1

DENTIN
 3

CONTENTS
 Introduction

 Development Of Dentin (Dentinogenesis)

 Physical Properties

 Chemical Properties

 Histological Structure Of Dentin

 Different Types Of Dentin

 Junctions Of Dentin

 Age And Functional Changes In Dentin

 Clinical Considerations

 Developmental Anomalies

 Conclusion
 4

INTRODUCTION
 Dentin is the mineralized and specialised connective tissue which is a derivative of the

dental papilla ,forms the bulk of the tooth and covered by the enamel in the crown

and cementum in the root.

 It is rigid but elastic tissue consisting of large number of small parallel tubules in a

mineralized collagen matrix and these tubules in turn consists of dentinal fluid and

cytoplasmic process of the odontoblasts.

 5

INTRODUCTION
 The dentin is formed throughout the life, increasing in thickness at the expense of the

dental pulp, which is reflected in the presence of an unmineralised layer of the

dentinal matrix at the pulpal surface known as predentin.

 Since it forms slightly before the enamel, it determines the shape of the crown,

including the cusps and the ridges ,and the number and the size of the roots.
 6

STAGES OF TOOTH DEVELOPMENT

 Development of tooth is a complex process initiated by the interaction between

epithelium and connective tissue.

 The epithelium lining the developing oral cavity is called the oral ectoderm and is

composed of stratified squamous epithelium.

 The connective tissue underlying the oral ectoderm is ectomesenchymal in nature

with neural crest cells.

Oral histology By A. R Tencate-8 th edition.

 DEVELOPMENT
7

• Components of tooth germ: Enamel organ, Dental papilla, Dental follicle/sac

EARLY
LATE
BUD
CAPBELL
BELL
STAGE
STAGE
STAGE
STAGE
 8

DENTINOGENESIS
 Dentin is formed by the cells called odontoblasts that differentiate from ectomesenchymal

cells of the dental papilla following an influence from the inner enamel epithelium.

 The actual development of dentin begins at the cusp tips after the odontoblasts have

differentiated and begin collagen production.

 STAGES: Formation of dentin is similar to that of bone and Cementum.

1) Synthesis of Organic matrix,

2) Subsequent Mineralization.

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 9

DENTINOGENESIS
DEPOSITION OF COLLAGEN MATRIX

 Initially the collagen fibers are of large diameter,discrete 0.1- 0.2μ Perpendicular to DEJ.

 Later the collagen fibers deposited are small in diameter, oriented perpendicular to tubules,

parallel to DEJ.

 Initially daily increments of approximately 4 μm of dentin are formed.

 Later this dentin production slows to about 1 μ/day.

 10

DENTINOGENESIS
Von Korffs’ Fibres:

 These fibers were found during the initial stages of dentinogenesis.

 They are larger diameter argryophillic collagen fibers consisting of type III collagen.

Oral histology By A. R Tencate-8 th edition.

 11

DENTINOGENESIS
MINERALIZATION: Begins once the matrix is about 5μ thick.

Various Matrix Proteins Influence Mineralization:

DPP- Binds to Ca, Controls Growth of Hydroxyapatite crystals

Osteonectin- Inhibits growth of Hydroxyapatite crystals, promotes their Binding to

Collagen

Gla-proteins, Phospholipids- Act as nucleators to concentrate calcium.

Proteoglycans- inhibit premature mineralization seen in predentin.

 12

DENTINOGENESIS
 Mineralization of dentin follows two different patterns histologically:

1. Globular or calcospheric calcification.

2. Linear calcification.

 Globular (or calcospheric) calcification involves the deposition of HA crystals in

several discrete areas of matrix which grows in mean time to form globular

masses.

 These globular masses gradually fuse together to form a homogenous mineralized

dentin.
 13

DENTINOGENESIS
 This pattern of mineralization is best seen in the mantle dentin region, where matrix

vesicles give rise to mineralization foci that grow and coalesce.

 In circumpulpal dentin the mineralization front can progress in a globular or linear

pattern

 When the rate of formation progresses slowly, the mineralization front appears more

uniform and the process is said to be Linear calcification.

 14

DENTINOGENESIS
 Root-dentin Formation:

 Begins once Enamel & Dentin formation reaches the future CEJ.

 Initiated by Cells of HERS which induce odontoblast differentiation.

 Collagen fibres are arranged parallel to the CDJ.

 It is comparitively less mineralized and contains less number of Tubules.

 Completion of root dentin does not occur in deciduous tooth until about 18 months after it

has erupted, and it is 2-3 yrs for Permanent Teeth.

 15

PHYSICAL PROPERTIES
 Dentin is pale yellow in colour and becomes darker with age and is less translucent and

contributes to the appearance of the tooth through the translucent enamel.

 Dentin is harder than bone and cementum but softer than enamel.

 Its organic matrix and tubular architecture provides it with greater compressive, tensile

and flexural strength than enamel.

 Dentin is permeable, and the permeability depends on the size and patency of the

tubules, which will decline with age.

 16

PHYSICAL PROPERTIES
 Compressive strength of dentin – 266MPa

 Tensile strength of dentin - 40MPa.

 Density 2.14gcm-3.

 Hardness 68 KHN.

 Dentin is comparatively elastic and its modulus of elasticity- 1.67x 10 6 psi.

 The hardness of dentin is one-fifth that of enamel.

 17

CHEMICAL PROPERTIES
15%

22%

20% 65% 45%

33%

By weight By volume
INORGANIC ORGANIC WATER
 18

CHEMICAL PROPERTIES
 ORGANIC COMPONENTS:
INORGANIC COMPONENTS
 Collagen–82% , mainly TYPE I & some amount of TypeIII and V.


• Calcium Hydroxyapatite: Ca10(PO4)6(OH)2
Non Collagenous Matrix Proteins- 18%
•Thin plate like crystals, shorter than enamel.
Phosphoproteins- DPP(Phosphoryn), Gla-Protein. Glycoproteins -
• 3.5 nm thick, 100 nm long.
DentinSialoprotein(DSP), Osteonectin, Osteocalcin ,(Seen in mineralized matrix)
• Salts- calcium carbonate, sulphate, phosphate etc.
Proteoglycans- Chondroitin SO4 (seen mainly in Predentin)
• Trace Elements- Cu, Fe, F, Zn
 Enzymes- Acid Phosphatase, Alkaline Phosphatase.

 Lipids- phospholipids, glycolipids etc. in traces.

 19

DENTINAL TUBULES:
HISTOLOGICAL STRUCTURE

 The course of the dentinal tubules follows a gentle curve in the crown and less so in

the root, where it resembles S in shape.

 These curvatures are called as primary curvatures.

 During the deposition of dentin, the odontoblast makes slight undulations that creates

wavy dentinal tubules, this waviness of the dentinal tubules is called secondary

curves.
 20

DENTINAL TUBULES
 The tubules end perpendicular at DEJ and CEJ.

 Branches of dentinal tubules near the terminals are referred to as terminal branches.

 Terminal branching is more profuse in the root dentin than in coronal dentin.

 Near the root tip and along the incisal edges and cusps, the tubules are

almost straight.

Cohens pathways of pulp -10th edition.

 21

DENTINAL TUBULES
 Clinical significance:

 Dentinal tubules make the dentin permeable, providing a pathway for the invasion of

caries.

 Microscopic examination of infected dentin shows that the dental tubules are packed

with micro-organisms well ahead of the decalcified intertubular dentin.

 Drugs and chemicals present in a variety of dental restorative materials can also

diffuse through the dentinal tubules and create pulpal injury.

 22

DENTINAL FLUID
 The dentinal fluid is present in a space called periodontoblastic space.

 Free fluid occupies 1% of superficial dentin.

 This fluid is an ultra filtrate of blood from the pulp capillaries, and its composition

resembles plasma in many respects. Ca content in dentinal fluid of predentin is 2-3 times

higher than in plasma.

 The outward fluid flows between the odontoblasts through the dentinal tubules and is

blocked peripherally by enamel on the crown and cementum on the root.

 23

DENTINAL FLUID
 Clinical significance: The slow outward movement of dentinal fluid is not sufficient to

activate the mechanoreceptor nerves responsible for dentin sensitivity.

 This slow outward fluid flow, about 0.02 ml/sec/ mm2, must increase to 1 to 1.5

ml/sec/mm2 before these nerves begin to discharge.

 Bacterial products or other contaminants may be introduced into the dentinal fluid as

a result of dental caries, restorative procedures, or growth of bacterial biofilms

beneath restorations.
 24

ODONTOBLASTS
 Odonoblasts are the derivatives of neural crest cells .

 Odontoblasts form a layer lining the periphery of the pulp and have a process

extending in to the dentin.

 In fully formed teeth, odontoblasts are arranged in a palisade pattern

 Histologically 3 functional states of odontoblasts can be seen:

1. Secretory odontoblasts

2. Transitional odontoblasts

3. Resting odontoblasts
Oral histology By A. R Tencate-8 th edition.
 25

ODONTOBLASTIC PROCESS
 In vital teeth, the odontoblasts are arranged as a continuous layer along the periphery

of pulp adjacent to pulpal surface of dentin.

 Each cell has a protoplasmic process that extends for varying distance into dentinal

tubule.

 These extensions are referred to as odontoblast process .

 These processes are 3-4µ in diameter at pulpal end and taper to 1µ near the

periphery.
 26

PERITUBULAR DENTIN
 Peritubular dentin is a zone of hyper mineralized dentin which surrounds the dentinal tubule.
•Acid etching agents and ethylene diamine tetra acetic acid used in
 This is also referred to as intratubular dentin because it is formed by the deposition along the
endodontic treatment enlarge the openings of the dentinal tubules by
inner aspect of dentinal tubules.
removing peritubular dentin and thus making the dentin more permeable.

 It is deposited
•Thebyabsence
odontoblast process
of intrafibrillar mineral in patients with dentinogenesis

imperfecta
and is 40% type 2 may
more mineralized andbe responsible for their softer dentin.
also

harder than the rest of the dentin.

 27

INTERTUBULAR DENTIN
 Forms main body of dentin and highly mineralized.

 Matrix consists of randomly arranged collagen fibers

around the dentinal tubules.

 Fibrils have striations at 64µm intervals.

 This dentin retains after decalcification.

 The hydroxyapatite crystals are formed along the fibers

with their long axis parallel to the collagen fibers.

Cohens pathways of pulp -10th edition.

 28

INTERTUBULAR DENTIN
 Clinical significance:

 Intertubular dentin determines the elasticity of the dental matrix.

 Sheath of Newmann : The Junction of peritubular Dentin and intertubular dentin reacts

differently to stains, acids and alkali treatments.

 Electron microscopic studies however do not confirm the existence of junctional

sheath.
 29

PREDENTIN
 The pulpal surface of dentin is lined by a layer of non mineralized dentin matrix,this layer

is comparable to osteoid of bone and is termed as predentin.

 It is a 2 to 6 µm unmineralized organic matrix layer , situated between the odontoblast

layer and the mineralized dentin.

 Presence of this layer has clinical significance because it covers

the mineralized dentin and protects in from being resorbed.

Oral histology By A. R Tencate-8 th edition.

 30

TYPES OF DENTIN
 Primary dentin :

 Forms most of the tooth and outlines the pulp chamber of the fully formed tooth.

 Mantle

 Circumpulpal

 Secondary dentin

 Tertiary dentin

Tencates 8th edition

 PRIMARY DENTIN
31

CIRCUMPULPAL
MANTLE DENTIN
DENTIN

B/n Mantle Dentin

Location Below DEJ and Predentin

Thickness 20µ 69nm

Mineralization Less more

Defects Less More

Larger- 0.1-0.2μ Smaller- 0.02-

Collagen fibers perpendicular to 0.05μ
the DEJ parallel to the DEJ.
Closely packed.
 32

SECONDARY DENTIN
 Narrow band of dentin bordering the pulp

 •Clinical
Develops significance:
after root completion.
•The continous formation of secondary dentin reduces the size of the pulp
 Contains fewer numbers of tubules than primary dentin.
chamber gradually.
 Usually•The
primary dentin
rate of and secondary
deposition dentin
of secondary are isseperated
dentin by roof
more at the a prominent
and floor contour
of the
pulp chamber causing reduction in the size of the pulp chamber and decrease
line which is formed due to a bend that develops as a result of sudden curve in the
in height of the pulp horn.
direction of dentinal tubules.

Oral histology By A. R Tencate-8 th edition.

 33

TERTIARY DENTIN
 It is also referred to as irregular secondary dentin,

reactive or reparative dentin formed in response to

stimuli such as attrition, abrasion, erosion, cavity

preparation.

 Tertiary dentin in contrast to physiological secondary

dentin is deposited on the pulpal surface of dentin only in

the affected area.

Orban’s oral histology and Embryology- 10th edition.

 34

JUNCTIONS OF DENTIN
 Dentin is bonded on the outer perimeter by enamel in the crown and cementum in

root and surrounds the pulp on inner perimeter.

Dentino-Enamel Junction Dentino-Cemental Junction

Oral histology By A. R Tencate-8 th edition.

 35

DENTINO ENAMEL JUNCTION

 It is seen as series of scallops in ground sections

 Electron microscope studies reveal, crystals of dentin

and enamel intermix in this junction

 Ridges are more pronounced in coronal dentin, where occlusal stress is more.

• clinical Significance: the scalloped DEJ also serves to reduce the chance of development of

cracks along the junction, because of the numerous changes in the direction of DEJ

• Branching of odontoblast process here results in increased sensitivity.

Oral histology By A. R Tencate-8 th edition.
 36

DENTINOCEMENTAL JUNCTION
 The CDJ is the point in the canal where cementum meets dentin; it is the point where

pulp tissue ends and periodontal tissues begin.

Clinical significance :
 TheIn CD
endodontic
junction is treatment, the containing
a wide zone canal preparation and
large quantities subsequent
of collagen and

obturation should
glycosaminoglycans terminate
,helps at the
to distribute theocclusal
apical loads
constriction,
to alveolarthe narrowest
bone.
diameter of the canal. This point is believed to coincide with the
 The cemental fibers intermingle with the dentinal fibers at the CD junction more in the
cementodentinal junction (CDJ)
cellular cementum than in acellular cementum.

Oral histology By A. R Tencate-8 th edition.

 37

INCREMENTAL LINES
 The incremental lines of von Ebner appear as a fine lines or striations in dentin.

 They run at right angles to the dentinal tubules and correspond to the incremental

lines in enamel or bone.

 These lines reflect the daily rhythmic, recurrent deposition of dentin matrix as well as

hesitation in the daily formative process.

 The distance between lines varies form 4-8µm

in the crown to much less in the root.

Oral histology By A. R Tencate-8 th edition.

 38

INCREMENTAL LINES
 The course of the lines indicates the growth pattern of the dentin.

 Analysis with soft xrays has shown this line to represent hypocalcified band.

 Contour lines of Owen:These are accentuated incremental lines.

 They occur due to disturbances in matrix formation and mineralization.

Orban’s oral histology and Embryology- 10th edition.

 NEONATAL LINES
39

 Usually seen in deciduous tooth and permanent first molar.

 Accentuated contour lines separate prenatal & postnatal dentin.

 Dentin formed before birth is usually better quality.

 Occurs both in enamel and dentin.

 A zone of hypocalcification, reflects an abrupt change in environment that occurs at

birth.

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 40

INTER GLOBULAR DENTIN

 Seen in circumpulpal dentin , just below the mantle dentin.

 Dentinal tubules pass uninterruptedly through this globular dentin.

Prominent & common in

 Vitamin D deficiency
 Rickets
 Fluorosis
 Hypoparathyroidism
 Hypothyroidism

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 41

GRANULAR LAYER
 Seen in the root dentin adjacent to the cementum in ground sections in transmitted light

known as Tomes granular layer.

 Occurs due to coalescing and looping of terminal portions of dentinal tubules

 Increases in amount from CEJ to root apex.

 They remain unmineralised like the intergloblar dentin.

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 AGE AND FUNCTIONAL 42

CHANGES
 The color of the dentin becomes darker with the age.

 The vitality of dentin is decreased in advancing age probably due to te decrease in

odontoblastic activity.

 Thickness of dentin increases as the age advances.

 Dental caries, abrasion, cutting of dentin will causes changes in dentin which may

result in development of dead tracts,sclerosis and reparative dentin.

Orban’s oral histology and Embryology- 10th edition.

 REPARATIVE DENTIN (IRREGULAR 43

SECONDARY DENTIN)
 Extensive tooth wear can result in substantial tissue injury, in such cases the

odontoblasts may either survive the injury or it may die.

 Reactionary/regenerated dentin is secreted from the existing odontoblasts, whereas

reparative/response/reactive dentin are from differentiated mesenchymal cells.

 May or may not have regular arrangement of tubules or no tubules at all.

 Sometimes the odontoblasts are trapped in the dentin and they are called

osteodentin..

Orban’s oral histology and Embryology- 10th edition.

 REPARATIVE DENTIN (IRREGULAR 44

SECONDARY DENTIN)
 The quality, quantity of reparative dentin depends on Intensity of stimulus, Vitality of

the pulp.

 Maximum rate of deposition: 3.5 microns per day.

Orban’s oral histology and Embryology- 10th edition.

 45

SCLEROTIC DENTIN
 Continuous depositin of intratubular dentin as a result of aging or in response to tooth

TYPES progressing
wear or slowly OF SCLEROTIC DENTIN:
dental caries, results in progressive reduction in lumen of the

Physiologic
dentinal tubules and ifsclerotic
continuesdentin: occursthe
obliterates duetubules.
to aging

Reactive sclerotic dentin: occurs due to irritants

 This dentin with obliterated tubules is called sclerotic dentin.

Eburnated dentin: A type of reactive sclerotic dentin where slow caries

has destroyed formerly overlying tooth structure, leaving, a hard,

darkened, cleanable surface..

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 46

SCLEROTIC DENTIN
 The refractive indices of occluded dentin are equalized and such areas become

transparent, and appears as transparent or light in transmitted light and dark in

reflected light.

 Sclerosis reduces the permeability of dentin and may help prolong pulp vitality.

 The presence of a hypermineralized surface layer, bacteria and sclerotic casts

obliterates the dentinal tubules and makes the dentin substrate less susceptible to acid

demineralization.

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 47

DEAD TRACTS
 Observed in ground section of tooth, these represents empty

tubules filled with air.

 Appear black in transmitted light & white in reflected light.

 They are formed due to loss of odontoblast process as a

result of caries, attrition, abrasion, erosion.

 These areas have decreased sensitivity and seen in mostly in

older teeth.

BERKOVITZ Oral Anatomy, Histology and Embryology - Mosby; 4th edition (January 27, 2009)
 48

CLINICAL
CONSIDERATIONS
DENTINAL HYPERSENSITIVITY
Dentin hypersensitivity is best defined as a 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.”

Ingles endodontics 7th edition

 49

THEORIES OF PAIN TRANSMISSION

NEURAL INNERVATION THEORY

 According to this theory, nerve fibers present within the dentinal tubules initiates

the impulses when they are injured and this causes the dentinal hypersensitivity.

Disputes About This Theory:

 Nerve fibers are present only in the predentin and inner dentinal zones.

 When pain-inducing substances like potassium chloride, acetylcholine are

applied to exposed dentin, they fail to elicit painful response , so rejected.

 THEORIES OF PAIN 50

TRANSMISSION
ODONTOBLASTIC RECEPTOR THEORY (Proposed by Rapp et al)

 This theory suggests that the odontoblasts or their processes are damaged when
•This theory also fell into disfavour as research has shown that the odontoblastic
external stimuli are applied to exposed dentin.
processes extend only partly through the dentin and not upto the DEJ.

 As a•Another
result valid finding
of this theyisconduct
that there were no to
impulses demonstrable
the nervesneurotransmitters
in the predentin likeand

acetylcholine
underlying in the
pulp from neural
where transmission
they proceed toofthe
pulp. Hence,
central this theory
nervous is no longer
system.
valid.
 THEORIES OF PAIN 51

TRANSMISSION
Hydrodynamic theory (proposed by brannstorm et al)

 This theory proposes that a stimulus causes displacement of the fluid that exists in the

dentinal tubules.

 The displacement occurs in either an outward or inward direction and this mechanical

disturbance activates the nerve endings present in the dentin or pulp.

 Brannstrom (1962) suggested that the displacement of the tubule contents is rapid

enough to deform nerve fiber in pulp or predentin or damage odontoblast cell.

 THEORIES OF PAIN 52

TRANSMISSION
 For hydrodynamic theory to be accepted as valid teeth presenting with

hypersensitivity must have dentinal tubules which are open at dentin surface and

patent till the pulp.

 SEM ,dye penetration studies have shown that there is a greater number and wider

tubules in hypersensitive dentin compared to non sensitive dentin.

 MANAGEMENT OF DENTIN 53

HYPERSENSITIVITY
 Two principal treatment options :

Desensitization by occluding the dentinal tubules.

 Formation of smear layer over exposed dentin

Desensitization by blocking the pulpal sensory nerves.
 Use of topical agents to occlude the exposed dentinal tubules
 Natural Process Contributing to Desensitization:
 Placement of restorations
Formation of reparative dentin by the pulp.
 Use of lasers
Obturation of tubules by the formation of mineral deposits (Dental sclerosis).

Calculus formation on the surface of the dentin.

54

DENTAL CARIES
 Progression of caries in dentin is different from overlying enamel because of structural

differences in dentin.

 Dentin contains less mineral content than enamel and possesses microscopic tubules

that provide a pathway for ingress of acids and egress of minerals.

 DEJ has least resistance to caries attack and allow rapid lateral spreading when caries

penetrated enamel.

 Dentinal caries is V shaped in cross-section with a wide base at the DEJ and apex

pointing apically.
 ZONES OF DENTINAL CARIES
Zone:-1 :-Normal dentin :

 Zone of fatty degeneration of Tome’s fibers.

 Formed by degeneration of the odontoblastic process.

 Otherwise dentin is normal and produces sharp pain on stimulation.

Zone:-2:-Sub transparent dentin:

 Intertubular dentin is demineralized.

 Dentinal sclerosis, i.e. deposition of calcium salts in dentinal tubules takes place.

 Damage to the odontoblastic zone process is apparent,There are no bacteria in this zone.

Hence, this zone is capable of remineralization.

55
 56

ZONES OF DENTINAL CARIES

Zone:-3:-Transparent dentin:

 Zone of dentinal caries that is softer than normal dentin and shows further loss of mineral

from the intertubular dentin.

 No bacteria are present, large crystals are present in the lumen.

Zone:-4:-Turbid dentin:

 Widening and distortion of the dentinal tubules which are filled with bacteria

 Dentin is not self-repairable, because of less mineral content and irreversibly denatured

collagen

 This zone should be removed during tooth preparation.

 ZONES OF DENTINAL CARIES:
Zone:-5:- Infected dentin:

 The outer most zone consisting of decomposed dentin ,that filled with great number of

bacteria .

 There is no recognizable structure to dentin and collagen and mineral seems to be

absent.The removal of infected dentin is essential for successful restorative

procedures .

57
 Infected Dentin Affected Dentin
more superficial layer of carious dentin. Deeper layer of carious dentin.

Light brown in colour. Dark brown in colour.

Soft and leathery consistency. Hard consistency.

Not sensitive to touch. Sensitive to touch

Collagen is irreversibly denatured. Collagen is reversibly denatured.

Has a high concentration of bacteria Has a low concentration of bacteria.

Stained by caries detecting dyes. Not stained by caries detecting dyes.

Not remineralizable. Remineralizable.

Should be removed. Should be retained.

58
 EFFECTS OF CARIES ON PULP 59

DENTIN ORGAN
 Type of decay : The more acute the decay process less effective the defensive repair

mechanism will be.

 Duration of the decay: The longer the duration in chronic decay ,the greater the chances

for repair ,provided the pulp chamber and the root canal system are not directly involved.

 Depth of involvement: for peripheral involvements we would anticipate either no pulpal

reaction at all or a reparative reaction in both acute and chronic lesions.

 Effective depth: is the area of minimum thickness of sound dentin separating the pulpal

tissues from the carious lesion, this is usually found in the deepest portion of the caries

activity.
 60

Clinical significance:

 Dentin permeability primarily depends on the RDT and the diameter of the tubules.

 Because the tubules are shorter, become more numerous and increase in diameter

closer to the pulp ,deep dentin is a less effective pulpal barrier than is superficial dentin

near DEJ or dentino cemental junction.

 61

The pulp-dentin organ may react against any stimulation or irritation in one of the following
ways

Healthy reparative Unhealthy reparative

reaction reaction Destructive
most favourable reaction Degeneration of the
odontoblasts., either by
reaction
consists of stimulation of
being poisoned or by being
PD organ to form
sclerotic dentin and
aspirated into the dentinal Most unfavourable
tubules,this is followed by response begins with
calcific barrier, followed the formation of the dead
by normal secondary loss of odontoblasts
tract in the dentin, and
dentin containing tubules complete cessation in the
and outer protective
formed from formation of secondary layer of the pulp.
odontoblasts. dentin.
 62

BONDING TO DENTIN:
 Adhesion to dentin remains still as a challenge because of its composition, the dentin

contains substantial amount of organic material and water.

 Ideally the adhesive should be hydrophilic to displace water and bond the dentin,

since most of the resins are hydrophobic the essential interface is important.

 The bonding agents bond the restorative resins to dentin mainly by micromechanical

bonding due to the formation of hybrid layer.

 CHALLENGES IN DENTIN 63

BONDING
• Structure of dentin.

• Smear layer.

• Dentin permeability.

• Changes due to caries, sclerotic dentin.

• Stresses at resin dentin interface.

 CHALLENGES IN DENTIN 64

BONDING
STRUCTURE OF
DENTIN
 Enamel contains 90% of hydroxyapatite crystals whereas dentin has only 50% and the

rest is constituted by water(25%) and type I collagen(25% by volume).

Adhesion can also be affected by remaining dentin thickness(RDT) as bond
 Dentinal tubules exert pressure of 25-30mmHg, thus creating decreased stability of
strength is greater for superficial dentin and it is lesser for deeper dentin
bond between composite resin and dentin.

 The number of dentinal tubules decreases from 45000 near the pulp to 20000 near

DEJ.

 Also the tubule diameter decreases from 2.37μm to 0.63μm near DEJ.
Hybridization of Dental Hard Tissues-nakabayashi
 65

SMEAR LAYER..

 Smear layer: formed when dentin

Smearis layer
cut or
is abraded consists
responsible for: of denatured collagen,

hydroxyapatite crystals,
•Physical debris
barrier1-for
3 bacteria
µm in thickness.
and bacterial products

•Restricting
 Acts as a natural bandagetheover
surface
cut area available
dentinal for because
surface diffusion of
it both
occludes many

dentinal tubulessmall and large

by smear plugs.molecules.

•Resistance to fluid movement.

 Smear layer may be deterrent to the bonding process, since it may serve as a barrier

•In vital teeth, the smear layer restricts the dentinal fluid
to the penetration of resin to the underlying dentin substrate.
from flushing the dentin surface.
Sturdevants 5th edition
 REMOVE OR RETAIN ??

REMOVE RETAIN

 Use of bonding agents that can penetrate

 The exposed collagen network provides

the smear layer and incorporate into

reactive groups that can chemically
bonding
interact with primers.
layer.
 Exposed collagen promotes
 Protective barrier.
micromechanical bonding to resin.
 Lowers dentinal permeability.
 Tubules are open for good retention.
 Lowers pulpal pressure.
66
 SMEAR LAYER..

 Opinions differ about the smear layer.

•Modifying the smear layer prior to bonding
 Some researchers consider it as a natural protective linerfor the pulp, while others

•Removal of smear layer prior to bonding

consider it as a source of microorganismswhich can cause pulp irritation.

•Dissolving
 More importantly the
it may smear
interfere withlayer and incorporating
the adhesion to dentin… it to the

bonding layer
 BONDING
68

DENTIN PERMEABILITY:
 It refers to the ease with which a substance can move into or across a diffusion

barrier. INTRATUBULAR INTERTUBULAR PERMEABILITY

PERMEABILITY
•Diffusion of monomer into demineralized
•The inmovement
 Variation permeabilityofaffects
fluidthe bonding mechanism of dentin.
intertubular dentin.
within dentinal tubules
•Demineralized
 The use of vasoconstrictors in local anethetics decreaseto expose the collagen
pulpal pressure and fibrils
reduce
•Responsible for the dentinal
of the dentinal matrix and to create diffusion
fluidsensitivity
flow in tubules.
pathways for monomer infiltration into long,
•Formation of resin tags
 Other factors are the radius, length ofcontinuous,
the tubules,interconnected, narrow
viscosity of the channels,
dentin fluid,the
or pores.
pressure gradient, the molecular size of the substances dissolved in the tubular

fluid,and the rate of removal of substances by the blood vessels in the pulp.
Hybridization of Dental Hard Tissues-nakabayashi
 69

FACTORS AFFECTING INTERACTION OF

DENTNAL PERMEABILITY AND MONOMER
DIFFUSION
Collagen fibril Noncollageno Primer
network us proteins solubility

•They are highly charged •HEMA can replace water in

•Resin monomers penetrate
molecules that bind to spaces around collagen
acid etched collagen via
water in demineralized fibrils, it can serve as a
spaces that can swell or
dentin. polymerizable solvent for
shrink depending on bonding
•Collagenous +non subsequently placed
condition.
collagenous proteins + adhesive monomers, given
GAG’s = hydrogel. sufficient diffusion time.
•Hydrogel-insoluble
hydrophilic polymer
 70

RS AFFECTING INTERACTION OF DENTNA

EABILITY AND MONOMER DIFFUSION
Fluid flow Tubular branching

• Areas with high tubule density that • Dentinal tubules permit adhesive

are in direct contact with pulp are monomers to flow.

difficult to dehydrate. • Most tubules contain lateral

• Multiple applications of primer allow branches that radiate 2-6 µm from

sufficient occlusion with resin lumen.

monomers to block diffusion of • These branches provide route for

water from the pulp. monomer infiltration.

 CHALLENGES IN DENTIN 71

BONDING
NGES IN DENTIN: SCLEROSED DENTIN

 Sclerotic dentin contains few, if any, patent tubules & therefore, has low permeability.

 It has areas of complete hypermineralization, without tubule exposure even when

etched.

 Thus, it is less receptive to the adhesive treatments than is normal dentin

Hybridization of Dental Hard Tissues-nakabayashi

 CHALLENGES IN DENTIN 72

BONDING
STRESSES AT THE RESIN-DENTIN INTERFACE:

 As composites polymerize,shrinkage occurs leading to stresses upto 7MPa.

 When the composite is bonded only to one surface, stresses are relieved by flow from

the unbonded surface.

 Davidson et al. postulated that minimum bond strength of 17-20 MPa to enamel and

dentin is needed to resist contraction forces of resin composite materials.

Hybridization of Dental Hard Tissues-nakabayashi

 HYBRID 73

LAYER
“ The structure formed in dental hard tissues (enamel, dentin, cementum) by demineralization of

the surface and subsurface, followed by infiltration of monomers and subsequent

polymerization” is known as Hybridized dental hard tissues; hybrid layer (Nakabayashi,

Pashley 1998)

 Also known as Resin-dentin Interpenetration / Interdiffusion Zone..

Hybridization of Dental Hard Tissues-nakabayashi

 74

ZONES OF HYBRID LAYER

Amorphous electron dense
layer denatured collagen or
very loosely arranged
collagen

Interfibrillar spaces in which

hydroxyapatite crystals have
been repalced by resin
monomer because of
hybridization process

Consists of almost
unaffected dentin with
partially demineralized zone
of dentin Hybridization of Dental Hard Tissues-nakabayashi
 75

DRY BONDING & WET BONDING

 Enamel should preferentially be dry to achieve good bonding, a certain amount of water

is needed to prevent the collagen fibrils in dentin from shrinking .

•“Dry Bonding” technique: It involves air drying of dentin after acid etching, and

 To applying
overcomeathis problem and
water-based maintain
primer, the structural
capable integrity of
of re-expanding theinterfibrillar
collapsed spaces in
collagen

themeshwork.
collagen network, 2 approaches are followed, depending on the primer of the

adhesive system. approach is to leave dentin moist, thereby preventing any collapse
•An alternative

and using an acetone-basedprimer, known for its water-chasing capacity. This

technique is commonly referred to as “Wet Bonding” introduced by Kanca& by

Gwinnett et al.

Sturdevant’s Art and Science of Operative Dentistry, 5th Edition

 MOIST VS DRY DENTIN FOR 76

BONDING
 Vital dentin is inherently wet; complete drying of dentin is difficult to achieve clinically.

 Water has been considered an obstacle for attaining an effective adhesion of resins to

dentin, so research has shifted toward development of dentin adhesives that are

compatible with humid environments.

 The “moist bonding” technique prevents the spatial alterations (i.e., collagen

collapse) that occur on drying demineralized dentin.

 Such alterations might prevent the monomers from penetrating the labyrinth of

nanochannels formed by dissolution of hydroxyapatite crystals between collagen

fibers. Sturdevant’s Art and Science of Operative Dentistry, 5th Edition

 MOIST VS DRY DENTIN FOR 77

BONDING
 The use of adhesive systems on moist dentin is made possible by incorporation of the

organic solvents acetone or ethanol in the primers or adhesives.

 Because the solvent can displace water from the dentin surface and the moist collagen

network, it promotes the infiltration of resin monomers throughout the nanospaces of

the dense collagen web.

 The moist bonding technique has been shown repeatedly to enhance bond strengths

because water preserves the porosity of collagen network available for monomer

interdiffusion.
Sturdevant’s Art and Science of Operative Dentistry, 5th Edition
 78

MOIST VS DRY DENTIN BONDING

 If the dentin surface is made too dry, collapse of the collagen

fibers and demineralized dentin takes place.

 This results in low bond strength because of ineffective penetration of the adhesive into

the dentin.

 If the dentin surface is too wet, because excess water can dilute the primer and

render

it less effective.

 Usually, a glistening hydrated surface without accumulation of

Sturdevant’s Art and Science of Operative Dentistry, 5th Edition

 79

PREPARATION

 Adequate cooling of bur cutting at high speed is essential to prevent histologic

changes in dentin & injury to underlying odontoblastic region .

 Desiccation, if occurring in vital dentin to the extent that moisture in Tome's fibers is

eliminated, will create a disturbance in the osmotic pressure of those dentinal tubules,

resulting in the aspiration of the nuclei.

 Vibrations which are produced during cavity preparation may cause microcracks in

enamel and dentin.

Text book of operative dentistry-Marzouk.-1 st edition

 80

OPERATIVE INSTRUMENTATION

 Cavity preparations should extend minimally into dentin whenever possible.

 Increasing the depth and width of the cavity preparation will increase the tendency of

the tooth to fracture due to loss of dentin support.

 During restorative procedures, the dentin must be protected by proper use of liners,

bases.

Text book of operative dentistry-Marzouk.-1 st edition

 81

DENTINOGENESIS IMPERFECTA
 It is characterized by excessive formation of defective dentin, which results in

obliteration of pulp chambers and root canals of tooth.

 The disease occurs in three forms—Type I,II,III

 The affected teeth have an opalescent hue with amber-like color after eruption; with

time they become brown or gray with a bluish reflection from enamel.

 Dentinoenamel junction is flat instead of scalloped and it causes poor locking between

enamel and dentin; because of this tooth enamel is quickly lost from the dentin

surfaces. Neville: Oral and Maxillofacial Pathology-3 rd edition

 82

DENTINOGENESIS IMPERFECTA
 Radiographically:

TREATMENT
bulbous crowns,cervical constriction, thin roots, early obliteration of
•VD Rebuilt By Non Precious Metal Castings.
roots canals and pulp chambers are present.
• Metal And Ceramic Crowns.

 Type I and Type •IIOverlay Dentures of pulp chamber due to abnormal

show obliteration

•Full Dentures
dentin formations.
•Implants
 Type III shows abnormally large pulp chamber (shell tooth).

Neville: Oral and Maxillofacial Pathology-3 rd edition

 TEETH)
83

 Characterized by normal enamel, abnormal denitn with atypical pulp morphology

 Witkop classified into following types:

 Type I – Radicular dentin dysplasia.

 Type II – Coronal dentin dysplasia.

Type I is more common.

 Both are hereditary origin and autosomal dominent type.

Neville: Oral and Maxillofacial Pathology-3 rd edition

 84

DENTIN-DYSPLASIA
Type I (Radicular):

 Both deciduous and permanent dentitions are affected.

 Exhibit normal morphology with slight amber translucency.

 Teeth show mobility and premature exfoliation due to short root.

 Radiographic features: Roots are short blunt and conical ,completely obliterated in

deciduous teeth and a cresent shaped pulp remnant in permanent teeth.

 Histologic features: Lava flowing around boulders and Cascades of dentin.

Neville: Oral and Maxillofacial Pathology-3 rd edition

 DENTIN-DYSPLASIA (ROOT LESS 85

TEETH)
 Type II (Coronal): It affects the both dentitions.

 The teeth have grey to yellowishbrown discolouration.

 Radiographic features: Pulp chambers of deciduous

teeth become obliterated ,abnormally large pulp

chamber seen in permanent teeth often described as

thistle tube.

 Histologic features: Deciduous teeth show

amorphous and atubular dentin, Permanent teethrd

Neville: Oral and Maxillofacial Pathology-3 edition
exhibit multiple pulp stones.
REGIONAL ODONTODYSPLASIA / 86

GHOST TEETH
 It is an unusual anomaly which affects the localized area in unusual manner.

 Maxillary anteriors are more commonly involved here.

 Effects both dentitions.

 The teeth affected are showing delay or failure to

eruption.

 The shape of teeth is altered, with irregular

mineralization

Neville: Oral and Maxillofacial Pathology-3 rd edition

 REGIONAL ODONTODYSPLASIA / 87

GHOST TEETH
 Radiographically teeth show marked reduction in radiodensity gives “Ghost teeth

appearance”.

 The enamel and dentin is very thin and pulp chamber is usually large.

 Histologically it is characterized by marked reduction in amount of dentin, widening of

predentin layer and large areas of interglobular dentin with irregular tubular pattern.

 Due to poor, cosmetic appearance extraction of teeth and restoration with prosthetic

appliances is usually indicated.

Neville: Oral and Maxillofacial Pathology-3 rd edition

 88

DENS-IN-DENTE
 Dens-in-Dente refers to a folding or invagination on the surface of the tooth towards

the pulp; which begins before the calcification of the tooth and eventually after

calcification.

 The defect is generally localized to a single tooth .

 Bilateral involvement (of the same tooth on either side of jaw) is often seen and

sometimes the defect can involve multiple teeth including the supernumeraries.

TYPES

 Dens-in-Dente is often broadly divided into two types : coronal type and radicular type.

Neville: Oral and Maxillofacial Pathology-3 rd edition

 89

DENS IN DENTE
 TREATMENT

 Early detection of the condition and restoration of the defect is the best treatment.

 In case of pulp involvement with or without apical pathology, endodontic treatment

should be attempted.

 However in more severe form of the defect, extraction of the affected tooth should be

done.

Neville: Oral and Maxillofacial Pathology-3 rd edition

 90

TETRACYCLINE PIGMENTATION
 Yellowish-Brown/grey Discoloration.

 Fluoresce Bright Yellow under U.V light.

 Deposited along Incremental lines of Dentin and to lesser Extent in Enamel.

Jordan and boksman 1984-op

 91

TETRACYCLINE PIGMENTATION
TREATMENT:

 Bleaching

 Laminate veneers

 Composite bonding
 SYSTEMIC DISTURBANCES 92

VITAMIN-D DEPENDENT RICKETS:

 The width or thickness of the predentin is increased.

 Improper and incomplete calcification of the regular dentin.

 Thick band-like areas of interglobular dentin can be seen histologically, which

correspond to the periods of active phase of the disease.

VITAMIN-D RESISTANT RICKETS(HYPOPHOSPHATEMIA):

 Increased amount of interglobular dentin formation.

 These teeth exhibit large pulp chambers and long pulp horns.

 The later may even extend to the dentino-enamel junction as narrow clefts.

Shafer’s text book of oralpathology-6th edition.

 DENTINAL ABNORMALITY DUE TO 93

SYSTEMIC DISTURBANCES
HYPOPHOSPHATASIA:

 Increased formation of interglobular dentin.

 Widening of the predentin.

JUVENILE HYPOPARATHYROIDISM:

 Multiple prominent incremental lines can be seen in the dentin.

 Histologically radicular dentin reveals many structural abnormality and there can be

areas of vascular inclusions in the dentin.

Shafer’s text book of oralpathology-6th edition.

 94

CONCLUSION
 The integrity of dentin is related to coronal strength and durability and can be

compromised by carious demineralization ,traumatic injury, wear, or poor restorative

techniques.

 Unlike the relatively homogenous nature of enamel, the dentinal substrate varies

considerably with location, age, and response to external stimuli.

 Differences in dentin permeability, wetness and dryness, hypermineralization, and

pathologic events complicate comparative research studies on dentin and on dentin

bonding systems.
 95

REFERENCES

 Text book of operative dentistry-Marzouk.-1st edition

 Neville: Oral and Maxillofacial Pathology-3rd edition

 Oral anatomy histology and embryology by B.K.B.Berkovitz -3rd edition.

 Ingles endodontics- 7th edition.

 Shafer’s text book of oralpathology-6th edition.

 96

REFERENCES
 Orban’s oral histology and Embryology- 10th edition.

 Oral histology By A. R Tencate-8th edition.

 Operative dentistry by Sturdevant -5th edition.

 Cohens pathways of pulp -10th edition.

97