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DENTI
N

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CONTENTS
INTRODUCTION
HISTORY
HISTOPATHOLOGICAL STAGES
DEVELOPMENT{DENTINOGENESIS}
PHYSICAL AND CHEMICAL PROPERTIES
STRUCTURE OF DENTIN
TYPES OF DENTIN
INNERVATION OF DENTIN
PERMEABILITY OF DENTIN
AGE AND FUNCTIONAL CHANGES
CLINICAL CONSIDERATIONS
DEVELOPMENTAL ANOMALIES
CONCLUSION 3
REFERENCES
Introduction

 A thick dentin layer forms the bulk of mineralized dental tissues. Dentin
is capped by a crown made of highly mineralized and protective enamel,
and in the root, it is covered by cementum, a structure implicated in the
attachment of the teeth to the bony socket.

• It is also called as substantia eburnea.

• Yellow in appearance, it greatly affects the color of a tooth due to the

translucency of enamel. 4
HISTORY

• 1771 - John Hunter described dentin as hard tissue.

• 1775 -Anton Von Leeuwenhoek described tubular structures.

• 1837 - Purkinje and Retzius explained about dentinal tubules.

• Cuvien gave the name “ivory” to dentin.

• 1891 - Von Ebner gave the term – Ebner’s lines . 5

 cap stage

Bud stage Early bell

Proliferation stage

Initiation HISTOPHYSIOL
OGICAL
Histodifferentiation
STAGES OF
TOOTH
Apposition DEVELOPMENT

Morphodifferentiation
Formation Advanced
of enamel bell stage 6

and dentin
INITIATION BUDSTAGE

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CAP STAGE/PROLIFERATION STAGE

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EARLY BELL STAGE/HISTODIFFERENTIATION

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ADVANCED BELL STAGE/MORPHO DIFFERENTIATION

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APPOSITION

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Dentinogenesis

*The formation of dentin is called dentinogenesis.

*Dentinogenesis takes place in two phases .First is formation of
organic collagen matrix followed by deposition of
hydroxyapatite crystals.
*At the beginning of dentinogenesis the odontoblasts elongate
and form tomes fibres or odontoblastic processes.

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• Odontoblasts then secrete matrix protein at the apical end of the cell and along its
process.
• The secreted matrix is collagenous and not mineralized hence it is Predentin.
• As the matrix is being secreted the odontoblasts move towards the centre of the
future pulp.
• The matrix that forms around the elongated cell process eventually mineralizes
and the odontoblastic process will lie within a dentinal tubule.

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• One of the key proteins involved in the mineralization and secreted by the
odontoblast is the dentin-phosphoprotein.
• Korff’s fibres have been described as the initial dentin deposition along the cusp
tips.
• MAP1B gene is responsible for odontoblast differentiation
• PHEX gene is responsible for dentin mineralization.

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 9
Radiography
Appears radiolucent than
enamel
because of lower mineral Viscoelastic properties
Colour content Withstand slight elastic deformation
Light yellow
Darkens with age
Modulus of elasticity:1.67×𝟏𝟎𝟔 PSI
Compressive strength :266MPa
Thickness-3-10 mm Specific gravity :2.14
Dentisty-22.1gm/mm
Hardness
Normal :68KHN
Carious :25KHN
Sclerotic :80KHN
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CHEMICAL COMPOSITION

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Organic substances:
• Type I collagenousfibrils
• Type V collagenousfibrils (minor)
• Non collagenousproteins: •dentin phosphoprotien(dpp)
•Dentin matrix protein 1 (DMP1)
•Dentin sialoprotein(dsp)
•Bone sialoprotein(bsp)
•Osteopontin, osteonectin
• proteoglycans
• phospholipids
• Growth factors: •bone morphogenetic proteins (BMP)
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insulin like growth factors (igfs)
transforming growth factors β(tgf-β)
Inorganic components:
• Inorganic component consists of hydroxyapatite crystals which are composed of
several thousand unit cells.
• Each unit cell have a formula of 3𝑐𝑎3 ℙ𝑜4 2 𝐶𝑎 0𝐻 2

• Crystals are plate shaped.

• Organic and inorganic substances are separated by either decalcification or
inceneration.

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 Dentinal tubules
• Peritubular
Odontoblastic • Intertubular
processes.

STRUCTURE
OF DENTIN • Incremental lines
of von ebner
• Neonatal lines
Dentino enamel junction
• Granular layer
Dentino cemental junction
Dentino pulpal junction
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DENTINAL TUBULES:
• The course of the dentinal tubules

Follow a gentle curve in the crown

Where it resembles an “S” shape.
• It starts at right angles at the pulpal
Surface, the first convexity of this
Doubly curved course is directed
Towards the apex of the tooth.
• These tubules end perpendicular to
The DEJ & CDJ.

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• It is almost straight near the root tip and along the
incisal edges and cusps

• Ratio between outer and inner surfaces of dentine is

About 5:1.

• No. Of tubules per square millimeter varies from

15000 at the DEJ to 65000 at the pulp – density and
Diameter increases with depth.

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• There are more tubules per unit area in the crown than in the root
• These dentinal tubules have
Lateral branches throughout dentin,
Which are termed canaliculi or microtubules
• A few odontoblastic processes
extend through the DEJ into the enamel
several millimetres.
• These are called enamel spindles.

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PERITUBULAR DENTIN

• The dentin that immediately surrounds the dentinal tubules is termed

Peritubular dentin

• Highly mineralised than intertubular dentin

Twice as thick in outer dentin(approx. 0.75μm) than
Inner dentin(approx. 0.4μm)

• Calcified tubule wall has an inner organic lining

Termed the lamina limitans which is high in
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Glycosaminoglycans (GAG).
INTERTUBULAR DENTIN
• Located between the dentinal tubules or more specifically between the zones of
Peritubular dentin
• One half of its volume is organic matrix, specifically collagen fibres
• The fibrils range from 0.5-0.2μm in diameter and
Exhibit crossbanding at 64μm intervals.
• Hydroxy apatite crystals are formed along the
fibres with their long axis oriented parallel to the
collagen fibres. Well mineralized
Provide tensile strength to dentin 24
INCREMENTAL LINES

• The incremental lines of von ebner or imbrications

Lines appear as fine lines or striations in dentin
Run at right angles to the dentinal tubules.

• These lines reflect the daily rhythmic, recurrent

Deposition of dentin matrix as well as hesitation
In the daily formative process.

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• The course of the lines indicates the growth
Pattern of the dentin.
• Some of these incremental lines are
accentuated because of disturbances in the
Matrix and remineralization process.
• Such lines are known as
contour lines of owen.
• These lines represent hypocalcified bands.

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 NEONATAL LINES
• In the deciduous teeth and in the first
Permanent molars, the prenatal and
Postnatal dentin is separated by an
Accentuated contour line, this is
Termed the neonatal line.
• This line reflects the abrupt
Change in environment that occurs at
Birth.
• The dentin matrix formed prior to birth is
Usually of better quality than that formed after
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Birth.
GRANULAR LAYER

• There is a zone adjacent to the cementum that

Appears granular known as tome’s granular layer.

• It slightly increases in amount from the cej to

The root apex.

• Caused by coalescing and looping of the terminal

Portions of the dentinal tubules.
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 DENTINO ENAMEL JUNTION
• First hard tissue interface to develop scalloped- with convexity towards dentin-
with concavity towards enamel.

• Scalloping greatest in cuspal area as occlusal

stresses are more

• Branching of odontoblastic process

Here will cause greater sensitivity.

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DENTINO CEMENTAL JUNCTION

• Firm attachment.
• Smooth in permanent teeth
• Scalloped in primary teeth.
• Intermediate zone called hyaline layer of
hopewell smith - cements the cementum to dentin.
• Endodontics- Termination of instrumentation as well
as obturation.

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 DENTIN PULP JUNCTION

• These junctions are mainly formed by the odontoblasts of pulp.

• These odontoblasts are joined by junctional complexes between
them.

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ODONTOBLASTIC PROCESSES
• Cytoplasmic extensions of the odontoblasts
The odontoblasts reside in the peripheral pulp at
the pulp-predentin border and their processes
Extend into the dentinal tubules.
• The processes are largest in diameter near the
pulp and taper further into dentin.
• The odontoblast cell bodies are approximately
7μm in diameter & 40μm in length.

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TYPES OF DENTIN

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PREDENTIN
• Located adjacent to the pulp tissues

• 2-6μm, depending on the activity of odontoblasts

• First formed dentin and is not mineralized

• The collagen fibres undergo mineralization at the

Predentin – dentin front, the predentin then
Becomes dentin and a new layer of predentin
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Forms circumpulpally
PRIMARY DENTIN
• Dentin that is formed prior to
Eruption of a tooth.
• Classified as orthodentin, the
Tubular form of dentin lacking
Of cells found in teeth of all
Dentate mammals.
• Secreted at a relatively higher rate.
• Constitutes major part of the
Dentin in the tooth.
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MANTLE DENTIN
• First layer of primary dentin to be deposited.

• Oldest dentin and produced adjacent to the enamel in the crown

• Can be recognized by the characteristic thick, fan shaped collagen fibres

deposited immediately subjacent to the basal lamina in histologic sections.

• Fibres run roughly perpendicular to the DEJ 150μm thick slightly less
mineralized than underlying dentin.

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• When viewed under polarised light, the mantle dentin (RED band) can be
differentiated from the circumpulpal dentin (purple with black dentinal
Tubules).

• This is due to difference in collagen fibres in mantle dentin.

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CIRCUMPULPAL DENTIN
• Formed after the layer of mantle dentin has been deposited.
• Hydroxy apatite crystals are deposited on the surface and within the fibrils and
continue to grow.
• As mineralization proceeds, resulting in an increased mineral content of dentin
Circumpulpal dentin is mineralized by calcospherites.
• As the calcospherites enlarge, they fuse with the adjacent calcospherites until the
dentin matx is completely mineralised.

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SECONDARY DENTIN
• formed after root completion.
• Narrow band of dentin bordering the pulp
Contains fewer tubules than
Primary dentin.
• There is usually a bend in the
Tubules where primary and
Secondary dentin interface.
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• Since it is formed after eruption, the odontoblasts
Slightly change direction which
Contributes to bending of dentinal tubules.

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TERTIARY DENTIN
• By pathologic process or operative procedures,
The odontoblastic processes are exposed or cut, the odontoblasts
Die or survive, depending on the extent of injury
• If they survive, dentin that is
Produced are called reactionary or regenerated
Dentin.
• Killed odontoblasts are replaced by the migration
Of undifferentiated cells arising in the deeper
Layers of the pulp to the dentin interface.
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• This newly differentiated odontoblasts then begin deposition of reparative
dentin to seal off the zone of injury as a healing process initiated by the pulp,
Resulting in resolution of the inflammatory process and removal of dead cells

• This type dentin produced by a new generation of odontoblast-like cells in

response to appropriate stimulus after the death of original odontoblasts is
Called reparative dentin.

• This reparative dentin has fewer and more twisted tubules than normal dentin.

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• Histological difference between reactionary and reparative dentin is that
reactionary dentin is deficient in acid proteins so it doesn’t stain.

• Reactionary dentin appears as either osteodentin type or orthodentin type

• Reparative dentin has structure-less mineralisation as in bone.

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INTERGLOBULAR DENTIN
• Sometimes mineralization of dentin begins in small globular areas that fail to
fuse into a homogenous mass.

• This results in zones of hypomineralisation between the globules. These zones

are called interglobular dentin.

• Forms in crowns of teeth in the circumpulpal dentin just below the mantle
dentin.
• Seen in dental anomlies (hypophosphatasia).

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• The dentinal tubules pass uninterruptedly, thus demonstrating a defect of
mineralization and not of matrix formation.

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INNERVATION OF DENTIN
• Nerve fibres were shown to accompany 30-70% of the odontoblastic process and
these are referred to as intratubular nerves.
• These nerves and their terminals are found in close association with the
odontoblasts process within the tubule.
• Theories of pain transmission through dentin
• 3 basic theories of pain conduction through dentin
• Direct neural stimulation
• Transduction theory
• Hydrodynamic theory

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DIRECT NEURAL STIMULATION
• According to which nerves in the dentin get stimulated.
DRAWBACKS:
• The nerves in dentinal tubules are not commonly seen and even if they are
present, they do not extend beyond the inner dentin.

• Topical application of local anaesthetic agents do not abolish sensitivity

• Hence this theory is not accepted.

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TRANSDUCTION THEORY

• According to which the odontoblasts process is the primary structure excited by

the stimulus and that the impulse is transmitted to the nerve endings in the inner
dentin.

DRAWBACKS:

• Since there are no neurotransmitter vesicles in the odontoblast process to

facilitate the synapse or synaptic specialization.

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THE HYDRODYNAMIC THEORY:

• This states that the stimuli cause

displacement of fluid that exists within the
dentinal tubules.
• The displacement occurs in either an
outward or inward direction and this
mechanical disturbance activates the nerve
endings in the dentine and pulp.

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PERMEABILITY OF DENTIN
• Tubular structure of dentin provides passage of
Solutes and solvents across dentin
• Lowest at the DEJ and highest at the pulp –
diameter increases with depth
• Divided into 2 categories
Transdentinal movement – fluid shifts in
Hydrodynamic stimuli.
Intradentinal movement – as occurs
Infilteration of hydrophilic resins into
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Demineralised dentin surfaces.
AGE AND FUNCTIONAL CHANGES IN DENTIN

VITALITY OF DENTIN

• Odontoblasts and its processes are an integral part of dentin.

• And so vitality is understood to be the capacity of the tissue to react to

physiologic and pathologic stimuli,dentin must be considered a vital tissue

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• Dentinogenesis is a process that continues through

Out life
• Although after the teeth have erupted and have
Been functioning for a short time, dentinogenesis
Slows and further dentin formation is at a slower
Rate. This is secondary dentin
• Pathologic changes in dentin such as dental caries,
Abrasion, attrition or the cutting of dentin in
Operative procedures cause changes in dentin. They
Are the dead tracts, sclerosis and the addition of
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Reparative dentin.
DEAD TRACTS

• The odontoblastic processes

Disintegrate and the empty tubules are
filled with air.
• Appear black in transmitted light and white in
Reflected light.
• Degeneration is often observed in areas of narrow
Pulp horns because of crowding of odontoblasts.

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• These degenerated empty areas demonstrate decreased sensitivity

• Seen to a greater extend in older teeth.

• Dead tracts are probably the initial step in the formation of sclerotic dentin.

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SCLEROTIC/TRANSPARENT DENTIN
• A sufficient stimuli (caries, attrition, erosion, cavity preparation)
generated, as a defensive mechanism result in deposition of
apatite crystals & collagen in dentinal tubules.

• results in obliteration of dentinal tubule lumen and it will

appear very much similar to peritubular dentin

• Absence of tubular structure makes it to appears transparent

• seen mainly elderly people 56

• Mainly seen in roots
• Mineral density of dentin is more.
• Found under slowly progressive caries.

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• DENTINAL FLUID
• Free fluid occupies 1% of superficial dentin and 22% of total volume of deep
dentin
• Ultrafiltrate of blood from pulp capillaries contains plasma proteins
Serve as a sink from which injurious agents can diffuse into the pulp
producing inflammatory response.
• Also serve as a vehicle for progress of bacteria from a necrotic pulp into
periradicular tissue.

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CLINICAL CONSIDERATIONS

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DENTINAL HYPERSENSITIVITY:

• Tooth hypersensitivity and more precisely dentinal sensitivity or

hypersensitivity is described clinically as an exalted response to non-
noxious sensory stimuli.

• Tooth hypersensitivity is not associated with actual tissue damage but

can involve potential tissue damage with constant erosion of enamel
and cementum along with concomitant pulpal response.

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• Tooth hypersensitivity is chronic condition with acute exacerbations.

• Tooth hypersensitivity differs from dentinal and pulpal pain in that

patients ability to locate the source of pain is very good.

• The pain is intensified by thermal changes and consumption of sweet

and sour food stuffs.

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AETIOLOGY:

Dentine may become exposed by either loss of enamel or cementum or

by loss of covering gingiva (recession). Loss of enamel occurs by
attrition, bruxism, abrasion, erosion associated with environmental or
dietary components particularly acids.

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MECHANISM OF DENTIN SENSITIVITY:

• Permeability of dentine is responsible for dentin sensitivity.

• Two mechanisms are responsible for the permeation of substances

across the dentine i.E. Diffusion and convection (transmission of heat
in liquid/gases by circulation carried on by the heated particles).

• Hydraulic conductance is the reciprocal of resistance. Thick dentine

has lower hydraulic conductance than thinner dentine. 63
Management

• Desensitizing materials - silver, nitrate, fluorides, strontium chloride,

bonding agents, citrates, oxalates,lasers etc.
• Acts by nerve desensitization, protein precipitation, plugging of
dentinal tubules.

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SMEAR LAYER & SMEAR PLUGS

• Smear layer - term most often used to describe the grinding debris
left on Dentin by cavity preparation
• Cutting debris when forced into dentinal tubules, it forms plugs
known as smear plugs
• Smear layer : 1-3 μm
• Smear plug : 40 μm
• Significance - lowers the permeability of
dentin surface.
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• The smear layer is not a stable structure.

• It must be removed in order to obtain optimal chemical and mechanical

bonding between restorative materials and tooth structures.

• It can be beneficial as restricts the flow of fluid through dentin and thus
decreasing its permeability.

• Alternative to its removal is incorporate it as an integral part of the

adhesive system.
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REMAINING DENTIN THICKNESS (RDT)

• Odontoblast injury increases as the cavity RDT decreases.

• Below 0.25 mm from DEJ the number of odontoblastic processes

decreases by 23%, and minimal reactionary dentin repair is observed.

• The ultrasonic micrometer is used to measure the remaining dentin

thickness.
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• Pashley (1979,81)reduction in dentin thickness increases permeability
(increase in number and diameter of tubules)
• With 0.5mm of dentin between base of cavity and pulp, decrease of
0.1mm produces more severe inflammation in low speed preparation
without coolant.
• With coolant the floor can be brought much closer to pulp (0.3mm)
• Medium size cavity{2mm} zinc phosphate base is preferred .
• Deep cavity {more than 2mm}– ZOE.

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DENTAL CARIES
• Tubule system helps in rapid spread of caries.
• Tubules form the pathway for the invading bacteria ,reaching the pupl
causes pain.
• Infected dentin - Demineralized & invaded by microorganisms
• Affected dentin -demineralized but not invaded by microorganism
• One must try to maintain that affected dentin

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INFECTED AND AFFECTED DENTIN

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 THERMAL AND CHEMICAL PROTECTION

• The exposed dentinal tubules are not insulated against bacterial

toxins, strong drugs, undue operative trauma, and unnecessary
changes.
• It is important to seal the exposed dentinal surface with nonirritating,
insulating substances.
• Thermal protection-base below the restoration.
• Chemical protection-cavity liners and varnish.

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 CAVITY FLOOR

• Elasticity of dentin absorbs and resists the force of mastication and

deformation.
• Mainly for amalgam, cast and pure gold restoration.

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 DIRECT AND INDIRECT PULP CAPPING

• The dentin is formed through out the life.

• The reparative dentin formation can be stimulated by cavity lining

materials (such as calcium hydroxide) forms reparative dentin within
3-4 weeks.

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DEVELOPMENTAL ANOMALIES

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DENTINOGENESIS IMPERFECTA:
*Autosomal Dominant condition.
*Effects both primary and permanent dentition.
*Clinically tooth appears to be -
i) Grey to Yellowish Brown
ii) Broad crowns with constriction of cervical area resulting in TULIP SHAPED
TOOTH
*Radiographically, teeth appears to be:
i) Solid
ii)Lacks pulp chamber and root canals
*Enamel will be easily broken leading to exposure of dentin that accelerates 75

attrition of teeth.
REVISED CLASSIFICATION OF DENTINOGENESIS IMPERFECTA :

• Dentinogenesis Imperfecta-1 - OPALSCENT DENTIN- Without

osteogenesis Imperfecta
• Dentinogenesis imperfecta- 2 -SHELL TEETH – Brandywine type of
dentinogenesis imperfecta

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DENTINOGENESIS IMPERFECTIA- 1
Other names:
 opalescent dentin
 dentinogenesis imperfecta without osteogenesis imperfecta
 opalescent teeth without osteogenesis imperfecta
 capdepont teeth.
Caused by:
• dssp gene mutation
• DSSP gene encodes –
 dental phosphoprotein
 dental sialoprotein
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CLINICAL FEATURES:
i) Blue- Grey or Amber brown coloured and Opalscent teeth
ii) Enamel may split readily from dentin when subjected to occlusal stress
RADIOLOGICAL FEATURES:
i) Bulbous Crowns
ii) Narrower roots than normal
iii) Completely obliterated/ Smaller than normal canals

In EDTA Soluble dentin portions – More GAGs observed

In EDTA insoluble dentin residues – Less GAGs observed
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DENTINOGENESIS IMPERCTIA –II
Other names :
a) Sheild’s type III
b) Brandy wine type Dentinogenesis Imperfecta
Incidence :
Dentinogenesis Imperfecta type II was found
in Brandywine triracial isolates in Southern Maryland . So called as Brandywine
type.
CLINICAL FEATURES:
i) Wearing off of crowns of Primary and Secondary teeth occurs rapidly
ii) Pulp exposures seen more frequently
iii) Amber coloured & smooth Dentin is seen 79
RADIOLOGICAL FEATURES :
i) In Primary dentition , Very large pulp chambers & root canals are seen during
first few years.
ii) As age progress, Pulp chamber size reduces.
iii) Permanent teeth will have large pulp spaces.
iv) SHELL like appearance of teeth on radiograph.
HISTOLOGICAL FEATURES:
i) Purely due to Mesodermal Disturbance.
ii) Irregularly tubules in dentin shows large areas of uncalcified matrix.
iii) Less number of tubules but larger in size are present leading to reduced dentin
volume.
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iv) Completely obliterated pulp chamber.

TREATMENT:

• Preventive care to prevent loss of enamel. So that , we can

prevent loss of dentin there by attrition of teeth.
• Even though we fill the teeth with restorative materials, those
fillings will remain temporarily because of “Smooth Dentin”.

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DENTIN DYSPLASIA:
• Autosomal Dominant disorder.
• Rare disturbance.
• Characterised by Normal enamel but Atypical dentin formation with abnormal
pulpal morphology.
CLASSIFICATION:
1. By SHIELDS
a) Type I Dentin Dysplasia
b) Type II Anamolous dysplasia of dentin
2. By WITKOP
a) Radicular dentin dysplasia ( Type I )
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b) Coronal dentin dysplasia ( Type II)
Dentin Dysplasia name given by RUSHTON.
OTHER NAMES: Root less teeth.
CLINICAL FEATUES:

TYPE - I TYPE - II
i) Both dentition affected. i) Both dentitions affected
ii) Clinically normal in colour and shape PRIMARY DENTITION:
of tooth. Clinically appears as Yellow,
iii) Occassionlly , Slightly amber Brown / Bluish grey Opalescent
translucency seen. appearance.
iv) Normal eruption pattern seen. SECONDARY DENTITION:
v) Abnormally short root. Clinically appears as Normal in
shape , colour.
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 RADIOLOGICAL FEATURES:

TYPE-I TYPE-II
i) Roots in both dentition appears as short i) Pulp chambers and Root canals are
, blunt , conical/ malformed similarly. completely obliterated in primary
ii) Pulp chambers and Root canals are dentition
completely obliterated in Primary ii) Pulp chambers and Root canals are
dentition and Crescent shaped pulpal abnormally large .
remnants seen in secondary dentition. iii) Pulp chambers in coronal portion of
teeth giving THISTLE TUBE
appearance.

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HISTOLOGICAL FEATURES:

TYPE-I TYPE-II
i) Portion of coronal dentin is normal. i) Primary dentin shows amorphous,
ii) Apical to this normal coronal atubular dentin in radicular portion
dentin , there will be calcified while coronal dentin is normal.
dentin present. ii) Secondary dentin shows normal
iii) LAVA FLOWING AROUND coronal dentin with MULTIPLE
BOULDERS appearance – PULP STONES.
Normal dentinal tubule
formation appears to be blocked so
that new dentin formed around
obstacles and few such charecteristic
appearance.

Treatment: No treatment . prognosis depends upon occurance of any periapical lesion.85

REGIONAL ODONTODYSPLASIA:
OHER NAMES:
i) Odontodysplasia
ii) Odontogenic Dysplasia
iii) Odontogenesis Dysplasia
iv) Ghost teeth
RATE OF INCIDENCE:
• Maxillary teeth >>> Mandibular teeth
• Among Maxillary teeth , Central Incisor>> Lateral Incisor > Canine.
• Among Mandibular teeth , Central Incisor >> Lateral Incisor > Canine.
• Both Primary and Secondary dentitions are affected.
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AETIOLOGY:
Presence of Latent Virus residing in Odontogenic Epithelium that
subsequently becomes active during Tooth Development.
CLINICAL FEATURES:
• Delay / total failure in eruption.
• Markedly altered tooth morphology.

RADIOLOGICAL FEATURES:
• Marked reduction in radio density.

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• Enamel, Dentin becomes very thin with abnormally large Pulp.
HISTOLOGICAL FEATURES:
• Marked reduction in amount of dentin.
• Widened predentin layer.
• Presence of large areas of interglobular dentin.

TREATMENT:
Extraction of teeth followed by Prosthesis due to Poor Cosmetic appearance.

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 INTRINSIC STAINS OF DENTINE
• Systemic causes – jaundice and porphyria
• Medications – tetracycline's (bright yellow fluorescence under uv
light) and fluorine
• Pulpal necrosis
• Pulpal remanants

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 DENS IN DENTE
• Dentin & enamel forming tissue invaginate the whole length of a
tooth.

• Radiographically- “tooth within a tooth.”

• Food lodges in the cavity to cause caries

which rapidly penetrates the distorted pulp
chamber.

• Endodontic treatment difficult- abnormal anatomy.

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 CONCLUSION

Dentin by its functions, structure, physical, chemical and optical

properties plays a crucial role in maintaining the enamel and
protecting the pulp, hence optimal importance should be given for its
preservation during restorative as well as endodontic procedures.
Although dentin and pulp have different structures, once they are
formed, they react to stimuli as a functional unit.

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REFERENCES:
• Orbans oral histology and embryology 13th edition[93-113]
• Tencates oral histology 5th edition.
• Satish Chandra Dental and oral histology with embryology 2nd edition[35-41
• Cohen pathways of pulp1st edition
• Neville and Damm oral and maxillofacial pathology text book.
• Sturdevent-the art and science of operative dentistry 10th edition
• Sanjay et.al, JCD, 2010. Dentin hypersensitivity: Recent trends in management
• Michel Goldberg et.al , Dentin: Structure, Composition and Mineralization,
journal of national institute of health, 2012.
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THANK YOU

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