THEORIES, ETIOLOGY AND

ZONES OF DENTAL CARIES.

BY. DR SHIVANI DUBEY

 CONTENT
 INTRODUCTION
 DEFINITIONS

 PART I

 THEORIES OF DENTAL CARIES

 ETIOLOGY OF DENTAL CARIES
 PART 2

 CLASSIFICATION OF DENTAL CARIES

 ZONES OF ENAMEL DEMINERALIZATION
 ZONES OF DENTINE DEMINERALIZATION
 REFERENCES
 INTRODUCTION
 Dental caries continue to be a greatest suffering on mankind,
despite wide spread preventive measures. Caries exert a
social, physical, mental and financial burden on a global
scale, with developing countries like India being affected the
most.

 WALTER LOESCHE (1986) termed caries as the “most

expensive infection that most individual have to contend with
during a life time”. The cost that Loesche talk about is not
only monetary loss. But the tooth loss resulting in
diminished chewing ability, pain suffering and cosmetic
defect.
 DEFINITION
 According to WHO caries is defined as a 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’S the microbial disease of calcified

tissue of the teeth, characterized by demineralization of the
inorganic portion and destruction of the organic substance of
the tooth.

 According to STUDERVANT, dental caries is defined as the

multifactorial microbiological disease, that result in localize
dissolution and destruction of calcified tissue of teeth.
 EARNEST NEWBURN stated “caries is not simply a continuous
and unidirectional process of demineralization of the mineral
phase, but appears to be cyclic, with periods of
demineralization immediately following metabolism of
fermentable substrate by the plaque flora, interspersed with
period of remineralization.”

 According to American Academy of Peadiartic Dentistry

2011-2012 definitions, Oral Health Policies and Clinical
Guidelines “ is biofilm (plaque) induced acid demineralization
of enamel or dentin, mediated by saliva.”
 THEORIES

 Dental caries has its origins rooted deep in history. Even as

early as 460 BC to 377 BC, toothache had been described as
the worst of tortures. Theories put forward to explain the
etiology of dental caries are :-

1. Worm Theory
2. Humors Theory
3. Vital Theory
4. Chemical Theory
5. Septic Theory.
6. Acidogenic Theory
7. Proteolytic Theory
8. Proteolysis-Chelation theory
9. Autoimmune Theory.
10. Sulfatase Theory
11. Complexing and Phospharilating theory.
 Worm Theory
 The earliest references to tooth decay and tooth ache came
from the ancient Sumerian text known as “Legend Of The
Worm”.

 According to an Assyrian legend, tooth ache was caused by

worm infestation, which drank the blood of teeth and fed on
their roots, as a punishment for offences committed against
God.
 The early history of India, Egypt and the writing of Homer
also make reference to the worm as the cause of the
toothache.

 Fumigation devices consisting of burning of loss and

byoyamus cane alkaloid were used by Chinese and Egyptians
for treatment of this disease.

 Rather, in 2700 B.C. the Chinese utilized acupuncture

technique to treat dental caries.
 2. HUMORS THEORY
 The legend of the worm faded over the early centuries as
Geek physicians advanced the Humoral Theory of disease.

 The ancient Greeks considered that a person’s physical and

mental constitution was determined by four element
1. Blood
2. Phlegm
3. Black bile
4. Yellow bile
 According to Galen, the ancient Greek physician and
philosopher, “dental caries is produced by internal action of
acid and corroding humors”.

 An imbalance in these humors results in disease.

 All disease including caries were explained by an imbalance

of these humors.
 3. VITAL THEORY

 Vital theory of tooth decay advanced towards the end of

the18th century which postulated that tooth decay originated
like bone gangrene, from within the tooth itself.

 A acceptance of this theory may have been the observation

that internal resorption occurs in some teeth.
 4. CHEMICAL THEORY
 In 17TH AND 18TH century, emerged the concept that teeth
were destroyed by acid formed in the oral cavity.

 The acid implicated were inorganic like sulfuric, nitric, citric

acids formed by decomposition of food in saliva.

 PARMLY proposed that an unidentified ‘chemical agent’

caused caries. He stated that the caries began on the enamel
surface in location were food putrefied and acquired
sufficient dissolving power.
 ROBERTSON (1835) proposed that dental decay was caused
by fermentation of food particles around teeth.
 5. SEPTIC THEORY
 IN 1843, ERDL described filamentous parasites in the
membrane removed from teeth.

 A few year later 1847 FICINUS , a physician also observed

filamentous organism in enamel cuticle (surface protein
membrane of teeth) and in carious lesions.

 Early microscopic observation of scraping from teeth and of

carious lesions by ANTONIO VAN LEEUWENHOEK (1632-1723)
indicated that the microscopic organism associated with the
carious process.
 DUBOS (1954) postulated that microorganism (animal culae)
can have toxic and destructive effects on tissue.

 Dental caries was then thought to develop as a result of

infiltration and decomposition of enamel cuticle, the inter-
prismatic substance of enamel and finally dentin.
 6. ACIDOGENIC THEORY
 In 1890 , W.D. MILLER put forward the ‘Acidogenic Theory’ or
‘Chemico- Parasitic’ theory to explain the occurrence of tooth
decay.

 He was the first well known scientist and investigator who

studied dental caries in detail and also published the result in
1882.

 According to MILLER dental decay is a chemo- parasitic

process that involve 2 stages:-
 Stage 1- is characterized by decalcification of enamel which
also result in destruction of dentine due to acid attack.

 Stage 2- is characterized by dissolution of softened residue

of enamel and dentin which is carried out by proteolysis
action of bacteria. The whole process is supported by
presence of carbohydrates, microorganism and dental plaque.

 This theory concluded that dental caries is a result of

decalcification of tooth structure due to acid produce by
‘parasite’ and ‘microorganisms’.
Critique of Acidogenic theory
a) Miller Acidogenic Theory was unable to explain the
predilection of specific sites on a tooth to dental caries. The
initiation of caries on smooth surfaces was not accounted
for, by acidogenic theory. The concept of dental plaque
adhering to tooth and serving to localize bacterial
enzymatic activity was discovered later.

b) Miller did not explain why some populations are caries free
and also the phenomenon of arrested caries was not
explained by this theory.
 7. PROTEOLYSIS THEORY
 The evidence given by Acidogenic theory was substantial but
not conclusive, an alternate explanation was given in form of
Proteolysis Theory.

 Workers like HYDER BOREDER (1878) and ABBOT (1879)

contributed to this theory. They sustained with an evidence that
the organic portion of tooth plays a major role in development of
dental caries.

 In 1944 GOTTLIEB proposed the ‘Proteolysis Theory’. According

to this theory the protein component of tooth is destroyed first,
prior to loss of minerals. The organic structure eg. Enamel
lamellae and enamel rods in enamel contains 0.58% of organic
matter of which 0.18% is keratin and 0.17% is soluble protein.
 The microorganism invade through enamel lamellae and acid
produced by microorganism causes damage to the organic
pathways in advance. The production of yellowish pigment,
produce by proteolytic bacteria, was only possible in
presence of dietary carbohydrate.
 LIMITATIONS –

 Proteolytic bacteria is uncommon.

 Till date no one has under physiological conditions,
successfully demonstrated significant loss of enamel tissue
through proteolytic activity.
 Enamel is highly structured tissue and the accessibility of
organic material to enzymatic action before decalcification is
restricted.
 Enamel can be dissolved under physiological conditions only
by demineralization with acids, chelating or complexing
agents.
8. PROTEOLYSIS- CHELATION THEORY.

 Some of the minor flaws of acidogenic and proteolytic theory

were addressed in Proteolysis- Chelation theory.

 This theory was introduced by SCHATZ and MARTIN (1955)

which was an extension of proteolysis theory. Theory implies
a simultaneous microbial degradation of organic component
(hence proteolysis) and dissolution of mineral of the tooth by
process of chelation.
 According to this theory, dental caries results from an initial
bacterial and enzymatic proteolytic action on the organic
matter of enamel without preliminary demineralization.

LIMITATION-

 Less than 1% of mature enamel is organic in nature and the

suggestion that this material upon degradation can give rise
to a significant concentration of chelate, sufficient to dissolve
up to 96% mineral matter has no experimental support.

 Hence this theory cannot be accepted as primary etiology of

dental caries.
9. AUTOIMMUNE THEORY.

 JACSON AND BURCH postulated the ‘Autoimmune theory’ of

caries development. According to them genetic structure of a
person is responsible for caries susceptibility or caries immunity.

 Based on the Burch’s ‘auto aggressive theory of the cause of

growth, disease and aging’.

 Jackson and Brush (1970) suggest that genes (partly inherited

and partly as a result of mutation) determine whether a site on
the tooth is at risk. An abnormal mitotic control protein has been
proposed that causes disorders of the odontoblasts as a random
event that leads to changes in the resistance of the enamel to
acid attack.
 The most widely accepted theory till today continues to be
acidogenic theory introduced by Miller. This can be best
understood by KEY’S TRIAD.

 The Key’s triad was introduced in 1960, The three factor

involved in the decay process are:
1) Tooth (host).
2) Substrate (fermentable carbohydrate).
3) Microorganism (bacteria)
 The Key’s triad was later modified To caries tetralogy by
NEWBURN (1982)-

4) Time
5) Saliva
 In 1997 Professor DOUGLASS BRATHALL devised the
cariogram model to illustrate the caries risk.

 According to Brathal the risk is expressed as ‘percent chance

to avoid caries’. A low percentage for example 5% risk. In
contrast, 90% chance indicate a very low caries risk.
Components of cariogram model include:

 Chance – the chance to avoid new cavities in the near future.

 Diet – frequency of eating as well as content of diet.

 Bacteria – plaque amount as well as type of bacteria.

 Susceptibility – Tooth resistance (fluorides and saliva

characteristics.

 Circumstances – past caries experience, systemic disease and

conditions.
 10. SULFATASE THEORY
 PINCUS (1950) advanced the sulfatase theory, where by
bacterial sulfatase hydrolyses the mucotin sulfate of enamel
and the chondroitin sulphate of dentine producing sulfuric
acid that causes decalcification of dental tissues.

 LIMITATION-

 The concentration of sulfated polysaccharides in enamel is

very small and not readily accessible as a substrate for
enzymatic degradation.
 This is highly unlikely hypothesis for the degradation of tooth
enamel.
11. COMPLEXING AND PHOSPHARILATING
THEORY.

 Given by LAURA in 1967.

 It can be readily demonstrated that uptake of phosphate by
plaque bacteria occurs during aerobic and anaerobic
glycolysis and the synthesis of polyphosphates.

 According to this theory “the high bacterial utilization of

phosphate in plaque causes a local disturbance in phosphate
equilibrium in plaque and tooth enamel resulting in loss of
inorganic phosphate from enamel.

 Soluble enamel complexing compound produced by bacteria

causes further tooth disintegration.
 LIMITATION-

 Saliva is an abundant source of inorganic phosphate for

bacterial utilization.

 Hence it is highly improbable that depletion of phosphate in

plaque by oral microbial metabolism result in phosphate
withdrawal from enamel.
 ETIOLOGY OF DENTAL CARIES
SUSCEPTIBLE TOOTH STRUCTURE:
 Healthy enamel is a non living yet dynamic calcified product
that appears to naked eye unchanged throughout life of the
individual.

 Although appearance of clinically normal teeth is relatively

constant over long periods of time, the tooth structure itself
undergoes continues change in both physiochemical and
morphologic properties as a result of constant interplay with
surrounding environment.
 It is important to realize that enamel, being essentially a
mineralized product, Is subject to the laws of solubility as in
any inorganic phase surrounding environment.

 Healthy enamel is the result of a relatively stable or favorable

equilibrium is disturbed by the superimposition of an altered
ecology (an exaggerated bias of one or a group of
environmental variables), the result will be dissolution of
tooth structure with eventual cavitations.

 Alternatively, an opposite and more favorable bias may result

in precipitation of inorganic mineral In sites of prior attack
(e.g reminrealization)
 Caries is basically the end result of a series of back and forth
shifts in chemical equilibrium of tooth structure which is
summation dictates condition more favorable to inorganic
dissolution than recrystalization.
 DIETARY CARBOHYDRATE
 Carbohydrate constitute the fuel of dental caries and as such
are essential ingredient for all types of carious activity.

 For carbohydrate to be active w.r.t caries, it must be

assimilated orally and in sufficient quantity to provide
abundant direct contact with the immediate environment of
the tooth surface.

 In this manner, dietary carbohydrates becomes available as a

substrate for local bacteria metabolism.
 If there is to be caries activity, there must be degradable
dietary carbohydrate, not only as a carbon source for
bacterial fermentation to organic acids, but also as a
substrate for ATP synthesis, necessary for bacterial survival
and proliferation.

 While the term carbohydrate is used in reference to the

general group of substrates for bacterial fermentation, it is
clear that this is far too broad.
 Specifically, the smaller disaccharide or monosaccharide units
are readily active in this respect. Thus, dietary carbohydrate
to be active as cariogenic substrate, must be either in readily
usable monosaccharide form or else easily broken down to
such by bacterial metabolic machinery at the site of carious
attack.
 ORAL BACTERIA
 The third essential factor of dental caries is the oral bacterial
component. Millions such microorganism act to ferment
dietary carbohydrate to acid and there by provide the
destructive agent necessary for demineralization of tooth
structure.
The Streptococci
 The streptococci have emerged as the dominant group of
microorganism involved in the pathogenesis of dental caries.

 FITZGERALD AND KEYES demonstrated that inoculation of

streptococcal microorganisms isolated from carious rodent
teeth would initiate caries in germ free rats and albino
hamster, provided the diet was rich in sucrose.

 The so called cariogenic streptococci are know known as

streptococcus mutans. The name was proposed by CLARKE in
1924.
 Streptococcus mutans is evenly found throughout population
of the world and can be found in almost all human mouths
from the time of tooth eruption until total tooth loss.

 One of the peculiar traits of the microorganism is its relative

inability to adhere to soft tissue. Colonization of S.mutans
does not occur easily nor at random but only on specific
areas that are relatively sheltered and free from the
mechanical action of mastication, soft tissue friction or tooth
cleansing devices
 Only s mutans has the ability to produce the extremely heavy
and viscous plaque associated with rampant interproximal
caries in rodent and humans.

 Its characteristic feature is tenacious adherence is

undoubtedly caused by copious amount s of extracellular
glucose polymers (glucans) produced as a byproduct of
sucrose metabolism.

 S mutans has a great importance in initiation of smooth

surface caries but relatively weak cariogenic status of these
microbes is related to their incapability to induce heavy
plaque formation.
The Lactobacilli
 Lactobacilli and other acidogenic microorganism are thought
to be significant with respect to smooth surface caries but
only after prior to demineralization and cavitations has taken
place.

 It is rare to find significance number of lactobacilli in direct

association with non cavitated “white spot”.

 Lactobacilli comes to prominence with plaque only after acid

condition becomes concentrated enough to drop pH level
below 5.5. at this time growth is more favorable to lactobacilli
than streptococcus species.
 GENETIC FACTOR
 Variation in amelogenin may contribute to caries
susceptibility.

 Having at least one copy of rare amelogenin marker allele is

associated with individuals with higher DMFT.

 Lactotransferrin A/G (exon 2, Lys/Arg) polymorphism is

associated with susceptibility to dental caries.

 Since beta defensin 1 (DEFB1) localizes in the oral cavity,

variation in DEFB1 is associated with caries.
 HOST FACTOR
 Morphology of teeth: Deep fissure are prone to accumulation
of food and development of caries.

 Intra-oral variation: the caries susceptibility of teeth varies in

following order:

Lower first molars> upper first molar > upper and lower
second molar> second bicuspids > upper incisors > cupids.

 Lower incisors and cupids are least susceptible to caries.

 Irregularities of arch forms: crowding and malaligned teeth
favor development of dental caries.

 Saliva quantity , viscosity, flow rate, composition buffering

capacity etc.
 SALIVA
 Saliva is not listed as one of the essential factors in dental
caries, saliva nevertheless constitute an extremely important
modifying variable which has considerable inhibitory effect on
the development of carious lesion.

 A number of mechanism are involved in the protective effect

such as mechanical via cleansing effect or chemical via
specific interaction of salivary constituents with bacteria,
acid, carbohydrate substrate or tooth surface.
Salivary flow rate
 The rate of salivary flow appears to be inversely proportional
to the degree of carious activity.

 As salivary flow rate increases there is greater tendency for

cariogenic substrate to be rinsed from tooth surface and thus
not remain at a given area for sufficient duration to allow to
degradation to lactic acid or synthesis of cariogenic
polysaccharides.

 Thus with heavier flow the salivary pH rises to 6.0 to value

greater than 7.0
 CURRENT CONCEPT
 Caries is perceived to be a prolonged imbalance in the oral
cavity such that factors favoring demineralization overwhelm
factors that favors remineralization or healing of tissues.

 Therefore to understand the caries process, it is necessary to

probe the reaction process that occurs at the surface.

 The mineral content of tooth surface is hydroxyapatite

[Ca(PO4)6(OH)2], which is equilibrium and neutral
environment saturated with calcium and phosphate.
 DEMINERALIZATION- The hydroxyapatite crystals react to
hydrogen ions at the critical pH and below. H+ ions react
with the phosphate group in the aqueous environment
immediately adjacent to the crystal surface with the
conversion of phosphate to hypophosphate by addition of
hydrogen ions being buffered at the same time. The
hypophosphate is not able to contribute to the normal
hydroxy-apatite equilibrium because it contains phosphate
not hypophosphate. Thus the hydroxyapatite crystal dissolve
and the process is termed demineralization.
 REMINERALIZATION- The demineralization can be reversed if
the pH is neutral and there are sufficient calcium and
phosphate ions in the immediate environment. Either apatite
dissolution can reach neutrality by buffering or the calcium
and phosphate ions in saliva can inhibit the process of
dissolution through the common ion effect. This enables
rebuilding of partly dissolved apatite crystals and is termed
remineralization.
 CONCEPT OF CRITICAL pH.

 The carious process is initiated by bacterial fermentation of

carbohydrates, leading to the formation of a variety of
organic acids and a fall in pH.

 Initially H+ will be taken up by buffers in plaque and saliva.

When the pH continues to fall (H+ increases), however the
fluid medium is depleted of (OH)- and phosphate ion which
react with H+ to form H2O and (HPO4)2-
 Stephan Plaque pH Response (Stephan 1940, 1944)
demonstrated the relationship between sugar exposure
resulting in the acidification of dental plaque and caries
experience.
 Therefore whenever surface enamel is covered by microbial
deposit the ongoing metabolic process within this mass can
cause fluctuation in pH and occasional steep fall in pH which
may result in dissolution of mineralized surface.

 The critical pH at which environment of enamel becomes

unsaturated and in addition that pH at sufficient high
concentration of un ionized acid are present to ensure the
inward diffusion of enough acid to extend to inner lesion.
PART 2
CLASSIFICATION OF DENTAL CARIES
 On the basis of clinical features and patterns, dental caries
may be classified according to three basic factors:
 Morphology, i.e. according to anatomical site of lesions. —
 Dynamics, i.e. according to severity and rate of progression
of lesions. —
 Chronology, i.e. according to age patterns at which lesions
predominate.

 In all probability, the different clinical types of caries have the

same underlying etiology, but the susceptibility of the
anatomical sites and the rate of progression of the lesions
vary widely from one tooth to another, and from one
individual to another.
 Based on location of lesion:

PIT AND SMOOTH SURFACE

FISSURE CARIES CARIES

LINEAR ENAMEL
CARIES ROOT CARIES
 Based on the tissue involved:

INITIAL CARIES

SUPERFICIAL CARIES

MODERATE CARIES

DEEP CARIES

DEEP COMPLICATED CARIES

 Based on virginity of lesion:
1) Primary / initial caries

2) Secondary/ recurrent caries

 Based on the progression of the lesion:

1. Progressive caries.

2. Arrested caries.
 Progressive caries is further classified as:

1.Rapidly progressive such as:

 Nursing caries
 Radiation caries

2. Slowly progressive.

 Based on extend of lesion:

 Incipient caries
 Occult caries
 Based on number of tooth surface involved:
 Complex
 Compound
 Simple

 Based on chronology:
 Early childhood caries.
 Adolescent caries
 Adult caries
WHO classification (1995):
 K02.0 –caries limited to enamel
 White spot lesion (initial caries).
 K02.1 – Caries extended into dentin
 K02.2 – Caries of cementum
 K02.3 – Arrested caries
 K02.4 – Odontoclasia
 Infantile melanodontia
 Melanodontia
 Excludes: internal and external resorption of teeth (K03.3)
 K02.8 – Other specified dental caries
 K02.9 – Dental caries unspecified.
Mount G.J and Hume (1997) classified
dental caries based on site and size.

 A) SITE
 Site 1: includes lesions of pits and fissures on occlusal
surfaces of the posterior teeth. These include the buccal
grooves of the mandibular molars, palatal grooves of the
maxillary molars.

 Site 2: includes lesions in the contact areas of posterior and

anterior teeth.

 Site 3: includes lesions originating in the gingival third of all

teeth.
 B) SIZE

Size 1 (mild): includes lesions which have progressed just

beyond remineralization.

Size 2 (moderate): includes larger lesions, with adequate tooth

structure to support the restoration.
Size 3 (enlarged): includes lesions in which the tooth structure
and the restoration are susceptible to fracture.

Size 4 (severe): includes lesions which have destroyed a major

portion of tooth structure.
VARIOUS CARIES CLASSIFICATION
SYSTEM:

1). G.V Black’s classification:

Greene Vardiman Black (1836- 1915) is one of the forefather of

modern dentistry. The caries classification system was
developed by G.V Black in early 1900s. This system divides
dental caries into several clases based on site of tooth.

CLASS 1: caries occurring on pits and fissures on facial , lingual

and occlusal surfaces of premolars and molars.

CLASS 2: caries affecting proximal surfaces of posterior teeth.

 CLASS 3: Caries occurring on the proximal surface of anterior
teeth.
 CLASS 4: caries involving proximal and incisal surfaces of
anterior teeth.
 Class 5: Caries occurring on facial and lingual surfaces in
cervical third of teeth.
 CLASS 6: (proposed by SHULZ) lesions on incisal edges of
anterior teeth and cusp tips of posterior teeth.
THE INCIPIENT CARIOUS LESION IN ENAMEL

 The first differential clinical sign of dental caries is the white

spot, so called because of the loss of translucency of the
affected area. The white spot is most easily observed when
the enamel is thoroughly dried.

 Clinically, no cavitations is evident but the surface may be

rougher than normal enamel as assessed by a dental probe.
The white spot is most frequently detected in the gingival
area of the buccal or labial surfaces of the clinical crown of a
tooth.
 A carious lesion on the smooth surface of enamel is conical
in shape with its broad base on enamel and the apex toward
the dentin
 Light microscopy studies of carious lesions of enamel
without cavitations have revealed four distinct zones which
represent varying degrees of hard tissue transformation
[Silverstone, 1977]. Starting from the advancing front of the
lesion these zones are classified as:

Zones of enamel demineralization

 - A translucent zone which is the advancing front of the
lesion.
 - A dark zone separating the translucent zone from the body
of the lesion.
 - The body of the carious lesion which is markedly
radiolucent.
 - A relatively intact enamel surface layer.
Zone 1 The Translucent Zone
 The advancing front of a carious lesion is represented by the
translucent zone. The first discernible signs of enamel
breakdown are seen in this area.

 Translucent zone is the first visible sign of caries & coincides

with 1 to 2% loss of minerals.

 It lies at the advancing front of the lesion.

 This zone appears structure less & is more porous than

sound enamel. It is not always present.
 It has pore volume of 1% compared with 0.1% in sound
enamel.

 In this zone, pores and voids form along the enamel prism
(rod), boundaries presumably because of the ease of
hydrogen ion penetration during the carious process.

 It appears structureless when perfused with quinolone

solution (having refractive index comparable to that of
enamel) and seen with polarized light (hence translucent).

 In this demineralization takes place (magnesium and

carbonates are dissolved).
Zone 2 The Dark Zone
 The dark zone lies deep to the body of the lesion and just
superficial to the translucent zone.

 The dark zone is adjacent and superficial to the translucent

zone. It is considered to be a positive zone.
 It does not transmit polarized light due to presence of many
tiny pores, too small to absorb quinoline. The smaller air or
vapor filled pores make region opaque. Total pore volume is 2-
4%.

 Some researchers speculated that dark zone is not really a

stage of breakdown of enamel; rather the dark zone may be
formed by deposition of ions into an area previously containing
larger pores.

 There is loss of crystalline structure in the dark zone

suggestive of process of demineralization and remineralization.

 A slight remineralization of enamel occurs in the dark zone,

which serves as an example of how the development of dental
caries is an active process with alternating changes.
Zone 3 The Body of the Lesion
 Deep to the relatively unaffected enamel surface layer is the
body of the carious lesion.

 It is the largest portion of the incipient lesion while in

dematerializing phase with enhanced striae of Retzius.

 It causes 24% mineral loss.

 It is the area of greatest demineralization.

 • It has largest pore volume from 5% at periphery to 25% at

the centre.
 The striae of Retzius are well marked in the body of lesion &
indicate preferential mineral dissolution along these areas of
relatively higher porosity.

 The first penetration of caries enters the enamel surface via

striae of Retzius.

 Bacteria may be present in this zone “if pore size is large

enough to permit their entry”.
Zone 4 The Surface Zone
 An important feature of the initial carious lesion is the
presence of an apparently intact enamel surface overlying an
area of subsurface demineralization.

 It is relatively unaffected by caries attack.

 It is thinner in active lesions and thicker in inactive lesions.

 It has lower pore volume than the body of the lesion (<5%)
and radiopacity comparable to unaffected enamel.
 The surface of normal enamel is hyper mineralized by contact
with saliva and has a greater concentration of fluoride ion
than the immediately subjacent enamel.

 The greater resistance of the surface layer may be due to a

greater degree of mineralization and/or a greater
concentration of fluoride in the surface enamel.

 There has been some attempts at implication of enamel

lamellae as pathways of invasion of proteolytic micro-
organisms and the subsequent development of caries.
THE INCIPIENT CARIOUS LESION IN
DENTIN.
 Progressing carious lesions penetrate the enamel, spread
laterally along the dentino-enamel junction and undermine
the enamel. The lesion invades the dentin following the
direction of the dentinal tubules. This pattern of invasion of
dentin results in a cone-shaped lesion with its base at the
dentino-enamel junction and apex towards the pulp.
Zones of dentin demineralization

 Zone 1: zone of fatty degeneration of Tomes’

fibers
 Zone 2: zone of dentinal sclerosis
 Zone 3: zone of demineralization of dentin.
 Zone 4: zone of bacterial invasion
 Zone 5: zone of decomposed dentin
Zone 1: Zone of fatty degeneration of Tomes’ fibers

 The most advancing front of dentinal caries.

 It is characterized by the presence of a layer of fat globules;

Hence stain red with Sudan red.

 Fat layer leads to impermeability of the dentinal tubules

trying to prevent further invasion of carious lesion.

 It favors sclerosis of dentin in zone of dentinal sclerosis.

Zone 2: Zone of dentinal sclerosis
 Layer of sclerotic dentin appears white in transmitted light.

 The sclerotic or translucent zone is located beneath and at

the sides of the carious lesion. It is almost invariably present,
being broader beneath the lesion than at the sides, and is
regarded as a vital reaction of odontoblasts to irritation or
carious invasion so as to prevent further penetration of
microorganisms.
 Formation of this zone is minimal in rapidly progressing
caries, and prominent in slow caries.

 Two patterns of mineralization have been described. The first

is the result of acceleration of the normal physiological
process of centripetal deposition of peritubular dentin which
eventually occludes the tubules.

In the second, mineral first appears within the cytoplasmic

process of the odontoblasts and the tubule is obliterated by
calcification of the odontoblast process itself. Sclerosed
dentin therefore has a higher mineral content.
 Dead tracts may be seen running through the zone of
sclerosis. They are the result of death of odontoblasts at an
earlier stage in the carious process.

 The empty dentinal tubules contain air and the remains of the
dead odontoblast process and such tubules can obviously not
undergo sclerosis. However, they provide ready access of
bacteria and their products to the pulp. To prevent this, the
pulpal end of a dead tract is occluded by a thin layer of
hyaline calcified material, sometimes called Eburnoid, which
is derived from pulpal cells.
 Beyond this, often very irregular, reactionary dentin may form
following differentiation of odontoblasts or odontoblast-like
cells from the pulp.
Zone 3: Zone of demineralization
 This zone lies above the zone of sclerotic dentin.

 There is the presence of pioneer bacteria-first of the

microorganisms penetrating dentinal tubules before there is
any clinical evidence of caries.

 The intertubular matrix is mainly affected by acid diffusing

from pioneer bacteria.

 Bacteria present in individual dentinal tubules are in pure

form (i.e. either completely cocci or completely bacilli; not in
mixed form)
 The softened dentin in the base of a cavity is therefore sterile
but, in clinical practice, it cannot be distinguished reliably
from softened infected dentin. It may be stained yellowish-
brown as a result of the diffusion of other bacterial products
interacting with proteins in dentin.
Zone 4: Zone of bacterial invasion
 It is characterized by the presence of microorganisms. In
early stage of cariesacidogenic microorganisms predominate
& in deeper layer- proteolytic microorganisms replace
acidogenic bacteria .

 In this zone the bacteria extend down and multiply within the
dentinal tubules, some of which may become occluded by
bacteria. There are always, however, many empty tubules
lying among tubules containing bacteria.
 The bacterial invasion probably occurs in two waves: the first
wave consisting of acidogenic organisms, mainly lactobacilli
produce acid which diffuses ahead into the demineralized
zone.
A second wave of mixed acidogenic and proteolytic
organism’s then attack the demineralized matrix. The walls of
the tubules are softened by the proteolytic activity and some
may then be distended by the increasing mass of multiplying
bacteria.

 The peritubular dentin is first compressed, followed by the

intertubular dentin, resulting in elliptical areas of proteolysis-
liquefaction foci. Liquefaction foci run parallel to the direction
of the tubules and may be multiple, giving the tubule a
beaded appearance. These changes are enhanced in the zone
of destruction. The bacteria may show varying degrees of
degeneration.
 It supports the hypothesis that initiation (by acidogenic
bacteria) and progression (by proteolytic microorganisms) are
2 distinct processes in caries development.
Zone 5: Zone of decomposed dentin

 It is the outermost zone.

 It consists of decomposed dentin filled with bacteria, acids &

enzymes.

 It must be removed during tooth preparation.

 If not treated, the lesion progresses towards the pulp. The

moment the microorganisms invade the pulp, a carious
exposure results. However, bacteria can be preceded by their
toxins which can give rise to an inflammatory response in the
pulp long before an exposure actually results.
REFERENCES
 Text Book of Pediatric Dentistry S.G DAMLE.
4-5th edition.

 Paediatric Dental Medicine Donald J Forrester.

 Nikkiforuk volume 1.

 Text book of Oral pathology Shafer’s 7th

edition.