GOOD MORNING!!!

DR.RINKU SHANKLESHA
DEPARTMENT OF CONSERVATIVE DENISTRY
AND ENDODONTICS.
1
KVGDC, SULLIA
Dentin

1
CONTENTS
 Introduction
 History
 Development (Dentinogenesis)
 Physical Properties
 Chemical Composition
 Structure of Dentin
 Types Of Dentin
 Age and functional changes
 Innervation of Dentin
 Clinical considerations
 Developmental anomalies
 conclusion

3
 HISTORY
• 1771 – John Hunter →hard tissue.

• 1775 – Anton Von Leeuwenhoek: Described tubular structures.

• 1837 -Purkinje and Retzius explained about Dentinal Tubules.

• Cuvien gave the name “Ivory” to Dentin

• 1867 – Neuman gave the term Neuman’s sheath

• 1891 – Von Ebner gave the term – Ebner’s growth lines or

Imbrication lines .

• 1906 – Von Korff gave the term – Korff’s fibres

4
 DENTINOGENESIS
• Process of Dentin
formation.

• Dentin-First Formed Dental

Hard Tissue –crown and
roots
• -Formation of Dentin
Precedes Enamel

• Late Bell stage.

LATE BELL STAGE
• Future cusp tips, Proceeds
Apically. 5
 STAGES
• Formation Of Dentin- similar to bone and
Cementum.
1. Synthesis Of Organic matrix
2. Subsequent Mineralization.

Carried out by- ODONTOBLASTS

6
 ODONTOBLASTS
• Cells Of Pulp.

• Derived - Dorsal Cranial Neural Crest,

Mesenchymal in origin.

• Lie along Dental papilla- Adjacent to

IEE.

• Tall columnar cells- length 25-40 µm ,

diameter 4-7 µm,

• Development- Initiated by epigenetic

influence of various signalling
molecules produced by Ameloblasts.

7
 ODONTOBLAST BIOLOGY
ECTOMESENCHYMAL CELLS- Undifferentiated, Flattened
Cells with a large Central Nucleus, Sparse Cytoplasm.

PRE-ODONTOBLASTS - small, ovoid cells with a high

nuc :cyt ratio poorly developed organelles.

SECRETORY ODONTOBLASTS. : Tall columnar cells , 40

µm length , 4-7 µm diameter, Large nucleus – with upto 4 nucleoli,
Abundant RER, Golgi apparatus, mitochondria ,secretory
granules- near the process.

TRANSITIONAL ODONTOBLASTS: Narrower, fewer

organelles, autophagic vacuoles

8
AGED ODONTOBLASTS: Reduction in length and cytoplasmic
Organelles, increase in number and size of lysosomes and
phagosomes, decreased secretory capacity, degenerate with age.

9
 FORMATION OF PRIMARY
DENTIN
Before Dentinogenesis-There
exists an acellular zone b/n the
IEE and Dental Papilla cells -
ground substance laid down by
the subodontoblastic cells.

The Cells of IEE become taller

and start differentiating into
Ameloblasts-polarity of cell
reverses.- Early Bell Stage.

10
They induce the differentiation of
odontoblasts, with reversal of
polarity.

Odontoblasts Develop variable no.

of small processes at the formative
end- start depositing Collagen
matrix- Predentin.

This induces the Ameloblasts to

start depositing Enamel matrix.

11
DEPOSITION OF COLLAGEN MATRIX
INITIALLY: large dia Type III
Collagen - 0.1- 0.2µ
VON KORFF’S FIBRES
-Cork Screw Shaped
-Perpendicular to DEJ
-Argyrophillic in nature.

LATER- smaller Fibrils-

perpendicular to Tubules,
parallel To DEJ.
12
As more matrix is formed- the Odontoblast
Migrates centripetally, towards the pulp.

A Single Prominent Process- Odontoblast

Process- (TOME’S FIBRES)- Tubular nature Is
established.

The rate of matrix production - about- 4-

8µ/day for Primary Dentin. And secondary
dentin -1µ/day
MINERALIZATION Begins once matrix is
about 5µ thick.
13
 Various Matrix Proteins Influence Mineralization:
• DPP- Binds to Ca, Controls Growth of H.A
Crystals
• Osteonectin- Inhibits growth of H.A crystals,
promotes their Binding to Collagen

• Gla-proteins, Phospholipids- Act as nucleators

to concentrate calcium.
• Proteoglycans- inhibit premature mineralization
seen in predentin.
CALCIFICATION OF MATRIX- initiated by
small crystallites within MatrixVesicles, budded from
odontoblasts.
14
 MATRIX VESICLES contain Alkaline Phosphatase
-↑ concentration of phosphates → combine with
Calcium →Hydroxyapatite Crystals.

Crystals- grow rapidly, rupture the matrix vesicles

Spread -clusters of crystallites → fuse with

adjacent clusters to form a continuous layer of
mineralized matrix
.Initially- on the surface of the collagen fibrils and
ground substance, later within the fibrils- aligned
with collagen.
15
PATTERNS OF MINERALIZATION
• GLOBULAR(CALCOSPHERIC) :Deposition of HA
crystals in several discrete areas of matrix at any one
time.
• Continued crystal growth → globular masses →
enlarge → fuse → single layer of calcified mass.
• MANTLE DENTIN- matrix vesicles.

16
RADIAL CRYSTAL GROWTH INTERGLOBULAR DENTIN
LINEAR : When the rate of Dentin
formation occurs Slowly -Mineralization
front appears more Uniform –
CIRCUMPULPAL DENTIN

LINEAR PATTERN

17
 ROOT DENTIN FORMATION
• Begins once Enamel& Dentin
formation reaches the future
CEJ.

• Initiated by Cells of HERS-

which induce odontoblast
differentiation.

• Collagen fibres- parallel to CDJ.

• Less mineralized, less no. of
Tubules.

• Complete- 18mths after

eruption-Primary
18
2-3 yrs -Permanent Teeth
 VASCULAR SUPPLY
• Provided by the Capillaries found in the subodontoblastic
layer of the pulp.
• Migrate between odontoblasts, and later - Regress.

19
PHYSICAL AND MECHANICAL
PROPERTIES
PROPERTY VALUE
COLOUR PALE YELLOW- WHITE
THICKNESS 3 - 10mm

MODULUS OF ELASTICITY 15-20GPA

HARDNESS 68 KHN
CARIOUS DENTIN 25 KHN
SCLEROTIC DENTIN 80 KHN
COMPRESSIVE STRENGTH 266 MPa
TENSILE STRENGTH 50 Mpa

PROPORTIONAL LIMIT 148 MPa

RADIOOPACITY LESS THAN ENAMEL 20
CHEMICAL COMPOSITION

BY WEIGHT BY VOLUME
15%

22%
20% 65% 45%

33%

INORGANIC ORGANIC WATER

21
 ORGANIC COMPONENTS
• Collagen – 82% , MAINLY TYPE I and some amount of Type
III and V.

• Non Collagenous Matrix Proteins- 18%

-Phosphoproteins- DPP(Phosphoryn), Gla-Protein.
-Glycoproteins- Dentin Sialoprotein,Osteonectin, Osteocalcin,
(Seen in mineralized matrix)
- Proteoglycans- Chondroitin SO4 (seen mainly in Predentin)

• Enzymes- Acid Phosphatase, Alkaline Phosphatase.

• Lipids- phospholipids, glycolipids etc. in traces.

22
 INORGANIC COMPONENTS
• Calcium Hydroxyapatite: CA10(PO4)6(OH)2
• Thin plate like crystals, shorter than enamel.
• 3.5 nm thick, 100 nm long.

• Salts- calcium carbonate, sulphate, phosphate

etc.
• Trace Elements- Cu, Fe, F, Zn

23
STRUCTURAL COMPONENTS
• Odontoblast
Process
• Dentinal Tubules
• Non mineralized
matrix- Predentin
• Mineralized matrix-
Peritubular and
Intertubular Dentin.

24
 DENTINAL TUBULES
• Most Striking Feature.
• From pulp to DEJ
• Occupy 1% superficial and 30%
volume of Deep Dentin.
• Size- varies with location.3-4µm near
pulp,1µ near the DEJ (ratio,5:1))
• Smaller branches- canaliculi (1µm in
dia, 2µm in length)-pathways of
exchange
• 1-2µ apart.

25
 PRIMARY CURVATURES

CROWN ROOT
Tubules exhibit Sigmoid curvatures-More prominent
in crown.
Least pronounced at cusp tips, incisal edges 26
 SECONDARY CURVATURES

At Increased Magnification- Secondary Curvatures.

27
Tubule density/ unit area - ↑es toward pulp.

A. - 50,000 to 90,000 / sqmm

pulpal surface

B. - 30,000 to 35,000/sqmm
middle dentine

C. - 10,000 to 25,000/sqmm
peripheral dentine

No. of Tubules / unit area – crown> root. 28

PERIODONTOBLASTIC SPACE
• Potential space between tubule wall and od.
Process.

• Contents - nerves, collagen fibrils, plasma

proteins, glycoproteins and mitochondria.

• Surface Area Tubule lumina - 1% at DEJ, 22 %

at Pulp(PASCHLEY-1996)

29
 Lamina Limitans
• Organic sheath or membrane lining the Dentinal
tubules
• seen in EM sections.

30
 DENTINAL FLUID
( Dentin Lymph)
• Occupies space b/n dentinal tubule and od. Process.
• Ultrafiltrate- pulp Capillaries

• Composition is similar to that of plasma..Ca content in

dentinal fluid of predentin is 2-3 times higher than in plasma.

• Tissue pressure of pulp- 14 cm of H2O, (10.3mm Hg).

(Ciucchi et al 1995) pressure gradient exists between pulp and
oral cavity -tends to flow outwards slowly
• Exposure of Tubules- tooth fracture or cavity prep.-Outward
movement → tiny droplets.-dehydrating the surface-rapid flow
31
of fluid-sensitivity.
• Slow outward flow of fluid (0.02nl//sec/mm -1-
1.5.microlitre/sec/mm for nerves to begin firing.

•Acts as barrier for microbes and toxins .

•Hydraulic transfer and relief of stresses in Dentin-
through the Periodontium and Enamel.
•Non vital Teeth- More brittle. (Carter et al 1983)

32
 PREDENTIN
• First Formed Dentin.

• A layer of Un Mineralized Matrix

• Thickness- 50 µ, 2-6µm wide

PREDENTIN
• Collagen and Non-collagenous
matrix proteins.

• Gradually Mineralizes.

• Thickness Remains Constant.

• Stains less intensely 33
 PERITUBULAR DENTIN
PERILUMINAL/INTRATUBULAR
. DENTIN
• Dentin that immediately surrounds the dentinal tubules

• Collar - ↑ Calcified Matrix – surrounds Dentinal tubules.

• ↓ collagen fibrils, ↑ sulfated proteoglycans.

• 40% more mineralized than ITD.

• Hardness of H. A. crystals-250 KHN

(Kinney Et al- 1996)

• Thickness-0.75µm- .4µm

• Lost in decalcified Sections, 34

 INTERTUBULAR DENTIN

• Main Body Of Dentin.

• 10 Secretory Product.
• Less mineralized
• Hardness of H. A
crystals -52KHN
(Kinney et al 1996)

35
Dentinal Tubule

Peritubular
Dentin

Intertubular
Dentin

36
 INTERGLOBULAR DENTIN
• Unmineralized islands within the
Dentin- formed due to failure of
fusion of mineral globules .

• In Circumpulpal Dentin- just

below Mantle Dentin,
• Subjacent to pits and fissures.
• .

• Tubules pass uninterrupted.

• Vitamin ‘D’ deficiency or

Hypophosphatasia
37
 INCREMENTAL LINES OF VON
EBNER/ IMBRICATION LINES
• Fine striations- perpendicular to
tubules.

• Daily rhythmic deposition of

Dentin-

• 4-8µ apart in crown, closer in root.

• 5 DAY INCREMENT-20µm

38
 LINES OF SCHREGER

Congruence Of PRIMARY CURVATURES of Dentinal tubules.

39
 CONTOUR LINES OF OWEN
• “Co-incidence of 2o
curvatures”
• ACCENTUATED
INCREMENTAL LINES
• Disturbance in matrix
formation
• Hypomineralized areas.
• Periods of illness/ GROUND SECTION
inadequate nutrition.
40
 NEONATAL LINE
• Accentuated Incremental
line
ENAMEL

• Primary teeth, permanent

first molars.
DENTIN
• Zone of hypo calcification

• Reflects abrupt change in

environment- At Birth.

• Dentin formed Before birth

-Better Quality

41
GRANULAR LAYER OF TOMES
• Granular zone-
• Ground sections- Root
Dentin in transmitted
light.
• Increases in amt. from
CEJ to Apex.
• Looping /coalescing of
Dent. Tubules.
• Hypomineralized areas.

42
 DENTINOENAMEL JUNCTION
• First hard Tissue Interface
To Develop
• Scalloped- with convexity
towards Dentin.
• Scalloping greatest in
Cuspal area →Occlusal
stress more
• Branching of Od. Process
here → ↑ed sensitivity.

43
 ENAMEL SPINDLES
• Odontoblast processes sometimes extend into the Enamel.

• Length is about 10—40 m

• Seen near Incisal edges

& cusp tips

• Appear dark
in ground sections

• Hypomineralized Areas

• Responsible for the Spread of Caries from Enamel to Dentin.

44
 DENTINO-CEMENTAL
JUNCTION
• Firm Attachment

• Smooth in Permanent teeth,

scalloped in 1o.

• Intermediate Zone- Hyaline layer

Of Hopewell Smith- Cements the
cementum to Dentin.

• Product Of HERS

• Endodontics- Apical Constriction

45
Termination of Instrumentation.
 TYPES OF DENTIN
• Primary dentin
– Mantle
– Circumpulpal

• Secondary dentin

• Tertiary dentin

46
 PRIMARY DENTIN
(Prior To Root Completion)
MANTLE CIRCUMPULPAL
LOCATION Below DEJ B/n Mantle Dentin
and Predentin.
THICKNESS 20 µ 68mm
MINERALIZATION ↓ ↑
DEFECTS ↓ ↑

COLLAGEN FIBRES Larger- 0.1-0.2µ Smaller- 0.02- 0.05µ

perpendicular to parallel to the DEJ.
the DEJ Closely packed.

47
 SECONDARY DENTIN
• Develops after root completion

• Narrow band- bordering the pulp

• Deposited more slowly- 1µ/day.

• Fewer tubules

• Bending of tubules at the 10 &

2° Dentin interface.

• Formed in greater amts.- roof of

pulp chamber- protecting the
pulp horns.

48
 TERTIARY DENTIN
• Localized formation of Dentin At pulp –Dentin
Border in response to noxious stimuli- Caries,
Trauma Attrition , Cavity Prep. Etc.

Also known as:

No continuity with 10 or 20
 Reactive Dentin,
Dentin so there is ↓ Dentin
 Reparative Dentin, permeability.
 Irritation Dentin, Quality Depends on :
 Replacement Dentin, •Intensity of stimulus.
 Adventitious Dentin, •Vitality of pulp.
 Defense Dentin 49
 TERTIARY DENTIN
REACTIONARY DENTIN REPARATIVE DENTIN

STIMULUS FOR MILD AGGRESSIVE

FORMATION

FORMATIVE CELLS SURVIVING POST MITOTIC NEW ODONTOBLAST- LIKE

ODONTOBLASTS CELLS FROM
PROGENITORS

STRUCTURE PHYSIOLOGIC DENTIN HETEROGENOUS:

CHANGE IN DIRECTION OF -TUBULAR (ORGANISED)
NEW DENTINAL TUBULES OSTEODENTIN
FIBRODENTIN
(DISORG)

SMITH ET AL (1994) 50
REACTIONARY DENTIN REPARATIVE DENTIN

The avg. daily rate of reparative dentin formation is about 2.8-3 µ/day-
acc to Stanley in 1996.
51
REPARATIVE DENTIN

52
 AGE AND FUNCTIONAL
CHANGES
• DEAD TRACTS
• DENTIN SCLEROSIS
• REPARATIVE DENTIN

53
DEAD TRACTS
• Represent Empty Tubules Filled
with air.

• Due to → Degeneration of
odontoblastic process (caries,
erosion, attrition etc.)

• Ground Sections

• Black in transmitted light, WHITE

IN REFLECTED LIGHT.

• Older Teeth-Areas of narrow

pulp horns. ↓ sensitivity. 54
 SCLEROTIC DENTIN
• Presence of irritating stimuli -Caries, Attrition, Erosion, Cavity

Preparation → Deposition of Apatite Crystals & Collagen in

Dentinal Tubules.

• Blocking of tubules- Defensive reaction.

• Filled with H. A - Obliteration of Lumen- Peritubular Dentin.

• Refractive indices are equalized- Transparent

• Elderly people – Mostly in Roots

55
 • Also seen- slowly
progressing Caries.

• Reduced Permeability

• Prolonged pulp vitality

• Resistant to Caries

• Forensic Odontology:One of
the criteria for age
determination using
Gustafson’s method.
SCLEROTIC DENTIN

56
 EBURNATED DENTIN
• Exposed portion of reactive sclerotic Dentin.
• Slow caries has destroyed overlying tooth
structure .
• hard , darkened , cleanable surface.
• Resistant to further caries Attack.

57
 REPARATIVE DENTIN
• Formed in response to
trauma, chronic
irritation etc.
• Provides protection to
the underlying pulp- by
Decreasing dentin
permeability.

58
 INNERVATION OF DENTIN
• Numerous Nerve Endings in
Predentin and Inner Dentin.
• 100-150µm from pulp.

• % of tubules innerveted Near Pulp

Horns –(40%)
• ↓ near CEJ- 1%

• Closely Associated with Odontoblast

Process.

• Arise from myelinated nerve fibers of

Dental Pulp- (Aδ fibres) Reach Brain
via Trigeminal N.

59
 PAIN TRANSMISSION THROUGH
DENTIN
• DIRECT NEURAL STMULATION
• TRANSDUCTION THEORY
• HYDRODYNAMIC THEORY

60
DIRECT NEURAL STIMULATION
• It was proposed by Scott
Stella in 1963

• Nerve endings in Tubules

are Directly Activated by
External Stimuli

• This view rests on the

assumption that Nerve
fibres Extend to DEJ.

• Not accepted

61
 TRANSDUCTION THEORY
• Odontoblastic Processes are
primary structures excited by
stimulus.

• Transmit impulse to Nerve

Endings

• Supported by evidence that

odontoblasts → Neural Crest
Origin

• Discarded -No synaptic Contacts

or vesicles - b/n odontoblasts and
axons.
62
HYDRODYNAMIC THEORY
• Most popular Theory

• Gysi (1900), Brannstrom

• Various stimuli such as Heat,

Cold, Air, Mechanical
Pressure →Movement
of Fluid Within Tubule
↓
• Activating the Free Nerve
Endings Associated with
Odontoblast and its Process

• Act as Mechanoreceptors-
Sensation is felt as pain.

63
64
 “Hypersensitivity”
• Unusual symptom of Pulp- Dentin Complex.

• Sharp Pain- easily localized.

• Etiology- Exposure of Dentinal tubules

loss of enamel- Attrition, abrasion, erosion etc.
loss of cementum- scaling and RP, Gingival Recession

• Best Explained by the Hydrodynamic Theory.

• Management - Block The Dentinal Tubules!!!

• Desensitising toothpastes-AgNo3, SrCl2, fluorides, Bonding Agents,

65
lasers etc.
 Dentin Permeability
• Highly Permeable- Tubular Nature

• TRANS DENTINAL- Movement-Through

entire thickness of Dentin- via tubules.
• INTRADENTINAL- Movement of
exogenous subst. into intertubular Dentin.-
seen during bonding.leading to passage of
irritants towards pulp.

• ↓Dentin thickness -↑Dentin permeability.

66
MORE PERMEABLE LESS PERMEABLE

DENTIN NEAR PULP DENTIN FURTHER AWAY

HORNS

AXIAL WALLS OF PULPAL FLOOR OF CLASS

CLASS II CAVITY II CAVITY

CORONAL DENTIN ROOT DENTIN

NORMAL DENTIN SCLEROTIC DENTIN

67
CLINICAL CONSIDERATIONS

69
 “Exposure of Dentinal Tubules”

• Tooth wear, fractures, caries,

cavity cutting procedures etc.
lead to exposure of Dentinal tubules.

• 1 mm of Exposed Dentin → Damage to 30,000 living

odontoblasts.

• Exposed Tubules- Should not be insulted!!

• Sealed- Bonding agents, varnishes or Restorations.

70
 Pulp protection
• Irritants from Restorative
Materials- Pulpal Damage

• Thermal Protection- Bases

below Restoration
• Chemical Protection- Cavity
liners and varnishes

71
 Dentinal Caries
• Tubular Nature of Dentin→ Rapid spread of Caries
Through Dentin.
• Lateral spread along DEJ→ Undermined Enamel.

ZONE 1 – Normal dentin

ZONE 2 – Sub transparent
ZONE 3 – Transparent dentin
ZONE 4 – Turbid dentin
ZONE 5 – Infected dentin

72
 Infected and Affected Dentin
INFECTED DENTIN AFFECTED DENTIN

SOFTENED AND SOFTENED ,

CONTAMINATED WITH DEMINERALISED BUT NOT
BACTERIA YET INVADED BY
BACTERIA
CONTAINS IRREVERSIBLY CONTAINS REVERSIBLY
DENATURED COLLAGEN – DENATURED COLLAGEN
STAINED BY CARIES
DETECTING DYE .
REQUIRES REMOVAL DOES NOT REQUIRE
REMOVAL
73
 Operative Instrumentation
Dentin- Treated with care during op. instrumentation
to prevent damage to the odontoblasts
• AVOID-
Excessive Cutting
Heat Generation
Continuous Drying – dislodgement -
aspiration into tubules.

• USE :
 Air- Water Coolant.
 Sharp hand Instruments- most
suitable
 Tungsten Carbide Burs to Cut vital
Dentin.- Less Heat generation.
74
 “Cavity Preparation”

• Cavity Floor → Dentin

• Dentin is RESILIENT → Absorbs and Resists

Forces of Mastication and Deformation – Grips the
rest. material.

• Grooves, coves, pins etc -completely in Dentin.

75
 “Vital pulp therapy”
• The reparative Dentin Formation can be stimulated by
cavity lining materials (such as Calcium hydroxide).

• Includes Direct and Indirect pulp capping

• Results in formation of reparative dentin .

• THE DENTINAL BRIDGE repair tissue that forms

across the pulpal wound.
• Sign of successful healing.

76
 “Bonding to Dentin”
• Adhesion to Dentin… A
CHALLENGE!!

• Due to - ↑organic content, tubular

nature and presence of Fluid.

• Further complicated by “Smear

Layer”- abraded dentin surfaces-
denatured collagen, HA crystals, SMEAR LAYER
debris.(1-4µm thick)

• It decreases dentinal permeability-

but interferes with bonding – should
77
be removed.
• Steps in Bonding:
- Conditioning
- Priming
- Application of Bonding Agent

Hybrid Layer Composed of collagen, Bonding

Agent and Resin

78
 “Endodontics”
• Secondary & Tertiary Dentin →obliteration of Pulp Chamber
& Root Canals.
• Endodontic treatment → Difficult.

• Periapical surgery- Root Resection- closer to 90o

to minimize no. of exposed tubules.

• Apical Dentin Chip Plug- Dentinal Chips compacted at apex

during Obturation- provides a “biologic seal”

79
DEVELOPMENTAL DEFECTS

80
 Dentinogenesis Imperfecta
Anomaly of Mesodermal Portion of the
Odontogenic Apparatus.

CLASSIFICATION:
(ACC. TO SHIELDS)
TYPE I- Assoc with. O.I.
Type II – Not Assoc with O.I
Type III- Brandy wine Type.

81
 TYPE I TYPE II TYPE III

CLINICAL Tulip Shaped teeth, Bluish- Amber appearance,

FEATURES grey- Yellow/Brown Excessive wear,
Translucent. Enamel Chips Multiple pulp
away→ Exposed dentin, Exposures.
rapid attrition.

RADIOGRAPHIC Partial/complete Shell teeth- Normal

FEATURES obliteration of pulp Enamel, Thin Dentin,
chamber , root canals Huge pulp Chambers,
short roots.
 TREATMENT

• In patient with DI, one must first ascertain which type

he/she are dealing with.

• Severe cases of DI type 1 associated Osteogenesis

imperfecta can present significant medical
management problems. Careful review of the patient's
medical history will provide clues as to the severity of
bone fragility based on the number of previous
fractures and which bones were involved.
• Patients not exhibiting enamel fracturing and
rapid wear crown placement androutine
restorative techniques may be used.

• Bonding of veneers may be used to improve

the esthetics.
• In more severe cases, where there is significant
enamel fracturing and rapid dental wear, the treatment
of choice is full coverage crowns.

However in case of D.I III with thin

root are not good cases for full coverage because of
cervical fractures.

• Occlusal wear with loss of vertical dimension –

Metal castings
Newer composites.
 Dentin Dysplasia (Root less teeth)
 Rare Dental Anomaly.

 Normal Enamel, Atypical

Dentin, Abnormal Pulp
Morphology

 CLASSIFICATION:
(Acc. To WHITKOP)

-TYPE I- RADICULAR
-TYPE II – CORONAL

86
 TYPE I(RADICULAR) TYPE II (CORONAL)

CLINICAL FEATURES Normal Morphology, Primary- yellow /brown-

Amber Translucency. grey.
Extreme Mobility and Permanent – normal.
Premature Exfoliation

RADIOGRAPHIC Deciduous - pulp Deciduous – pulp

FEATURES chambers completely chambers obliterated
obliterated, short conical Permanent -
roots. “thistle tube” appearance
Permanent – crescent
shaped pulp chambers-
Difficulty in locating
canal orifices.

87
 Regional Odontodysplasia
• Maxillary Anteriors

• CLINICAL
FEATURES: delay or
failure of eruption,
irregular shape.

• RADIOGRAPHIC
FEATURES: “Ghost
Teeth.” 88
 Treatment:
• No treatment required
• Meticulous oral hygiene
• Extraction / Endodontic treatment
• Prosthetic rehabilitation
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.
90
 Tetracycline Pigmentation
• Yellow- Brown/grey
Discoloration.

• Fluoresce Bright
Yellow under U.V
light.

• Deposited along
Incremental lines of
Dentin and to lesser
Extent in Enamel.
91
RESPONSE OF DENTIN TO RESTORATIVE
PROCEDURE AND MATERIALS

1) SMEAR LAYER:
The smear layer is an amorphous , relatively smooth layer of
microcrystalline debris with a featureless surface that cannot
be seen with the naked eye [ Pashley DH 1984]

The cutting of dentin during cavity preparation produces

microcrystalline grinding debris that coats the dentin and
clogs the orifices of the dentinal tubules. This layer of debris
is termed as smear layer.
• Reduces sensitivity and permeability

• Interferes with the apposition or adhesion of dental

materials to dentin

• Has a potential to provide a media for recurrent caries

and bacterial irritation of the pulp

Methods of removal of smear layer from root canals

before obturation is the alternative use of a chelating
agent(disodium ethylenediamine tetra acetic acid EDTA)
or weak acid i.e. (10 % citric acid) followed by thorough
canal rinsing with 3 to 5 % NaOCl.
2) Restorative procedures can affect the permeability of
remaining dentin

• Minimal effects are transmitted to the pulp if the remaining dentin

thickness is 2mm or more.

• For an amalgam restoration in a deep tooth preparation a total of

1- 2 mm of underlying dentin is preferred.

• For a non metallic restoration which has better insulating

properties than a metallic one, 0.5 – 1mm of dentin or liner / base
is sufficient.
• Approximately a 20 fold increase in permeability is seen from
extending a cavity preparation that is 3 mm from the pulp to
0.5 mm

• An acid etchant can increase the permeability by 4- 5 folds as

tubule apertures are enlarged.

• Loss of coronal enamel or cervical cementum exposes dentin

and can produce hyperalgesic response.

• Cementation and impression procedures exert tubular pressure

which results in odontoblastic displacement.
3) THERMAL AGENTS:

• Degree of heat produced depends on instrument

type, speed of rotation , cavity depth, effectiveness
of cooling.

• Metal restorations without insulating base and liner

& heat produced by setting cements irritate pulp by
dehydration of dentinal tubule.
4) CHEMICAL AGENTS:
• Sterilization and disinfecting chemicals applied to the dentin
produce odontoblastic injury

• Alcohol &chloroform produce thermal irritation by evaporation

and dehydrate dentinal tubules

• Hydrogen peroxide may travel through dentinal tubules of deep

cavity preparations and into the pulp producing emboli and
perhaps even arresting circulation.

• Dentin conditioning agents: classic acid etchant used on dentin de

mineralize Peritubular dentin which widens the tubule increasing
permeability.
• The acid should be passively applied for short periods 5-15 secs

• This technique leaves behind smear plugs in tubule apertures

• The intact collagen framework interacts with hydrophilic priming

agents which penetrate through the remnant smear layer and into
the Intertubular dentin and fills the spaces left by the dissolved
apatite crystals. This allows acrylic monomers to form an
interpenetrating network around dentin collagen. Once
polymerized , this layer produces what Nakabayashi (1992)
referred to as HYBRID ZONE( Interdiffusion zone or
Interpenetration zone) 0.1 to 5 um deep.
• ACID LIQUID COMPONENTS OF CEMENTS: Initial
acidity of zinc phosphate, silicate , zinc polycarboxylate and
glass ionomer cements produce pulpal irritation.

• ACRLIC MONOMER: Produces shrinkage and is unable to

seal effectively produces pulpal irritation

• EUGENOL: Anti inflammatory activity through the inhibition

of prostaglandin synthesis

• Antibacterial

• Anodyne effect through desensitization and blockage of pain

impulse.

• ZOE is found to be the most effective sealing agent

5. RESTORATIVE MATERIALS:
A restoration placed in a cavity preparation can develop
contraction gaps between the restoration and the cavity wall.
This gap then fills with fluid from the outflow of tubules or saliva
from external surface. An environment is created for bacterial
growth and failure of restoration .
CONCLUSION…!!!
 REFERENCES
• Orbans’ Oral Histology and Embryology-G.S Kumar – Twelfth
Edition
• Ten Cate’s Oral Histology- Development, structure and Function-
Antonio Nanci- Sixth Edition.
• Pathways of the pulp- Cohen. Hargreaves- Ninth Edition.
• Shafer’s Textbook of Oral Pathology- Shafer, Hine, Levy-5th
Edition.
• Oral and Maxillofacial Pathology- Neville-3rd Edition.
• The art and science of Operative dentistry- Theodore Sturdevant- 4th
Edition.
• An Atlas and Textbook of Oral Anatomy and Histology- Berkovitz.
• Tooth Wear and sensitivity Clinical Advances in restorative
Dentistry-Martin Addy, Graham Embery, W Michael Edgar
102
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