1883- W.D. Miller found bacterial involvement in the
development of caries.
1891- G.V. Black put forth the concept of Extension for
1907- Mckaley in Colorado springs noticed decreased
incidence of caries in patients with mottled enamel.
1917- GV Black laid down the basic tenets for the design
of cavities prescribed for restoring carious lesion.
1945- sorbitol was recommended as a substitute for sucrose
due to its reduced fermentation .
1945- air abrasion was 1st described by Dr. Robert Black.
1951- S.S White Company- Air dent air abrasion unit.
1966- Markley modification of the cavity designs laid by Black
to more conservative preparation .
1969 : invention of glass ionomer cements (reported in 1971
by Wilson & Kent).
1974- Brudevold influence of fluoride.
1977- Simonsen introduced preventive resin restoration.
Mid 1980s- ART was pioneered in Zimbabwe and
1980- tunnel restoration was reintroduced by Hunt &
1997- new classification of caries by G.J. Mount and
The history of understanding caries in human has passed
through two distinct era.
The first , which is lasted until the twentieth century and may
still ongoing today, is the observational era.
The second, which is developed and revolutionized our
understanding of the causes and treatment ,is scientific
Still caries management is in gray year, in terms of
restoration and preventive dentistry.
Al Ismail et al, Dental caries in the second
millennium, journal of dental education
Dental caries is a microbial disease of the calcified tissues of
the teeth, characterized by demineralization of the inorganic
portion and destruction of the organic substances of the
Dental caries is the disease produced by metabolic end
products of certain micro organisms that results in dissolution
of inorganic components of enamel ,dentin and cementum
and degradation of their organic structure .
Dental caries is defined as a localized post eruptive,
pathological process of external origin, involving
softening of hard tooth tissues, and proceeding into
the formation of cavity.
It is an infectious microbial disease of the teeth that
results in localized dissolution and destruction of the
It is the most prevalent chronic disease affecting the human race. Once it
occurs, its manifestations persist throughout life even though the lesion is
There are practically no geographic areas in the world whose inhabitants
do not exhibit some evidence of dental caries.
It affects persons of both sexes in all races, all social- economic straits and
every age group.
It usually begins soon after the teeth erupt in the oral cavity. Persons who
never develop carious lesions are designated “caries free”. No satisfactory
explanation of their cario resistance has been found.
Hundreds of dental research investigators for more than a century have
studied various aspects of dental caries problems. Despite this extensive
investigation, Many aspects of etiology are still under observation and
efforts at preventions have been partially successful .
A detail of a tooth (to the right = enamel). It is covered
by plaque, which consists mainly of bacteria. Plaque is
often found close to the gum, in between teeth, in
fissures and at other "hidden" sites.
When sugar and other fermentable carbohydrates
reaches the bacteria, they form acids which start to
dissolve the enamel - an early caries lesion occurs
due to loss of Calcium and Phosphates
When sugar consumption has ceased, saliva can
wash away sugars and buffer the acids. Calcium
and Phosphates can again enter the tooth. The
process is strongly facilitated by fluorides
A CAVITY occurs if the Demineralization "wins" over the Remineralization over time
1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.
1.Based on anatomical site
2.Based on progression
3.Based on virginity of lesion
4.Based on extend of caries
5.Based on tissue involvement
6.Based on pathway of caries spread
7. Based on number of tooth surface involved
8. Based on chronology
9 .Based on whether caries is completely removed or not during treatment
10.Based on tooth surface to be restored
11.Black’s classification and Finn's modification
13.G.J Mount classification
OCCLUSAL(PIT AND FISSURE
LINEAR ENAMEL CARIES
Highest prevalence of all caries bacteria
rapidly colonize the pits and fissures of the
newly erupted teeth.
These early colonizers form a “bacterial
plug” that remains in the site for long time
,perhaps even the life of the tooth .
Type & nature of the organisms prevalent in
the oral cavity determine the type of
organisms colonizing the pit & fissure.
• Numerous gram positive cocci, especially dominated by
s.sanguis are found in the newly erupted teeth.
• The appearance of s.mutans in pits and fissures is usually
followed by caries 6 to 24 months later.
• Sealing of pits and fissures just after tooth eruption may be
the most important event in their resistance to caries.
• Shape, morphological variation and depth of pit and fissures
contributes to their high susceptibility to caries.
• Caries expand as it penetrates in to the enamel.
NANGO (1960):Based on the alphabetical description of shape–
I & U type: self cleansing and somewhat caries resistant.
V type: narrow slit like opening with a larger base as it extend
towards DEJ .Caries susceptible; also have a number of
K type: also very susceptible to caries.
Entry site may appear much smaller than
actual lesion, making clinical diagnosis
Carious lesion of pits and fissures develop
from attack on their walls.
In cross section, the gross appearance of
pit and fissure lesion is inverted V with a
narrow entrance and a progressively wider
area of involvement closer to the DEJ.
Less favorable site for plaque attachment, usually
attaches on the smooth surface that are near the
gingiva or are under proximal contact.
In very young patients the gingival papilla
completely fills the interproximal space under a
proximal contact and is termed as col. Also
crevicular spaces in them are less favorable
habitats for s.mutans.
Consequently proximal caries is less lightly to
develop where this favorable soft tissue
The proximal surfaces are particularly susceptible to caries
due to extra shelter provided to resident plaque owing to the
proximal contact area immediately occlusal to plaque.
Lesion have a broad area of origin and a conical, or pointed
extension towards DEJ.
V shape with apex directed towards DEJ.
After caries penetrate the DEJ softening of dentin spread
rapidly and pulpally.
Linear enamel caries ( odontoclasia ) is seen to occur in the
region of the neonatal line of the maxillary anterior teeth.
The line, which represent a metabolic defect such as
hypocalcemia or trauma of birth, may predispose to caries,
leading to gross destruction of the labial surface of the teeth.
Morphological aspects of this type of caries are atypical and
results in gross destruction of the labial surfaces incisor
The proximal root surface, particularly near the cervical
line, often is unaffected by the action of hygiene
procedures, such as flossing, because it may have
concave anatomic surface contours (fluting) and
occasional roughness at the termination of the enamel.
These conditions, when coupled with exposure to the
oral environment (as a result of gingival recession),
favor the formation of mature, caries-producing
plaque and proximal root-surface caries.
Root-surface caries is more common in older patients.
Caries originating on the root is alarming because
1. it has a comparatively rapid progression
2. it is often asymptomatic
3. it is closer to the pulp
4, it is more difficult to restore
The root surface readily allows plaque formation in the absence of good
The cementum covering the root surface is extremely thin and provides
little resistance to caries attack.
Root caries lesions have less well-defined margins, tend to be U-shaped
in cross sections, and progress more rapidly because of the lack of
protection from and enamel covering.
Acute caries is a rapid process involving a large number of teeth.
These lesions are lighter colored than the other types, being light
brown or grey, and their caseous consistency makes the
Pulp exposures and sensitive teeth are often observed in patients
with acute caries.
It has been suggested that saliva does not easily penetrate the
small opening to the carious lesion, so there are little opportunity
for buffering or neutralization.
• These lesions are usually of long-standing involvement, affect a
fewer number of teeth, and are smaller than acute caries.
• Pain is not a common feature because of protection afforded to
the pulp by secondary dentin
• The decalcified dentin is dark brown and leathery.
• Pulp prognosis is hopeful in that the deepest of lesions usually
requires only prophylactic capping and protective bases.
• The lesions range in depth and include those that have just
penetrated the enamel.
Caries which becomes stationary or static and does not show any
tendency for further progression.
Both deciduous and permanent affected.
With the shift in the oral conditions, even advanced lesions may
become arrested .
Arrested caries involving dentin shows a marked brown pigmentation
and induration of the lesion [the so called ‘eburnation of dentin’]
Sclerosis of dentinal tubules and secondary dentin formation
Exclusively seen in caries of occlusal
surface with large open cavity in
which there is lack of food retention.
Also on the proximal surfaces of tooth
in cases in which the adjacent
approximating tooth has been
A primary caries is one in which the
lesion constitutes the initial attack on
the tooth surface.
The designation of primary is based
on the initial location of the lesion on
the surface rather than the extent of
• This type of caries is observed around the
edges and under restorations.
• The common locations of secondary caries
are the rough or overhanging margin and
fracture place in all locations of the mouth.
• It may be result of poor adaptation of a
restoration, which allows for a marginal
leakage, or it may be due to inadequate
extension of the restoration.
• In addition caries may remain if there has
not been complete excavation of the
original lesion, which later may appear as a
residual or recurrent caries.
Recurrent carious lesion are mostly located on the
gingival margins of classII and classV restorations.
Overhangs, are predisposing factors for plaque
accumulation and development of recurrent caries.
The development of recurrent caries is unrelated to
Ivar A. Mjor et al ,Clinical diagnosis of
recurrent caries,Journal of American
Dental Association 2005;136:1426-1433.
Incomplete removal of caries is beneficial specially
in case of deep carious lesion in terms of risk of
pulpal exposure, post-operative pulpal symptoms,
overall failure, and caries progression.
Risk of failure is similar in complete or incomplete
F.Schwendicke et al, Incomplete caries
removal, Journal Of Dental Research
The early caries lesion, best seen on the
smooth surface of teeth, is visible as a
Histological the lesion has an apparently
intact surface layer overlying subsurface
Significantly may such lesion can undergo
remineralization and thus not an
indication for restorative treatment
These white spot lesion may be confused initially with white
developmental defects of enamel formation, which can be
differentiated by their position [ away from the gingival
margin], their shape [unrelated to plaque accumulation] and
their symmetry [they usually affect the contra lateral tooth].
Also on wetting the caries lesion disappear while the
developmental defect persist.
It is believed that bite wing and OPG radiographs
along with noninvasive adjuncts like fiber optic
transillumination (FOTI),laser luminescence,
electrical resistance method (ERM) are used for
diagnosis these occlusal lesions.
These lesion are not associated with microorganisms
different to those found in other carious lesion.
These carious lesion seem to increase with increasing
Occult carious lesion are usually seen with low caries
rate which is suggestive of increase fluid exposure.
It is believed that increased fluid exposure encourages
remineralization and slow down progress of the caries in the pit
and fissure enamel while the cavitations continues in dentine, and
the lesions become masked by a relatively intact enamel surface.
These hidden lesions are called as fluoride bombs or fluoride
Recently it is seen that occult caries may have its origin as pre-
eruptive defects which are detectable only with the use of
Once it reaches the dentinoenamel
junction, the caries process has the
potential to spread to the pulp along
the dentinal tubules and also spread
in lateral direction.
Thus some amount of sensitivity may
be associated with this type of lesion.
This may be generally accompanied
1. Initial caries
2. Superficial caries
3. Moderate caries
4. Deep caries
5. Deep complicated caries
Dental caries can be divided into 4 or 5 stages
Initial caries: Demineralization without structural defect.
This stage can be reversed by fluoridation and enhanced
Superficial caries (Caries superficialis):Enamel caries,
wedge-shaped structural defect. Caries has affected the
enamel layer, but has not yet penetrated the dentin.
3. Moderate caries (Caries media): Dentin caries. Extensive
structural defect. Caries has penetrated up to the dentin
and spreads two-dimensionally beneath the enamel defect
where the dentin offers little resistance.
4. Deep caries (Caries profunda): Deep structural defect. Caries
has penetrated up to the dentin layers of the tooth close to
5. Deep complicated caries (Caries profunda complicata) :Caries
has led to the opening of the pulp cavity (pulpa aperta or
caries involving only one
caries involving two surfaces
caries that involves more than
two surfaces of a tooth
Early childhood caries
Early childhood caries(ECC) would
include, two variants: Nursing
caries and rampant caries.
The difference primarily exist in
involvement of the teeth
[ mandibular incisors ] in the
carious process in rampant caries
as opposed to nursing caries.
Type I(MILD )
Involves molars and incisors
Seen in 2-5 years
Causecariogenic semisolid food +lack of oral hygiene
Type II (MODERATE)
Unaffected mandibular incisors
Soon after first tooth erupts
Causeinappropriate feeding +lack of oral hygiene
All teeth including mandibular incisors
Causemultitude of factors
Emma O’ Keefe confirmed that factors occurring
during the first year of life affect ECC. Also found
that maternal factors influence bacterial acquisition,
whereas colonisation was mediated by oral health
behaviour and practices and feeding habits.
Emma O’Keefe, Early childhood
caries,Evidence based dentistry
Seen in infant and toddler
Affects primary dentition
Mandibular incisors are
Pacifier dipped in honey/other
Seen in all ages, including
Affects primary and Permanent
Mandibular incisors are also
Sticky refined CHO
This type of caries is a variant of rampant caries where the
teeth generally considered immune to decay are involved.
The caries is also described to be of a rapidly burrowing type,
with a small enamel opening.
The presence of a large pulp chamber adds to the woes,
causing early pulp involvement.
With the recession of the gingiva and sometimes decreased
salivary function due to atrophy, at the age of 55-60 years,
the third peak of caries is observed.
Root caries and cervical caries are more commonly found in
Sometime they are also associated with a partial denture
Residual caries is that which is not
removed during a restorative procedure,
either by accident, neglect or intention.
Sometimes a small amount of acutely
carious dentin close to the pulp is
covered with a specific capping material
to stimulate dentin deposition, isolating
caries from pulp.
The carious dentin can be removed at a
Most widespread clinical utilization
O for occlusal surfaces
M for mesial surfaces
D for distal surfaces
F for facial surfaces
B for buccal surfaces
L for lingual surface
Various combinations are also possible, such as MOD –for mesio-
Class 1 lesions:
•Lesions that begin in the structural defects
of teeth such as pits, fissures and defective
Occlusal surface of molars and premolars.
Occlusal two thirds of buccal and lingual
surfaces of molars and premolars.
Lingual surfaces of anterior tooth.
Class 2 lesions:
They are found on the proximal surfaces of the bicuspids
Class 3 lesions:
Lesions found on the proximal surfaces of anterior teeth
that do not involve or necessitate the removal of the
Class 4 lesions:
Lesions found on the proximal surfaces of anterior teeth
that involve the incisal angle.
Class 5 lesions:
Lesions that are found at the gingival third of the facial
and lingual surfaces of anterior and posterior teeth.
Class 6 (Simon’s modification):
Lesions involving cuspal tips and incisal edges of teeth.
Class1 : cavities involving the pits and fissure of molar
teeth and the buccal and lingual pits of all teeth.
Class 2: cavities involving proximal surface of molar teeth
molar teeth will access established from the occlusal
Class 3: cavities involving proximal surfaces of anterior teeth
which may or may not involve a labial or a lingual extension.
Class 4: a restoration of the proximal surface of an
anterior tooth which involves the restoration of an incisal
Class 5: cavities present on the cervical third of all teeth,
including proximal surface where the marginal ridge is not
included in the cavity preparation.
In this classification the shape and depth of the caries
lesion scored on a four point scale
D1. clinically detectable enamel lesions with intact (non
D2. Clinically detectable cavities limited to enamel.
D3. Clinically detectable cavities in dentin.
D4. Lesions extending into the pulp.
•This new system defines the extent and complexity of a
cavity and at the same time encourages a conservative
approach to the preservation of natural tooth structure.
•This system is designed to utilize the healing capacity of
enamel and dentine.
Pits, fissures and enamel defects on occlusal
surfaces of posterior teeth or other
Proximal enamel immediately below areas in
contact with adjacent teeth.
The cervical one third of the crown or
following gingival recession, the exposed
Size1:Minimal involvement of dentin just beyond treatment
by remineralization alone.
Size2: Moderate involvement of dentin. Following cavity
preparation, remaining enamel is sound, well supported by
dentin and not likely to fail under normal occlusal load. The
remaining tooth structure is sufficiently strong to support
Size 3: The cavity is enlarged beyond moderate. The remaining
tooth structure is weakened to the extent that cusps
or incisal edges are split, or are likely to fail or left
exposed to occlusal or incisal load. the cavity needs to
be further enlarged so that the restoration can be
designed to provide support and protection to the
remaining tooth structure.
Size4: Extensive caries with bulk loss of tooth structure has
•Radiography is frequently associated with xerostomia due to
decreased salivary secretion, an increase in viscosity and low
•This and other causes of decreased salivary secretion may
lead to a rampant form of caries, including the significance of
saliva in preventing caries.
Three types of defects due to
1. Lesion usually encircling the neck of
teeth amputation of crowns may
2. Begins as brown to black
discoloration of tooth .Occlusal
surface and incisal edges wear away.
3. Spot depression which spreads from
any surface .
Caries causes damage by demineralization and
dissolution of tooth structure
sucrose +cariogenic plaque
lowering of ph(if below 5.5)
dissolution of tooth mineral
In caries active individual ph remains below 5.5 for
20-50 mins following single exposure to sucrose.
WORMS – According to the ancient
Sumerian text, toothache was caused by a worm
that drank the blood of the teeth and fed on the
roots of the jaws.
This legend of the worm was discovered on one
of many clay tablets excavated near Niffer, Ur, and
other cities within the Euphrates valley of the
lower Mesopotamian area and estimated to date
from about 5000 BC. Oracle bones from the shang
dynasty, dating before 1000 BC, bear the Chinese
character for caries.
The idea that caries is caused by a worm was
almost universal at one time, as evidenced by the
writing of Homer and popular lore of China,
India, Finland, and Scotland .
GUY DE CAHULIAC (1300- 1368)-The greatest surgeon of
middle ages believed that worms caused dental decay .As a
cure he advocated fumigation with seeds of leek, onion and
hyoscyamus. The Chinese and Egyptians used fumigation in
earlier times, and fumigation devices continued to be used in
England as early as the nineteenth century.
HUMORS – The ancient Greeks considered that a persons
physical and mental constitution was determined by the
relative proportions of the four elemental fluids of the body
- blood, phlegm, black bile, and yellow bile which
corresponds to the four humors –sanguine, phlegmatic,
melancholic and choleric .All diseases, including caries could
be explained by an imbalance of those humors.
The vital theory regarded dental caries as originating within the
tooth itself, analogous to bone gangrene.
This theory proposed at the end of eighteenth century, remained
dominant until the middle of the nineteenth century .
A clinically well known type of caries is characterized by
extensive penetrations into the dentin, and even into the pulp,
but with a barely detectable catch or a fissure.
Parmly (1819) rebelled against the vital theory and proposed
that an unidentified “chemical” agent was responsible for
caries .He stated that caries began on the enamel surface in
locations where the food putrefied and acquired sufficient
dissolving power to produce the disease chemically.
Support for the chemical theory came from Robertson (1835)
and Regnart (1938) who actually carried out experiments with
different dilutions of organic acids (such as sulphuric and
nitric) and found that they corroded enamel and dentin.
1843 erdl described filamentous parasites in the “ surface
membrane” of teeth.
Shortly thereafter Ficinus ,a Dresden physician observed
filamentous microorganisms ,which he called denticulate in
material taken from carious activities .He implied that these
bacteria caused decomposition of the enamel and then the
Neither erdl nor ficinus explained how these organisms
destroyed tooth structure.
This theory is a blend of the above two theories, because it
states that caries is caused by acids produced by
microorganisms of the mouth. it has been customary to credit
this theory to W. D miller (1890), whose writings and
experiments helped to establish this concept on a firm basis.
The work of W. D Miller (1853-1907) at the university
of Berlin has a most profound effect on the understanding of
caries etiology and subsequent caries research.
In a series of experiments Miller demonstrated the following facts,
Acid was present within the deeper carious lesions, as shown
by reaction on litmus paper.
Different kinds of foods (bread, sugar, but not meat) mixed with
saliva and incubated at 37 ⁰C could decalcify the entire crown
of a tooth .
Several types of mouth bacteria (at least 30 species where
isolated) could produce enough acid to cause dental caries.
Lactic acid was an identifiable product in carbohydrate –saliva
incubation mixtures .
Different microorganisms (filamentous ,long and short bacilli
,and micrococci ) invade carious dentin .
Miller concluded that no single species of microorganism
caused caries but rather that the process was mediated by an
oral microorganism capable of producing acid and digesting
According to this theory , the organic component is most
vulnerable and is attacked by hydrolytic enzymes of
microorganisms ,this precedes the loss of the inorganic phase .
Gottlieb (1944) maintained that the initial action was due to
proteolytic enzymes attacking the lamellae ,rod sheaths ,tufts
and walls of the dentinal tubules.
o He suggested that a coccus, probably staphylococcus aureus
,was involved because of the yellow pigmentation that he
considered path gnomonic of dental caries .
Frisbie (1944) also described caries as a proteolytic process
involving depolymerization and liquefaction of the organic
matrix of enamel. The less soluble inorganic salts could then
be freed from their “organic bond” favoring their solution, by
acidogenic bacteria that secondarily penetrate along widening
paths of ingress .
Pincus (1949) contended that proteolytic organisms first
attacked the protein elements ,such as the dental cuticle and
then destroyed the prism sheaths. The loosened prisms
would then fall out mechanically.
He also suggested that sulfatases of gram-negative bacilli
hydrolyzed “mucoitin sulfate” of enamel or chondrotin
sulphate of dentin and produced sulfuric acid . The released
sulfuric acid could combine with the calcium of the mineral
It should be noted that the composition of the organic
components of enamel does not resemble that of connective
tissue and an abundance of sulphated polysaccharides has
not been demonstrated. The pincus’ theory remains
,therefore ,without experimental support.
According to this theory, decalcification is mediated by a
variety of complexing agents ,such as acid anions ,amines
,amino acids ,peptides polyphosphates ,and carbohydrate
derivatives .oral karatinolytic bacteria are thought to be
involved in the process. Differences in the keratin content of
the enamel in children with high caries and low caries
experience are considered important . It should be noted
that only a small fraction of the protein of enamel bears any
resemblance to the keratin of hair.
Schatz and Martin challenged the chemo-parasitic theory
advocated the proteolysis – chelation theory and stated that
acid may prevent tooth decay by interfering with growth and
activity of protolytic bacteria .
Dental caries is a multifactorial disease in which there is interplay
of three principle factors – the HOST ( primarily the saliva and
teeth ) , the MICROFLORA , and the SUBSTRATE , or diet . In
addition a fourth factor TIME must be considered in the etiology of
For caries to occur , conditions within each of these factors must
be favorable . In other words caries requires a susceptible host, a
cariogenic oral flora , and a suitable substrate .
Micro flora: Acidogenic bacteria that colonize the tooth
Host: quantity and quality of saliva, the quality of the
Diet: intake of fermentable carbohydrates, especially
sucrose, but also starch.
Time: Total exposure time to inorganic acids produced
by the bacteria of the dental plaque.
Bacteria metabolize sugars and produces acid.
pH decreases and enamel demineralised.
Bacterial colonization and acid production increases without
Demineralisation vs. Remineralisation.
Saliva refers to the mixture of secretions in the oral cavity .
The mixture consists of fluids derived from the major salivary
glands ( Parotid , submandibular , sublingual ) from the minor
glands of the oral mucosa and traces from the gingival
There is no doubt that saliva significantly influences the
caries process as evidenced by animal experiments in which
the salivary glands are surgically extirpated . It is only fair to
point out that removal of salivary glands is a drastic procedure
affecting, in addition to saliva other factors which in
themselves influence caries development. These factors
include 1) Difference in food and water consumption 2) Longer
eating time 3) Greater food retention 4) Possible alterations in
the bacterial flora of the mouth . 5)Maturation of the enamel .
Tooth morphology and arch form
A susceptible host is one of the factors required for caries to
occur . Tooth morphology has long been recognized as an
important determinant . For example attempts to induce caries
in dogs have been unsuccessful mainly because of the wide
spacing and the conical shape of the teeth .
On the basis of clinical observation it is known that the pit and
fissure areas of the posterior teeth are highly susceptible to
caries . Food debris and microorganisms readily impact in the
Certain surfaces of the tooth are more prone to decay whereas
other surfaces rarely show decay . For eg. In mandibular first
molar the likelihood of decay in descending order is occlusal ,
buccal , mesial , distal and lingual , whereas in maxillary first
molars the order is occlusal , mesial , palatal , buccal and distal.
An intraoral variation exists in susceptibility to caries
between different tooth types . The more susceptible
permanent teeth are the mandibular first molars closely
followed by the maxillary first molars and the mandibular and
maxillary second molars . The second premolars , the maxillary
incisors and the first premolars are the next in sequence ,
whereas the mandibular incisors and canines are the least
likely to develop lesions .
Irregularities in arch form , crowding , and overlapping of
the teeth also favor the development of carious lesions .
There is good evidence to indicate that enamel surface is
more caries resistant than the sub surface .
A pumping mechanism has been proposed whereby matter
is transported from the inner enamel to the surface zone
and from the surface zone to the saliva .
There is net movement of inorganic mineral phase from
the inner enamel to the oral cavity. The surface enamel
appears unaltered simply because it is continuously being
regenerated by precipitation of solid phases .
However , when “white spots” have been examined by
scanning electron microscopy , the initial stage of such
active carious lesions has been characterized by openings
in the outer enamel surfaces through eroded focal holes .
Accordingly , the concept of a relatively ineffective surface
layer , described in transverse sections examined by micro
radiography or light microscopy , needs revision in view of
the surface defects, which represents signs of focal
By transmission electron microscopy , the enamel surface is
seen to be dented by irregular destruction of appetite
crystals . Small micro defects starting at the enamel surface
and reaching the deeper enamel layers have been observed .
Changes of the enamel such as decrease in density and
permeability and an increase in nitrogen and fluoride
content, occurs with age .
These alterations are part of the post eruptive “maturation”
process whereby teeth become more resistant to caries with
The concentration of fluorides of the surface layer of enamel
increases as the fluoride concentration of the drinking water
increases, and such enamel is less soluble in acids.
Furthermore , the higher the fluoride concentration of the
water supply , the lower the prevalence of caries .
Microorganisms implicated in the etiology of dental caries must be
acidogenic as well as acidouric to initiate carious lesions.
In enamel the microorganisms must be able to colonize the tooth
surface and survive in competition with less harmful species
,forming bio films –the so called Dental Plaque .
As early as 1960 ,Fitzgerald and keys showed that certain
microorganisms isolated from human dental plaque when
inoculated in germ-free rodents on a high –sucrose diet ,resulted
in the spread of rampant caries. Therefore dental caries should be
regarded as an infectious transmissible disease .
Three cariogenic bacteria
S.mutans, s.sobrinus, s.sanguinis, s.salivariaus, s.milleri
While not the first colonize the tooth, studies have shown
S.mutans to be the main culprit in dental caries
There is abundant support for the so –called specific plaque hypothesis
,introduced by Loesche(1982,1986) ,which proposes that some specific
species of the plaque flora be regarded as major pathogens in the etiology of
dental caries . Included in the major pathogens are those bacteria associated
with caries in humans and also able to induce carious lesions in experimental
animals .The most important are the mutans streptococci, there are seven
species, of which two s.mutans and s.sobrinus ,are closely associated with
caries in humans .
The second genus closely associated with caries is lactobacillus ,commonly
isolated from carious dentin .
Also associated with the etiology of dental caries ,but considered to be less
cariogenic than s.mutants ,s. sobrinus .and lactobacillus, are actinomyces
odontologica, actinomyces naeslundii, and some other species of mutant
Dental caries is a bacterially based disease. When it progresses,
acid produced by bacterial action on dietary fermentable
carbohydrates diffuses into the tooth and dissolves the carbonated
hydroxyapatite mineral—a process called demineralization.
Pathological factors including acidogenic bacteria (mutans
streptococci and lacto- bacilli), salivary dysfunction, and dietary
carbohydrates are related to caries progression.
Protective factors—which include salivary calcium, phosphate and
proteins, salivary flow, fluoride in saliva, and antibacterial
components or agents— can balance, prevent or reverse dental
Caries progression or reversal is determined by the balance between
protective and pathological factors.
Fluoride, the key agent in battling caries, works primarily via topical
mechanisms: inhibition of demineralization, enhancement of
remineralisation and inhibition of bacterial enzymes.
Fluoride in drinking water and in fluoride-containing products reduces
caries via these topical mechanisms.
Antibacterial therapy must be used to combat a high bacterial
challenge.For practical caries management and prevention or reversal of
dental caries, the sum of the preventive factors must outweigh the
John D.B. Featherstone, science and practice of caries
prevention, JADA 2000;131:887-898
In 1924 Clarke isolated a streptococcus that predominated in many
human carious lesions and that he named streptococcus mutans
because of its varying morphology. Clarke noted that s.mutans
adhered closely to tooth surfaces in artificially induced caries .For the
next 40 years, s.mutans was virtually ignored , until the 1960s when
it was “ rediscovered” and its prevalence in plaque confirmed .
Characteristics of this group of streptococci have been described
.They are non motile , catalase-negative, gram –positive cocci in short
or medium chains . On mitis-salivarius agar they grow as highly convex
to pulvinate (cushion –shaped)colonies. These colonies are opaque
;the surface resembles frosted glass.
These s.mutans variants also posses caries –inducing properties ,and
when re-isolated from infected animals they may resume the original
rough colonial form.
When cultured with sucrose they form polysaccharides that are
insoluble or can be precipitated with one part ethanol .This
property of forming insoluble extra cellular polysaccharides from
sucrose is regarded as an important characteristic contributing to
the caries –inducing properties of s.mutans.
Mutants of s.mutans ,which lack the ability to synthesize
insoluble glucans or to stick to glass surfaces, do not cause smooth
Streptococcus mutans exhibits several important properties ;
1) it synthesizes insoluble polysaccharides from sucrose
2) it is a homo fermentative lactic acid former .
3) it colonizes on tooth surfaces
4) it is more aciduric than other Streptococci
cariogenic strains of S.mutans contain lysogenic bacteriophage
,which has not been isolated from non cariogenic strains . Non
cariogenic mutants of S.mutans are unable to adhere to glass and
have decreased ability to form insoluble polysaccharide .If this
mutants are infected with lysogenic phages , they are transformed
, acquiring the ability to adhere and form abundant insoluble
s.mutans isolates can be grouped into three “chemotypes” based on
differences in the composition of the cell wall. Atleast seven sero types of
S.mutans have been found . Compared to s.sanguis ,s mutans is more
aciduric and can reproduce in a culture medium at a pH as low as 4.3.
S.mutans forms a homogenous group , based on physiological
,ecological ,and morphological characteristics ,and has been recognized
as a distant species by the National Communicable Disease Center
.However ,analysis of the guanosine and cytosine content and
hybridization studies on the homologies of the DNA isolated from strains
of s.mutans revealed significant differences . These cariogenic organisms
,though phenotypically similar ,are genetically heterogeneous ,and were
therefore divided into five genotypes or “genospecies”.
However, because their nucleic acid base content and
sequence are too disparate ,these “mutans –like” organisms
have been divided into separate species , namely s.mutans,
streptococcus rattus ,streptococcus sobrinus ,streptococcus
ferus of the “mutans –group”.
s.mutans, s.rattus ,and s.cricetus have been accepted and
appear on the Approved Lists of Bacterial Names.
S.mutans and S.sobrinus are most commonly found in
human plaque . S.cricetus and s rattus are less common in
humans ,and s.ferus only occurs in rats .
Lactobacilli are gram positive ,non spore –forming rods that
generally grow best under micro aerophilic conditions.
Isolation and enumeration of oral lactobacilli have been
facilitated by use of selective agar medium which suppresses
the growth of other oral organisms by its low pH (5.4) .
Lactobacilli are found mostly as transients in the mouth of
infants . Lactobacilli represents about 1% of the oral flora.
L.casei and L.fermentum are the most common oral species. T
he population of oral lactobacilli is influenced by dietary habits.
A favorite habitat of lactobacilli is in the dentin of deep carious
Lactobacilli and its role in caries.
Lactobacilli, or organisms resembling lactobacilli have been
reported in the oral cavity ever since Miller enunciated the chemo
parasitic theory. In 1925, Bunting and his collaborators claimed that
bacillus Acidophilus was the specific etiological factor responsible for
the initiation of caries. Subsequent investigators have isolated other
types of lactobacilli besides L. acidophilus in saliva, plaque, and
Small anaerobic lactobacilli (L minutus) have been isolated
consistently from pockets of patients with chronic periodontitis. The
genus lactobacillus includes many species with a broad range of
guanosine + cytosine content. The following are the most commonly
encountered in the mouth.
The following are the most commonly encountered in the mouth.
L. casei L. fermentum
L. acidophilus Actobacillus brevis
Lactobacillus plantarum Lactobacillus buchneri
Lactobacillus salivarius Lactobacillus cellobiosus
In isolates of lactobacilli from human carious dentin, the
homofermentative out numbered the heterofermentative variety.
It was argued that lactobacilli are both acidogenic and aciduric and could,
therefore, multiply in the low pH of plaque and carious lesions. Using
selective culture media , counts of lactobacilli in the saliva could be
correlated with the prevalence of dental caries. Furthermore the growth site
of lactobacilli was reported to correspond to the sites of clinically diagnostic
• When such lesions were restored, most of the growth sites of the lactobacilli
Acceptance of the doctrine that lactobacilli were the
etiological agents of dental caries was not universal, however
as more information on the microbial composition of dental
plaque became available it was found that lactobacilli
constitute only a minor fraction (1/10000) of the plaque flora
Amount of acid that can be formed by the relatively small
number of lactobacilli present in plaque is almost insignificant
in comparison with that produced by other acidogenic oral
micro organisms. In humans lactobacilli can be isolated from
the saliva, tooth surfaces, dorsum of the tongue, vestibular
mucosa, and hard palate.
L.acidophilus is most frequently isolated from saliva.
Lactobacilli have a relatively low affinity for the tooth surface.
The establishment of oral lactobacilli coincides with the
development of carious lesions. L casei is the predominating
lactobacillus in dental plaque and carious dentin. Fitzgerald
interprets such data to mean that lactobacilli are more a
consequence than a cause of caries initiation.
Actinomyces is a gram –positive ,nonmotile ,non-spore-
forming organisms occurring as rods and filaments that vary
considering in length . Filaments are usually long and slender
and are branching .
The species that have been found in the oral cavity are:
Facultative anaerobic Anaerobic
A. naeslundii A .israelii
A. viscosus Actinomyces meyeri
All species of Actinomyces ferment glucose ,producing
mostly lactic acid ,lesser amounts of acidic and succinic acid
,and traces of formic acid.
Most interest has centered on A.viscosus and A naeslundii
because of their ability to induce root caries, fissure caries ,and
periodontal destruction when inoculated into gnotobiotic rats .
A viscosus has been separated into two ,and A naeslundii into
four ,serological types.
Actinomyes is a good plaque former ,capable of adhering to
wires and forming tenacious deposits on the teeth.
It is the most common group of microorganisms isolated
from the sub gingival micro flora and from plaque of human
root surfaces caries.
It is found in the supragingival plaque of all children and
comprises about 50 % of all cells present.
A naeslundii predominates in the tongue ,salivary flora ,and
in the plaque of young children ,while plaque from teenagers
and adults has a higher proportions of A viscosus.
Ingestion of food may affect oral-dental health care by both systemic and
local mechanisms .
Nutritional effects are mediated systemically ; dietary effects are mediated
locally in the oral cavity .
The systemic effects results from the absorption and circulation of nutrients
to all cells and tissues and may be mediated through influences on
development of teeth , the quality and quantity of salivary secretions ,
improved host resistance and improved function .
Dietary constituents exert their local effects by influencing the metabolism
of oral flora and by modifying salivary fluids and indirectly the qualitative
aspects of salivary secretion .
Dental caries is a interaction between diet, cariogenic flora and
tooth of the host.
Significant, also , is the fact that the tooth is relatively passive in
the caries process. The environmental challenge to teeth from
products of bacterial substrate reactions is often the most
important variable in the caries process. Thus , even teeth that
are well formed and mineralized cannot withstand a strong
environmental challenge from the chemical by-products of a
highly cariogenic flora and a high concentration of the substrate
in the oral cavity .
Also diets and eating patterns change with age, making it difficult
to assess nutrition influences on dental tissue .
Metabolism of Vitamin D : Vit. D along with Parathyroid hormones and
calcitonin play primary roles in regulating the concentration of calcium
and inorganic phosphate in the plasma and extracellular fluids ,by
regulating the movement of these ions in and out of cell and in
controlling mineralization of bones and teeth .
Enamel Hypoplasia : Enamel Hypoplasia is the most common abnormality
of development and mineralization of human teeth . The lesion is
characterized by a quantitive defect in enamel tissue resulting from a
undetermined metabolic injury to the formative cells - Ameloblasts .
Recent evidences have suggested that the etiology of enamel hypoplasia
is highly specific and linked with disorders of calcium and phosphate
haemostasis .Enamel hypoplasia was found in conditions characterized
bu hypocalcaemia but not in those characterized by hypophosphotemia .
( Nikiforuk and Fraser , 1981 ) .
Clinically enamel hypoplasia is seen as a roughened surface
with discreet pitting or circumferential band like irregularities
which post eruptively acquire a yellow brown stain.
Enamel hypoplasia is clinically significant not only because of
its disfiguring and the restorative treatment cause ,but
because it may effect caries susceptibility.
Mellanby (1936) reported that there is a strong co-relation
between hypoplasia in the teeth of British school children and
caries susceptibility . Similarly , various other studies by Allen ,
1941 ; Bibby , 1943 ; Carr , 1953 have reported similar
The only member of the vitamin B complex which has been associated
with caries is pyridoxine ( Vitamin B6) . The vitamin has been stated to
reduces caries in rats . But the effect was not confirmed on monkeys .
( Cole et al , 1980 )
These experiments do not suggest that deficiency of pyridoxine is
responsible for caries but that large unphysiological doses , in which
pyridoxine is being used as a drug rather than as a vitamin reduces caries
by modifying the oral flora .
Deficiency of essential fatty acids in man is rare and
evaluation of the role of these nutrients on caries rates is not
Fat consumed post eruptively in diets of animals , has been
co-related with caries reduction .
( Williams et al , 1982 )
where Kwashiorkor is prevalent .
Low intake of cariogenic food .
Shaw, 1970 and Navia, 1979 showed that protein
deficiency induced in rats caused:
-smaller teeth ,
-a delay in eruption ,
- and a greater susceptibility to caries .
These may be due to reduced salivary flow and therefore
reduced total buffering capacity , reduced remineralization
and anti-bacterial activity.
Intolerance to disaccharide or monosaccharide occurs because of a
deficiency of a specific enzyme involved in the metabolism of sugar.
A condition known as hereditary fructose intolerance provides direct
link between sugar ingestion and dental caries.
Hereditary fructose intolerance
In 1959 Froesch described an inborn error of fructose metabolism
transmitted by an autosomal recessive gene .
Episodes of pallor, nausea vomiting ,coma and convulsions
following ingestion of fruit containing fructose or cane sugar.
Tolerance test shows marked hypoglycemia(8mg/100ml, a sharp
increase in blood fructose concentration ,and drop in serum
Persons with Hereditary fructose intolerance show a
strikingly reduced dental caries experience when
compared to a controlled population of the same
Constituents : Polysaccharides and Sugars
• The four carbohydrates starch, sucrose , fructose and
glucose comprise the greatest proportion of foods consumed
• The main polysaccharide(starch) is not highly cariogenic in
animals or man at least in some circumstances.
Excessive and frequent use of highly fermentable mono-and
disaccharides is correlated with high caries rate.
While Glucose , Fructose , Lactose and Mannose have been shown
to be cariogenic in animal experiments, they are usually minor
constituents of human foods as they are present only in dried fruits ,
honey and milk .
Sucrose is by far the commonest dietary sugar consumed and is
considered ARCH CRIMINAL OF ORAL CAVITY.
Physical Properties of Foods and Cariogenicity
Some important physical properties that determine food texture
1) Mechanical properties : hardness , cohesiveness , viscosity ,
2) Geometric properties: particle size and shape.
3) others : moisture and fat contents .
• From a dental stand point the physical properties of food may
have significance by affecting food retention , food clearance ,
solubility and oral hygiene .
• Adhesive properties of foods have been measured and
correlated with their retention in the mouth after ingestion .
The high fibrous , cellulose content of plant foods exert a
mechanical cleansing action on teeth
The physical texture and chemical composition of food is known to
effect salivary flow rates .Saliva that is rapidly flowing is more
alkaline than the resting saliva and more super saturated with
calcium and phosphate and thus may be more caries inhibitory.
Physical properties of food , particularly those that improve the
cleansing action and reduce the retention of food within the oral
cavity and increase saliva flow , are to be encouraged in everyday
diets . However , clinical evidence that consumption of these food
items will significantly reduce caries , is lacking.
saliva incubated with refined foods caused a greater
dissolution of tooth enamel than when incubated with
unrefined foods .
Mixtures that included bran , wheat germ , unrefined treacle
and cane juice contained protective factors .
The protective substance identified was Phytate – a
polyphosphate, which when applied to tooth enamel reduces
its solubility and has caries inhibiting effects.
Some dietary items are highly acidic and affect the pH in
plaque and saliva .
Natural foods such as lemons , apples , fruit juices and
carbonated beverages , are sufficiently acidic as to cause
demineralization of enamel that is in prolonged contact with
Prime culprit of Dental decay and Periodontal diseases .
Plaque – a soft adherent collection of salivary products and
bacterial colonies on the teeth .
It accumulates on the surface of the teeth continuously
throughout the life span.
Eliminating this disease producing material is by continuously
removing it by tooth brush and dental flossing.
Unrestricted plaque growth
that may promote the
accumulation of pathogenic
bacterial species .
High frequency sucrose
exposure is the single most
important factor in
producing a cariogenic
The factors that control the presence of individual species in
plaque are termed ecological determinants.
- Host resistance
- extent and nature of shelter for bacteria
- host diet
- oral hygiene
- status of the dentition
- and composition of the oral flora .
These various factors can be viewed as links in a chain of
reactions eventually leading to caries.
Plaque growth begins approximately six hours after the
thorough cleaning of the teeth.
The first phase of plaque development is the deposition of
adherent products from the saliva.
Composed of mucin, which forms the thin adherent layer on
the teeth called the pellicle .
Once the pellicle has been formed on the clean tooth
surface, bacteria that inhabit the oral cavity attach
themselves to the pellicle. After attachment ,the bacteria
multiplies to form large masses of bacterial colonies.
These begin to occur approximately eighteen hours after
thorough cleaning of the teeth and continue until the plaque
is fully mature at the end of three weeks.
Mature plaque consists primarily of bacteria of various types.
Some bacteria produce harmful chemical substances and
others produce substances that are needed by neighboring
bacteria to survive.
Still other organisms produce adherent substances that are
interspersed with the bacteria and hold the plaque intact on
Supra gingival plaque consists of a different combination of bacteria than
Sub gingival plaque.
The bacteria in supra gingival plaque is capable of producing acids that
can erode the surface of the tooth and also thrive in an acidic
The sub gingival plaque consists of bacteria that do not grow well in the
presence of acid. It does not produce acids, but rather other chemical
compounds that penetrate the soft gingival tissue and cause it to become
Therefore, supra gingival plaque, because of its acidic nature, is
responsible for dental caries. Sub gingival plaque because of its capacity
to produce substances that are toxic to soft tissues, is responsible for
Streptococcus mutans is one of the first organisms to attach
to the pellicle and multiply.
The streptococci are capable of producing both
polysaccharides and acids from carbohydrates.
These polysaccharides help attach the streptococci to the
The acid they produce is capable of demineralizing the
enamel layer of the tooth.
Other organisms in dental plaque produce various
substances that help the bacteria mass attach to the pellicle.
The plaque because of its thickness and density prevents
acid produced within it from being diluted by saliva or
neutralized by chemicals contained in the saliva.
Therefore the acid rather concentrated adjacent to the tooth
surface can break down the enamel more quickly.
Once the caries process is initiated, another organism,
lactobacillus, can become retained in the decayed area. Since
the lesion is acidic, these organisms thrive and like those of
streptococcus mutans, they convert sugar to acid, which in
turn attacks tooth structure.
The small lesion had has been divided into zones based upon its
histological appearance when longitudinal ground sections are
examined with light microscope.
It is subdivided into 4 zones
Translucent zone at the inner advancing front of the lesion.
Dark zone lies superficial to the translucent zone.
The Body of the lesion is the third zone and lies between the dark
zone and the apparently undamaged enamel surface..
Unaffected zone is the fourth zone and is superficial to the lesion .
Early smooth surface caries ,ground section visualized by polarized light after Imbibition
with quinoline The dark zone shows positive birefringence (golden brown) and surrounded
by peripheral translucent zone (left), In white. The Body of the lesion has become positively
birefringent while the surface zone appears to be unaffected as shown negative (blue –green)
birefringence (middle) .In the dry specimen the surface zone still shows some negative
bifrengerence indicating that it has lost not more than approx 1% of its mineral content, in
contrast to the 25% mineral loss more deeply (right).
The deepest zone and represents the advancing front of the
Has a structure less appearance when perfused with quinoline
solution and examined with polarized light .
Pores or voids form along the enamel prism (rod) boundaries,
presumably because of the ease of hydrogen ion penetration
during the carious process.
When these boundary area voids are fitted with quinoline
solution, (same R.I as enamel) the features of the area disappear.
The pore column of translucent enamel caries is 1%, 10 times
greater than normal enamel.
The next deepest zone is dark zone
because it does not transmit polarized
light. The light blockage is caused by the
presence of many tiny pores too small to
These smaller air or vapor filled pores
make the region opaque.
The total pore volume is 2% to 4% .
There is some speculation that the dark
zone is not really a stage in the sequence
of the breakdown of enamel, rather the
may be formed by deposition of ions into
an area previously only containing large
Experimental remineralization has demonstrated increase in
the size of the dark zone at the expense of the body of the
lesion. There is also a loss of crystalline structure in the
dark zone, Suggesting of a process of demineralization and
The size of the dark zone is probably an indicator of the
amount reminerlization that has recently accoured .
The body of the lesion is the largest
portion of the incipient lesion. It has pore
volume , varying from 5% at the
periphery to 25% at the center.
The striae of Retzius are well marked in
the body of the lesion indicating
preferential mineral dissolution along the
areas of relatively higher porosity.
The first penetration of caries enters the
enamel surface via the striae of Retzius.
The inter prismatic areas and these cross-
striations provide access to the rod
(prism) cores, which are then
Bacteria may be present in this zone if the
pore size is large enough to permit their
Early smooth surface caries ; ground section
shows the body of the lesion, containing
Enhanced striae of retzius ,enclosed
between the dark and peripheral translucent
zones and the intact surface.
It is relatively unaffected by the caries attack.
It has lower pore volume than the body of the lesion (less than
5%) and a radiopacity comparable to unaffected adjacent enamel.
It has been hypothesized that hyper mineralization and increased
fluoride content of the superficial enamel are responsible for the
relative immunity of the enamel surface. However removal of the
hyper mineralized surface by polishing fails to prevent the
reformation of a typical well mineralized surface over the carious
lesion. Thus, the intact surface over incipient caries is a
phenomena of the caries demineralization process rather than any
characteristics of the superficial enamel.
As the enamel lesion
shaped defects in the
surface zone can be seen
by SEM. These are the
first sites where bacteria
can enter into a carious
Arresting the caries
process at this stage
results in a hard surface
that may at time be
rough though cleanable.
Caries advancement in dentin
proceeds through three
1) Weak organic acids
demineralize the dentin.
2) Organic material of the
dentin ,collagen degenerates
3) The loss of structural integrity
is followed by invasion of
Deepest area is normal dentin which has tubules with
odontoblastic process that are smooth and no crystals in the
The inter tubular dentin has normal cross banded collagen
and normal dense apatite crystals.
No bacteria in the tubules.
Stimulation of dentin (eg :by osmotic gradient, a bur, a
dragging instrument or air blow) produces a sharp pain.
Zone of demineralization of the inter tubular dentin and
initial formation of very fine crystals in the tubule lumen at
the advancing front.
Odontoblastic process damage is evident.
No bacteria are found in this zone.
Stimulation of dentin produces pain.
Dentin is capable of remineralization.
This dentin is softer than normal
dentin and shows further loss of
mineral from the inter tubular
dentin and many large crystals in
the lumen of the tubules.
Stimulation produces pain.
Intact collagen can serve as a
template for the remineralization
of the inter tubular dentin and thus
this region is capable of self repair ,
provided the pulp remains vital.
Zone of bacterial invasion and is marked by widening and
distortion of the dentinal tubules which are filled with bacteria.
There is very little mineral present and the collagen is irreversibly
Dentin in this zone will not self repair .This zone cannot be
remineralized and must be removed before restoration.
Outer most decomposed dentin
that is teeming with bacteria.
No recognizable structure to the
dentin and collagen ,and minerals
Removal of infected dentin is
essential to sound, successful
restorative procedure as well as
prevention of spreading of
INFECTED DENTIN AFFECTED DENTIN
1) Softened demineralized Softened demineralized
dentin teaming with bacteria dentin not yet invaded by bacteria
2) Collagen is irreversibly Collagen cross linking
3) Cannot be remineralized Acts as a template for
4)Soft necrotic tissue followed Softer than normal dentin
by dry leathery dentin. Flakes discolored but does
away with instrument. not flake easily
5)Dyes – 1% Acid red in propylene
glycol .Stains only irreversible
denatured collagen. Does not stain
Infected dentin Affected dentin
Zone of Fatty
Aims of prevention (Sturdevant):
1. Limiting pathogen growth & metabolism
2. Increasing resistance of tooth surface to demineralization
3. Caries control methods which include operative
There are three levels of prevention of dental caries.
1. Primary prevention – is defined as
“actions taken prior to the onset of the disease, which
removes the possibility that the disease will ever
2. Secondary prevention - is defined as
“actions which halt the progress of a disease at its
incipient stage and prevents complications.”
. Tertiary prevention- is defined as
“ all measures available to reduce or limit impairments
& disabilities, minimizing suffering caused by
existing departures from good health & to promote
the patients adjustments to the irremediable
Essentials of Preventive and
Community dentistry. Soben Peter.
Primary prevention Secondary
Health promotion Specific
visit to dental
water, use of
By improving oral hygiene
By diet modification
By use of salivary stimulants
Pit and fissure sealants
Plaque free tooth surfaces do not
Oral hygiene procedures
Daily personal oral hygiene recommended for good hygiene
and for control of gingival diseases
Total length: 6.0-7.5 inches
Length of brushing plane: 1-1.25 inches
Width of brushing plane: 5/16-3/8 inch
Filament height: 7/16 inch
Soft: .007 inch
Medium: .012 inch
Hard: .014 inch
Any brush which allows pt. to comfortably
access all tooth surfaces is acceptable
although a medium brush with small head
Powered brush – physically handicapped.
Brush at least twice daily with toothpaste
for effective plaque removal.
Toothbrush to be replaced every 3
months or when bristles become
Oral-b professional care™ 8000 series
Oral-b sonic complete
Oral-b advancepower™ 900 series
Roll – modified stillman technique
Vibrator-stillman,charters, or bass method(sucular).
Circular – the fones technique
Vertical – the leonard technique
Horizontal – the scrub technique
Method - bristles are directed apically at 45 ⁰ to long axis of
tooth, gentle force applied into sulcus.
Use gentle but firm vibratory strokes without removing
bristle ends from sulcus. At least 20 vibrations.
The tips of the bristles should be forced to enter the gingival
sulcus and the embrasures as far as possible.
Apply the brush to the next group teeth.
The entire stroke is repeated at each position around the
maxillary and mandibular arches, both facially and lingually.
Approximal surfaces and malaligned teeth or these are
additional cleaning required
(1)dental floss or tape
(4)single tufted brushes
Nylon, yarn or teflon; waxed or unwaxed
Waxed preffered in young where interdental papilla fills
About 15-18 inches taken.
Wrap the two ends of the floss around the middle fingers of
Thumb and index finger used to control the floss.
Both thumbs are manipulated to floss maxilla.
Both forefingers are manipulated to floss mandible.
Cone shaped brushes with nylon
Used when there are wide
interdental spaces and also for
cleaning around bridges.
Brush selected should be slightly
larger than the gingival
Useful aids in malaligned teeth.
Highly effective in the lingual surface of mandibular
premolars, where tongue impedes toothbrush.
May provide access to furcation areas and isolated areas of
It is removal of a shallow, enamel developmental fissure
or pit to create a smooth ,saucer–shaped surface that is
self cleansing or easily cleaned.
Fissure depth less than ¼ to 1/3 the thickness of the
Developmental faults are removed with the side of a
flame shaped diamond stone, leaving a smooth surface.
Usually available as paste form.
Can be used in conjunction with tooth brushing.
Aid in cleaning and polishing tooth surfaces.
Not necessary to effectively remove dental plaque.
Some dentifrices contain abrasives that help remove stain and
polishing agents that restore tooth luster.
Some have a compound added to reduce calculus formation
and fluoride can be added to prevent dental caries.
Free fluorides should be available in the paste not to the
ingredients in the abrasive system.
They can also contain desensitizing agents that are beneficial
to patients with tooth sensitivity such as exposed dentin
Helpful in identifying areas of plaque retention.
Tablet or solution form. A red dye (erythrosin) is most
A two-tone dye has the advantage of differentiating mature
dental plaque (stains blue) from newly formed bacterial
plaque (stains red).
Used after toothbrushing to improve plaque control
Professional tooth cleaning measures
Selective removal of plaque by the dentist using
mechanically driven instruments like contra-angled handpiece
with bristle brush and fluoride prophylaxis paste.
1) Substances which alter the surface of tooth structure
d. Silver nitrate.
e. Zinc chloride and potassium ferrocyanide.
2) Substances which interfere with carbohydrate
degradation through enzymatic reaction/alterations
a. Vitamin K.
3) Substance which interfere with bacterial growth
a. Urea and ammonium compounds
d. Caries vaccine
Highly effective against plaque microorganisms causing
gingivitis and periodontal disease.
Prevents bacterial adhesion on tooth surface.
0.12% mouth rinse at bedtime for 2 weeks
1% gel or 40% varnish professionally applied .Once a week for
several weeks reduces caries incidence in high risk patients.
It helps in remineralization of incipient caries.
'Vaccine' is an immunobiological substance designed to produce
specific protection against the given disease. It stimulates the
production of protective antibody and other immune
o First developed by Williams 1944 using a lactobacillus
o Bowen in 1976 demonstrated monkeys immunized by whole
live cells of S.mutans developed lesser caries.
o Underwood and Miller published in 1881 bacteria are
involved in the pathogenesis of dental caries was clearly
expressed in a paper .
The subcellular component which are currently being seriously
proposed as vaccines are
(a) Glucosyltransferases (GTF)
(b) Wall associated proteins.
(d) Glucan- binding protein.
(Adapted from Slots & Taubman, 1992)
Glucan binding protein
*PBP: Pellicle Binding Protein
Sucrose Glucose Fructose
(Adapted from Slots & Taubman, 1992)
I: Insoluble form or GTF-B and GTF-C
S: Soluble form or GTF-D
GTF Binding Glucans
(Adapted from Slots & Taubman, 1992)
(Adapted from Slots & Taubman, 1992)
Two purified proteins from the surface of S. mutans serotype c
are currently being suggested for use as dental caries
1. Antigen I/II or B described by Lehner and his colleagues,
2. Antigen A - a small molecular weight cell wall protein
Group of the extracellular enzymes involved in synthesis of polymer
(glucans) from sucrose.
Genes responsible for glucan synthesis in S. mutans are gtfB, gtfC, and
Inactivation of the gtfD gene has also resulted in a mutant gene with
lower cariogenicity on smooth surfaces
Passive administration of antibody to GTF in diet can also protect rats
from experimental dental caries.
Thus, presence of antibody to glucosyltransferase in oral cavity prior to
infection can significantly influence the disease outcome, presumably
by interference with one or more of the functional activities of the
Adhesins are the receptors which allow S.mutans to bind
Adhesins from two principal human pathogens,
Streptococcus mutans and Streptococcus sobrinus have been
Numerous immunization approaches have shown that active
immunization (with intact antigen) or passive immunization
can protect subjects from dental caries
The ability of mutans streptococci to bind to glucan is
presumed to be mediated, at least in part, by cell wall-
associated proteins (GBP).
Protection can be achieved by either subcutaneous injection of
GbP in the salivary gland region or by mucosal application by
the intranasal route.
Saliva samples from young children often contain IgA antibody
to GbP, indicating that initial infection with S. mutans can lead
to natural induction of immunity to this protein.
Recombinant Vaccines/Attenuated Expression Vectors-
Attenuated mutant Vectors such as Salmonella, which contain
plasmids expressing recombinant peptides, can target the
vaccine to appropriate inductive lymphoid tissue for mucosal
- other vaccine approach which may intercept more than one
aspect of mutans streptococcal molecular pathogenesis is
chemical conjugation of functionally associated
protein/peptide components with bacterial polysaccharides.
-Added to the value of including multiple targets within the
vaccine is that conjugation of protein with polysaccharide
enhances the immunogenicity polysaccharide entity.
-Subcutaneous injection with conjugate-induced systemic IgM
and IgG antibody responses to both peptide and polysaccharide,
which could be boosted upon subsequent injection.
o Heart cross-reactive antigens (HCRA )have been identified in
S. mutans , which when injected in animals may damage to
the heart. Streptococcus mutans antibodies, possibly reacts
with, the myosin component of the heart tissues .
o The precise timing and number of injections which might
ultimately be required in children has not yet been
o Apart from logistic consideration of availability of patients
and coordination with other vaccine programmers,
fundamental details of the level and longevity of immune
responses in humans are not yet known.
Unlike traditional vaccines, which are injected directly into
the bloodstream, the nasal spray vaccine works by way of the
mucosal immune system—an antibody-producing “factory”
that resides in the body’s mucosal surfaces, such as the lining
of the respiratory, digestive, and urogenital tracts.
Shivkumar et al,dental caries vaccine,Indian
Journal of Dental Resident 2009;20:99-106
Dietary sucrose has two important detrimental effects on
1 – frequent ingestion provide stronger potential for S.Mutans
2 – Mature plaque exposed to sucrose rapidly metabolizes
into organic acids lowering pH.
Diet modification recommended for pt. With active caries and
those with high caries risk.
Points considered at the
Measures to reduce caries risk
and/or to stop ongoing caries
Frequency of meals Number of meals+ snacks should be
kept on a low level.
Elimination of sugars and
consistency of food
Sugars should be eliminated as fast as
possible. Foods needing active chewing
lead to an increased salivation, which
Fermentable carbohydrates Polysaccharides, disaccharides and
monosaccharides, but the capacity
differs between different products.
Protective and favorable elements
Fluorides ,calcium, phosphates, fats
Sugar substitutes Use of sugar substitutes results in a
lower acid formation.
ADEQUACY OF DIET
Determine the number of servings of food in each of the basic five food
groups and compare this with the recommended number of servings.
MILK- contain lactose ....Least cariogenic
CHEESE- casein phosphatase give anticariogenic property
TEA - green and black tea
Prevent S.Mutans from binding to sucrose
Increase concentration of amino acids and ammonia neutralizing
Bacteriostatic, as they are nonfermentable
Increase salivary flow, enhance remineralization
When the salivary glands are capable of secreting, chewing gum
stimulates salivary flow.
A chewing gum containing xylitol or chlorhexidine ( or both) may be
Patients with dry mouths in whom the salivary glands are irreparably
damaged and cannot secrete , are not helped by chewing but may
benefit from an artificial saliva spray containing calcium, phosphate ,and
o Finnish name for Xylitol is "koivusokeri", or birch sugar.
o Imfeld classified the caries preventive features of xylitol into ‘passive’ and
o ‘Passive’ properties - surround its non fermentability by oral
microorganisms, and thus its substitution in the diet is effectively sugar
o ‘Active’ properties- include disturbance of bacterial metabolism, growth
or adhesion, or a role in facilitating remineralization of lesions.
o Regular use of chewing gum has been shown to be a means of
promoting remineralization, due to the accompanying enhancement of
salivary flow and buffer capacity.
British Dental Journal 2003;194( 8):429-436
Have anticariogenic activity as shown in laboratory, animal
and human in situ experiments
[Reynolds et al., 1999, 2003., Shen et al., 2000]
CPP stabilizes amorphous calcium phosphate and also
localizes it at the tooth surface thus leading to increased rate
of remineralization than with ACP alone.
Promotes remineralization of
enamel subsurface lesions with
Improves crystallinity and
lowers microstrain than normal
18.8 mg of CPP-ACP complex
significantly remineralizes 2
times better than control sugar-
free gums (Shen et al 2001)
Topical crème with bio – available calcium and phosphate.
A water based, sugar free crème containing CPP – ACP
Saliva has important role in
Xerostomia patient increased caries
risk is seen.
Gums, paraffin waxes, or salivary
substitutes can be prescribed as
Malic acid, pilocarpine etc is effective
in the treatment
Sugar free chewing gum, ascorbic acid
also helps in salivary flow.
Fluoride therapy is the delivery of fluoride to the teeth
topically or systemically in order to prevent tooth decay.
Mechanism of action
Precipates fluorapatite into tooth structure from the calcium
and phosphate ions present in saliva. Fluorapatite makes
enamel more resistant to caries attack.
Helps in mineralization of hypo mineralized areas that are
often present in a newly erupted tooth.
Fluoride ingested during tooth development makes teeth
slightly smaller with shallow fissures and decreased cusp
Effects of fluoride
Increases resistance of enamel to caries.
Increases rate of post operative maturation.
Enhance remineralization of incipient caries.
Interferes with bacterial enzymatic process and prevents
Modifies tooth morphology when ingested during tooth
School water fluoridation
Fluoride tablets and drops
Self applied solution
Fluoridated community water
Children with developing
Optimum level – 1 ppm
public water supply must be available.
School water fluoridation
Optimum level 4.5 – 5.5 ppm.
Fluoride tablets and drops.
Contain sodium fluoride or calcium fluoride.
Amount required varies according to age, weight and
dietary pattern of child.
AGE FLUORIDE CONTENT IN
DRINKING WATER (PPM)
0-0.3 0.3-0.6 > 0.6
0.25-2 YRS 0.25 0 0
2-3 YRS 0.5 0.25 0
3-13 YRS 1.0 0.5 0
› 200-350 mg Fl/kg of salt
43% reduction in DMFS with
200 ml milk/day (7 ppm) for
Clinician applies a thin layer onto teeth.
Application time is several minutes.
Patient avoids eating for several hours and avoids brushing
till next morning.
Varnish sets on contacting moisture.
Only tooth brushing needed before applying.
Disadvantage – temporary tooth color change
AGENTS USED – Naf in organic lacquer.
Difluorosilane in polyurethane lacquer and chloroform.
[A] fluoride dentifrices
Sodium fluoride, stannous fluoride and sodium
Usually contain 1000 ppm of fluoride.
Cleared from mouth by spitting rather than rinsing and used
twice a day.
[B] fluoride mouth rinses
Sodium fluoride and acidulated phosphate fluoride.
Additive effect when used along with topical or systemic
Age Type of dentifrice used
<4yrs Fluoridated dentifrice not recommended.
4-6yrs Brushing twice with non-fluoridated and once with
6-10yrs Brushing once with non-fluoridated and twice with
>10yrs Brushing thrice a day with fluoridated dentifrice.
1 – high dose/low frequency
Used best in weekly rinsing programs in schools
2 – low dose/high frequency
Used best by individual patients at home
High caries risk/caries active pt. Should rinse daily.
Optimal application time in the evening.
10 ml used for 1 min after which eating or drinking should be delayed
for 1 hour.
Fluorides are less effective in preventing pit and fissure
Sealants have 4 important preventive effects:
#Mechanically fills pits and fissures with an acid resistant
#Deny cariogenic organisms their habitat.
#Render pit and fissure easier to clean.
#Arrest incipient carious lesion.
“Sealants have been shown to be effective to have long-term retention to
cause regression of active lesions, and to be superior to amalgam
restoration in terms of time requirements”
High risk for caries patients.
Recently erupted molars with deep, retentive pits and fissures.
Teeth with signs of incipient occlusal caries.
Adult patients with suspicious fissures.
1.Glass ionomer sealants (type iii)
'Laser' is an acronym for 'light amplification by
the stimulation emission of radiation'. Its
theoretical basis was postulated by Albert
First tooth exposed to laser light was in 1960.
Laser light in dentistry is a unique, non-ionizing
form of electromagnetic radiation that can be
employed as a controlled source of tissue
stimulation, cutting or ablation, depending on
specific parameters of wavelength, power and
Laser treatment particularly in combination with topical fluoride
application (NaF, APF), increase resistance against caries, desensitization
of hypersensitive dentine (Er:YAG) and improve marginal seal under
composite resin (Nd:YAG).
C02-laser = Caries inhibition up to 82.7%
Er:YAG-laser = Reduction in surface lesion depth (root surfaces 39%,
primary enamel surfaces 56%)
Nd:YAG-laser (with Duraphat) = Caries inhibition (pits and fissures 43%,
smooth surfaces 80%).
Defintion of caries activity (Messer, Aus Dent J, 2000)
“the rate at which dentition is destroyed by
caries, represented by the sum of the new
carious lesions and enlarged lesions per unit
› To determine the need and extent of preventive measures
› Indicator of patient cooperation
› Aid in timing of recalls
› Determine success of therapeutic measures
› Motivate and monitor the effect of education programs.
› To identify high risk groups/individuals
› Aid in determination of prognosis
› Precautionary signal to orthodontist
› Guide to insertion of expensive restorations
Lactobacillus colony count test
Buffer capacity test
Fosdick calcium dissolution test
S.mutans level in saliva test-screening tests
Caries risk test
Hadley - 1933
number of bacteria in saliva by counting the number
of colonies appearing on Tomato Peptone Agar or
› Saliva collected
› 1:10 & 1:100 dilution made
› Spread on agar plate
› Incubated for 3-4 days at 37 C
0-1000 Little or none
> 10,000 Marked
No. of colonies
Measures the rapidity of acid formation when saliva
inoculated in glucose agar
› saliva sample is collected.
› Media contains
peptone 20 gms
Dextrose 20 gms
Sodium chloride 5 gms
Agar 16 gms
Bromocresol green 0.02 gms
CARIES ACTIVITY COLOR CHANGE
High 24 hrs
Medium 48 hrs
Slight 72 hrs
Immune no change>72 hrs
Modification of snyder test
Uses less agar i.e 5ml per tube
Saliva is directly drooled into tubes
Incubated for 4 days at 37deg C
Color change is noted from bluish green to yellow
Measures the activity of the salivary enzyme
Sample is mixed with an indicator ie diazoresorcinol
Changes in color measured after 30 secs & 15 mins
COLOUR TIME SCORE CARIES ACTIVITY
Blue 15 min 1 Non conducive
Orchid 15 min 2 Slightly conducive
Red 15 min 3 moderate conducive
Red Immediately 4 Highly conducive
Immediately 5 Extremely conducive
5 ml of saliva measured into a beaker.
pH of saliva adjusted to 7.0 by addition of lactic acid
Level of lactic acid is re-recorded
Lactic acid is then added to sample until a pH of 6.0
The number of ml of lactic acid needed to reduce
the pH from 7 to 6 is a measure of buffer capacity
DENTOBUFF STRIP SYSTEM
blue 6.0 or more high
green 4.5 - 5.5 medium
yellow 4.0 or less low
more than 0.25 normal
0.1 - 0.25 low
less than 0.1 very low
25 ml of gum stimulated saliva is collected
Placed in an 8 inch test tube with 0.1 gm of powdered human
Tube shaken for 4 hrs, then again analyzed for calcium content
The amount of enamel dissolution increases as the caries
DEWARS TEST- pH is measured
Saliva/ tongue blade method
S. mutans adherence method
S. mutans dip-slide methods
S. mutans replicate technique
Plaque samples placed in ringers solution
Samples are shaken until homogenized
Plaque suspensions streaked across a mitis salivarius agar plate
Aerobic incubation at 37 C for 72 hrs, the cultures
are examined under microscope
GRADE COLONIES/10 FIELDS
2 < 8
3 ≥ 8
Saliva/plaque samples obtained using
Inoculated on Mitis salivaris agar for 48
hrs at 37 C
Counts of more than 100 CFU are prop to
greater than 106 colonies per ml of saliva
by conventional methods
STRIP MUTANS TEST-Jensen & Bratthall
Saliva inoculated in MS broth for 24 hrs at 37 C
After growth, the supernatant removed
Cells adhering to the glass examined macroscopically
SCORE NO OF COLONIES
- No growth expressed
+ Few deposits from 1-10
++ Scattered deposits of smaller size
+++ Numerous minute deposits & more than 20
large deposits (indicates > 105 CFU/ml)
Procedure A: DENTOCULT SM
› Saliva on agar coated slide
› Bacitracin disks on the slide, incubate for 48 hrs
› Colony density (small blue colonies) compared with
2- 105 to 106
Procedure B: CARIESCREEN SM
› Bacitracin tablet in buffered diluent in which saliva is
› Dip-slide coated with MS agar placed in vial
› Incubate for 48 hrs at 37 C
› Use reference colony density chart that shows
10,000, 50,000, 100,000, 250,000, 500,000, 1,000,000
To localize S. mutans on tooth surfaces
Imprint of tooth surface taken with impression matrix
Incubated at 37 C overnight
Observe directly for growth on the matrix at specific
e.g.- occlusal/root surfaces
Recently advocated - new, quick, effective test
CRT has 2 components:
two-in-one dip-in-slide test which identifies counts
of Mutans & Lactobacilli
Stimulated saliva is applied to dip-in-slide
Incubated for 48 hrs at 37 deg C
•Available in strip form, which changes color to
indicate whether the patient has a high, medium or
low buffering capacity.
•This occurs within 5 mins.
I. Hand cutting instruments:- The cutting instruments are used to
cut hard and soft tissues of the mouth. Excavators are used for
removal of caries and refinement of the internal parts of the
cavity, chisels are used primarily for cutting enamel.
The four subdivisions of excavators are ordinary hatchet , Hoes,
angle formers and spoon excavators.
Chisels are intended primarily for cutting enamel . They are
grouped as :-
straight, slightly curved, biangle
gingival marginal trimmer.
Majority of the caries removal procedures on enamel
and dentin is accomplished by using rotary
Five factors are potentially responsible for the
discomfort and pain that is associated with cavity
sensitivity of vital dentin
pressure on tooth
bone conducted noise and vibration
high pitched noise of air turbine handpiece
Development of high temperature at cutting
R.D. Black originally developed air abrasion in 1945.
He preliminary investigation into other alternative
pseudo mechanical method for removal of caries. It
involved bombarding the tooth surface with high
velocity particles, conventionally aluminum oxide was
carried in a stream of air.
Depending on the natural of the abrasive used this
technique has the ability of abrading efficiently both
sound dentin and enamel.
In this method there is no rise in temperature.
This is a relatively pain free procedure.
Polycarbonate resin or aluminum hydroxyl appetite mixtures
might be more selective in carious dentin removal leaving
healthier sound tissues virtually unscratched.
A recent development from the original ultrasonic is the
use of high frequency sonic air scalars with a modified
abrasive tips a technique known as Sono Abrasion.
The tips described an elliptical motion with a transverse
distance between 0.08- 0.15mm and a longitudinal
movement of between 0.055- 0.135mm.
They are diamond coated on one side using 40 micro
meter grit diamond an are cooled using water irrigant at
a flow rate of between 20 –30 ml/min.
currently there are three different instrumental tips.
A length ways halved torpedo shaped 9.5 mm long
and 1.3 wide.
A small hemisphere 1.5mm in diameter
A small hemisphere 2.2 mm in diameter.
If the applied pressure air is too great, the cutting
efficiency is reduced due to damping and oscillation.
Air polishing is a process by which water soluble particles of
sodium bicarbonate to which tri calcium phosphate, is
added to improve the flow characteristics, are applied onto
a tooth surface using air pressure.
It has been suggested that air polishing would be used for
the removal of carious dentine at the end of cavity
In 1976 Goldman & Kronman reported on the possibility of
removing caries material chemically using N- Mono glycine
and N- Mono Chloro Aminobutryt.
Caries dentin softened by this is readily removed by lightly
abrading its surface with an applicator tip.
Carisolv consists of two carboxy methyl cellulose base
gels . A red gel containing 0.1 M .Amino Acids Nacl,
NaoH and erythrosine .
second containing sodium hypo chlorite.
The two are thoroughly mixed in equal parts at room
temperature before use and applied using hand
instruments on to the exposed carious dentine ,left for
60 seconds prior to gently but firmly abrading away the
softened dentine to leave a hard caries –free cavity.
Since the development of the first ruby laser by MAIMAN in
1960 researchers postulated that it could be applied to
cutting both hard and soft tissues in the mouth.
The efficacy of lasers will depend on numerous factors
including the wavelength characteristics, pulse energy,
Lasers that are currently been investigated for more
selective hard tissue abrasion include
Er. YAG & ND. YAG
Carbon dioxide lasers
› Argon Freon
› Xenon : Chlorine
Dye Enhanced laser ablasion
British Dental Journal 2000; 188: 476–482
Featherstone John D.B,The science and
practice of caries prevention,JADA
The clinical management of dental caries has been
primarily directed at the treatment of the
consequences of the diseases process by placing
restoration and not at curing the disease.
The widespread use of fluorides has dramatically
reduced the prevalence of dental caries and the rate
of progression of the carious lesion. These changes
permit dentist to adopt to more conservative
management strategies directed at prevention and
cure of dental caries.