CARIOLOGY

CARIOLOGY- Classification,Etiopathogenesis,Caries
pattern in primary and permanent teeth in
children,Diagnosis and Management KARISHMA.S

contents
 INTRODUCTION
 CLASSIFICATION
 ETIOLOGY
 THEORIES
 HISTOPATHOLOGY
 CARIES PATTERN IN PRIMARY AND PERMANENT TEETH
 DIAGNOSIS
 MANAGEMENT
 CONCLUSION
 REFERENCES

INTRODUCTION
Dental caries is still a major health problem in most of the countries
affecting about 60-90% of the school children and majority of the aults
Ii is most prevalent oral disease in several Asian and latin American
countries,while it appears to be less common and less severe in most
African countries.

DEFINITION:
According to Sturdevant: Dental caries is a infectious microbiologic disease
of the teeth that results in localized dissolution and destruction of calcified
tissues.
According to WHO: It is defined as localized post eruptive pathological
process of external origin involving softening of the hard tooth tissue and
proceeding to the formation of cavity.

According to Shafer, Hine,Levy: It is defined it as a ―microbial
disease of the calcified tissues of the teeth, characterized by
demineralization of the inorganic portion and destruction of the
organic substance of the tooth.
According to Ernest Newbrun (1989): “Dental caries is defined as a
pathological process of localized destruction of tooth tissues by
microorganisms.”

CLASSIFICATION
G.V.Black’s Classification:
 Class-I: - caries on the occlusal surfaces of molars and
premolars
- occlusal 2/3 of the buccal and lingual surfaces of
molars
- lingual surfaces of the anterior teeth.
 Class-II: - lesions found on the proximal surfaces of
molars and premolars
 Class-III: - lesions found on the proximal surfaces of
anterior teeth, but do not involve the incisal angle

 Class-IV: - lesions found on the proximal surfaces of anterior teeth and
involving incisal angle
 Class-V: - lesions found on the gingival third of the facial and lingual
surfaces of anterior and posterior teeth.
 Class-VI: - were not included in Black’s classification
- proposed by WJ Simon in 1956
- lesions on the incisal edge and cusp tips of the teeth

According to Sturdevents: He has classified dental caries mainly according to 3
criterion: 1)– Location. 2)– Extent. 3)– Rate.
According to Location:
Primary caries.
Caries of Pit & Fissure
origin.
Caries of enamel smooth
surface origin.
Backward caries.
Forward caries.
Residual caries.
Root surface caries.
Secondary (recurrent)
caries.
According to Extent:
Incipient caries (reversible).
Cavitated caries (irreversible).›
According to Rate (speed) of caries spread:
Acute (rampant) caries.
Chronic (slow or arrested) caries.

Mount G. J.(1997) classified dental caries based on site and size.
A) Site
 Site 1: includes lesions on pit & fissures of posterior teeth, buccal
grooves of mandibular molars, palatal grooves of maxillary molars&
erosion lesions on incisal edges
 Site 2: includes lesions in contact areas of posterior and anteriors.
 Site 3: includes lesions originating in gingival third of all teeth

B) Size
 Size 0: small and early enough to be remineralized lesion with only
residual stain
 Size 1: (mild) includes lesions which have passed just beyond
remineralization
 Size 2: (moderate) includes larger lesions, with adequate tooth
structure to support restoration
 Size 3: (enlarged) includes lesions in which tooth structure &
restoration are susceptible to fracture
 Size 4: (severe) includes lesions which have destroyed a major
portion of tooth structure

WHO Classification:
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 cavitated)
surfaces
D2. Clinically detectable cavities limited to enamel
D3. Clinically detectable cavities in dentin
D4. Lesions extending into the pulp

Classification according to Mc Ghee
 Superficial caries- surface of enamel affected
 Simple caries – penetration into DEJ
 Deep seated caries – cavity of sufficient depth
 Caries with almost exposed pulp – large well defined cavity
 Caries with pulp involvement
 Caries with perforation laterally or through the floor of the pulp
 Loss of crown of the tooth from caries
 Caries of remaining root
Suzamme M & Jerry R McGhee (1977) Infection and Immunity

INTERNATIONAL CARIES DETECTION AND ASSESSMENT SYSTEM
(ICDAS)
ICDAS was developed to bring forward the current understanding of the process
of initiation and progression of dental caries to the field of epidemiological and
clinical research.This system allows us to record the severity and incidence of the
caries in its continuum.

ETIOLOGY
 The oral cavity houses more than 250 microbial species.
 Unlike oral epithelium, the epithelium of the tooth does not shed and
toothmorphology has many areas inaccessible to physiological clearance
mechanisms.Thus, a tooth becomes an ideal place for the stubborn adherence
for many of these species.
 This colonization occurs as a string of methodical adhesion, succession,and
progression.
 Numerous references on dental caries including early theories have attempted
to explain its etiology.

There are three major hypothesis for the etiology of dental caries:
 the specific plaque hypothesis
 the nonspecific plaque hypothesis
 the ecological plaque hypothesis
› The specific plaque hypothesis has proposed that only a few specific
species, such as Streptococcus mutans and Streptococcus sobrinus, are
actively involved in the disease.

 On the other hand, the nonspecific plaque hypothesis maintains that caries
: outcome of the overall activity of the total plaque microflora, which is
comprised of many bacterial species.
 The ecological plaque hypothesis suggests caries is a result of a shift in the
balance of the resident microflora driven by changes in local
environmental conditions.

 S. mutans, e.g., species of Veillonella, Lactobacillus, Bifidobacterium,
Propionibacterium, low-Ph, Non-S. mutans streptococci, Actinomyces,
and Atopobium, also may play an important role in caries production.
 Actinomyces spp. And non-S. mutans streptococci may be involved in
the initiation of the disease.

 Evidence of dental caries in relatively few teeth found in skull
fragments of our earliest known direct ancestors, the pithecanthoporus
 Prevelance of dental caries did not change significantly during 2000
years or more from beginning of Iron age to Medieval period(1066-
1500 AD)
However, many theories have evolved through years of investigation and
observation;
› the acidogenic theory
› the proteolytic theory
› proteolysis-chelation theory,
are among many which have stood the test of time.
THEORIES OF DENTAL CARIES

Theories of formation of caries:
Early theoires
The legend of worms:
 The earliest reference to tooth decay is from ancient sumerian
text – LEGEND OF WORMS
 Given in 5000 b.c
 Stated that worms are responsible for causation ofcaries

Endogeneous theories:
 Also called humoral theory
 Proposed by Greek physicians
 Stated that caries produced by internal action of acids and corroding
humors
 Imbalance in humors
Vital theory:
 Tooth was thought to be source of problem and caries started from within
tooth

Exogenous theories
Chemical theory:
 Parmly in 1820
 Stated that dental decay affected externally
 Unidentified chymal agent is responsible
Septic theory:
 Proposed by Underwood and Miller :1880
 Acid capable of causing decalcification was actually
produced by bacteria , which feeds on organic fibrils of dentin

Parasitic theory:
 Theory proposed by Erdl
 First to relate microorganisms as causative agent is Erdl in 1843
 Fincus, in 1847, a German physician attributed dental caries to DENTICOLAE
 Generic name proposed to decay related organisms
 Theory stated that living micro organisms caused the disintegration in both
enamel and dentin.
Chemico-parasitic theory:
 Also called acidogenic theory
 Proposed by Willought D Miller in 1884
 Stated that dental decay is a chemico-parasitic process

Two stages :
 decalcification of tooth substance
 dissolution of softened residue
This theory is the back bone of current knowledge of understanding
etiology of dental caries
Draw backs in theory:
 Prediliction of certain specific sites on a tooth
 Why some populations are caries free
 Doesnt explain phenomenon of arrested caries
 Theory implicates the study of role of carbohydrates, microorganisms,
acids and dental plaque

Proteolytic theory:
 Bodecker , in 1878, demonstrated – certain enamel structures are
made up of organic material such as enamel lamellae and
enamel rod sheaths
 Serves as a path way for entry of micro organisms
 Pincus (1949) contended that proteolytic organisms initially
attacked the protein elements, such as dental cuticle,and then
destroyed the prism sheaths,after which the loosened prisms
would fall off mechanically.
 Sulfatases of Gm –ve Bacilli hydrolysed Mucoitin sulfate to
produce Sulfuric Acid,which combined with Ca of the mineral
phase.

Preoteolysis Chelation theory:
 This theory proposed by Schatz et al (1955)
 The breakdown products of this organic matter have chelating properties and there
by dissolve the minerals in enamel.
 This results in the formation of substances which may form soluble chelates with the
mineralized component of the tooth and thereby decalcify the enamel at a neutral or
even alkaline pH.
 Enamel also contains other organic components besides keratin, such as
mucopolysaccharides, lipid and citrate, which may be susceptible to bacterial attack and
act as chelators.

Sucrose chelation theory:
 Egglers-Lura (1967) 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
intermediates require inorganic phosphate, which is
subsequently removed from the enamel by phosphorylating
enzymes.

Auto immune theory:
 It suggests that few odontoblasts cells at some specific sites within the
pulp of few specific teeth are damaged by the autoimmune
mechanisms.
 For this reason, the defence capacity and integrity of overlying enamel
and dentin in those specific areas are compromised and they can be the
potential sites for caries development.

Role of plaque as etiologic factor:
 Soft, translucent and tenaciously adherent material accumulating on
the surface of teeth is commonly called as plaque
 90% contains bacteria and its byproducts
Adherence of micro organisms :
 Few specialized microorganisms primarily streptococci adhere onto the
tooth surfaces
 Bacteria contains receptors
 Adhere to even other filamentous and spiral bacteria forming colonies

Plaque communities and habitats :
 Dorsum of tongue : S.salivarius
 Teeth : S.sanguis and S.mitis
 Habitat - Predominant species
 Mucosa - S.mitis, sanguis, salivarius
 Tongue - S.salivarius, mutans and sanguis
 Teeth - S.sanguis(non carious)
 Acids : initially decalcify the enamel have a pH: 5.5 to 5.2 or less and
areformed in the plaque material,
 which has been described as an organic nitrogenous mass of microorganisms
firmly attached to the tooth structure

Role of carbohydrates :
 Cariogenic carbohydrates are dietary in origin
 Cariogenicity varies with :
• Frequency of ingestion,
• Physical form,
• Chemical composition,
• Routes of administration and presence of other
food constituents
 Sticky solid carbohydrates are more cariogenic
 They in detergent foods are less damaging

 Ones which are rapidly cleared by saliva are less cariogenic
 Plaque organisms produce little acid from the sugar alcohols sorbitol or
mannitol.
 The acids involved in the initiation of the caries process are normal
metabolic by-products of the microorganisms and are generated by the
metabolism of carbohydrates.
 Carbohydrates fed entirely by stomach tube or intravenously are not
cariogenic
 Meals high in fat, protein and salt reduce retentiveness of
carbohydrates
 Refined pure carbohydrates are more cariogenic
 Bacteria + sugar + teeth – organic acids = caries

Streptococcus mutans :
 First isolated by CLARKE in 1924
 Catalase –ve , gram +ve cocci
 Cariogenic strains contain lysogenic bacteriophage
 Serotypes a to h
 Polymerize glucose and fructose moieties of sucrose to glucans
and fructans

Extra cellular polymers:
 Homopolymers of glucans – dextran and mutan are synthesized
by S.mutans
 Mutan- important constituent of plaque, less soluble and
resistant to acid attack
 Fructans are highly soluble , degraded by plaque bacteria

Lactobacilli :
 Gram +ve non spore forming rods
 Acidogenic and aciduric
 Produce lactic acid
Oral actinomyces :
 Gram +ve filamentous organisms
 A.naesulundi and viscosus – facultative anaerobes
 A. Israeli and odontolyticus – strict anaerobes

Role of acids :
 Exact mechanism of carbohydrate breakdown to form acid by
bacterial action is not known
 Probably occurs due to enzyme breakdown of sugars
 Acids formed are chiefly lactic acid and butyric acid
 The localization of acids upon tooth surface is more important in
cariogenic process.
 Monosaccharides and disaccharides – greatest fall in pH

Current concepts in etiology of caries :
Three primary factors:
• the host
• the microbial flora
• the substrate
A fourth factor — the time — must be considered in any
discussion of the etiology of caries.
In other words, Caries requires a susceptible host, a cariogenic
flora and a suitable substrate that must be present for a
sufficient length of time.

In the epidemiological model, a disease state is due to interplay of three primary factors
(Keyes and Jordan, 1960): The host, the agent or recruiting factor and environmental
influences.
KEYS TRIAD

Newbrun in 1982 postulated that many secondary factors
also influence the rate of progression of caries.
• Interaction between three primary factors is essential for
the initiation and progression of caries: A susceptible host
tissue, the tooth; microflora with a cariogenic potential;
and a suitable local substrate to meet the requirements of
the pathodontic flora.
• The tooth is the target tissue destroyed in the dental caries
process. The cariogenic oral flora, which is localized to
specific sites on teeth, is the agent that produces and
secretes the chemical substances The local substrate
provides the nutritional and energy requirement for the
oral microflora, thereby permitting them to colonize,
grow, and metabolize on selective surfaces of teeth. The
third factor, the resistance of the tooth, is obviously
important since this determines the overall effects of the
attack.

Host factors and components:
 Tooth 1)Composition
2)Morphologic characteristics
3)Position
 Saliva 1)Composition
2)ph
3)Buffering capacity
4)Antibacterial factors
5)Quantity and viscosity
 Diet 1)Physical factors (quality of diet)
2)Local factors carbohydrate, vitamin and
3)Frequency
4)oral clearance
 Systemic and other conditions

Caries may be considered as a continuous dynamic process.
› Involving repeating periods of demineralization by organic acids of
microbial origin and subsequent remineralization by salivary
components(or therapeutic agents).
› but in which overall oral environment is imbalanced toward
demineralization.

Socioeconomic status:
 low socioeconomic status has an impact on carious process.
 Caries rate among individuals living below poverty level is higher.
 Lack of access to care among poor exacerbates condition because dental
caries is more likely to remain untreated.
Barriers to dental care may include :
 Limited income
 Lack of value placed on dental health
 Lack of knowledge of oral care,
 And transportation limitations.

WINDOW OF INFECTIVITY: Caufield 1993
› First windowof infectivity, 7-31 months: Teeth erupt
Provide virgin habitat for bacteria.
› Second window of infectivity.(Krass 1967, Edrman 1975)
› 6-12 yrs: Permanent teeth erupt
Provide new habitat for bacteria

Caries progression:
› Time for progression from incipient caries to clinical caries (cavitation)
on smooth surfaces is estimated to be 18 months+/- 6 months .
› Peak rates : 3 years after eruption of tooth. (incidence)
› Poor oral hygiene and frequent exposures to sucrose can produce
incipient lesions in as little as 3 weeks.
› Caries development in healthy individuals is usually slow in comparison
to compromised persons

Demineralization-remineralization Concept:
 Dental caries is not a result of a single acid attack caused by the acid formed as
a result of fermentation of dietary substrates by the oral microflora. Rather it is
an outcome of the imbalance occurring in the demineralization -
remineralization cycle that is continuously operating in the oral cavity.
 This balance is governed by a number of factors which is either caries
promoting (promotes demineralization) or caries inhibiting (promotes
remineralization). These factors have been depicted in.
 An important point to be mentioned is all these factors are present in every
individual’s oral cavity but in different proportions determining the direction of
the demineralization-remineralization cycle.

Stephan Curve:
• In 1940’s, Dr Robert Stephan, an officer in the US
Public Health Service, suggested there was a
continuous change in salivary pH following
consumption of foods and beverages, especially with
fermentable carbohydrates.
• Stephan curve is a graph published by Stephan
and Miller in 1944 which reflected the fall in
salivary pH following a glucose rinse.
• The graph has four landmarks viz: resting pH, the
rapid fall in pH, the critical pH and the recovery
phase.

RESTING PLAQUE pH:
This describes plaque that has not been exposed to fermentable carbohydrates for
approximately 2 hours and generally has a pH of between 6 and 7. The resting
plaque pH value for an individual tends to be stable and may remain so for long
periods. One example of an exception is if antibiotics have been taken, which may
alter the oral flora.

DECREASE IN PLAQUE pH:
After exposure of dental plaque to fermentable carbohydrates, the pH
decreases rapidly. The rate at which the pH decreases is due in part to the
microbial composition of dental plaque. In general, if more acidogenic,
aciduric bacteria is present in plaque, the pH would lower more rapidly.
 The rate of pH decrease is also dependent on the speed with which
plaque bacteria are able to metabolize the dietary carbohydrate.
 Another factor that affects the rate of pH decrease is the buffering
capacity of unstimulated saliva.

Critical pH:
The critical pH is the pH at which saliva no longer remains saturated
with calcium and phosphate, thereby permitting the hydroxyapatite in
dental enamel to dissolve. It is the highest pH at which there is a net
loss of enamel from the teeth, which is generally accepted to be about
5.5 for enamel.
Increase in plaque pH:
The low pH remained for some time, taking 30 to 60 minutes to return
to its normal pH The gradual recovery of the plaque pH is influenced
by various factors. These include the buffering capacity of saliva,
whether fermentable carbohydrate remains in the mouth and the
diffusion of acids from plaque into saliva or teeth.

Acc to Llory et al., 1972:
 Despite the continuous flow of saliva, Dental plaque can accumulate
at a rapid rate of (10-20 mg/day) in the absence of oral hygiene
procedures but the rate of plaque accumulation appears to be even
more rapid in patients with xerostomia.
 Dental plaque developed for 12 hours or less, enamel
demineralization resulting from a single exposure to sucrose will be
remineralized by within10 minutes.
 4 hours are required for enamel repair resulting from a exposure to
sucrosein presence of dental plaque that is 48 hours old.

HISTOPATHOLOGY
Macroscopic changes of enamel
SMOOTH SURFACE CARIES:
 Loss of transparency- opaque chalky region (white
spot)
 In slowly progressing & arrested lesions-Brown or
yellow pigmentation.
 Longitudinal section – cone shaped with apex
pointing towards dentin (smooth surface).

Pit & fissure caries:
• Fissure shapes – V,U,I,J,K.
• Caries start on both sides of fissure walls and not at base – extend
perpendicular to DEJ.
• Brown stains – newly erupted- underlying decay; older individuals-
arrested or remineralized zones.
• Cone shape – base towards dentin; apex-enamel surface.
• No apparent break in enamel surface.

The following 4 histological zones of an enamel lesion
Clearly explains the development of enamel caries:
 Zone 1: Translucent zone
 Zone 2: Dark zone
 Zone 3: Body zone
 Zone 4: Surface zone

Zone 1: translucent zone
It is the deepest zone representing the advancing front of enamel
caries.
Pores or voids form along the enamel prism(rod) boundaries (due
to easy H+ ion penetration)
 It appears structureless when perfused with quinolone solution
(having refractive index comparable to that of enamel) and seen
with polarized light (hence translucent)

Zone 2: Dark zone
 Situated near the advancing front just superficial
to the translucent zone
 Presence of many tiny pores block light transmission.
 These smaller air or vapor-filled pores make the region opaque.
(2-4% pore volume) It shows a +ve birefringence in polarized light
 Loss of crystalline structure suggesting the process of
DEMINERALIZATION AND REMINERALIZATION IN THIS ZONE.

Zone 3: Body zone
 Body of Lesion Occupies major portion of the lesion , AREA OF MAX
DEMINERALIZATION
The body of the lesion is positively bi refringent.
This is the largest zone which exhibits enhanced striae of Retzius.
( >5-25% pore volume )
Striae of Retzius is the primary point of entry of carious lesion into
rod/prism cores of enamel)

Zone 4: surface zone
 Relatively unaffected by caries (only partial demineralization)
 Because surface of enamel is relatively immune to caries (due to
hypermineralization- because of saliva contact , and higher surface
F-content)
 Its pore volume is lower than the body of lesion.(1 to <5% pore
volume)

After the involving the ENAMEL, the carious lesion progresses to the
DENTINAL STRUCTURE.
Caries advancement in dentin proceeds through 3 STAGES :
1) Demineralization of dentin (by weak organic acids)
2) Degeneration and dissolution of organic material of dentin ,
mainly collagen fibers (type I)
3) Bacterial invasion after the loss of structural integrity caused
due to 1 and 2).

Histologically , 5 zones of early dentinal caries progression can be
seen (listed pulpally to occlusally)
 Zone 1: zone of fatty degeneration of Tomes’ fibers
 Zone 2: zone of dentinal sclerosis
 Zone 3: zone of decalcification of dentin
 Zone 4: zone of microbial invasion
 Zone 5: zone of decomposed dentin

Zone 1: zone of fatty degeneration of Tomes’ fibers
 Most advancing front of dentinal caries characterized by the
presence of a layer of fat globules
 Formed by degeneration of the odontoblastic process
 Otherwise dentin is normal and produces
sharp pain on stimulation.

Zone 2: zone of dentinal sclerosis
It is the layer of sclerotic dentin ( deposition of calcium salts in dentinal
tubules takes place) which appears white in transmitted light
 There are no bacteria in this zone hence, this zone is capable of
REMINERALIZATION. Prevents further penetration of
microorganisms
 Formation of this zone is minimal in
rapidly progressing caries,and prominent
in slow caries.

Zone 3: zone of decalcification
 This zone lies above the zone of sclerotic dentin
 Initial decalcification of only the walls of the dentinal tubules
 Presence of PIONEER BACTERIA- first of the microorganisms
penetrating dentinal tubules before there is any clinical evidence of
caries.
 Bacteria present in individual dentinal tubules are in pure form
(i.e. either completely cocci or completely bacilli ,not in mixed
form)

Zone 4: zone of microbial invasion
 Characterized by the presence of
microorganisms in early stage of caries-
acidogenic microorganisms in deeper layer-
proteolytic microorganisms replace
acidogenic bacteria and
Supports the hypothesis that initiation (by
acidogenic bacteria) and progression ( by
proteolytic microorganisms ) are 2 distinct
processes in caries development.

• During initiation phase- in the early stage when caries is not deep ,
Acidogenic bacteria predominant which utilizes carbohydrate for their
metabolism
• Later in progression phase – as the caries goes deeper , less and less of
carbohydrate substrate available
• Hence acidogenic bacteria are replaced by proteolytic microorganisms
which uses dentinal protein for their metabolism.
• This is zone should be removed during tooth preparation.

Zone 5 : zone of decomposed dentin
Outermost zone
 Consists of decomposed dentin due to acids and enzymes
and filled with bacteria
Great number bacteria dispersed in this decomposed granular
matter.
It must be removed during tooth preparation.

PATTERNS OF CARIES IN PRIMARY
AND PERMANENT TEETH

Shape of the propagating lesion was summarized by Kidd & Fejerskov
 AT APPROXIMAL SURFACE Triangular shape in the enamel
with a base at the
enamel surface and a vertex at the
enamel –dentine (ED) junction
 Another ‘TRIANGLE’ is then observed at the DENTINE, with a base at the ED junction and
a vertex deep in the dentine.
 OCCLUSAL SURFACE, i.e. A PIT It has the shape of a triangle with a
vertex at the
pit (enamel surface) and a base at the
ED junction
Rene Fabregasand Jacob Rubinstein. On the initial propagation of dental caries J. R.
Soc. Interface 11: 20140809

Pattern of decay in nursing bottle caries
ETIOLOGY:
Due to nursing bottle containing milk or milk formula, fruit juice or
sweetened water
 Sometimes it occurs due to sugar or honey-sweetened pacifier

PATHOGENESIS:
child is put on bed at afternoon nap time or at night with nursing
bottle containing milk or a sugar containing beverage
milk or sweetened liquid becomes pooled around maxillary
anterior teeth
carbohydrate containing liquid provide an
excellent culture medium for acidogenic
microorganisms

• The intraoral decay pattern of nursing caries is characteristic and
pathognomonic of the condition.
• The 4 maxillary incisors are most affected, while the 4 mandibular
incisors usually remain sound.
• The other primary teeth, the canines, first molars, and second
molars may exhibit involvement depending upon how long the
carious process remains active
PATTERN

 Initially, the maxillary incisors develop a band of dull
white demineralization along the gum line that goes
undetected by the parents.
 As the condition progresses, the white lesions develop
into cavities that girdle the necks of the teeth in a
brown or black collar
 In advanced cases, the crowns of the 4 maxillary
incisors may be destroyed completely leaving decayed
brownish-black root stumps
 Conversely, the 4 mandibular incisors remain
unaffected

• Rampant caries is a suddenly appearing, rapidly burrowing type of
caries resulting in early pulp involvement, in which more than 10
new lesions appear every year on healthy teeth surfaces which are
generally immune to caries
Rampant caries is of the following three types –
 Nursing bottle rampant caries,
 Adolescent rampant caries and
 Xerostomia-induced rampant caries.
Rampant caries :
Rampant caries is seen at any
age and seen in both primary
and permanent dentition

NURSING BOTTLE RAMPANT CARIES :
 Nursing bottle caries is an type of rampant caries, which is
demarcated because of age factor which is seen in infants and
toddlers

ADOLESCENT RAMPANT CARIES –
When rampant caries occurs in adolescent age, it is called
adolescent rampant caries.
 During adolescence, some children habitually put chocolates,
toffees and biscuits in their mouth and go to sleep. Such patients
suffer from adolescent rampant caries.
The adolescent rampant caries has the same pattern as that of
nursing bottle caries.

Dental caries in adolescents associated with caffeinated carbonated
beverages Robert F. Majewski DDS, MS
Dental caries is an infectious disease involving all age groups. Adolescence is a period in which the risk for dental
caries remains especially high. Many factors, some unique to the teenage years, contribute to the initiation and
progression of dental caries in this age group. One factor with the potential for being significant is the adolescent
diet, especially the high consumption of sugars. One product that tends to contribute to the amount of sugar
ingested is carbonated beverages. Many soft drinks also contain significant amounts of caffeine. Regular caffeine
ingestion may lead to increased, even habitual, usage. It is suggested that the combination of the consumption of
highly sweetened soft drinks and habitual usage of caffeine may significantly increase a susceptible adolescent’s
potential for developing dental caries.
• Oral hygiene – As supervised home tooth-brushing
sessions and professional care may decrease in
frequency, there may be an increase in potential for
dental caries and periodontal disease
• Dietary habits –In this age group there is often a pattern
of irregular meals, frequent snacking, and consumption of
higher amounts of confectionery20 with a corresponding
decrease in consumption of healthier foods.
• Marketing and advertising –soft drink vending machines
on school property, along with other measures to increase
students exposure to the beverages
• Soft drink consumption – There is further concern that as
teens have increased their consumption of soft drinks
their consumption of milk has decreased by 40%
• Caffeine – Many carbonated beverages contain
caffeine.It is possible that the presence of caffeine in the
beverages consumed by adolescents is a major
contributor to the tendency for frequent, even habitual,
ingestion of such beverages
• Sugar
• Acidity of soft drinks

Conclusion: Adolescents consume a high amount of soft drinks, generally highly
sweetened, acidic, and often containing caffeine. The habitual ingestion of such
beverages could be a significant factor in the development and progression of dental
caries in susceptible individuals.

• The patient had the habit of frequent eating and taking milk and
biscuits just before going to sleep. This resulted in adolescent
rampant caries.
• Extensive carious involvement seen in maxillary anterior teeth

Arrested Caries :
Is a type of dental caries affecting teeth which are basically caries
which has become stationary or non-progessive or static without
any signs of further progression or extending in to enamel or dentin
structure
It is usually self cleansable and seen on lingual and labial surfaces
of the tooth
Due to self cleansable property there is lack of food retention in
arrested area

• CLINICAL FEATURES:
• Both deciduous + permanent are affected
• Large open cavities , brown-stained polished appearance + hard

• ARRESTED CARIES is usually hard and glossy
• It is due to the fact that the top layer of soft and decalcified enamel
is lost due to masticatory movements and forces
• And this leads to brownish/black discoloration and polished/shiny
surface which is hard in consistency
• SCLEROSIS of dentinal tubules is seen and secondary dentin
formation occurs in arrested caries.
• If arrested caries involves dentin it is
called EBURANATED DENTIN

• Initial carious lesions are the so-called "white spot" lesions
• which implies that there is a subsurface area with most of the
mineral loss beneath a relatively intact enamel surface
White spot" lesions :
Incipient lesions/White spot lesions are
active lesions which continue to
progress under acid attack whereas an
arrested lesions does not progress.

• Clinically, early caries lesion in enamel is initially seen as a white
opaque spot and is characterized by being softer than the adjacent
sound enamel and is increasingly whiter when dried with air
• Enamel defect with a relatively intact surface layer (SL) and some
subsurface damage due to acid formed from plaque on tooth surface.
• The shape of the white-spot lesion is determined by the distribution of
the microbial deposits between the contact facet and the gingival
margin, which results in a kidney shaped appearance.

On the proximal smooth surface there will typically be an interdental
facet area surrounded by an opaque area extending in the cervical
direction. The cervical border of the lesion is formed according to the
shape of the gingival margin

Radiation induced caries :
• Radiotherapy to the head and neck region causes xerostomia and salivary
gland dysfunction which dramatically increases the risk of dental caries
and its sequelae
• Radiation therapy (RT) also affects the dental hard tissues increasing
their susceptibility to demineralization following RT.
• Postradiation caries is a rapidly progressing and highly destructive type
of dental caries
• Radiation-related caries and other dental hard tissue changes can appear
within the first 3 months following Radiation therapy.

DIFFERENT TYPES OF RADIATION CARIES.
• A. Type 1 are lesions affecting the cervical aspect of the teeth and
extending along the cementoenamel junction.
• B. Type 2 presents with demineralized and worn occlusal
surfaces.
• C. Type 3 lesions present as color changes in the dentin. The
crown is dark brown/black, along with occlusal wear

Fluoride bomb :
• The various synonyms are ‘HIDDEN CARIES’, ‘FLUORIDE
BOMBS’, AND ‘FLUORIDE SYNDROME ’AND ‘PRE ERUPTIVE
CARIES’
• Occult caries is defined as the occlusal caries which cannot be
diagnosed clinically because the occlusal surface appears to be
ostensibly intact and shows radiolucencies in dentin.
Poornima P et al. An Insight to Occult Caries- An Overview with a Novel Approach in the Management J Oral Hyg Health
2015, 3:3

• The term ‘hidden caries’ or ‘occult caries’ denote those lesions that
cannot be detected by clinical examination alone
• In some teeth, these lesions have been discovered on routine
radiographs before their eruption into the oral cavity and these
are often referred to as ‘pre-eruptive caries’,
• The incidence of caries involving occlusal aspects
has been increased in children almost making 80% of
new lesions
International Journal of Contemporary Dental and Medical Reviews (2015), Article ID 020215, 4 Pages

XEROSTOMIA-INDUCED RAMPANT CARIES
 It is often associated with salivary gland hypofunction due to
irradiation of the head and neck region
 Lack of production of saliva
 Increased acidity
 Reduced remineralizing potential
 Shift towards cariogenic flora
 Reduced buffer capacity and secretory immunoglobulin A
 Carious lesion develops as early as 3 months after onset of
xerostomia

Pit and Fissure Caries :
CLINICAL FEATURES:
Appears brown or black
Feel slightly soft
Catch a fine explorer point
Enamel bordering the pit and fissure may appear opaque and
bluish white as it becomes undermined

• Lateral spread of caries at DEJ as well as penetration into dentin
along dentinal tubules may be extensive without fracturing away
overhanging enamel
• There may be large carious lesion with only a tiny point of
opening

Cervical, Buccal, Lingual or Palatal Caries :
 Usually extends from area opposite gingival crest occlusally to
convexity of tooth surface
 Extends laterally towards proximal surfaces
 Usually occurs on cervical area
 Gradually becomes excavated
 Typical cervical lesion is a crescent shaped
cavity beginning as slightly roughened chalky area

Root surface caries lesions :
also known as cemental caries
• involves both dentin + cementum
• Increase in number of people exhibiting gingival recession with
clinical exposure of cemental surface

• INITIAL ROOT CARIES :
• White at first then may become light brown to yellow.
• Shallow, spreads laterally. Without patient symptoms.
• ACTIVE, PROGRESSING ROOT CARIES :
• Yellowish, light brown.
• Soft or leathery on probing with light pressure.
• Its covered by visible plaque.
• Its primarily detected by the presence of softness and cavitation.

INACTIVE ROOT CARIES:
• Well-defined , Dark brownish or black in color
• May be rough or smooth shiny surface but its cleanable.
• Hard on probing with moderate pressure.
• Usually not covered with plaque
• Its seen in patients (usually older) whose oral hygiene and diet in
recent years are good

Caries-risk Assessment for Infants, Children, and Adolescents

Caries-risk Assessment and Management for Infants, Children,
and Adolescents

Caries management by risk assessment: A review on current strategies for
caries prevention and management S. Uma Maheswari, Jacob Raja,1 Arvind Kumar, and R. Gnana Seelan
J Pharm Bioallied Sci. 2015 Aug; 7(Suppl 2): S320–S324
The current trend in treating dental caries is using nondestructive risk-based caries management strategies
rather than focusing on the restorative treatment alone. Currently, there have been many changes in
understanding of the multifaceted nature of caries process and its management. Caries Management by
Risk Assessment (CAMBRA) which is an evidence-based approach focuses on determining many factors
causing the expression of disease and take corrective action.With this modern CAMBRA protocol, a novel
treatment plan can be designed to arrest dental caries thereby decreasing the chance of cavitation. The
initial caries lesions can be diagnosed with modern diagnostic aids and with the help of CAMBRA,
reestablishment of the integrity of the tooth surface early on in the caries process will bring great rewards
for patients.
DISEASE INDICATORS: The four disease indicators
 Visible white spots on smooth surfaces
 Last 3 years restorations placed in the oral cavity as a result of caries
 Lesions approximating enamel visible on dental radiographs
 Carious cavitation lesions are showing radiographic penetration into the dentin.

 Clinical Examination
 Caries Lesion Activity Assessment and Diagnosis
 Risk Factors
 Bacteria
 Saliva
 Diet
 Protective Factors(fluoridated water; regularly using fluoridated toothpaste,
low-fluoride oral rinses and xylitol; and receiving topical applications of
fluoride, chlorhexidine, and calcium phosphate agents.)
 Lesion Arrest and Repair(Along with fluorides calcium based strategies with
casein phosphopeptide amorphous calcium phosphate containing chewing
gums and more recently bioactive glass that react with the oral environment
and releases calcium and phosphate ions.)
 CAMBRA clinical guidelines recommend the use of xylitol to control S.
mutans for patients over 6 years of age who are at moderate to extreme risk for
caries.

 Resin Sealants and Infiltrants
 Antimicrobial Agents(Antimicrobial agents destroy or suppress the growth or multiplication
of microorganisms, including bacteria. CAMBRA clinical guidelines recommend the use of
antimicrobials for patients over 6 years of age who are classified as being at high or
extreme risk for caries.)
 Habits
Conclusion:
The strategies used for treating dental caries should have individualized consideration of the
underlying disease process for each patient. Many factors such as bacteria, carbohydrate diet,
and host response, cause initiation of dental caries, and its progression. Assessment of the caries
risk of the individual patient is a critical component in determining an appropriate
management strategy.
For low-risk patients the considerations must be given for remineralization, the arrest of
incipient caries or pit, and fissure sealant application, which provides ultimate conservation of
tooth.
For high-risk patients the preservation of the tooth structure and slow caries progression,
minimal intervention program can be considered.
There is a great variation in the interplay between all known and unknown factors that are
involved in caries development and the strategy have to be balanced with the clinician's

METHODS OF CARIES DETECTION
IN VIVO
1. Visual examination
2. Tactile examination
3. Radiographs-Conventional ,
Digital
and Xeroradiography *
4. Fiber optic transillumination.
5. Optical methods - Fluorescence,
light
scattering
6. Electronic resistance measurements
7. Ultrasonics
8. Dyes
IN VITRO
Single tooth measurements
1. Chemical analysis
2. Cross sectional microhardness
testing
3. Polarized light rpicroscopy
4. Traditional transverse
microradiography(TMR)
5. Microprobe analysis
Methods for sequential
measurements
on tooth slabs
1. Iodine absorbitometry
2. Longitudinal microradiogrpahy
3. Light scattering
4. Surface microhardness

Visual examination:
 The Visual examination of caries
encompasses the use of criteria such as
detection of white spot ,discolouration
and frank cavitation; Visual examination
on its own and without aids can be quite
unreliable.

ICDAS two-digit coding method:
A two-number coding system is suggested to identify restorations/sealants with the
first digit, followed by the appropriate caries code, for example: a tooth restored
with amalgam, which also exhibits an extensive distinct cavity with visible dentin
will be coded 4 (for an amalgam restoration) and 6 (for a distinct cavity); an
unrestored tooth with a distinct cavity would be 06.
Gugnani, Neeraj et al. “International Caries Detection and Assessment System (ICDAS): A New Concept.” International journal of
clinical pediatric dentistry vol. 4,2 (2011): 93-100.

In an study, approximal surfaces of 20 teeth were
examined by two researcher to compare ICDAS
II criteria with radiography in detecting caries.
While sensitivity of ICDAS II is better,
specificity of it is worse than radiography. Thus,
they reported that ICDAS II should be preferred
as caries diagnostic method in populations at
high risk of caries whereas radigraphy should be
preferred in population at low risk of caries.
Ekstrand et al. (2011) revealed that ICDAS can
detect and assess approximal caries that can be
seen with intraoral examination more successful
than radiography
The reliability and accuracy of two methods for proximal caries detection and depth on directly visible proximal surfaces: an in vitro
study.Ekstrand KR, Luna LE, Promisiero L, Cortes A, Cuevas S, Reyes JF, Torres CE, Martignon S Caries Res. 2011; 45(2):93-9.

Tactile examination:
The explorer and the floss to certain extent have been used for the tactile examination
of the tooth .
The explorer can be of different varieties such as:
1. Right angle probe [No.6]
2. Back action probe [ No. 17]
3. Shepherds crook [No. 23]
4. Cow horn with curved ends [no. 2]
Use of floss as an adjunct to tactile sensation:
Pickard (1961) has suggested the use of floss for detection of caries.when there is a
history of food packing between the teeth, the fraying of a piece of dental floss,when
it is passed through an apparently normal contact area points out that the area is the
site of early carious detection.

Radiographs
The carious area attenuates less radiation than the intact tooth surface so that
the film in the area of its image receives a higher exposure and thus is darker
on the processed radiograph.
The appearance of caries on various surfaces in the following order:
Interproximal > Occlusal > Buccal >Lingual > Cemental.
Conventional radiographs:
Though conventional radiographs [Bitewing and IOPA] are most frequently
used for the detection of caries, they are associated with drawbacks that it
presents a 2-D image of an object, may cause overlapping of the teeth due to
faulty angulation ,more so with the use of bisecting technique and may also
miss the initial lesion.

Advances
Digital Radiography either with Charge coupled device technology or
Storage phosphor screen technology has been used and is said to have
added advantages such as:
 Less image resolution.
 Less radiation required
 The image detector is generally larger.
 Detector life-span is unknown.
 The image is immediately available
 Hard copy image is less diagnostic
 Image can be electronically transferred.
 Image may be enhanced.

Xeroradiography :
 Xeroradiography is a technique that uses the xerographic copying
process to record images produces by diagnostic x-rays.
 It has also been used with the advantages of less radiation and edge
enhancement along with its wide latitude of exposure.
 The principal difference between xeroradiography and conventional
radiography is that ,in xero radiography the image formation is
achieved by a photoelectrostatic process and not by photochemical
process.

Fiber optic transillumination (FOTI)
With increasing concern about the use of ionizing radiation,the search continued for
an alternative to bite-wing radiographs for the diagnosis of proximal caries.
An alternative diagnostic syatem that has been advocated is the use of fiberoptic
transillumination(FOTI).
The principle of transillumination is that there is a different index of light
transmission for decayed and sound tooth. Since tooth decay has a lower index of
light transmission than the sound tooth structure, an area of decay shows up as a
darkened shadow that
follows the decay along the path of dentinal tubules.

The use of FOTI has been proved to be effective, specialty when used in the anterior
region. The usage in the posterior region is associated with some difficulty. It has
been thus advocated as an adjunct to visual and radiographic methods.
LIMITATIONS:
It can be used only for approximal surfaces:secondary caries cannot be
diagnosed.

Digital imaging fiber-optic transillumination(D-
FOTI):
 This is a digitized and computed version of
the FOTI.While FOTI was designed for
detection of approximal and occlusal caries,
digital imaging fiber-optic transillumination
DIFOTI is used for detection of both incipient
and frank caries in all tooth surfaces.

 DIFOTI can also be used to detect fractures, cracks, and
secondary caries around restorations.
 DIFOTI uses white light to transilluminate each tooth and to
instantly create highresolution digital images of the tooth. It
is based on the principle that carious tooth tissue scatters
and absorbs more light than surrounding healthy tissue.
 Decay near the imaged surface appears as a darker area
against the more translucent brighter background of
surrounding healthy anatomy.

Quantitative Light-induced Fluorescence
 Another dental diagnostic tool for detection of early carious lesions is quantitative
light-induced fluorescence (QLF), which is based on auto-fluorescence of teeth.
 When the teeth are illuminated with high intensity blue light, the resultant
autofluorescence of enamel is detected by an intraoral camera which produces a
fluorescent image.
 The emitted fluorescence has a direct relationship with the mineral content of the
 enamel.
 Thus, the intensity of the tooth image at a demineralised area is darker than the
sound area.

 The software of QLF systems can process the
image to provide user quantitative parameters
such as lesion area, lesion depth,and lesion
volume.
 These parameters can detect and differentiate the
lesions at very early stages, and make the QLF
system more sensitive to changes of caries over
time.
 QLF uses a blue light (488 nm) to illuminate the
tooth, which normally fluorescence a green
colour.
 Teeth should be dried before its application.

Laser fluorescence—DIAGNODent:
 The DIAGNODent (DD) instrument (KaVo, Germany) is another device
employing fluorescence to detect the presence of caries.
 Using a small laser the system produces an excitation wavelength of 655 nm
which produces a red light. This is carried to one of two intra-oral tips; one
designed for pits and fissures, and the other for smooth surfaces.
 The tip both emits the excitation light and collects the resultant fluorescence.

 Unlike the QLF system, the DD does not produce an image of the tooth;
instead it displays a numerical value on two LED displays.
 The first displays the current reading while the second displays the peak
reading for that examination.

Electronic resistance measurements:
 The low conductance of the tooth is primarily caused by the enamel. At
locations where the Porevolume of the enamel is larger, the electrical
conductance increases considerably.
 When a potentia1of less than one volt is applied, the resistance of above
600,000 ohms indicates that the tooth is caries free. A resistance below 250
000 ohms indicates that canes involving the dentin is present.
 Recently, site specific and surface specific measurements have been found to be
useful in the detection of caries in the precavitation stage as well

ULTRASONICS:
 Ultrasonics is the use of sound waves for detection and this offers considerable
potential as a diagnostic instrument.
 With the use of this instrumentation, sonic velocity and specific acoustic
impedance can be determined for the dentin and enamel as well as for
the soft tissue and bone.
 The velocity of sound on the enamel surfaces has been found to be Vs= 3,143 121
m/s. Comparing with a radiographic and visual inspection , it has been found that
white spot lesions with no radiolucencies or radiolucencies confined to the enamel
produced no detectable or weak surface echoes .
 All sites with visible cavitation and dentinal radiolucencies produced echoes with a
substantially higher amplitude

DYES:
 Various dyes have been used in the detection of enamel caries
[Calcein.Zyglo ZL-22],and dentin caries [Fuschin,Acid red system,9-
Aminoacridine]
 Though the use of dyes for the detection of carious dentin is used in the
removal of the same, concern has been expressed that the use of dyes is
associated with excessive removal of the dentin
 The use of the dye is based on the fact that increased porosity -through the
development of capillary like microvoids -is the earliest change in
the carious lesion.
 Very fluid solutions, that can strongly wet the enamel can be used to deposit
a fluorescent material in these pores.
 Other methods such as Micro-air abrasion, Infrared camera , Tuned
aperture computed tomography have also been developed for the detection
of caries.

MICRO AIR ABRASION:
 Developed in 1940s as an alternative to the slow
speed,belt driven handpieces.
 This system uses a narrowly focused particle
stream that abrades tooth structure in
proportion to the particle size,air pressure and
nozzle distance employed.
 Short bursts from the device reveals the
underlying decay that has been masked by the
stain

Other advances include:
 Infrared camera
 Videoscope/endoscope
 Tuned aperture computed tomography
 Magnetic resonance micro imaging
 Optical coherence tomography
 Terahertz Pulse Imaging
 CBCT
 Midwest caries ID
 Ultrasound carrier detector

Evaluation of different Diagnostic Modalities for Diagnosis of Dental Caries:
An in vivo Study Iram Zaidi Rani Somani Shipra Jaidka Int J Clin Pediatr Dent. 2016 Oct-Dec; 9(4): 320–325
AIM:The aim of this study was to compare and evaluate the efficacy of different diagnostic aids for
diagnosis of dental caries and to compare the validity in terms of sensitivity and specificity of all four
diagnostic modalities for diagnosis of caries.
MATERIALS AND METHODS: Occlusal surfaces of 100 primary and permanent molars were examined
using the four diagnostic systems (visual, intraoral camera, DIAGNOdent, and DIAGNOdent with dye).
These results were compared with operative intervention gold standard. Sensitivity and specificity were
calculated for each diagnostic system for both enamel and dentin caries. Interrater agreement was calculated
for each diagnostic system using kappa statistics.
RESULTS: For both enamel and dentin caries, the highest sensitivity values were provided by
DIAGNOdent (0.91 and 0.72) and lowest for visual examination on wet surface (0.60 and 0.50). For both
enamel and dentin caries, the specificity was found to be highest for intraoral camera on dry surface and
lowest for visual examination. The DIAGNOdent gave the highest value of interrater agreement (kappa),
i.e., 0.816 as compared with 0.03 for visual examination.
CONCLUSION: The study clearly demonstrated that DIAGNO-dent was the most accurate and valid
system tested for the detection of occlusal caries. It has the advantage of quantifying the mineral content,
helping to improve the diagnostic efficacy and treatment and accurate assessment of fissures where the
visual examination alone is not adequate, thus complementing the traditional dental examination.

Aims:
 Management of existing emergency
 Arrest and control of the carious process
 Institution of preventive procedures
 Restoration and rehabilitation
Factors affecting management:
 Extent of the lesion
 Age of the patient
 Behavioral problems
MANAGEMENT:

1st visit:
 All lesions should be excavated and restored.
 Indirect pulp capping or pulp therapy procedures can
be evaluated by further investigation.
 If abscess is present it can be treated through drainage.
 X-rays are advised to assess the condition of the
succedaneous teeth.
 Collection of saliva for determining the salivary flow
and viscosity.
 Application of fluoride topically.
Treatment:

 Parents should be questioned about child’s feeding
habits.
 Should be asked to try weaning the child from using
the bottle as a pacifier while in bed.
 Should be instructed to clean the child’s teeth after
every feed.
 Adviced to maintain a diet record for 1week.
PARENT COUNSELLING:

2nd visit:
 Analysis of diet chart and explanation of the disease process
of the child’s teeth with a simple equation.
 Isolate sugar factors from the diet chart and control sugar
exposure by intelligent use.
 Reassess the restoration and redo if needed.
 Caries activity tests can be started and repeated at monthly
intervals to monitor success of treatment.

3rd and subsequent visit:
 Restoring all grossly decayed teeth
 Endodontic treatment
 In case of unrestorable teeth, extractions can
be done followed by space maintenance.
 Crowns can be given for grossly decayed or
endodontically treated teeth.
 Review and recall after every 3months.

Early screening for signs of caries
development, starting from the first year of
life,could identify infants and toddlers
showing the risk of developing early
childhood caries.
 3 general approach:
 Community based
 Professional based
 Home based
PREVENTION

 The art and science of operative dentistry ,3rd
edition,Sturdevant.
 Textbook of pedodontics – 1st ed. Shobha tandon.
 Cariology: Ernest Newbrun, 3rd edn.
 Text book of oral pathology – shafer, 4th edn.
 Diagnosis and risk prediction of dental caries , vol 1. –
Per Axelsson
 Nikhil Marwah-Textbook of Pediatric Dentistry 3rd
edition.
 Dental Caries Aetiology, Pathology and Prevention –
L.M.Silverstone,N.W.jhonson
REFERENCES

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