dental caries; short notes

1. Created by Vinayak Pathak
(OVO)

2. INTRODUCTION
• Throughout the history of man, diseases have come
and diseases have disappeared. For most of the
diseases, it has been possible to clearly identify the
underlying cause.
• But for other diseases, it may be more difficult to
explain the reason and this is particularly true for
diseases with multifactorial background like dental
caries.
• Word “caries” derived from Latin word meaning ‘rot’
or ‘decay’.
• Dental caries has been recognized throughout history and exists
around the world, although the prevalence and severity varies in
different populations. The ultimate effect of caries is to
breakdown enamel and dentine and to open a path for bacteria
to reach the underlying tissues. This causes infection and
inflammation of the pulp and later of the periapical tissues.
Infection can spread from the periapical region to the jaw and
beyond.

3. Definition (According to
SHAFER/1993):-Dental caries is an
irreversible microbial disease of the calcified
tissue of the teeth, Characterized by
demineralization of the inorganic portion and
destruction of the Organic substance of the
tooth, which often lead to cavitation.
OTHER def:- (based on current
concept)
Dental caries is a multifactorial, transmissible,
infectious oral disease caused primarily by the
complex interaction of cariogenic oral flora
(biofilm) with fermentable dietary
carbohydrates on the tooth surface over time.
Traditionally, this tooth-biofilm-
carbohydrate interaction has been
illustrated by the classical Keyes-
Jordan triad/diagram.

4. Factors affecting caries prevalence:-
Race:- black have fewer carious lesion than whites.
Age:- children in the middle and lower middle socioeconomic groups showed
a trend towards higher caries incidence.
Gender:- in permanent teeth, F > M of same age, this is bcz the teeth of the
girls erupt earlier age than to the teeth of boys.
Conversely, the caries experience in deciduous teeth is greater in males.
Familial :- siblings of individual with high caries susceptibility are caries active
and vice-versa.
Parents with low caries , children also have low caries.

5. Etiology of dental caries:-
There is no universally accepted opinion of the etiology of
dental caries.
It depends on complex inter-relationships b/w the following
five critical parameters:-
• Biofilm
• Tooth habitat
• Diet
• Saliva
• Oral hygiene

6. To better understand the current concept of
the etiology of caries, following theories were
given:-
1. The legend of worms
2. Endogenous theory
3. Chemical theory
4. Parasitic theory
5. Miller’S chemico-parasitic theory or the
Acidogenic theory
6. The proteolytic theory
7. The proteolytic-chelation theory
8. Sucrose chelation theory
9. Autoimmune theory.

7. MILLER’S CHEMICO-PARASITIC THEORY/ ACIDOGENIC
THEORY (most accepted theory)
• It state that caries is caused by acids produced by micro-org.
of the mouth
• W.D Miller hypothesis:- he stated that “dental decay is a
chemico-parasitic process consisting of two stages, the
decalcification of enamel, which results in its total destruction
and the decalcification of dentin as a preliminary stages,
followed by dissolution of the softened residue. In case of
enamel, however, the second stage is practically wanting the
decalcification of enamel signifying its total destruction”

8. In a series of experiments Miller demonstrated the
following facts:
1. Acid was present with in the deeper carious lesion, as shown by reaction
on litmus paper.
2. Different kinds of foods (bread, sugar but not meat) mixed with saliva and
incubated at 37°C could decalcify entire crown of a tooth.
3. Several types of mouth bacteria (at least 30 species were isolated) could
produce enough acid to cause dental caries.
4. Lactic acid was an identifiable product in carbohydrate saliva incubation
mixtures.
5. Different kinds of micro-organisms invade carious dentin.
6. Miller concluded that no single species of microorganism caused caries,
but rather that the process was meditated by an oral microorganism
capable of producing acid and digesting protein.

9. The significance of W.D. Miller’s observation is that he
assigned an essential role to three factors in the caries
process: the role of micro-org. in acid production and
proteolysis; the carbohydrate substrate; and the acid which
causes the dissolution of tooth minerals.
Drawback :- the theory was unable to explain the predilection
of specific sites on a tooth to dental caries and the initiation
of smooth surfaces was not accounted by this theory. It
doesn’t explain why some populations are caries-free and the
phenomenon of arrested caries.

10. The role of carbohydrates in dental caries:-
• the +nce of readily fermentable carbohydrates has been thought to be
responsible for their loss of caries resistance.
• The early curde studies of miller showed that when teeth were
incubated in mixtures of saliva and bread or sugar, decalcification
occurred. There was no effect on the teeth when meat or fat was used
in place of the carbohydrates.
• Sticky solid carbohydrates are more caries-producing than those
consumed as liquid.
• Polysaccharides are less easily fermented by plaque bact. than
monosaccharides and disaccharides.
• The etiology of dental caries involves an interplay b/w the oral bact.,
local carbohydrates and the tooth surface.
Bact. + sugars + teeth  organic acids  caries

11. The Role of Microorganisms:
Although there are differences of opinion as to how and which microorganisms,
produce carious lesions. It is uniformly agreed that caries cannot occur without
microorganisms, the over whelming evidence implicating microorganisms in the
etiology of caries is summarized below:
• Germ free animals do not develop caries.
• Antibiotics fed to animals are effective in reducing the incidence and severity of
caries.
• Totally unerupted and un exposed teeth do not develop caries, yet when exposed to
the oral environment and microflora can become carious. Rarely, impacted 3rd molars
with soft tissue covering are found to be carious, in which case a sinus tract to the
oral cavity can be found.
• Oral bacteria can demineralize enamel and dentin invitro and produce caries like
lesions.
• Microorganisms have been histologically demonstrated invading carious enamel and
dentin. They can be isolated cultivated from carious lesions.

12. Role of dental plaque (biofilm):-
• Plaque is a thin, transparent film produced on the tooth surface and it
consists predominantly of micro-org suspended in salvary mucins and
extracellular bacterial polysaccharides.
• There is also +nce of desquamated epithelial cells, leukocytes, and food
debris etc. in it.
• As the plaque matures with S. Mutans group becomes more
predominant within the plaque. These orgs. rapidly metabolize the
carbohydrates and produce organic acids.
• Demineralization of enamel beings in the pH range of 5.0 to 4.5

13. THE PROTEOLYTIC THEORY:-
This theory was first proposed by Gottelib in1944 and this theory
stated that “the proteolytic enzyme liberated by cariogenic bact.
Cause destruction of the organic matrix of enamel.
Limitations:- the carious lesion cannot be reproduced in vitro by
the proteolytic mech.
Proteolytic bact. Are very uncommon in the oral cavity.
This theory cannot explain the role of sucrose,pH, fluoride etc. in
dental caries.

14. Contributing factors in dental caries:-
1.Intrinsic factors:
tooth factors
2. Extrinsic factors:-
saliva factor,
diet factor,
systemic factors,
immunity.

15. CLINICAL ASPECTS OF DENTAL
CARIES :-
CLINICAL TYPES:-
1. Pit and fissure caries:-
• Occurs in the developmental pits and fissure of the
teeth.
• Areas includes occlusal surfaces of molars,
premolars and buccal, lingual surfaces of molars
and lingual surfaces of maxillary incisors.
• Appear brown or black.
• When examined by fine explorer tip a “catch point”
is often felt where the explorer tip catches the
area.

16. 2. Smooth surface caries:-
Occurs in relation to the smooth
surfaces of the teeth. Eg.-
proximal surfaces or gingival
areas of the buccal and lingual
aspect of tooth.
Well-demarcated as chalky-white
opacity of the enamel with no
loss of continuity of the surface.

17. 3. Incipient caries :-
• Definition :- initial carious
lesion limited to the enamel
is called incipient caries and
is characterized by a virtually
intact surface but a porous
subsurface.
• Clinically incipient caries
appear as “chalky-white”.

18. 4.Rampant caries:-
• There is an acute fulminating
type of carious process, which is
characterized by simultaneous
involvement of multiple number
of teeth in multiple surfaces.
• Rapid coronal destruction occurs
within a short span of time,
causing early involvement of the
pulp.
• Common age group 4-8yrs of
the deciduous teeth and 11-
19yrs for the permanent teeth.

19. 5.Nursing bottle caries:-
• Acute carious lesion which
occurs among children who
take nursing bottle for a
considerably longer
duration of time, preferably
during sleep.
• Commonly occurs in the
upper anterior teeth.

20. 6.Chronic caries:-
• Progresses at a slower
rate
• It rarely causes pulp
involvement cz the pulp
gets sufficient time to
produce sec. dentine to
protect itself.

21. 7.Arrested caries
:-
• It is a lesion whose
progression is
ceased after the
initial development
• It occurs both in
enamel and dentine.

22. 8.Recurrent caries:-
• Beings around the
margins or at the
base of a pre-
existing defective
restoration.

23. 9.Forward caries :-
• When a caries lesion progresses unidirectionally from
enamel into the dentine and pulp, it is called as
forward caries.
10. Backward caries:-
• These lesion also initially progresses from enamel into the
dentin, where the spread laterally and involve a wide area.
• Later on, these lesions proceed in a backwards direction
from dentin back to the enamel and affect the enamel once
again at a different location.

24. 11. Root caries:-
• There are carious lesions which involve the cemental wall of the
exposed root surfaces of teeth.
12. Radiation caries:-
• Patients receiving large doses of radiation for the treatment of
malignant lesions in the head and neck region, often develop a
specific type of large “caries-like lesion” in the cervical areas of
the teeth.
• The lesion being a few weeks to few months after radiotherapy.
• They often surround the entire crowns of the affected teeth.

25. # HISTOPATHOLOGICAL ASPECTS OF DENTAL CARIES
Histological features of early enamel caries
• There will be loss of interprismatic or inter-rod substances with
increase in the prominence of enamel rods.
• Appearance of transverse striations of the enamel rods due to
segmental demineralization.
• Dark lines often appear at right angles to the enamel rods,
suggesting segments.
• Accentuation of the incremental striae of Retzius often occurs.

26. Histological features of advanced enamel caries
+nts several zones in the tissues:-
Zone I :- Translucent zone
• Deepest zone
• First recognizable
• Slightly more porous than the normal sound enamel and
1% by vol. spaces
• Pores are larger than the usual smaller pores seen in
normal enamel.

27. ZONE II :- DARK ZONE
• Located just superficial to the translucent zone
• Dark appearance is due to the excessive
demineralization of the enamel due to caries
• Narrower in rapidly advancing caries and wider in slowly
advancing caries.
• Contains 2-4% pore vol
• Reveals some degrees of remineralisation of the caries
enamel

28. ZONE III:- BODY OF THE LESION
• Situated b/w dark zone and surface layer of the
enamel and it represents the area of greatest
demineralization
• Pore vol b/w 5-25%
• Contain apatite crystals larger than those of
normal enamel
• Shows increased prominence of the Striae of
Retzius

29. ZONE IV:- SURFACE ZONE
• About 40micrometer thick
• In untreated cases the surface enamel often gets
destroyed and a cavity is formed
• Surface remineralisation results from active
precipitation of mineral ions derived from both
plaque and the saliva.

30. ULTRASTRUCTURAL STUDIES OF ENAMEL CARIES
• Suggest that the initial dissolution of enamel beings
along prism boundaries and later on there is
demineralization occurring both within and b/w the prism
which results in an increased in the intercrystalline gap.
• Along with dissolution there is also remineralisation of the
enamel due to the combined effects of demineralization
and remineralisation of enamel

31. HISTOLOGY OF DENTINAL CARIES
Histologically +nts five zones in the tissue
ZONE I :- NORMAL DENTINE
• Innermost layer of the carious dentine
• Dentinal tubules appear normal
• Evidence of fatty degeneration of the Tomes process
• No crystals in the lumen of the tubules
• No bact. In the tubules
• Intertubular dentine has normal cross-banded collagen and
normal dense apatite crystals

32. ZONE II:- SUB TRANSPARENT DENTINE
• Zone of dentinal sclerosis and characterized by the
deposition of very fine crystal structure within the
dentinal tubules at the advancing front
• Superficial layer shows areas of demineralization and
damage of the odontoblastic processes
• No bact in the tubules
• This dentine capable of remineralisation

33. ZONE III:- TRANSPARENT DENTINE
• Appear transparent due to demineralization of dentine
• Softer than normal dentine
• Loss of mineral ions from intertubular tubules
• Large crystals within the lumen of the dentinal tubules
• No bact in the tubules
• Cross-banded intertubular collagen still intact

34. ZONE IV:- TURBID DENTINE
• This zone called turbid dentine and is marked by
the widening and distortion of the dentinal
tubules which are packed with micro-org.
• Zone cannot undergo self repair or
remineralisation
• Must be removed before restoration

35. ZONE V:- INFECTED DENTINE
• Outermost zone of carious dentine
• Characterized by complete destruction of the dentinal
tubules
• In this zone the areas of decomposition of dentine which
occur along the direction of the dentinal tubules are called
the liquefaction foci of miller.
• Transverse clefts +nt
• In this zone bact may no longer remain confined within the
dentinal tubules and they invade and destroy the peri and
intratubular dentin. In the process, the entire dentinal str
becomes destroyed.

36. CARIES ACTIVITY TEST
1. Synder test
2. Salivary Reductase Test
3. Salivary buffering capacity test
4. Microbiological test
5. S. mutans DIP-SLIDE method
6. Enamel solibility test

37. METHODS OF CARIES PREVENTION
1. Limit substrate
2. Modify oral microflora
3. Plaque disruption
4. Modify tooth
5. Stimulate salivary flow
6. Restore tooth surface

38. CARIES VACCINE
• It will prevent the ability of microorganism to colonies on to the tooth
surface.
• Alter the pattern of polysaccharide metabolism by bacteria and
thereby reduce their adhering capacity on to the tooth surface.
• It can reduce ability of microorganism to produce acids also.
• It can reduce caries by helping in the process of killing the cariogenic
microorganism.
• The vaccine are usually given at the age of about 6 months, before the
eruption of the deciduous tooth.
• Passive immunization against caries can also be done by injecting
specific IgG class of antibody against the S. Mutans.

39. References :-
• Shafer’s 5th edition
• Neville 2nd edition
• Purkit 3rd edition
• Google