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GOOD MORNING!!!

DR.RINKU SHANKLESHADEPARTMENT OF CONSERVATIVE DENISTRY

AND ENDODONTICS.KVGDC, SULLIA

Dentin

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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

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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 fibres4

DENTINOGENESIS

• Process of Dentin

formation.

• Dentin-First Formed Dental

Hard Tissue –crown and

roots

• -Formation of Dentin

Precedes Enamel

• Late Bell stage.

• Future cusp tips, Proceeds

Apically. 5

LATE BELL STAGE

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 signallingmolecules produced by Ameloblasts.

•

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8

ODONTOBLAST BIOLOGYECTOMESENCHYMAL 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

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AGED ODONTOBLASTS: Reduction in length and cytoplasmic

Organelles, increase in number and size of lysosomes and

phagosomes, decreased secretory capacity, degenerate with age.

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.

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11

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.

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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.

DEPOSITION OF COLLAGEN MATRIX

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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

As more matrix is formed- the Odontoblast

Migrates centripetally, towards the pulp.

MINERALIZATION Begins once matrix is

about 5µ thick.

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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.

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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.

.

MATRIX VESICLES contain Alkaline Phosphatase

-↑ concentration of phosphates → combine with

Calcium →Hydroxyapatite Crystals.

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.

16RADIAL CRYSTAL GROWTH INTERGLOBULAR DENTIN

17

LINEAR PATTERN

LINEAR : 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.

• Complete- 18mths after

eruption-Primary

2-3 yrs -Permanent Teeth 18

VASCULAR SUPPLY• Provided by the Capillaries found in the subodontoblastic

layer of the pulp.

• Migrate between odontoblasts, and later - Regress.

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PHYSICAL AND MECHANICAL

PROPERTIESPROPERTY 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

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BY VOLUME

45%

22%

33%

BY WEIGHT

20%

15%

65%

INORGANIC ORGANIC WATER

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.

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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

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STRUCTURAL COMPONENTS

• Odontoblast

Process

• Dentinal Tubules

• Non mineralized

matrix- Predentin

• Mineralized matrix-

Peritubular and

Intertubular Dentin.

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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.

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CROWN ROOT

PRIMARY CURVATURES

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Tubules exhibit Sigmoid curvatures-More prominent

in crown.

Least pronounced at cusp tips, incisal edges

SECONDARY CURVATURES

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At Increased Magnification- Secondary Curvatures.

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A. - 50,000 to 90,000 / sqmmpulpal surface

B. - 30,000 to 35,000/sqmmmiddle dentine

C. - 10,000 to 25,000/sqmmperipheral dentine

Tubule density/ unit area - ↑es toward pulp.

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

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)

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Lamina Limitans

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• Organic sheath or membrane lining the Dentinal

tubules

• seen in EM sections.

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

of fluid-sensitivity. 31

• Slow outward flow of fluid (0.02nl//sec/mm -1-

1.5.microlitre/sec/mm for nerves to begin firing.

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•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)

PREDENTIN• First Formed Dentin.

• A layer of Un Mineralized Matrix

• Thickness- 50 µ, 2-6µm wide

• Collagen and Non-collagenous

matrix proteins.

• Gradually Mineralizes.

• Thickness Remains Constant.

• Stains less intensely 33

PREDENTIN

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)

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Dentinal Tubule

PeritubularDentin

IntertubularDentin

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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

Hypophosphatasia37

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

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LINES OF SCHREGER

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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.

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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

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ENAMEL

DENTIN

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.

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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.

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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.

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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

Termination of Instrumentation.45

TYPES OF DENTIN

• Primary dentin

– Mantle

– Circumpulpal

• Secondary dentin

• Tertiary dentin

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PRIMARY DENTIN

MANTLE CIRCUMPULPAL

LOCATION Below DEJ B/n Mantle Dentin and Predentin.

THICKNESS 20 µ 68mm

MINERALIZATION ↓ ↑

DEFECTS ↓ ↑

COLLAGEN FIBRES Larger- 0.1-0.2µperpendicular to

the DEJ

Smaller- 0.02- 0.05µ parallel to the DEJ.

Closely packed.

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(Prior To Root Completion)

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:

Reactive Dentin,

Reparative Dentin,

Irritation Dentin,

Replacement Dentin,

Adventitious Dentin,

Defense Dentin49

No continuity with 10 or 20

Dentin so there is ↓ Dentin

permeability.

Quality Depends on :

•Intensity of stimulus.

•Vitality of pulp.

TERTIARY DENTINREACTIONARY DENTIN REPARATIVE DENTIN

STIMULUS FOR FORMATION

MILD AGGRESSIVE

FORMATIVE CELLS SURVIVING POST MITOTIC ODONTOBLASTS

NEW ODONTOBLAST- LIKE CELLS FROM

PROGENITORS

STRUCTURE PHYSIOLOGIC DENTINCHANGE IN DIRECTION OF NEW DENTINAL TUBULES

HETEROGENOUS:-TUBULAR (ORGANISED)

OSTEODENTINFIBRODENTIN

(DISORG)

50SMITH ET AL (1994)

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REPARATIVE DENTIN REACTIONARY DENTIN

The avg. daily rate of reparative dentin formation is about 2.8-3 µ/day-

acc to Stanley in 1996.

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

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• 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.

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SCLEROTIC DENTIN

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

60

PAIN TRANSMISSION THROUGH

DENTIN

• DIRECT NEURAL STMULATION

• TRANSDUCTION THEORY

• HYDRODYNAMIC THEORY

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,

lasers etc. 65

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

67

MORE PERMEABLE LESS PERMEABLE

DENTIN NEAR PULP

HORNS

DENTIN FURTHER AWAY

AXIAL WALLS OF

CLASS II CAVITY

PULPAL FLOOR OF CLASS

II CAVITY

CORONAL DENTIN ROOT DENTIN

NORMAL DENTIN SCLEROTIC DENTIN

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.

72

ZONE 1 – Normal dentin

ZONE 2 – Sub transparent

ZONE 3 – Transparent dentin

ZONE 4 – Turbid dentin

ZONE 5 – Infected dentin

INFECTED DENTIN AFFECTED DENTIN

SOFTENED AND

CONTAMINATED WITH

BACTERIA

SOFTENED ,

DEMINERALISED BUT NOT

YET INVADED BY

BACTERIA

CONTAINS IRREVERSIBLY

DENATURED COLLAGEN –

STAINED BY CARIES

DETECTING DYE .

CONTAINS REVERSIBLY

DENATURED COLLAGEN

REQUIRES REMOVAL DOES NOT REQUIRE

REMOVAL

Infected and Affected Dentin

73

Operative Instrumentation

• AVOID-Excessive CuttingHeat GenerationContinuous 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

Dentin- Treated with care during op. instrumentation

to prevent damage to the odontoblasts

“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,

debris.(1-4µm thick)

• It decreases dentinal permeability-

but interferes with bonding – should

be removed.77

SMEAR LAYER

• 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 FEATURES

Tulip Shaped teeth, Bluish-grey- Yellow/Brown Translucent. Enamel Chips away→ Exposed dentin, rapid attrition.

Amber appearance, Excessive wear, Multiple pulpExposures.

RADIOGRAPHICFEATURES

Partial/complete obliteration of pulp chamber , root canals

Shell teeth- Normal Enamel, Thin Dentin, 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,

Amber Translucency.

Extreme Mobility and

Premature Exfoliation

Primary- yellow /brown-

grey.

Permanent – normal.

RADIOGRAPHIC

FEATURES

Deciduous - pulp

chambers completely

obliterated, short conical

roots.

Permanent – crescent

shaped pulp chambers-

Difficulty in locating

canal orifices.

Deciduous – pulp

chambers obliterated

Permanent -

“thistle tube” appearance

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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