2. DENTAL CARIES
1. DEFINITION
2. THEORIES OF DENTAL CARIES
3. ETIOLOGY
4. CLINICAL ASPECTS OF DENTAL CARIES
5. HISTOPATHOLOGY OF DENTAL CARIES
6. DIAGNOSIS OF DENTAL CARIES
7. METHODS OF CARIES CONTROL
3. DEFINITION
Dental caries is defined as a microbial
disease of the calcified tissues of the teeth,
characterized by demineralization of the in-
organic portion and the destruction of the
organic substances of the teeth.
Affects persons of both genders in all races,
all socioeconomic strata and every age
group.
5. A. THE EARLY THEORIES:
a] The legend of worms
b] Endogenous theories
c] Chemical theories
d] Parasitic theories
B.
a] Miller’s Chemo-parasitic / Acidogenic theory
b] The proteolytic theory
c] The sucrose-chelation theory
6. A. THE EARLY THEORIES:
a) The legend of Worms:
The earliest reference to tooth decays is
probably from the ancient Sumerian text
known as the ‘The legend of Worms'.
This dates from about 5000 B.C.Euphrates
valley of the lower Mesopotamian area.
The idea that caries is caused by worms was
universal as is evident from the writings of
Homer who made a reference to worms as
the cause of toothache.
7. b)Endogenous theories:
It was advocated by Greek
physicians, who proposed that dental
caries is produced by internal action
of acids and corroding humors. And
an imbalance in these humors
resulted in disease.
8. c) Chemical theory:
In the 1820s observed that dental decay
affected externally, not internally, as had
been claimed.
It was proposed that an unidentified ‘chymal
agent’ was responsible for caries.
Support for the chemical theory came after
Robertson in 1835 proposed that dental
decay was caused by acid formed by
fermentation of food particles around the
teeth.
9. d) Parasitic theory:
Apparently the first to relate
microorganisms to caries on a causative basis
as early as 1843 was Erdl who described
filamentous organisms in the membrane
removed from teeth.
Shortly thereafter, Ficnus in 1847, a German
physician in Dresden, definitely attributed
dental caries to ‘denticolae’ the generic term
he proposed for decay related
microorganisms.
10. B. 1) MILLER’S CHEMICO-PARASITIC THEORY
(ACIDOGENIC THEORY):
W D Miller, an American, in beginning of
1890 gave the following hypothesis in
which he stated:
“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 stage, followed by dissolution
of the softened residue.
11. The acid which affects this primary
decalcification, is derived from the
fermentation of starches and sugar
lodged in the retaining centres of the
teeth.
Subsequently, he isolated numerous
microorganisms from the oral cavity,
many of which were acidogenic and
some were proteolytic.
12. The significance of W D Miller’s
observation is that he assigned an
essential role to three factors in the
caries process :
-the oral microorganisms in acid
production and proteolysis;
-the carbohydrate substrate; and
-the acid which causes dissolution of
tooth minerals.
× Miller's chemico-parasitic theory is the
backbone of current knowledge and
understanding of the etiology of dental
caries.
13. Miller’s 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 for by this theory.
Also miller’s theory doesn’t explain
why some populations are caries-free
and the phenomenon of arrested
caries
14. 2) THE PROTEOLYTIC THEORY
Offered as an alternative explanation is the
proteolytic theory where it has been
proposed that the organic or protein
elements are the initial pathway of invasion
by microorganisms.
It has been established that enamel
contains approx. 0.56% organic matter, of
which 0.18% is a type of keratin, 0.17% a
soluble protein, possibly a glycoprotein, and
the remainder citric acid and peptides.
15. Heider and Wedl, Bodecker, Abbot
demonstrated that certain enamel
structures are made up of organic
material, such as enamel lamellae and rd
sheaths.
Baumgartner and Fleischmann
demonstrated that microorganisms could
invade the enamel lamellae, and stated
that acids produced by these bacteria
were capable of destroying the inorganic
portion of the enamel.
16. Gotlieb(1944) and Gottlieb, Diamond and
Applebaum(1946) postulated that caries is
essentially a proteolytic process:
-the microorganisms invade the organic
pathways and destroy them in their advance.
-They did admit that acid formation
acccompanied the proteolysis
-Gotlieb held that yellow pigmentation was
characteristic of caries and that this was due
to pigment production by proteolytic
organisms.
17. Pincus proposed that Nysmuth’s membrane
and other enamel proteins are
mucoproteins, yielding sulphuric acid upon
hydrolysis.
-Gram-ve bacilli capable of producing the
enzyme sulphatase.
-This enzyme releases the combined
sulphuric acid from the mucoprotein, but
only reluctantly unless the protein is first
hydrolyzed to free the polysaccharide.
-The liberated acid dissolves the enamel,
combining with the calcium to form calcium
sulphate
18. Manley and Hardwick attempted to
reconcile the two chief theories concerning
the etiology of dental caries.
They pointed out that, while the
acidogenic and the proteolytic mechanisms
may be seperate and distinct , they need
not be.
Many bacteria produce acid from
carbohydrate substrate, some bacteria
capable of producing acid form
carbohydrate may even degrade protein in
the absence of carbohydrate.
19. On this basis there may be two types of
carious lesion
In one type, microorganisms invade enamel
lamellae, attack the enamel and involve the
dentin before there is clinical evidence
In the other, no enamel lamellae are present
and there is alteration of enamel prior to
invasion produced through decalcification by
acids formed by bacteria in a dental plaque
overlying the enamel. The early lesion
produced are those typically described as
“chalky enamel”
20. 3) SUCROSE-CHELATION THEORY
Eagglers-Lura proposed that sucrose itself, and
not the acid derived from it, can cause
dissolution of enamel by forming an ionized
calcium saccharate.
The theory is that calcium saccharates and
calcium complexing intermediaries require
inorganic phosphate which is subsequently
removed from enamel by phosphorelating
enzymes
24. TOOTH
a) Susceptible tooth surface:
• non-self cleansable areas are more prone ,as they
provide stagnation areas for dental plaque
• Pits & fissures have the highest prevalence ,
provide mechenical shelter for m.org
• Proximal areas immediately gingival to contact
area are the next common site, as they are
protected from effects of mastication, tongue
movement and salivary flow
25. • Enamel at the cervical aspects of the teeth near
the gingiva and exposed root surface are other
potential site for plaque retention
• Plaque retention can also occur near the
margins of existing restorations if they are
rough, overhanging or exhibit wide marginal
gaps
• Crowding
26. b) Biochemical characteristics of teeth:
•The enamel surface of a newly erupted tooth is highly
susceptible to caries because of highly carbonate content of
enamel crystals.
•Any deficiencies of vit-A and D, minerals like calcium
phosphorus and flourides predisposes to caries occurrence.
•Devlopmental disturbances of enamel hypoplasia or
hypomineralization
•With age, the surface enamel becomes more resistant to
caries because of posteruptive maturation ,
•flouride, zinc and nitrogen level increases , provides
resistance to caries
27. DENTAL PLAQUE
•Soft, translucent, tenaciously adherent mass
accumulating on tooth surface
•Composed of an aggregate of bacteria, salivary
glycoprotiens and inorganic salts
•Also called “microbial biofilm”
•Dental plaque associated with dental caries has
high concentration of streptococcus mutans and
lactobacillus acidophilus(acidogenic bacterias)
28. •Diet rich in sucrose favours the accumulation of
strep.mutans in plaque
•Sucrose rich environment allows the strep.mutans to
produce large amount of extracellular polysacharide like
glucan, which enables the bacteria to tenaciouly adhere to
tooth surface and limits the salivary buffers.
•With the local environment being highly acidic,
dissolution of the tooth surface begins
• once the tooth surface becomes cavitated, filamentous
bacteria with poor adhesion abilities like lactobacilli
becomes established in lesion
29. DIET
•Less fibrous, more refined, soft and sticky diet
favours the stagnation of food on tooth surface
•Chemically diet is composed of carbohydrates
which are cariogenic.
•Modern diet contains more of refined
carbohydrates (sucrose,fructose,glucose,etc)
makes it more cariogenic
30. •Modern diet lacks of phytates, which is
anticariogenic
•Another factor promoting caries is the
comsumption of snacks between meals, this
lowers the plaque pH for prolonged time leads to
dvelopment of caries.
•Protective factors in diet against caries are:
calcium lactate(cheese), milk, flourides, vit-D & B6
31. TIME
•Significant factor
•During long intervals of undisturbed plaque
stagnation, the plaque pH is lowered down ,
favours the production of organic acids that
demineralize tooth structure
32. SALIVA
•Has a protective role in preventing caries
•Helps to flush away food debris and
bacteria
•Buffers the acids released , due to its
bicarbonate concentration, phosphate
content and presence of sialin
33. •Antimicrobial property due to the presence of
lysosomes, immunoglobulinA, lectoperoxidase,
lactoferrin, salivary protien and mucin
•Helps in remineralization of early caries lesions
due to presence of calcium, phosphate and
flouride.
•Salivary flow reduced-------> increased incidence
of caries
•Xerostomia – high risk of caries
34. SYSTEMIC HEALTH:
•Any condition which predisposes to poor oral
hygiene can increase the incidence of dental caries
eg; neurological disorders, mental retardation
•Caries risk is highly associated with sjogren’s
syndrome
•Prolonged use of drugs like anti depressants,
antihistamine, diuretics, etc, may cause xerostomia,
which predisposes occurrence of caries
35. •Diabetes mellitus is associated with increased
risk of caries
•Pt under going radiotherapy or chemotherapy
are prone to caries due to reduction in adult
flow
SEX:
•Females are more susceptible to caries than
males due to early eruption of teeth
36. HEREDITY:
•May be related to his genetic makeup.
•Several studies have demonstrated that caries
may be inherited from parents, especially mother
to child
•It has been shown that children are frequently
colonized with strains of streptococcus mutans
identical toi strains carried by their mothers
37. RACE:
•Related to their culture and dietary influences
GEOGRAPHIC INVOLVEMENT:
•Regions where there is high content of phosphate in food
and water, caries prevalance is less
OCCUPATIONS:
•Where frequent food sampling is required eg; bakery
workers, confectionary industry workers, etc
•Where regular meals scheduke is disturbed eg; night shift
workers, truck drivers, etc
40. Acc. to whether its new or recurrent lesion:
1. Primary caries(Initial)
2. Secondary caries(Recurrent)
Acc. to extent of caries:
1. Incipient caries (Reversible)
2. Cavitated caries (non reversible)
Acc. to the pathway of
caries:
1.Forward caries
2.Backward caries
41. Acc. to number of tooth surface involved
1.Simple caries
2.Compound caries
3.Complex caries
Acc. to treatment and restoration design
1. Class-I caries
2. Class-II caries
3. Class-III caries
4. Class-IV caries
5. Class-V caries
6. Class-VI caries
42. Acc. to the age of patient:
1. Nursing bottle caries
2. Adolescent caries
3. Senile caries
Acc. to the tooth surface to be restored:
1.Occlusal
2.Mesial
3.Distal
4.Facial
5.Buccal
6.Lingual
* combination of above are possible
43. WORLD HEALTH ORGANISATION(WHO) SYSTEM:
- the shape and depth of the lesion can be scored on
a four point scale
D1- Clinically detectable enamel lesion with intact
surface
D2- clinically detectable cavities limited to enamel
D3- clinically detectable cavities in dentine
D4- lesions extending into pulp
44. A NEW CLASSIFICATION OF CARIES
LESION BASE ON SEVERITY (DEPTH)
Over time, to determine whether the caries risk is high, moderate
or low
E0 – No lesion
E1 – Lesion on outer half of enamel
E2 – Lesion extended into inner half of enamel
D1 – Lesion in outer 1/3 of dentin
D2 – Lesion in middle 1/3 of dentin
D3 – Lesion in inner 1/3 of dentin
45. PITS & FISSURE CARIES
Occlusal surface of molars &
premolars – buccal & lingual surface
of molars & lingual surface of
maxillary incisors.
Early caries appears brown or black –
slightly soft – provides catch
The enamel around caries may
appear opaque bluish -> undermined
Lateral spread of caries at the D.E.J –
May cause a large caries lesion with
small point of opening
46. SMOOTH SURFACE CARIES
Proximal surface to teeth or on gingival 1/3 of buccal &
lingual surfaces (non-self cleansing areas)
Usually starts below the contact point of teeth
It appears as a yellow or brown area, initially,
As caries goes occurs on buccal or lingual surfaces
Extents from area opposite the gingival crest to the
height of contour of the tooth.
It may extend laterally towards the proximal surface &
also beneath free margin of the gingival
This typical cervical lesion is a crescent shape cavity and
is always an open cavity
47.
48. ACUTE DENTAL CARIES
Rapid clinical course
Early pulpal involvement
Occurs mostly in children & young adults
(dentinal tables are large and open and
don’t show sclerosis)
Dentin has a light yellow color
Pain is present
49. CHRONIC DENTAL CARIES
Progresses slowly
Late pulpal involvement
More seen in adults
The entrance of lesion is larger than acute
More entry of saliva
Less food retention
Dentin is dark – brown- cavity is shallow –
minimum softening of dentin
Cavity is not undermined, as pain is usually
absent.
50. RECURRENT CARIES
Usually occurs around the
restoration
May be due to inadequate extension
of cavity or poor adaptation of
restoration that produces leaky
margin & has retention of food
51. ARRESTED CARIES
This kind of caries become stationary and does not progress
further if affects both deciduous & permanent dentition
The superficial dentin is soft decalcified but gradually gets
burnished (shinny) and has a brown polished appearance is
hard
This is called Eburnation, of dentin sclerosis of dentinal
tubules & secondary dentin formation are seen.
Another type of arrest carries seen on proximal surface of
teeth when adjacent tooth is extracted
It shows brown area at or below the contact point of tooth
This type of caries is early caries which get arrested after
extraction due to formation of self-cleaning area.
52. RAMPANT CARIES
This is defined by massler as suddenly appearing wide
spread rapidly burrowing type of caries resulting in
early involvement of the pulp and affecting those
teeth which are usually regarded as immune to dental
decay
it is seen ion patients which suffer from xerostemia or
drymouth
this caries is atypical and cervical area is attacked
involving cementum and dentin
it progresses inwards until the crown is removed
there is a heavy brownish black discoloration of tooth
in children this is called as nursing bottle caries.
53.
54. ROOT CARIES
Called as cementum caries
Defined as soft progressive lesion found
anywhere on thereof surface that has lost gingival
attachment and is exposed to the oral cavity
Enamel may also be involved if it is undermined
during progress of the lesion
Dental plaque & micro-organisms are the main
cause of lesion
Teeth most frequently affected are:- mandibular
molar premolar – maxillary canine
Mandibular incisor are least affected
55. In the maxillary teeth the proximal surfaces are
mostly affected – in mandibular arch buccal surface
mostly affected
The lesion starts in cementum by sub surface
deminirelization with an intact surface layer.
The cementum is easily attacked due to it’s greater
porosity & high organic contain
The development of lesion is same as that of
enamel caries.
56.
57. INCIPIENT CARIES (REVERSIBLE)
It is the first evidence of caries activity in the enamel
which has not extended to the DEJ and enamel is hard &
intact, it appears opaque white when air-dried and it can
be demineralized if immediate corrective measures after
the oral environment including plaque removal control
58. CAVITATED CARIES (NON-REVERSIBLE)
Enamel surface is broken
lesion is advanced into dentin
Remineralization is not possible
Treatment by tooth preparation are
restoration indicated
59. BACKWARD CARIES
When the spread of caries along
the DEJ exceeds the caries in the
contiguous enamel, caries
extends
into this enamel from the junction
is
called as backward caries
60. FORWARD CARIES
Whenever the caries come in enamel is larger or at least
the same size as that is dentin
61. RESIDUAL CARIES
caries that remains in completed tooth preparation
whether by operator intention or by accident
It is not acceptable if at the DEJ or on the prepared
enamel tooth wall
It may be acceptable
when it is affected
dentin, specially near
the pulp
62.
63. OCCULT OCCLUSAL CARIES
It Represents dentinal caries – only on radiographs –
unrecognized on visual examination
Prevalence – 2.2% to 50%
This caries may start as fissure caries, that after
misdiagnosis progressed to early caries
The dentinal radiolucency may present in affected
teeth even before the teeth erupted, as pre eruptive
into a coronal resorptive defects
65. a] ENAMEL CARIES
On smooth enamel surface , the earliest
macroscopic evidence of incipient caries is the
appearance of an area of decalcification
beneath the dental plaque which resembles a
smooth chalky white area.
Scott and his assocites, has revealed that the
first change is usually a loss of the
interprismatic or inter-rod substance of the
enamel with increased prominence of the
rods.
66. •In some instances, the initial change seems to
consist of roughening of the ends of the enamel
rods, suggesting that the prism may be more
susceptible to early attack.
•Another change in early enamel caries is the
accentuation of the incremental striae of
Retzius.
•due to loss of minerals which causes the
organic structure to appear more prominent.
67. Early smooth surface
caries. Ground section
shows body of lesion,
enhanced striae of
Retzius, between the
dark zone and
peripheral translucent
zone.
68. There may also be accentuation of perikymata.
As this process advances and involves deeper layers
of enamel
It forms a triangular or actually a cone-shaped
lesion with the apex toward the DEJ and base
toward the surface of the tooth.
There is eventual loss of continuity of the enamel
surface, and the surface feels rough to the point of
an explorer.
69. The roughness is caused by the disintegration of the
enamel prisms after decalcification of the
interprismatic substance and the accumulation of
debris and microorganisms over the enamel rods.
The small lesion has been divided into different zones
based upon its histological appearance when
longitudinal ground sections are examined with the
light microscope.
Four zones are clearly distinguishable, starting from
the inner advancing front of the lesion.
70. * Zone 1: The transluscent zone.
Lies at the advancing front of the enamel lesion
first recognizable zone of alteration from normal enamel.
About half of the lesions demonstrate a transluscent
zone at their advancing front, which is seen only when a
longitudinal ground section is examined in a clearing agent
having a refractive index identical to that of enamel.
Quinoline is more suitable since its refractive index is
identical to that of enamel(RI 1.62).
When ground section is examined under transmitted light,
after imbibition with quinoline, the translucent zone
appears structureless.
It is not always present.
71. By means of polarized light it has been shown
that this zone is slightly more porous than
sound enamel, having a pore volume of 1%
compared with 0.1% in sound enamel.
Chemical studies carried out on various zones
showed that the fluoride content of transluscent
zone enamel was found to be increased relative
to adjacent sound enamel.
72. The overall findings suggested that carious
that attack had preferentially removed
magnesium and carbonate rich mineral
from translucent zone and not organic
material.
73. * Zone 2: The dark zone.
It has been referred to as the positive zone,
because it is usually present.
This zone is formed as a result of
demineralization and appears dark brown in
ground sections examined by transmitted light
after imbibition with quinoline.
Polarized light studies showed that the dark
zone has a pore volume of 2-4%
74. These effects have been shown to be due to the
presence of very small pores in the zone besides the
relative large pores that are present in the first stage,
the translucent zone.
If a ground section is examined in an aqueous
medium having a small molecule which penetrates
the micro pores, the dark zone is no longer seen.
75. * Zone 3: The body of the lesion.
This zone lies between the relatively unaffected
surface layer and the dark zone.
It is the area of greatest demineralizaiton.
In polarized light, the zone shows a pore volume of
5% in spaces near the periphery, to 25% in the center
of the intact lesion.
When a longitudinal ground section is examined in
quinoline with transmitted light, the body of the
lesion appears relatively translucent compared with
sound enamel.
76. * Zone 4: Surface zone.
When examining a small initial carious lesion with the
polarizing microscope, the surface zone is an important
feature.
Quantative studies of the surface layer indicate the partial
demineralization equivalent to about 1-10% loss of mineral
salts has taken place and the pore volume of the surface zone
is less than 5% of spaces.
The greater resistance of the surface layer may be due to a
greater degree of mineralization and/or a greater
concentration of fluoride in the surface enamel and perhaps a
greater amount of insoluble protein in the surface enamel.
The surface zone remains intact and also well mineralized
because it is a site where calcium and phosphate ions,
released by subsurface dissolution, become reprecipitated.
This process is referred to as remineralization.
77. CARIES OF THE DENTIN
Caries of the dentin begins with the natural spread of
the process along the DEJ and the rapid involvement
of great numbers of dentinal tubules, each of which
acts as a tract leading to the dental pulp along which
the microorganisms may travel at a variable rate of
speed.
* Early dentinal changes
The initial penetration of the dentin by caries may
result in alterations in the dentin previously described
as dentinal sclerosis or ‘transparent dentin’.
78. This dentinal sclerosis is a reaction of vital dentinal
tubules and a vital pulp in which there is calcification
of the dentinal tubules that tends to seal them off
against further penetration by microorganisms.
The formation of sclerotic dentin is minimal in rapidly
advancing caries and is most prominent in slow
chronic caries.
The term ‘transparent dentin’ has been applied
because of the peculiar transparent appearance of
the tooth structure when a ground section is viewed
by transmitted light.
By reflected light the sclerotic dentin appears dark.
79.
80. The appearance of fatty degeneration of Tomes’
dentinal fibers, with the deposition of fat globules
in these processes, precedes even the early
sclerotic dentinal changes.
Two types of lipid staining have been seen,
one of which is more superficial and probably of
bacterial origin.
The other type may be due to unmasking of lipids
present in the intratubular dentin, by
demineralization.
81. The rate at which the carious destruction
progresses tends to be slower in older
adults than in young persons because of
the generalized dentinal sclerosis that
occurs as a part of the aging process.
In the earliest stages of caries, when only a
few tubules are involved, microorganisms
may be found penetrating these tubules
before there is any clinical evidence of the
carious process.
These have termed ‘pioneer bacteria’.
82. The initial decalcification involves the walls of the
tubules, allowing them to distend slightly as they
become packed with masses of microorganisms.
It is evident that these microorganisms as they
penetrate farther and farther into the dentin, become
more and more separated from the carbohydrate
substrate upon which the bacteria responsible for the
initiation of the disease depend.
The high protein content of the dentin would favor
the growth of those microorganisms which have the
ability to utilize this protein in their metabolism.
Thus proteolytic organisms would appear to
predominate in deeper caries of the dentin, while
acidogenic forms are more prominent in early caries.
83.
84. * Advanced dentinal changes
A thickening and swelling of the sheath of
Neumann may sometimes be noted at irregular
intervals along the course of involved dentinal
tubules.
Tiny ‘liquefaction foci’ described by Miller, are
formed by foccal coalescence and breakdown of a
few dentinal tubules.
This focus is an ovoid area of destruction parallel
to the course of the tubules and filled with necrotic
debris which tends to increase in size by expansion.
This produces compression and distortion of
adjacent dentinal tubules so that their course is bent
around the ‘liquefaction focus’.
85. In areas of globular dentin, decalcification and confluence of
dentinal tubules occur rapidly.
The destruction of dentin through a process of decalcification
followed by proteolysis occurs at numerous focal areas which
eventually coalesce to form a necrotic mass of dentin of a
leathery consistency.
Clefts are rather common in this softened dentin, although they
are rare in chronic caries, since the formation of a great deal of
softened necrotic dentin is unusual.
These clefts extend at right angles to the dentinal tubules and
appear to be due to extension of the carious process along the
lateral branches of the tubules or along the matrix fibres which
run in this direction.
The cleft account for the manner in which carious dentin often
can be excavated by peeling away thin layers with hand
instruments.
86. As the carious lesion progresses, various zones of
carious dentin may be distinguished which grossly
tend to assume the shape of a triangle with the apex
toward the pulp and the base toward the enamel.
Beginning pulpally at the advancing edge of the lesion
adjacent to the normal dentin, these zones are as
follows:
Zone 1: zone of fatty degeneration of Tomes’ fibres
Zone 2: Zone of dentinal sclerosis characterized by deposition
of calcium salts in dentinal tubules.
Zone 3: Zone of decalcification of dentin, a narrow zone,
preceding bacterial invasion.
Zone 4: Zone of bacterial invasion of decalcified intact dentin.
Zone 5: Zone of decomposed dentin.
87. * Secondary dentin involvement
The carious involvement of secondary dentin does
not differ remarkably from the involvement of the
primary dentin, except that it is usually somwhat
slower because the dentinal tubules are fewre in
number and more irregular in their course, thus
delaying penetration of the invading microorganisms.
Sooner or later, however, the involvement of the pulp
results with ensuing inflammation and necrosis.
Occasionally, caries will spread laterally at the
junction of the primary and secondary dentin and
produce a seperation of the two layers.
89. METICULOUS CLINICAL EXAMINATION:
Careful examination under clean and dry condition with
good illumination can reveal varios signs of caries like:-
- brown discoloration of pits and fissures
- opacity beneath pits and fissures or marginal ridges
- frank cavitation of the tooth surface
90. TACTILE EXAMINATION:
• Use of dental explorer may help in detection of dental caries.
•Tactile findings suggestive of caries are:
- softness at the base of a pit and fissures
and discontinuity of enamel surface
- catch at the explorer tip
- cavitation at base of pit and fissure
•Cautions:excassive pressure with explorer can cause
cavitation where was not present earlier
infective m.org may be transferred to uninfected
area
91. RADIOGRAPHIC EXAMINATION:
-Conventional , intraoral periapical and bitewing
radiograph are employed to daignose dental
caries
- bitewing is of more duagnostic value
Uses of bitewing:
• detecting proximal caries
•Examinig many teeth in one radiograph
•Checking cervical margin of restoration
•Monitering the progress of arrest caries
92. Scoring the progress of caries on bitewing:
0= sound enamel
1= radiolucency only in enamel
2= radiolucency in enamel extending upto
DEJ
3= radiolucency in enamel and outer half of
dentine
4= radiolucency in enamel reaching inner
half of dentine
93. Cervical burnout:
“a radiolucent appearance
mimicing proximal caries seen at cervical aspect
of teeth. This is perfectly a normal appearance
at the gap between the dense enamel over the
crown of the tooth and the crest of the alveolar
ridge where xray pass tangentially through the
root dentine.
94. TOOTH SEPARATION:
•To detect initial proximal caries, separation of the
contacting teeth can be achieved using wedges or
mechanical separator
•Once the proximal surface is accessible, visual
examination and gentle probing may help in diagnosis of
the carious lesion
95. FIBEROPTIC TRANSILLUMINATION:
•Carious lesion have lowered index of light transmission,
when teeth are examined with the fiberoptic light
source, caries appears as a dark shadow
•After drying the tooth, a fiberoptic probe can be placed
in the buccal or lingual embrassures directly beneath the
contact area between two adjacent teeth.
•If caries is present , dark shadow is seen beneath the
marginal ridge
•Non invasive
•No radiation hazard
•No permanent record
•Difficulty in placing probe
96. XERORADIOGRAPHY:
•Image is recorded on an aluminium plate coated with a
layer of selenium particles
•These selenium particles are charged uniformly and
stored in a unit called condition
•When x-ray is passed onto the film , it causes selective
discharge of the particles which forms a latent image.
•This is converted into positive image by a process known
as development in the processper unit
•Less radiation exposure
•No wet processing
•Electric charge over the film may cause discomfort
97. DIGITAL RADIOGRAPHIC METHODS:
• offers more superior means of detecting caries
•Can be obtained by 2 methods
i)video recording and digitization of a conventional
radiograph
ii)direct digital radiography
•The direct digital radiography system was RVG
•It uses a charged couple device which works like a miniature
video camera
•This records images produced by conventional x-ray and
stores it in the computer memory for image processing and
viewing
•Reduced radiation dose ,no need of dark room,no processing
error, instant image visualization and can be magnified
98. COMPUTER AIDED RADIOGRAPHIC METHOD:
•This method uses the measurement potential of
computers in assessing and recording the size of carious
lesions.
•Provides graphic visualization of the size and
progression of the carious lesion especially approximal
caries.
•Computer software have been developed for automated
interpretation of digital radiographs in order to
standardize image assessment
•Helps in monitering the carious process
•Time consuming and expensive
99. DIGITAL FIBEROPTIC TRANSILLUMINATION:
•New technique which combines fiberoptic
transillumination and digital ccd camera.
•Images captured by the camera are sent to a
computer for analysis, which produces digital images
that can be viewed
•This method overcomes the shortcomings of FOTI
•Non invasive
•Can detect incepient and recurrent caries very early
•Does not measure the depth of the lesion
100. METHODS OF CARIES CONTROL
The control of dental caries presents one of the greatest
objectives that must be met today by the dental
profession.
The suggested methods of control may be classified into
three general types:
1. Chemical measures
2. Nutritional measures, and
3. Mechanical measures
101. CHEMICAL MEASURES
• Chemicals used for caries control include:
• Substances which alter the tooth surface or tooth
structure
• Substances which interfere with carbohydrate degradation
through enzymatic alteration
• Substances which interfere with bacterial growth and
metabolism
•
* Substances which alter the tooth surface or tooth structure
• The exposure of the teeth to fluoride through profesional
application of fluoride solutions, gels, foams and varnishes
plus exposure from dentrifices and other fluoride
preparations used at home is beneficial in preventing dental
caries.
102. Fluorine
• The history of fluorine and dental caries dates from
the recognition by GV Black and Frederick S Mckay
that teeth with even a severe degree of mottled
enamel have a greater immunity to dental caries
than normal teeth.In biological mineralized
tissues such as bone and teeth, it occurs as the
apatite salt of fluoridated hydroxy-apatite.
Fluorine has been administered principally in
two ways: through the communal water supply
and by topical application.
103. Mechanism of action of ingested fluoride
The mechanism of action of fluoride in the drinking water has
been discussed by many workers, and several theories have
been proposed. Since fluoride inhibits enzymes by inactivating
the coenzyme portion of the enolase system, and specifically
by inhibing the conversin of 2-phosphoglyceric acid to (enol)
phosphopyruvic acid, it has been thought to protect against
caries by preventing carbohydrate degradation.
The most widely accepted theory on the mechamism of
action of ingested fluoride is that of alteraiton of the structure
of the developing tooth through systemic absorption of the
element.
The exact means whereby fluoride would alter the tooth
structure to resist caries has not been completely established,
but it is probably through the incorporation of fluorine in the
crystal lattice structure of enamel, with the formation of a
fluorapatite producing less acid soluble enamel.
104. Fluoride supplements
Where communal water fluoridation is not feasible, fluoride tablets,
drops, or lozenges have been proven definitely to be effective
cariostatic agents, provided such supplements are taken on a daily
basis from birth to about 14 years.
The correct dosage in prescribing fluoride supplements depends on
two factors: the age of the child and the existing fluoride
concentration in the water supply.
For young infants, drops are more convenient and can be added to
foods such as cereals or beverages such as milk formula, or juices.
For older children, whose primary teeth have erupted, fluoride tablets
or lozenges are indicated as these provide both systemic benefits
when swallowed an topical benefits as they are swished around the
mouth.
The concentration of total fluoride in human milk is about 0.05 ppm
and cow’s milk about 0.1 ppm. Nevertheless, in most cases there is
no need to supplement breastfed children who reside in optimally
fluoridated areas.
105. Topical application of fluoride
The second manner in which fluoride is used for the prevention
of dental caries is by topical or local application to the teeth.
Although the exact mechanism is not known, it appears that
there is formation of either a calcium fluoride or a calcium
fluorapatite.
Professionally applied topical fluoride preparations usually
contain 2% sodium fluoride, 8% stannous fluoride, or 1.23%
acidulated phosphate fluoride.
Sodium Fluoride
It was first proposed by Knutson et.al. which involved first the
cleaning of the teeth with pumice paste followed by a four minute
topical application of 2% sodium fluoride solution at pH 7.
The initial topical application was then followed by three similar
applications at weekly intervals, except that no prophylazis was
carried out at these subsequent visits. The treatment series was
recommended at ages 3,7,10, and 13 years.
106. The disadvantage of this technique was that the patient had to make
four visits to the dentist within a relatively short time.
However, sodium fluoride as a topical agent had many advantages in
that it is chemically stable, has an acceptable taste, non irritating to
gingiva and does not discolor the teeth.
Stannous fluoride
The advantages of using SnF2 were rapid penetration of tin fluoride
and formation of a highly insoluble tin fluorophosphate complex on
enamel surfaces.
The disadvantages of aqueous SnF2 far outweighed advantages in
that it is unstable and should be prepared fresh for every treatment,
its naturally low pH make it astringent, it produces discoloration of
the teeth particularly in hypocalcified areas and the solution has a
metallic taste.
In order to overcome some of the disadvantages of a freshly
prepared 85-10% solution of SnF2, stannous fluoride gel containing
0.4 % SnF2 in methyl cellulose and glycerin base was developed.
However, for fluoride ion to be released, the gel should be diluted
with water following its application to the teeth.
107. By far the most useful fluoride therapy is the application of
acidulated phosphate fluoride (APF) in the form of a solution
or gel. The use of these agents provides a 25-40% reduction in
caries.
APF agent has to be applied for four minutes usually in a
disposable tray applicator. APF agents have a pH of
approximately 3 and contain 1.23 % fluoride and 0.1M
orthophosphoric acid.
The low pH favors more rpid fluoride uptake by enamel and
the presence of the orthophosphate prevents enamel
dissolution by the common ion effect.
108. The application of these solutions or gels is often preceded by a coronal
polishing. This removes exogenous stains and plaque but doesn’t affect the
cariostatic potential of topical fluoride gel.
To allow topical fluoride to react with the enamel for more time and
thereby increase its uptake, fluoride varnishes have been developed.
One of the most effective means of caries reduction involves the daily self
application of 0.5 % fluoride gel (5000ppm F) about 40% of the
concentration used for professional office applications in custom fitted trays
for five minutes.
This form of self therapy is best suited for high caries risk patients who are
sufficiently motivated to confirm to the daily regimen.
It is appropriate for those school going children and for patients who have
received therapeutic radiation in the headand neck region.
109. Fluoride dentifrices
This is another method of applying fluoride. Although fluoride
containing mouthwashes, lozenges and chewing gums have all been
suggested, and in some cases tested, there is no evidence to indicate
that their use produces any benificial effect.
Sodium Monoflurophosphate (MFP) has been used as a therapeutic
agent in dentrifices and in the USA, MFP at 0.76% or 1000 ppm is the
most commonly used therapeutic ingredient in commercial
toothpastes.
110. Fluoride mouthwashes or rinses
There has been extensive clinical trial of mouthwashes or rinses
containing fluoride used either as a mouthwash to flush the oral
cavity, or in a few instances by application with a toothbrush in
effort to prevent dental caries.
For geographic areas where t is impossible to fluoridate the water
supplies because of the lack of a central water system, alternative
measures should be considered in the form of school based fluoride
mouth rinse program.
American Dental Association has recognized neutral sodium
fluoride and acidulated phosphate fluoride rinses as effective caries
preventive agents (1975) as well as stannous fluoride rinse(1980).
Since the rinsing can be performed as an individual caries
preventive measure at home or as a school based group preventive
program, the dentist must be familiar with the different techniques
involved, because they vary considerably with the different
circumstances and objectives.
111. BIS-BIGUANIDES
Chlorhexidine have received the most attention as potential
anticaries agents, since they have been shown to be effective
antiplaque agents. It has been shown by in vitro studies that
chlorhexidine is adsorbed onto the tooth surfaces and salivary
mucins, and then released very slowly in an active form.
Unfortunately , it has a bitter taste, produces a brownish
discoloration of hard and soft tissues and may produce a
painful desquamation of mucosa.
Due to stringent food and drug regulation, it is still not
available for patient use.
.
112. SILVER NITRATE
The earlier workers believed that the silver plugged the
enamel, either the organic invasion pathways such as the
enamel lamellae or the inorganic pathways, combining with
the soluble inorganic portion of enamel to form a less soluble
combination
ZINC CHLORIDE AND POTASSIUM FERROCYANIDE
Gottlieb in accordance with his theories of the importance
of the protein matrix of the enamel in the dental caries
process, proposed that the use of a solution of zince
chloride and potassium-ferrocyanide-would effectively
impregnate the enamel and seal off caries invasion pathway.
113. B. NUTRITIONAL MEASURES
On an individual basis, the dentist, dental hygienist
and/or dietician consultant can provide information
on safe foods and drinks.
But the ultimate responsibility for diet modification
lies in the individual. Voluntary dietary restriction
may suit some patients and certainly reduce caries
as evidenced by persons who have hereditory
fructose intolerance.
The function of the dental office personnel in diet
modification is one of counselling, providing
information, motivation and encouragment.
The diet used in caries prevention is essentially a
healthy, adequate, balanced diet and resembles a
normal diet except for the exclusion of a few food
components and eating practices.
114. Changes in dietary habits are reflected within a couple of
weeks in corresponding reductions in the numbers of oral
lactobacilli and streptococcus mutans.
Follow up visits are adivsed so that the patients diet can be
rechecked and further modifications adopted if necessary.
The control of dental caries through nutritional or dietary
means is impossible to achieve on the basis of a mass
prevention program and, for this reason, is relatively
unimportant in public health preventive dentistry is contrast
to fluoridation of water supplies.
The chief nutritional measure advocated for the control of
dental caries is restriction of refined carbohydrate intake. Only
the most cooperative patient will adhere rigidly to the type of
diet designed to reduce sugar consumption drastically.
For this reason, clinical studies on large groups of patients for
the purpose of ascertaining the extent of caries reduction that
would occur with restriction of sugar consumption are difficult
to carry out.
115. PHOSPHATE DIETS
Stralfors mixed 2% dibasic calcium phosphate into the
bread , flour, and sugar used in a school lunch program in
Sweden and obtained a significant reduction in caries
incidence in the maxillary incisors over a two year period.
Ship and Mickelsen found no meaningful reduction in the
caries attack rate of children consuming a diet in which
flour used in the preparation of bakery products was
supplemented with 2% calcium acid phosphate for three
years.
The cariostatic superiority of sodium dihydrogen phospate
over calcium acid phosphate was attributd to the greater
systemic action of the sodium salt as demonstrated by
radiophosphorus uptake studies on sound and carious
enamel.
116. PIT AND FISSURE SEALANTS
Pits and fissures of occlusal surfaces are among the
most difficult areas on teeth to keep clean and from
which to remove plaque.
Because of this, it was suggested many years ago that
prophylactic odontomy, the preparation of cavities in
these areas and their restoration by some material
such as amalgam before extensive decay had
developed, be carried out. In this way, these caries
susceptible pit and fissure areas would be made less
susceptible to subsequent caries.
The sealant is not necessarily required to fill the
entire depth of the fissure, but it must extend along
its entire length, bonding firmly at the fissure entry.
117. A major breakthrough in the efforts to produce an
effective sealant occurred when Buonocore reported
greatly improved retention of an acrylic filling material
to an enamel surface that had been etched with a 50%
phosphoric acid solution.
The etchant, referred to as a conditioning agent,
removes surface layers and a part of the enamel surface
to about 5-10um and thereby produce surface
irregularity into which the resin material penetrate and
polymerize.
118. CONCLUSION
Diagnosis prevention and treatment of dental caries must
be the foremost objectives of operative dentistry.
-Research efforts in understanding the caries process,
maximizing the benefits of fluoride and chlorohexidine
use, and perhaps, developing anti caries vaccines must
be continued
-patient education and motivation in the prevention and
treatment of dental caries must be stressed.
Finally the clinical treatment of cavitated carious teeth must
be accomplished judiciously and appropriately.
