Dental caries is caused by acid-producing bacteria in dental plaque that metabolize sugars from the diet. As the bacteria lower the pH, minerals are dissolved from tooth enamel and dentin, leading to cavitation. The primary bacteria involved are mutans streptococci. Risk factors include frequent sugar consumption. Early lesions appear as white spots on smooth surfaces or pits and fissures. Untreated, caries progresses through enamel and into dentin, forming zones of demineralization and bacterial invasion.

2. Is defined as a bacterial
disease of the calcified tissues
of teeth characterized by
demineralization of the
inorganic and destruction of
organic substance of the tooth.

3.  It’s a complex and dynamic process involving ,
for example , physio-chemical processes
associated with movement of ions across the
interface between the tooth and the external
environment as well as biological process
associated with the interaction of bacteria in
the dental plaque with the host defense
mechanism

4. Etiology of dental caries :
There are various theories regarding the etiology
of dental caries have been proposed , but
there is now overwhelming support the
acidogenic theory which proposed that acid
formed from the fermentation of dietary
carbohydrates by oral bacteria leads to
progressive decalcification of the tooth
substance with a subsequent disintegration of
organic matrix

7. Role of bacteria and dental plaque
:
 Bacteria are essential for the development of
dental carries. They are present in dental
plaques which are found on most teeth
surfaces.
 Now , a plaque is a biofilm consists of variety
of different species of bacteria embedded in
a matrix derived from salivary mucin and
extracellular polysaccharide polymers
(glucose and fructose) synthesized by these
organisms.

8.  Dietary sugars diffuse rapidly through plaque
where they are converted by bacterial
metabolism to acids ,like: lactic acid , acetic
acid, and propionic acid. But mainly lactic acid.
 The pH may fall by as much as 2 units within
10 min. after ingestion of sugars , and then
slowly rises back to it’s normal value during the
next 30-60 min.

9.  At critical pH of 5.5 mineral ions are liberated
from the hydroxyapatite crystals of the enamel
and diffuse into the plaque.
 Ions may diffuse back into the enamel
(fluoride).

10. Microbiology of dental caries :
 No single bacteria.
 Members of the ‘mutant streptococci’ group
are the most efficient cariogenic organisms.

11. Cont.
 Other bacteria for example lactobacilli may be
important in further progression of the lesion.
 Lactobacillic are also the pioneer organism in
dentine caries.

12. Role of Carbohydrates :
 The evidence of the relationship between
carbohydrate and dental caries :
1. The increasing prevalence of dental caries in
the developing countries and the increasing
availability of sucrose in their diet.

13. 2. The decrease in prevalence of caries during
WWII because of sugar restriction followed
by arise to previous levels when sucrose
become available.
3. The Hopewood house study – a children
home in Australia where sucrose and white
bread were virtually excluded from the diet ,
the children had low caries rate which
increased dramatically when they moved out
of their house.

17. Pathology of dental caries
:

18.  Dental cries can be classified according to :
1. The site of the lesion.
2. The rate of the attack.

19. Site of the lesion
 Pit or fissure :
Occurs on the occlusal surface of molars and
premolars on the buccal and lingual surface of
molars and lingual surface of maxillary incisors.
Early caries may be detected clinically by brown
or black discoloration of a fissure in which a
probe “stick” .

20.  Smooth surface caries
Occurs on the approximal surface and on the
gingival third of the buccal and lingual surface.
approximal caries begins just below the contact
point as a well-demarcated chalky-white
opacity of the enamel.

21.  Cemental or root caries :
This occurs when the root face is exposed to the
oral environment as a result of periodontal
disease , usually shallow , saucer shaped with
ill-defined boundaries.
 Recurrent caries :
This occurs around the margin of at the base of a
previously existing restoration.

22. Rate of attack
 Rampant or acute caries :
This is rapidly progressing caries involving many
of all of the erupted tooth. (rapid coronal destruction)
 Slowly progressive or chronic caries :
This type progresses slowly and involves the
pulp much later than in acute caries.

23. Cont.
 Arrested caries:
This is caries of enamel or dentine , including
root caries that becomes static and shows no
tendency for further progression

24. Enamel caries
 The early established lesion (white spot) in
smooth surface enamel caries is cone shaped
with the apex pointing towards the
amelodentinal junction.
 In ground section it consists of series of zones
, depending on the degree of demineralization.

26. Zones:
1. Translucent zone
 The first recognizable histological change.
 More poruos than normal enamel , contain 1
% by volume of spaces compared with the
0.1 % pores volume in normal enamel.

27.  Mg and carbonate when compared with normal
enamel.
 Some times missing.

28. Cont enamel zone
 Dark zone :
 2-4% by volume of pores.
 It is thought that the dark zone is narrow in
rapidly advancing lesion and wider in more
slowly advancing lesions when more
reminiralization may occur.

29.  Body of the lesion :
5-25% by volume of pores.
Highly mineralized and having higher fluoride
level and lower Mg level0

30. Surface zone
 This is about 40 µm thick and shows
surprisingly little change in early lesion.
 Highly meniralized and having higher flouride
level and lower Mg level.

31. Histopathologenesis of the early
lesions
1. Development of a subsurface translucent
zone which is unrecognizable clinically and
radiologicaly.
2. The subsurface translucent zone enlarges
and a dark zone develops in it’s center.

32. 3.As the lesion enlarges more mineral is lost and
the center of the dark zone becomes the body
of the lesion ,the lesion is now clinically
recognizable as a white spot.
4.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.

33. 5. When the caries reaches the amelodentinal
junction it spreads laterally , underminig the
adjacent enamel , giving the bluish-white
appearance.
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 to form a
cavity.

34. Dentine caries
 Dentine differ from enamel is that it’s a living
tissue as such can respond to caries attack
(Reactionary . Tertiary)

35.  Caries of dentine develops from enamel caries
, when the lesion reaches the amelodentinal
junction lateral extension results in the
involvement of great numbers of tubules.
 The early lesion is cone shaped with base at
adj

36. Zone of dentine caries
 Zone of sclerosis:
Beneath the sides of the serious lesion.
Sclerosed dentine has a higher mineral content.
 Zone of demineralization
The intertubular matrix in mainly affected by a
wave of acid produced by bacteria in the zone
of bacteria invasion.

37.  Zone of bacterial invasion
Bacteria extended down and multiply within the
dental tubules , some of which may become
occluded by bacteria.
 Zone of destruction
Cracks of clefts containing bacteria and necrotic
tissue also appears at right angles to the
course of the denital tubules forming
transverse clefts.