from
the junctional areas between the prismatic
and interprismatic enamel.
• The translucent zone is sometimes missing.

15. Dark Zone
• This zone contains 2-4% by volume of
pores. Some of the pores are large, but
others are smaller than those in the
translucent zone, suggesting that some
remineralization has occurred due to
reprecipitation of mineral lost from the
translucent zone.

16. • It is thought that the dark zone is
narrow in rapidly advancing lesions and
wider in more slowly advancing lesions
when more remineralization may occur.
• Also called possitive or true zone as its
always present.

17. Body Of The Lesion
• This zone has a pore volume of between 5%
and 25%, and also contains apatite crystals
larger than those found in normal enamel.
• The lost mineral is replaced by unbound
water and to a lesser extent by organic
matter, presumably derived from saliva and
microorganisms.
• There is increased prominence of the striae
of the retzius in the body of the lesion.

18. • Form the bulk of the lesion.
• Area of greatest demineralization.

19. Surface Zone.
• This is about 40 micro meter thick and
shows surprisingly little change in early
lesions. The surface of normal enamel
differs in composition from the deeper
layers, being more highly mineralized and
having, for example, a higher fluoride level
and lower magnesium level, and so
understanding of possible chemical changes
in this zone is difficult.

20. • The surface zone remains relatively normal
despite subsurface loss of mineral,
because it is an area of active
reprecipitation of mineral derived both
from the plaque and from that dissolved
from deeper areas of the lesion as ions
diffuse outward.

21. Histopathology.
• Development of a subsurface translucent
zone, which is unrecognizable clinically
and radiologically.
• The subsurface translucent zone enlarges
and a dark zone develops in its center.

22. • As the lesion enlarges more mineral is lost
and the center of the dark zone becomes
the body of lesion. This is relatively
translucent compared with sound enamel
and shows enhancement of the striae of
retzius, interprismatic markings, and cross
striations of the prisms. The lesion is now
clinically recognizable as a white spot.
• The body of the lesion may become stained
by exogenous pigments from food, tobacco,
and bacteria. The lesion is now clinically
recognizable as a brown spot.

23. 5. When the carries reaches the amelodentinal
junction it spreads laterally, damaging the
adjacent enamel, giving the bluish white
appearance to the enamel as seen clinically.
Although lateral spread can occur before
cavitation, it is more common and more
extensive in lesions with cavity formation.

24. • 6. With progressive loss of mineral a
critical point is reached when the enamel
is no longer able to withstand the loads
placed upon it and the structure breaks
down to form a cavity. Carries progression
is slow process and it usually takes several
years before cavitation occurs.

25. Remember Confusion Is Always
Awesome.
(khubaib Shaikh).
Reference: Oral Pathology 4th audition
by J.V Soams & J.C Southam.