You can neither win

nor lose if you don't

run the race
- David Bowie

Good morning
STRU CTU RE O F

DENTI
N PRESENTED BY
DR. ABHISEK GURIA
1ST YEAR MDS
D E P T. O F C O N S E R V A T I V E D E N T I S T R Y A N D E N D O D O N T I C S
 Contents
 Introduction
 History
 Dentinogenesis
 Formation of organic matrix
 Mineralization
 Odontoblast
 Odontoblastic process
 Odontoblastic biology
 Pre-odontoblasts
 Secretory odontoblasts
 Transitional odontoblasts
 Aged odontoblasts
 PATTERNS OF MINERALIZATION
 Globular pattern
 Linear patter
 Vascular supply
 Nerve supply
 Physical & chemical properties
 Chemical composition
 Organic component
 Inorganic component

 Structural components
 Primary curvatures
 Secondary curvatures
 Peri-odontoblastic space
 Lamina limitans
 Peritubular dentin
 Intertubular dentin
 Predentin
 Primary dentin

 Secondary dentin

 Tertiary dentin

 Reactionary dentin

 Reparative dentin

 Interglobular dentin

 Granular layer

 Dentinoenamel junction

 Cementodentinal junction

 Enamel spindle

 Incremental lines
 Incremental lines of Von Ebner

 Lines of Schreger

 Contour line of Owen

 Neonetal line
 Dentinal fluid
 Dentin permeability
 Age changes
• DEAD TRACTS
• DENTIN SCLEROSIS
• EBURNATED DENTIN
• Clinical considerations

 Hypersensitivity
 Direct neural stimulation theory
 Transduction theory
 Hydrodynamic theory
 Modulation theory

 Pulp dentin complex

 Dentinal caries
 Infected and Affected Dentin
 Remaining dentin thickness
 Cavity preparation
 Operative Instrumentation
 Pulp protection

 Vital pulp therapy

 Indirect pulp capping
 Direct pulp capping

 Bonding to Dentin
 Dentin in Endodontics
 Apexification & apexogenesis
 Smear layer
 Developemental anomalies

 Dentinogenesis imperfect

 Dentin dysplasia

 Regional odontodysplasia

 Dense in dente

 Tetracyclin staining

 Conclusion
 Referances
INTRODUCTION
 Second layer of the tooth
 Structure that provides the bulk and general
form of the tooth
 determines the shape of the crown, including
the cusps and ridges
 closely resembles bone
 Said to be a living tissue
 HISTOR
Y
• 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

DENTINOGENESIS
 STAGES
1. Synthesis Of Organic matrix
2. Subsequent Mineralization.

•Carried out by- ODONTOBLASTS

 ODONTOBLASTS

• Cells Of Pulp, 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.
ODONTOBLASTIC PROCESSES

 Cytoplasmic extensions of the odontoblasts

 Extend into the dentinal tubules

 largest in diameter near the pulp and

taper further into dentin

 The odontoblast cell bodies are approx.

7µm in diameter & 40µm in length
ODONTOBLASTIC PROCESSES
ODONTOBLAST BIOLOGY

• PRE-ODONTOBLASTS

• SECRETORY ODONTOBLASTS

• TRANSITIONAL ODONTOBLASTS

• AGED ODONTOBLASTS
FORMATION OF PRIMARY DENTIN
The Cells of IEE become taller
and start differentiating into
Ameloblasts

Reversal of polarity – early bell

stage

Induce differentiation of
odontoblast

Odontoblastic process developes and start

depositing collagen matrix – predentin

Ameloblasts to start depositing Enamel

matrix
DEPOSITION OF COLLAGEN MATRIX
INITIALLY:

•Large dia Type III Collagen

•VON KORFF’S FIBRES
-Cork Screw Shaped
-Perpendicular to DEJ
-Argyrophillic in nature.

LATER
• smaller Fibrils- perpendicular to
Tubules
• parallel To DEJ.
Odontoblast migrates twards the pulp

Odontoblast Process- (TOME’S FIBRES)-

Tubular nature is established.

MINERALIZATION Begins once matrix is

about 5µ thick.
CALCIFICATION OF MATRIX- initiated by
small crystallites within MatrixVesicles

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
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.
PATTERNS OF MINERALIZATION
GLOBULAR(CALCOSPHERIC) pattern :

• 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

RADIAL CRYSTAL GROWTH INTERGLOBULAR DENTIN

LINEAR pattern

• when the rate of dentin formation occurs

slowly
• mineralization front appears more
uniform – Circumpulpal Dentin
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.
VASCULAR SUPPLY
• Provided by the Capillaries found in the subodontoblastic
layer of the pulp.
• Migrate between odontoblasts, and later - Regress.
 INNERVATION OF DENTIN

• Numerous Nerve Endings

in Predentin and Inner Dentin.

• Closely Associated with Odontoblast Process.

• Arise from myelinated nerve fibers of Dental Pulp-

(Aδ fibres) Reach Brain via Trigeminal N.
 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
CHEMICAL
COMPOSITION

BY WEIGHT BY VOLUME
15%

22%
20% 65% 45%

33%

INORGANIC ORGANIC WATE

R
1. ORGANIC COMPONENTS

• Collagen – 82% ,
• MAINLY TYPE I and some Type III and V.

• Non Collagenous Matrix Proteins- 18%

-Phosphoproteins- DPP(Phosphoryn), Gla-Protein.

-Glycoproteins- Dentin Sialoprotein,Osteonectin,
Osteocalcin
- Proteoglycans- Chondroitin SO4 (seen mainly in
Predentin)
• Enzymes- Acid Phosphatase, Alkaline Phosphatase.

• Lipids- phospholipids, glycolipids etc. in traces.

Growth factors:

• Bone morphogenetic proteins (BMP)

• Insulin like growth factors (IGFs)
• Transforming growth factors β (TGF- β
2. 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

• Trace Elements- Cu, Fe, F, Zn

33
STRUCTURAL COMPONENTS

• Odontoblast
Process
• Dentinal
Tubules
• Non
mineralized
matrix-
Predentin
• Mineralized matrix-
Peritubular and
 DENTINAL
TUBULES
• From pulp to DEJ
• resembles an S shape
• Ratio btwn outer and inner
surfaces of dentine is about
5:1
• Smaller branches- canaliculi -
pathways of exchange

• More tubules per unit area in

the crown than in the root
Tubule density/ unit area - ↑
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.

 PRIMARY CURVATURES

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

At Increased Magnification- Secondary Curvatures.

PERI-ODONTOBLASTIC SPACE

• Potential space between tubule wall and od. Process.

• Contents - nerves, collagen fibrils, plasma proteins,

glycoproteins and mitochondria.
 Lamina Limitans
• Organic sheath or membrane lining the Dentinal tubules
• seen in EM sections.
 PREDENTIN
 Located adjacent to the pulp tissues

 2-6µm, depending on the activity of

odontoblasts

 First formed dentin and is not

mineralized

• Stains less intensely

 PERITUBULAR DENTIN
•PERILUMINAL/ INTRATUBULAR DENTIN
• Immediately surrounds the dentinal tubules

• Collar - ↑ Calcified Matrix

• ↓ collagen fibrils, ↑ sulfated proteoglycans.

• 40% more mineralized than ITD.

• Hardness of H. A. crystals-250 KHN

(Kinney Et al- 1996)
• Thickness- 0.75µm- 0.4µm
• Lost in decalcified Sections
INTERTUBULAR DENTIN

• Main Body Of Dentin.

• 10 Secretory Product.
• Less mineralized
• Hardness -52KHN
• (Kinney et al 1996)
• The fibrils exhibit crossbanding
at 64µm intervals
Dentinal
Tubule
Peritubular
Dentin

Intertubular
Dentin
 INTERGLOBULAR DENTIN

• Unmineralized islands- due to

failure of fusion of mineral
globules .

• In Circumpulpal Dentin
• Subjacent to pits and fissures.

• Tubules pass uninterrupted.

• Vitamin ‘D’ deficiency or

Hypophosphatasia
 TYPES OF
DENTIN
• Primary dentin
– Mantle
– Circumpulpal

• Secondary dentin

• Tertiary dentin
• Reparative dentin
• Reactionary dentin
 PRIMARY DENTIN
(Prior To Root Completion)
MANTLE CIRCUMPULPAL
LOCATION Below DEJ B/n Mantle Dentin
and Predentin.
THICKNESS 20 µ 68nm
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
PRIMARY DENTIN
 MANTLE DENTIN
• First layer of primary dentin

• under polarised light, mantle

dentin (RED Band) can be
differentiated from the
Circumpulpal dentin (Purple
with black dentinal tubules)

 due to difference in collagen

fibres in mantle dentin
CIRCUMPULPAL DENTIN

 After mantle dentin has been deposited

 Major part of primary and secondary dentin

 mineralised through calcospherites in the

mineralisation front between predentin and
mineralizing dentin
 SECONDARY DENTIN

• after root completion

• Narrow band- bordering the pulp

• Deposited 1µ/day.

• Fewer tubules

• Bending of tubules at the 10 & 2°

Dentin interface.

• greater amounts at roof of pulp

chamber- protecting the pulp horns.
52
 TERTIARY DENTIN
• Localized At pulp – in response to noxious
stimuli
No continuity with 10 or 20 Dentin so
Also known there is ↓ Dentin permeability.
as:
Reactive Dentin, Quality Depends on :
Reparative
Dentin, • Intensity of stimulus.
• Vitality of pulp.
Irritation Dentin,
Replacement
Dentin,
Adventitious
 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

Rate of deposition= 2.8-3 µ/day

GRANULAR LAYER OF TOMES

• In Root Dentin

• Increases in amt. from CEJ to

Apex.

• Looping /coalescing of
Dent. Tubules.

• Hypomineralized areas.
 ENAMEL SPINDLES
• Odontoblast processes sometimes extend into the Enamel.

• Length is about 10- 40 m

• near Incisal edges &

cusp tips

• Dark in ground
sections

• Hypomineralized

• Spread of Caries from

Enamel to Dentin.
 INCREMENTAL LINES OF VON
EBNER/ IMBRICATION LINES

• Fine striations- perpendicular to

tubules.
• Daily rhythmic deposition

• 4-8µ apart in crown,

closer in root.
• 5 DAY INCREMENT-
20µm
 LINES OF SCHREGER

Congruence Of PRIMARY CURVATURES of Dentinal tubules.

 CONTOUR LINES OF OWEN

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

• Primary teeth, permanent

first molars.

• Zone of hypo calcification

• Reflects abrupt change in

environment- At Birth.

• Dentin formed Before birth-

Better Quality
 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 →
sensitivity.
 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

• Apical Constriction- Termination of

Instrumentation. 45
 DENTINAL
FLUID
( Dentin Lymph)

• Occupies space b/n dentinal tubule and od.

Process.
• Ultrafiltrate- pulp Capillaries

• Ca content is 2-3 times higher than in plasma.

• Tissue pressure of pulp- 14 cm of H2O,

• (Ciucchi et al 1995) pressure gradient -tends to
flow outwards slowly
• Exposure of Tubules - Outward
movement → dehydrating the
surface-rapid flow of fluid - sensitivity.

• Slow outward flow of fluid (0.02

nl/sec/mm to 1-1.5.microlitre/sec/mm
for nerves to begin firing.

• Acts as barrier for microbes and toxins

.
 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.

 MORE PERMEABLE LESS PERMEABLE

DENTIN NEAR PULP HORNS DENTIN FURTHER AWAY

AXIAL WALLS OF CLASS PULPAL FLOOR OF CLASS II

II CAVITY CAVITY

CORONAL DENTIN ROOT DENTIN

NORMAL DENTIN SCLEROTIC DENTIN

AGE AND
FUNCTIONAL
CHANGES

• Dead tracts

• Dentin sclerosis

• Eburnated dentin
 DEAD TRACTS

• Empty Tubules Filled with

air.

• Due to → Degeneration
of odontoblastic
process

• Black in transmitted light,

WHITE IN REFLECTED
LIGHT.

• Older Teeth - Areas of

 SCLEROTIC DENTIN
• Presence of irritating stimuli → 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

 • Also seen- slowly
progressing Caries.

• Reduced Permeability

• Prolonged pulp
vitality

• Resistant to Caries

• Forensic Odontology: One

of the criteria for age
determination using
SCLEROTIC DENTIN Gustafson’s method.
 EBURNATED DENTIN
• Exposed portion of reactive sclerotic Dentin.

• Slow caries has destroyed overlying tooth structure

• hard , darkened , cleanable surface.

• Resistant to further caries Attack.

CLINICAL CONSIDERATIONS

Hypersensitivity
Pulp dentin complex
Dentinal caries
Infected and Affected Dentin
Remaining dentin thickness
Cavity preparation
Operative Instrumentation
Pulp protection
Vital pulp therapy
Bonding to Dentin
Endodontics
Smear layer
 Hypersensitivity
• Unusual symptom of Pulp- Dentin Complex.

• It is a condition characterized by short , sharp

pain arising from exposed dentin in response to
stimuli typically thermal , evaporative , tactile,
osmotic or chemical and which cannot be
ascribed to any other form of dental defect or
pathology . ( Holland et al 1997)

• Sharp Pain- easily localized.

• Etiology-
Exposure of Dentinal tubules
loss of enamel
Direct neural Transduction
stimulation theory

Hydrodynami Modulation
c theory theory
DIRECT NEURAL STIMULATION
• 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.
•Drawbacks:

• No nerve endings in dentinal tubules

• Topical application of local anaesthetic
agents do not abolish sensitivity
 TRANSDUCTION THEORY
• By Thomas 1994
• Odontoblastic
Processes are primary
structures excited by
stimulus.

• Transmit impulse to
Nerve
Endings

• Supported by evidence
that odontoblasts
→ Neural Crest Origin

Drawbacks:
• No synaptic Contacts or
 HYDRODYNAMIC THEORY
• Gysi (1900), Brannstrom
• Various stimuli heat, cold,
airblast dessication or
mechanical or osmotic
pressure affect fluid
movement in the dentinal
tubules.

• Activating the Free Nerve

Endings Associated with
Odontoblast and its Process

• Act as Mechanoreceptors-
 MODULATION THEORY

• Nerve impulses in the pulp are modulated

through the liberation of polypeptides from the
odontoblasts, when injured.

• Alter permeability of the odontoblastic cell

membrane through hyperpolarisation,

• So that pulp neurons are more prone to

discharge upon receipt of subsequent stimuli
• Management - Block The Dentinal Tubules!!!

• Desensitising toothpastes-
• AgNo3, SrCl2, fluorides, Bonding Agents, lasers etc.
Suggestion for patients

• Avoid gingival recession due to plaque

deposition by practicing good oral hygiene

• Avoid using large amount of dentifrice

• Avoid hard bristled tooth brushes

• Avoid brushing with excessive pressure

• Avoid excessive flossing or incorrect use

• Avoid picking at gums

 Pulp dentin complex

• Orbans(1980) stated that “The pulp lives for

the dentin and the dentin lives by the grace
of the pulp. Few marriages in nature are
marked by a greater interrelationship. Thus it
is with the pulp and the four functions that it
serves: namely, the formation and the
nutrition of dentin and the innervation and
defense of the tooth.”
• Based on this Nanci (2005) has stated that the
pulp and dentin can no longer be studied as two
separate entities but must be viewed as the
 Dentinal caries

• Zone1: Zone of fatty degeneration

(from pulp)
• Zone2: DENTINAL sclerosis
• Zone3- Dentin decalcification
• Zone4: Decomposed dentin.
 Remaining dentin
thickness
• From base of the cavity to roof of pulp

• Methods of measurement
• Radiographic method
• CBCT
• Electrical resistance
• Prepometer

RDT influence treatment outcome

• 1 mm of residual root dentine following post preparation is claimed to
reduce the risk of root fracture
• Pulpal toxicity of certain materials (eg zinc oxide eugenol) reduces with
increasing dentine thickness
• Bond strength of resin-based adhesive systems
reduces as the dentine thickness reduces.

• Hydraulic conductance of radicular dentine

decreases with increasing distance from the
pulp

• Heat-induced pulpal injury following curing with

light-emitting diode units or from burs during
caries removal is more likely with reduced
dentine thickness.
• Minimal effects are transmitted to the pulp if RDT is 2mm or
more.

• For an amalgam restoration 1- 2 mm is preferred.

• For a non metallic 0.5 – 1mm of dentin or liner / base is

sufficient.

• Approximately a 20 fold increase is seen from extending a

cavity preparation that is 3 mm from the pulp to 0.5 mm

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

tubule apertures are enlarged.
 “Cavity Preparation”

• Cavity Floor → Dentin

• Dentin is RESILIENT → Absorbs and

Resists Forces of Mastication and
Deformation – Grips the restorative
material.

• Grooves, coves, pins etc -completely in

Dentin.
 Operative Instrumentation
• To prevent damage to the odontoblasts

AVOID-
Excessive Cutting
Heat Generation
Continuous Drying

USE :
 Air- Water Coolant.
 Sharp hand Instruments
 Tungsten Carbide Burs to Cut vital
Dentin
 Pulp protection
• Irritants from Restorative
materials- pulp damage

• Need for pulp protection

1. Mechanical protection
2. Barrier to chemical
components
3. Thermal protection
4. Galvanic protection
5. Adequate seal at
interface
71
 1) 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.
2) CHEMICAL
AGENTS:
• Alcohol &chloroform
• produce thermal irritation by evaporation and dehydrate
dentinal tubules

• Hydrogen peroxide
• may travel through dentinal tubules into the pulp
producing emboli and perhaps even arresting circulation.

• Dentin conditioning agents:

• widens the tubule increasing permeability.
• 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

• Anodyne effect through desensitization and blockage of pain

impulse.
• Thermal Protection- Bases below
Restoration
• Base: materials that are used to
replace missing dentin or to block
out undercuts in preparation for
indirect restorations.

• Chemical Protection- Cavity sealers,

liners
• Sealers : materials that provide
protective coating to the walls of the
prepared cavity.
• Eg: cavity varnish, resin bonding agent

• Liners: these are cement coating of

minimal thickness, which serve as a
physical barrier to bacteria
• Eg: calcium hydroxide, GIC
 “Vital pulp therapy”
• The reparative Dentin Formation can be stimulated by
cavity lining materials (such as Calcium hydroxide).

• Direct Indirect pulp capping

• Indirect pulp capping

• THE DENTINAL BRIDGE repair tissue that forms

across the pulpal wound.
INDIRECT PULP CAPPING

• Definition
• A procedure wherein the deepest layer of the
remaining affected carious dentin is covered
with a layer of biocompatible material in order
to prevent pulpal exposure and further trauma
to pulp.

• Performed as single or two-step approach.

 DIRECT PULP CAPPING

• DEFINITION :

•A procedure in which the exposed vital pulp is

covered with a protective dressing or base
placed directly over the site of exposure in an
attempt to preserve the pulpal vitality.
 INDICATIONS

• Iatrogenic mechanical exposure of pulp in an

asymptomatic vital tooth

• Small carious exposures in an asymptomatic

permanent tooth with an incomplete root
formation.

• Radiographically no thickening of PDL space

and no evidence of peri-radicular lesion.
CONTRAINDICATIONS

• Large carious exposures in symptomatic

permanent tooth

Materials used
• Calcium hydroxide
• Theracal
• MTA
• Biodentin
 CALCIUM HYDROXIDE
• Pulpdent paste and Dycal

HEALING WITH CALCIUM HYDROXIDE

• Zone of obliteration
• Zone of coagulation necrosis
• Zone of dentin bridge formation
• Line of demarcation
 “Bonding to Dentin”
• Adhesion to Dentin… A
CHALLENGE!!

• Due to - ↑organic content,

tubular nature and presence
of Fluid.
• Further complicated by
“Smear Layer”
SMEAR
• It decreases dentinal LAYER
permeability- butinterferes
with bonding
• 1949, Dr. Hagger, a Swiss chemist used first dental
adhesive “cavity seal”

Generations of bonding agent

• 1st gen - 1956
• Use glycerol-phosphoric acid & dimethacrylate (NPG GMA)
• Reduce bond strength

• 2nd gen - 1970

• formation of ionic bond between calcium and
chlorophosphate groups
• Still fail to remove smear layer
• 3rd gen- Late 1970s
• Acid etching

• 4th gen -1980s

• Total etch tech
• Etchant, primer, bonding agent
• Technique sensitive
• All bond 2, 3, scotchbond multipurpose

• 5th gen - 1990s

• 1 bottle system (primer + adhesive)
• Excite, all bond plus, clearfill new bond
6th gen- early 2000s
• “self-etching primers”,
• 1 step 2 bottle (etchant& primer +
adhesive)
• Lower bond strength
• Clearfil ac, g bond, adper scotchbond ac

7th gen- early 2005

• one-bottle self-etching system
• Reduced long term strength
• One coat 7.0, xeno iv, adper easy one

8th gen- 2010

• voco America introduced voco
futurabond DC, contains nano fillers
 “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”
APEXIFICATIO
N
• Definition : Its defined as a method to induce a calcific
barrier across an open apex of an immature, pulpless
tooth.

Objective
• formation of an apical “calcific barrier” against which
obturation can be achieved.

Apexogenesis
• Refers to a vital pulp therapy procedure to encourage
physiological development and formation of root apex
 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]

• Has a potential to provide a media for recurrent

caries
and bacterial irritation of the pulp

• 2–5 lm thick
 Methods of removal of smear layer

• Chelating agent EDTA

• Weak acid i.E. (10 % citric acid)

• Thorough canal rinsing with 3 to 5 % NAOCL.

• Ultrasonic removal with 1% Naocl

• Laser removal (ne:yag, er:yag, co2 laser)

DEVELOPMENTAL DEFECTS
 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
 TYPE TYPE II TYPE III
I

• Tulip Shaped teeth,

Bluish- grey- Amber
CLINICA
Yellow/Brown appearance,
L
Translucent. Excessive wear,
FEATUR
Enamel Multiple pulp
ES
• Chips away→ Exposures.
Exposed dentin,
rapid attrition.

Partial/complete Shell teeth-

RADIOGRAP obliteration of Normal Enamel,
HIC pulp chamber , Thin Dentin, Huge
FEATURES root canals pulp Chambers,
short roots.
 TREATMEN
T
• first ascertain which type he/she is dealing with.

• Severe cases of DI type 1

• 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 and
routine 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
 TYPE I(RADICULAR) TYPE II (CORONAL)

Normal Morphology,
CLINICAL FEATURES Amber Translucency. Primary- yellow
Extreme Mobility and /brown- grey.
Premature Permanent – normal.
Exfoliation

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

• Maxillary Anteriors

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

• RADIOGRAPHIC
FEATURES: “Ghost
Teeth.”
 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.
 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.
CONCLUSION…!!!

 Although dentin and pulp have different

structures, once they are formed, they react to
stimuli as a functional unit.

 Exposure of dentin through attrition, caries or

trauma produces profound pulpal reactions that
tend to reduce permeability and stimulate
formation of additional dentin.
 REFERENCES
1. Orbans oral histology and embryology – 12th edition
2. Ten Cate’s Oral Histology- Development, structure and
Function- Antonio Nanci- Sixth Edition.
3. Pathways of the pulp- Cohen. Hargreaves- Ninth Edition.
4. Shafer’s Textbook of Oral Pathology- Shafer, Hine,
Levy-5th Edition.
5. Oral and Maxillofacial Pathology- Neville-3rd Edition.
6. The art and science of Operative dentistry- Theodore
Sturdevant- 4th Edition.
7. An Atlas and
andTextbook of Oral
sensitivity Anatomy
Clinical and Histology-
Advances in
Berkovitz. restorative
Dentistry-Martin Addy, Graham Embery, W Michael Edgar
8. Tooth Wear
THANK
YOU!!!!