Seminar 1 Dentin

DENTIN
BY DR. SHREYA POKIYA {PG-|}

DEPARTMENT OF PEDIATRIC AND PREVENTIVE DENTISTRY
DENTIN
Physical characteristics Innervation of dentin
Chemical properties Permeability of dentin
 Histology Structures Age and functional changes
Development of dentin Clinical considerations
Primary dentin
Secondary dentin
Tertiary dentin
INTRODUCTION
•Dentin is a bonelike tissue present in both crown and root of teeth.
•Dentin provides bulk & general form of tooth.
•It is unique hard tissue with tubules throughout its thickness.
•Dentin is vital tissue containing cell process of odontoblast and neurons.
ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

PHYSICAL AND CHEMICAL PROPERTIES
• Color : light yellowish which get darker with age.
•Property : viscoelastic
•Hardness : enamel > dentin > bone
•Permanent teeth> primary teeth.
• Dentin is harder in centre than in peripheries.
•Radiolucency : dentin > enamel ( low mineral content)

THICKNESS:
•Ranges from 3-10mm
•Thickness greater in boys .
•Increases during puberty.
•Varies not only from tooth to tooth but also on different surfaces of same tooth.
•Ratio of thickness between outer and inner surfaces of dentin is 5:1

Hack dentistry website and youtube channel
ORGANIC MATRIX(35%)
INORGANIC MATRIX(65%)
•Collagenous fibrils embedded in •Consist hydroxyapatite

mucopolysaccharides . (proteoglycans ,
glycosaminoglycans) •Each HA composed of several thousands unit cells
•Principle collagen fibres is type-1 •Formula of cell : 3Ca3(PO4)2. Ca(OH)2
•Matrix proteins are similar in dentin and •Plate shaped crystals, smaller than HA crystals of
bone ; but dentin sialoproein (DSP)and enamel.
dentin phospho-proteins (DPP) are •Small amount of phosphates, carbonates, sulfates.
Present only in dentin.
•In compared to enamel , crystals are rich in
•Matrix contains various growth factors , carbon & poor in calcium.
which help in mineralization of dentin.

Ground substance
Phosphpo- Growth factors

protein
Proteoglycans Glycoproteins
Transforming growth
factor
Dentin FGF
Chondroitin sulfates Dentin sialoproteins IGFs

phosphoprotein(dpp BMPs
Osteonectin )
EGF
Decorin PDFG
Osteopontin Gamma PLGF
biglycan VEFG
Carboxyglutamate AGF

HISTOLOGIC STRUCTURE
On microscopic view , structure present in dentin are following:
1. Dentinal tubules
2. Peritubular and intertubular dentin
3. Interglobular dentin
4. Incremental growth lines
5. The granular layer of Tomes
6. Pre dentin
7. Odontoblast process
8. Dentinal fluid

HISTOLOGICAL STRUCTURE
orban's oral histology & embryology 14th edition

DENTINAL TUBULES

•Odontoblast processes run in canaliculi that traverse the dentin layer and
are referred to as dentinal tubules.
•Dentinal tubules extend through the entire thickness of the dentin from
the dentinoenamel junction to the mineralization front .
•It forms a network for the diffusion of nutrients throughout dentin.
•Follow an S-shaped path from the outer surface of the dentin to the
perimeter of the pulp in coronal dentin.
•S-shaped curvature is least pronounced beneath the incisal edges and
cusps.
•Biconvex (1st convexcity towards apex) – Primary curvature
•Gradually Straighter – Apical or cuspal region
•Smaller curvatures along entire course – Secondary curvature
TEN CATE’S ORAL HISTOLOGY 9TH EDITION

- Diagram illustrating the curvature, size, and
distance between dentinal tubules in human
outer (A), mid (B), and inner dentin (C).
- The tubules are approximately 1 μm in
diameter at the dentinoenamel junction (DEJ),
1.5–2 μm midway through dentin, and 1.5–3
μm at the pulp.
- Bacterial penetration (D) follows line of least
resistance to reach the pulp.

•The tubules are farther apart in the peripheral layers and are more
closely packed near the pulp
•Numbers of tubules range from 59,000 to 76,000 per square millimeter
at the pulpal surface, with approximately half as many per square
millimeter near the enamel
•The ratio between the numbers of tubules per unit area on the pulpal
and outer surfaces of the dentin is about 4:1.
•The dentinal tubules have lateral branches throughout dentin, which are
termed canaliculi or microtubules.
• A few odontoblastic processes extend through the dentinoenamel
junction into the enamel for several millimeters. These are termed
Enamel spindles

•Due to tubular nature of dentin there is an unusual
degree of permeability that can enhance a carious process
•Tubules in carious lesions may fill with bacteria and
appear darkly stained in histologic sections.
•The processes in these tubules may disintegrate or
retract, leaving behind an empty tubule, called DEAD
TRACT.
•Reparative dentin seals off such dead tracts at their
pulpal extremity, thereby protecting the pulp from
infection.

SUMMARY OF DENTINAL TUBULES
• Wider & closer near pulp
• Father apart & narrower near DEJ & CEJ Arrangements
• Enclosed by highly mineralized wall- peritubular dentin

• Biconvex (1st convexcity towards apex) – primary curvature
• Gradually Straighter – apical or cuspal region
• Smaller curvatures along entire course – secondary curvature
Course
• Lateral branches – along its course

• Terminal branches – near DEJ Branches

PERITUBULAR DENTIN

•The dentin that immediately surrounds the
dentinal tubules is termed Peritubular dentin.
•Forms the walls of the tubules
•Hypermineralized than intertubular dentin.
•It is twice as thick in outer dentin (0.75 µm) than
in inner dentin (0.4 µm).
•The deposition of the minerals occurs in the
inner wall of the tubule rather than on the outer
wall. So called INTRATUBULAR DENTIN

• In demineralized dentin visualized with a light microscope, the tubule diameter will therefore appear
similar in inner and outer dentin because of the loss of the peritubular dentin. This is important
clinically, as etching of a cavity floor will open up the tubules.
•Between the odontoblastic process and the peritubular dentin, a space known as Periodontoblastic
space is reported to be present. This space contains the dentinal fluid.
•Dentinal tubules increase in size by the loss of intratubular or peritubular dentin. This dentin is
subject to decalcification by caries or acid cleansing of the cavity, which removes the smear layer.
This dentin is about 40% more highly calcified than the remainder of the dentin.

INTERTUBULAR DENTIN

•Dentin located between the dentinal tubules
•It represents the primary formative product of the odontoblasts
•Consists of a tightly interwoven network of type I collagen fibrils
(50 to 200 nm in diameter) in and around which apatite crystals
are deposited.
•The fibrils are arranged randomly at roughly right angles to the
dentinal tubules.
•The ground substance consists of noncollagenous matrix proteins.

SCLEROTIC DENTIN

•Dentinal tubules that have become occluded with calcified material.
•When this occurs in several tubules in the same area, the dentin assumes a
glassy appearance and becomes translucent, so called as translucent
dentin.
•The amount of sclerotic dentin increases with age and is most common in
the apical third of the root and in the crown midway between the DEJ and
the surface of the pulp.
•Sclerosis reduces the permeability of dentin, it may help to prolong pulp
vitality.

INTERGLOBULAR DENTIN

•Interglobular dentin is the term used to describe areas of
unmineralized or hypomineralized dentin where globular zones
of mineralization have failed to fuse into a homogeneous mass
within mature dentin.
•Prevalance is seen in:
1)Vitamin D deficiency
2) High fluoride exposure at the time of dentin formation
•Most common in circumpulpal dentin
•Irregularity of dentin mineralization and not of matrix
formation( the normal architectural pattern of the tubules
remains unchanged)

INCREMENTAL LINES

•The incremental lines of von Ebner appear as fine lines or striations
in dentin.
•It runs at right angles to the dentinal tubules and correspond to the
incremental lines in enamel or bone
•The distance between lines varies from 4 to 8 mm in the crown to
much less in the root.
•The daily increment decreases after a tooth reaches functional
occlusion.
•The course of the lines indicates the growth pattern of the dentin.

•Lines formed by increments over several days
(possibly every 5 days), resulting in 20um lines.
•A 2-µm organic matrix of dentin is deposited in a
12-hour cycle (daily deposition is approximately
4 µm)
•Some of the incremental lines are accentuated
because of disturbances in the matrix and
mineralization process. They are known as
contour lines of Owen it represents
hypocalcified bands

NEONATAL LINE

•In the deciduous teeth and in the first permanent molars, where dentin is formed partly
before and partly after birth, the prenatal and postnatal dentins are separated by an
accentuated contour line.
•This is termed as NEONATAL LINE
•It is seen in enamel as well as dentin .
•This line reflects the abrupt change in environment that occurs at birth.
•It may be a zone of hypocalcification

THE GRANULAR LAYER OF
TOMES
•When dry ground sections of the root dentin are visualized in
transmitted light, a zone adjacent to the cementum appears granular
•This is known as Tomes granular layer.
•Increase in granularity occurs from the cementoenamel junction to the
apex of the tooth.
•The zone is the result of a coalescing and looping of the terminal
portions of the dentinal tubules.

•Tomes’ granular layer and interglobular dentin have similarities
in their formation but they differ in their mineral content.
•Tomes’ granular layer highest concentrations of calcium and
phosphorus.
•Interglobular dentin a higher content of sulfur.
•Recent studies relate Tomes’ granular layer as a special
arrangement of collagen and noncollagenous matrix proteins at
the interface between dentin and cementum

PRE DENTIN
•First formed dentin
•Location : adjacent to pulp
•2- 6µm wide (depends upon odontoblast activity)
•Non mineralized
•Mineralization occurs at the predentin-dentin junction,
and predentin becomes a new layer of dentin.

ODONTOBLAST PROCESS
•The odontoblast processes are the cytoplasmic extensions of the
odontoblasts
•Odontoblast cells reside in the peripheral pulp at the pulp –
predentin border and their processes extend into the dentinal
tubules
•The odontoblast cell bodies are approximately 7 µm in diameter
and 40 µm in length.
•Diameter near the pulp 3–4 µm, taper to approximately 1 µm
further into the dentin.
•The odontoblastic processes narrow to about half the size of the
cell as they enter the tubules

•The odontoblast process have microtubules (20 µm) and
small filaments (5–7.5 µm)
•The microtubules and intermediate filaments run
longitudinally throughout the tubules.
•Occasionally mitochondria, dense bodies resembling
lysosomes, microvesicles, and coated vesicles that may open
to the extracellular space are also seen
•The odontoblast processes divide near the dentinoenamel
junction and extend into enamel as enamel spindles.
•Periodically along the course of the processes, side branches
(lateral branches) appear that extend laterally into adjacent
tubules

DENTINAL FLUID
•Between the odontoblastic process and the peritubular dentin a space called
periodontoblastic space
•This space contains the Dentinal Fluid
•The normal flow of the fluid is outwards from the pulp.
•Composition:- similar to plasma, calcium content in dentinal fluid of
predentin is 2-3 times higher than that of dentin .Fluid has a higher K+ and
lower Na+ content.
•Dentinal sensitivity is explained on the basis of this fluid movement.
•Barrier for bacterial toxins.

DENTINAL JUNCTION
DENTINOENAMEL JUNCTION
•The junction between the enamel and dentin is irregular and scalloped
•The convexities face the dentin whereas the concavities face the
enamel.
•A membrane performativa is seen between the enamel and dentin
during tooth development. After calcification starts, this membrane
disappears and the interface is called dentinoenamel junction

2. CEMENTODENTINAL JUNCTION
The terminal apical area of cementum where it joins the internal root dentin is called cementodentinal
junction(CDJ)

TYPES OF DENTIN
Classification
Dentin
Acc . to developmental
Acc. to location Acc. to mineralization
pattern
- Intertubular -Globular dentin

-Primary
-Intratubular -Interglobular dentin
- Secondary
-Mantle dentin -Toms granular layer
-Tertiary
-Circumpulpal dentin -Sclerotic dentin

PRIMARY DENTIN
•Dentin which is formed before root completion is known as primary
dentin.
•The primary dentin are of two types
1) Mantle dentin(20µm wide)
2) Circumpulpal dentin(50-200 nm)
•Primary dentin, which outlines the pulp chamber and is referred to
as circumpulpal dentin
•Outer layer of coronal dentin is referred to as mantle dentin which
differs in process of mineralization and in the structural
interrelation between the collagenous and noncollagenous matrix
components.

Difference between mantle dentin and
circumpulpal dentin

SECONDARY DENTIN
•Secondary dentin is a narrow band of dentin bordering the pulp and
representing that dentin formed after root completion.
•Contains fewer tubules than primary dentin.
•Secondary dentin is formed more slowly than primary dentin
•It does not formed uniformly and appears in greater amounts on the roof and
floor of the coronal pulp chamber, where it protects the pulp from exposure
in older teeth.
•It does not form in response to any external stimuli, and it appears very much
like primary dentin.
•Apical dentin shows irregularity of dentinal tubules of both primary and
secondary dentin.

CLINICAL CONSIDERATION :-
•The changes in the pulp space, clinically referred as
pulp recession and it is important in determining the
form of cavity preparation for certain dental
restorative procedures.
•For example, preparation of the tooth for a full crown
in a young patient presents a substantial risk of
involving the dental pulp by mechanically exposing a
pulp horn.
• In an older patient the pulp horn has receded and
presents less danger.

TERTIARY DENTIN
• Tertiary dentin is reparative response, or reactive dentin.
• Localized formation of dentin on the pulp–dentin border.It formed in reaction to
trauma such as caries or restorative procedures.
• It is produced only by those cells directly affected by the stimulus.
• Tertiary dentin may have tubules continuous with those of secondary dentin,
tubules sparse in number and irregularly arranged, or no tubules at all.
• The cells forming tertiary dentin line its surface or become included in the
dentin; referred to as osteodentin.
• Tertiary dentin is subclassified as;-
REACTIONARY DENTIN deposited by preexisting odontoblasts
REPARATIVE DENTIN formed by newly differentiated odontoblast-like cells.

•Reparative dentin at times resembles bone more than dentin and is then
termed osteodentin
CLINICAL CONSIDERATION :-
•The sensitivity of dentin is an important clinical consideration after
placement of a restoration that conducts heat or cold.
•Dentin responds to such stimuli by deposition of reparative dentin and by
changes in the dentin tubules underlying the restoration. The sensitivity of the
tooth will diminish after a few weeks because of these changes.
ESSENTIALS OF ORAL HISTOLOGY AND EMBRYOLOGY , CLINICAL APPROACH BY JAMES K. AVERY

SUMMARY

FORMATION OF DENTIN
PATTERN OF DENTIN FORMATION
Spreads down from Root dentin begins to form Root dentin formation
Begins at bell stage cusp slope to cervical at slight later stage and it By the time tooth completes at 18th
in papillary tissue requires proliferation of reaches its functional months after tooth
loop of enamel organ epithelial cell( hertwig’s
adjacent to concave position; two third of eruption in deciduous
& dentin thickens epithelial root sheath)
teeth whereas it
tip of inner enamel around pulp to initiate root dentin formation
until all coronal prolongs upto2-3 years
epithelium at cusp tip differentiation of root is completed.
dentin is formed. odontoblasts. in permanent teeth.
TEN CATE,’S ORAL HISTOLOGY 9TH EDITION

Odontoblast differentiation
Expression of signaling molecules and growth factors in the cells of the inner enamel epithelium
dental papilla cells are small and undifferentiated as well as separated from the inner enamel epithelium by an
acellular zone that contains some fine collagen fibrils.
inner enamel epithelium reverse polarity
ectomesenchymal cells rapidly enlarge and elongate to become preodontoblasts
Volume of cytoplasm increases to accommodate protein-synthesizing organelles to convert preodontoblasts

into odontoblasts .
newly differentiated cells are highly polarized, with their nuclei positioned away from the inner enamel
epithelium.

DENTINOGENESIS
•Dentin is formed by odontoblasts that differentiate from ectomesenchymal cells of the dental
papilla.
•The dental papilla is the formative organ of dentin
2 step process :1) organic matrix formation
2) mineralization

FACTORS INVOLVED IN DENTINOGENESIS
TGF (transforming growth factor), IGF (insulin like growth factor)and BMP help in organization of odontoblast cytoskeleton.
DPP (dentin phosphoprotein): highly anionic,binds to calcium and transports it to mineralization front,controls the growth of apatite
crystals
Osteonectin: inhibits growth of apatite crystals but promotes its binding to collagen
Osteopontin: promotes mineralization
Gla protein: seeds or nucleators to attract and concentrate calcium
Proteoglycans: inhibit premature mineralization in predentin
THE NEWER GENES INVOLVED:

MAP1B-odontoblast differentiation
PHEX-dentin mineralization

ORGANIC MATRIX FORMATION
•First sign of dentin formation is the appearance of large-diameter collagen fibrils (0.1 to 0.2 µm
in diameter) called von Korf 's fibers.
• Fibers consist of collagen type III associated with fibronectin which originate among the
odontoblasts, extend toward the inner enamel epithelium, and fan out in the structureless ground
substance.
•It continues to increase in size and produce smaller collagen type I fibrils that oriented parallel to
the future dentinoenamel junction.
•Ultimately, layer of mantle predentin is formed.

Von Korff's fibers appear as convoluted, bluish threadlike structures that originate deep between
odontoblasts

•As the matrix formation continues, the odontoblast process lengthens like
dentinal tubule.
•Initially daily increments of approximately 4 µm
•This continues until the crown is formed and the teeth erupt into
occlusion.
•After this time, dentin production slows to about 1 µm/day.
•After root development is complete, dentin formation may decrease
further

MINERALIZATION
Mineralization is achieved by continuous deposition of
mineral, initially in the matrix vesicle and then at the
mineralization front.
Dentin mineralization can be observed in 2 patterns:
1) Globular calcification
2) linear calcification

The plasma membrane of odontoblasts , extends stubby processes into the forming extracellular matrix
Develops a cell process, called as odontoblast process or Tomes’ fiber
It buds off a number of small, membrane-bound vesicles known as matrix vesicles
The mineral phase first appears within the matrix vesicles as single crystals believed to be seeded by phospholipids
present in the vesicle membrane
Crystals grow rapidly to form a continuous layer of mineralized matrix.
Deposition of mineral lags behind the formation of the organic matrix so that a layer of organic matrix, called
predentin, always is found between the odontoblasts and the mineralization front
After mineral seeding, noncollagenous matrix proteins produced by odontoblasts come into play to regulate mineral
deposition. In this way coronal mantle dentin is formed in a layer approximately 15 to 20 µm thick onto which then is
added the primary (circumpulpal) dentin.

1) Globular (or calcospheric) calcification
• Best seen in mantle dentin region.
Deposition of crystals in Ultimately various

Globular masses are
several discrete area of globular masses fuse to
formed which
matrix by heterogenous form single calcified
continues to grow
capture in collagen mass

2) Linear calcification
• When the rate of formation progresses slowly, the mineralization
front appears more uniform, and the process is said to be linear.
Matrix
Vesicles give
This foci grows
rise to
and coalesce
mineralization
foci

FORMATION OF ROOT DENTIN
•The epithelial cells of Hertwig’s root sheath initiate the
differentiation of odontoblasts that form root dentin
•Begins when enamel and dentin formation reach the future
CEJ.
•Collagen fibers – parallel to the CDJ.
•It is less mineralized and has less number of tubules.
•Completed after 18 months of eruption in primary teeth and 2-3
yrs of eruption of permanent teeth.

Difference between crown and root dentin formation
ROOT FORMATION H,F. THOMAS' DEPARTMENT OF PEDIATRIC DENTISTRY, UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER, SAN ANTONIO, TEXAS. USA
Similarly differences have been described in the biochemical composition of root dentin when
compared with crown
For example, differences between crown and root odontoblasts in the quantity and quality of
the phosphoproteins synthesized.
Also, lower levels of both α1, and α2 chains of type I collagen mRNA have been described in root
odontoblasts
ROOT FORMATION H,F. THOMAS' DEPARTMENT OF PEDIATRIC DENTISTRY, UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER, SAN ANTONIO, TEXAS. USA
SECONDARY DENTINOGENESIS
•Secondary dentin is deposited after root formation is completed.
•It is formed by the same odontoblasts that formed primary dentin.
•It is laid down as a continuation of the primary dentin.
•It forms at a much slower pace than primary dentin.
•Histologically it demarcated by a demarcation line of less regular organization of
dentinal tubules.

TERTIARY DENTINOGENESIS
•Tertiary dentin is deposited at specific sites in response to injury by
damaged odontoblasts or replacement cells from pulp.
•The rate of deposition depends on the degree of injury; the more severe
the injury, the more rapid the rate of dentin deposition.
•As a result of this rapid deposition, cells often become trapped in the
newly formed matrix, and the tubular pattern becomes grossly distorted
•During its formation, production of collagen, DSP(dentinsialoprotein),
and DMP1(dentin matrix protein1) appears to be downregulated,
whereas that of BSP(bone sialoprotein) and osteopontin is upregulated .

INNERVATION OF DENTIN
•Nerve fibers were shown to accompany 30%–70% of the odontoblastic
process and these are referred to as intratubular nerves.
•Dentinal tubules contain numerous nerve endings in the predentin and inner
dentin
•Most of these small vesiculated endings are located in tubules in the coronal
zone, specifically in the pulp horns.
•The primary afferent somatosensory nerves of the dentin and pulp project
to the main sensory nucleus (subnucleus condalis) of the mid brain.
•The nerve endings are packed with small vesicles, either electron dense or
lucent.

PERMEABILITY OF DENTIN
•The density and diameter of the dentinal tubules increases with dentin depth from the DEJ
to the pulp region.
•The permeability of dentin is lowest at the DEJ and highest at the pulpal ends.
•The permeability of dentin is related to the functional diameter of the dentinal tubules; the
greater the functional diameter, the higher the flow rate and thus the rate of permeation.
•Tubules are consequently cone shaped and permit increased permeability from the cavity
wall or floor to the pulp.
•Lateral and terminal branching of dentinal tubules also increase permeability.
•loss of the odontoblastic process results in increased permeability.
•Higher osmotic pressure is the only protective feature for pulp.

Clinical significance:-
•Peritubular dentin is more highly calcified than is the intertubular, the etching of a cavity causes
an increase in the diameter of the tubule.
•Permeability factor is a major consideration in cleansing of the cavity preparation and the
placement of a cavity liner to prevent microleakage.
•Reduction in dentin permeability would lessen the sensitivity of dentin.
• The odontoblasts act as barriers for entry of bacteria or their toxins.

Factors affecting :-
A) Normal appositional growth of intratubular dentin,
B) Deposition of calcium phosphate crystals e.g. whitlockite in the tubules in the translucent zone ahead of
the demineralised areas of caries, sometimes referred to as caries crystals,
C) the coagulation of plasma proteins (fibrin) from pulpal blood vessels in the tubules beneath a recently cut
cavity
D) pathological precipitation of intratubular materials i.e. mineral deposits, collagen fibrils, proteoglycan
linings and bacteria
E) the formation of a smear layer of dentin debris on its cut surface during cavity preparation.
DENTIN PERMEABILITY-FARID BIN CHE GHAZALI -ARTICLE FROM THE MALAYSIAN JOURNAL OF
MEDICAL SCIENCES
DIFFERENCE BETWEEN PRIMARY AND
PERMANENT TEETH DENTIN
SHOBHA TANDON TEXTBOOK OF PEDODONTICS-2ND EDITION

AGE CHANGES
2 Most evident changes that are witnessed with advancing age is:
1) increase in dentin thickness due to continuous , gradual deposition of secondary dentin
2) Increased sclerosis or obliteration of dentinal tubules during which minerals are added into the
tubules with an associated decrease in the amount of dentinal fluid, reduced sensitivity and
permeability .
Stimuli for formation of secondary dentin can be either physiological or pathological ; therefore
age and functional changes are consider together.

Pathological effect of dental caries, abrasion, attrition or cutting with operative procedures
cause following changes:
1) Dead tracts
2) Sclerosis
3) Reparative dentin

DEAD TRACTS
•The odontoblastic processes disintegrate in dried ground
section, and the empty tubules are filled with air.
•They appear black in transmitted and white in reflected
light
•Loss of odontoblast processes may also occur in teeth
containing vital pulp as a result of caries, attrition, abrasion,
cavity preparation, or erosion

•Their degeneration is often observed in the area of narrow pulpal
horns because of crowding of odontoblasts. Dentin areas
characterized by degenerated odontoblast processes give rise to
dead tracts.
•These areas demonstrate decreased sensitivity and appear to a
greater extent in older teeth.
•Dead tracts are initial step in the formation of sclerotic dentin

SCLEROTIC DENTIN
• In cases of caries, attrition, abrasion, erosion, or cavity preparation,
sufficient stimuli are generated to cause collagen fibers and apatite
crystals to begin appearing in the dentinal tubules.
• Transparent or sclerotic dentin can be observed in the teeth. of elderly
people, especially in the roots.
• The sclerosis of radicular dentin begins at the apex in the dentin 
progresses inward and coronally  roots become more brittle and may
fracture during extraction
• It reduces the permeability of the dentin and may help prolong pulp
vitality.
• It appears transparent or light in transmitted light and dark in reflected
light

REPAIRATIVE DENTIN
If by extensive abrasion, erosion, caries, or operative procedures the odontoblast
processes are exposed or cut
If odontoblasts survive If odontoblasts die
Replaced by the migration of

Reactionary or regenerated
undifferentiated cells arising in
dentin
deeper regions of the pulp to the
dentin interface

•This action to seal off the zone of injury occurs as a healing process initiated by the pulp, resulting in
resolution of the inflammatory process and removal of dead cells
•Characterized as having fewer and more twisted tubules than normal dentin
•Bacteria, their toxic products , chemical substances from restorative materials, migrate down the
tubules to the pulp, and stimulate pulpal response leading to reparative dentin formation.
•Nestin and Notch protein, which are expressed in young odontoblasts and in sub-odontoblastic layer
during odontogenesis, are absent in adult tissue but are re-expressed during reparative dentin formation.
It is suggested that transforming growth factor-beta (TGF-β) is involved in the production of tubular dentin
bone morphogenetic protein (BMP) is involved in the production of osteodentin.

SUMMARY

CLINICAL CONSIDERATION
•Tooth wear , fractures , caries , cavity cutting procedures etc. lead to exposure of dentinal tubules
•1 mm 2 of dentin exposure can lead to damage to 30,000 living cells.
•Exposed tubules should not be insulted by bacterial toxins, strong drugs, undue operative trauma,
unnecessary thermal changes, or irritating restorative materials
•Exposed dentin surface should be sealed with a nonirritating, insulating substance.
Eg : Bonding agents ,Varnishes ,Restorations

DENTIN HYPERSENSITIVITY
•According to Holland et al. Dentin hypersensitivity is 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.
•Various studies showed that the incidence of dentin hypersensitivity in most population ranges between 10-30%
of the general population.
•Age range varies from 20-50 years with the peak incidence occurring at the end of the third decade and decreases
during the fourth and fifth decades of life.
•The higher incidence is reported in females than in males which may reflect hormonal influence and dietary
practices.
•Commonly involved teeth : Canines and premolars of both the arches.
•Buccal aspect of cervical area is the commonly affected site
BUBTEINA N, GAROUSHI S (2015) DENTINE HYPERSENSITIVITY: A REVIEW. DENTISTRY 5: 330. DOI:10.4172/2161-1122.1000330

Theories of pain transmission through dentin

DIRECT NEURAL STIMULATION THEORY
affect nerve
endings within the
dentin tubules
Thermal, or
through direct
Mechanical stimuli
communication
with the pulpal
nerve endings
BUBTEINA N, GAROUSHI S (2015) DENTINE HYPERSENSITIVITY: A REVIEW. DENTISTRY 5: 330.

DOI:10.4172/2161-1122.1000330
•Although this theory has been reinforced by the presence of unmediated nerve fibers in the outer
layer of root dentin and the presence of putative neurogenic polypeptides, it is still considered
theoretical with lack of solid evidences to support it.
•Topical application of local anesthetics do not abolish sensitivity.
•Whether intratubular nerves are involved in dentin sensitivity is not known

DOI:10.4172/2161-1122.1000330
TRANSDUCTION THEORY :- RAPP ET AL.
Cause the sensation of pain

Transmit impulses via
odontoblasts act as receptor from the nerve endings
synaptic junctions to the
cells located in the pulpo-dentin
nerve terminals
border

DOI:10.4172/2161-1122.1000330
•Evidence for the odontoblast transducer mechanism theory is deficient and unconvincing.
•This is because the majority of studies have shown that odontoblasts are matrix forming cells and
they are not considered to be excitable cells, and no synapses have been revealed between
odontoblasts and nerve terminals.

DOI:10.4172/2161-1122.1000330
3) Hydrodynamic theory
The hydrodynamic theory is currently accepted mechanism of dentin hypersensitivity which has been proposed by Brännström in 1964.
The exposed dentin surface is subjected to thermal, chemical, tactile or evaporative stimuli
fluid flow within the dentinal tubules will be increased which change pressure.
alteration in pressure excites pressure-sensitive nerve receptors across the dentin.
response of the excited pulpal nerves, mainly in intradentin fibers, will be depended
upon the intensity of stimuli in pain production

•Scanning electron microscopic (SEM) examination of hypersensitive dentin
surface reveals the presence of widely open dentin tubules which is
considered consistent with the hydrodynamic theory.
•Number and the diameter of the dentin tubules are considered important
factors in initiating pain
•Higher the number and greater the diameter of the open dentin tubules ,
more intense will be the pain.
•It has been noted that triggers such as cold stimuli stimulate fluid to flow
away from the pulp creating more rapid and rigorous neural responses than
heat stimuli, which cause somewhat sluggish fluid flow towards the pulp

DOI:10.4172/2161-1122.1000330
DOI:10.4172/2161-1122.1000330
ETIOPATHOGENESIS
loss of protective covering over the
dentin
due to loss of enamel via attrition,

Lesion localization
abrasion, erosion
gingival recession which can be due

to tooth brush abrasion, pocket
reduction surgery, tooth
Dentin hypersensitivity
preparation for crown, excessive
flossing or secondary to periodontal
diseases.
after the protective covering of

smear layer is removed leading to
Lesion initiation
exposure & opening of dentinal
tubule.
DENTIN HYPERSENSITIVITY AND ITS MANAGEMENT: A REVIEW TUSHARLUTHRA, SANDEEP GUPTA, SUDHANSHU BHARADWAJ, ASHISH CHOUBEY, HITENDRA YADAV, HARIMRAN SINGH
Clinical features of Dentinal hypersensitivity
•Pain is the most common clinical feature associated with dentin hypersensitivity
•Intensity of pain varies from mild discomfort to severe sensitivity.
•Character of pain: rapid in onset, sharp in character and is of short duration.
•External stimuli which can elicit pain include:-
Thermal stimuli – Hot/cold food and beverages , Cold blast of air
Osmotic stimuli – Sweet food.
Acidic stimuli – Citrus fruits , Acidic beverages , Medicines
Mechanical stimuli – Toothbrush , Dental instruments
DESENSITIZING AGENTS
CLASSIFICATION
Based on Mode Based on

of mechanism of
administration action
Cover or
Nerve Protein Periodontal soft
At home In office plugging Dentin Sealers laser
desensitization precipitants tissue grafting
dentinal tubules
•Nerve desensitization:- e.g., potassium nitrate
•Cover or plugging dentinal tubules:- calcium hydroxide , Calcium phosphate , Calcium
carbonate , Calcium silicate
•Protein precipitants:- formaldehyde , glutaraldehyde , silver nitrate , strontium chloride
hexahydrate , Zinc chloride
•Dentin Sealers :- Glass ionomer cements ,Composites , Dentinal adhesives , Resinous dentinal
desensitizers , Varnishes , Sealants, Methyl Methacrylate
REMAINING DENTIN THICKNESS
•RDT between the floor of cavity preparation and pulp chamber is
important factor to determine the pulpal response
•2mm RDT will provide adequate insulating barrier against irritants
•RDT decreases  pulpal response increases
•At RDT of 0.75 mm, effects of bacterial invasion are seen
•When RDT is 0.25 mm, odontoblastic cell death is seen
NISHA GARG.AMIT GARG TEXTBOOK OF ENDODONTICS-3RD EDITION

Effect of remaining dentin thickness on tooth
NISHA GARG.AMIT GARG TEXTBOOK OF ENDODONTICS-3RD EDITION
INFECTED AND AFFECTED DENTIN
INFECTED DENTIN AFFECTED DENTIN
Superfical layer which is soft and leathery in Deeper layer which is hard in consistency and
consistency and dark brown in colour. light brown in color.
Collagen irreversibly denaturated Reversibly denaturated
High concentration of bacteria Donot contain bacteria
Must be removed,not remineralizable. Donot require removal

PULP PROTECTION
Deep dentin is very porous and susceptible to desiccation
Thin remaining wall of dentin
provides protection from
Heat generated by rotary instruments
Noxious ingredients of various restorative

materials,
Thermal changes conducted through

restorative materials
Forces transmitted through materials to the

dentin
Galvanic shock
ingress of bacteria and/or noxious bacterial

toxins through microleakage.
STURDEVANT’S ART AND SCIENCE OF OPERATIVE DENTISTRY / ANDRÉ V. RITTER, EDWARD J. SWIFT, JR., HAROLD O. HEYMANN, V. GOPIKRISHNA - A SOUTH ASIA ED -
DENTIN ADHESIVES
• They are intermediate materials that can be connected with both dentin tissue and composite resin and are developed to help
ensure the connection between dentin tissue and composite resin surfaces and the retention of restoration, to prevent
microleakage and to prevent dentin sensitivity that may occur after restoration by covering dentin tubules
• Properties of Dentin Adhesives Enamel/dentin bonding systems used to perform adhesive bonding are today called “adhesive
systems”.
Properties sought in adhesive systems:
• Prevention of microleakage and secondary caries,
• To be able to withstand stresses caused by polymerization shrinkage and under chewing forces,
• Micromechanical and chemical bonding to enamel and dentin tissue,
• To be able to connect to enamel and dentin tissue as well as to be able to connect to metal and porcelain,
• Easy application on moist surfaces (Wet-bonding),
• Easy clinical application without technical precision,
• Preventing post operative sensitivity by closing all or part of the dentin channels.
Development of Dentin Bonding Systems from Past to Present- Review article Mağrur
KAZAK1, Nazmiye DÖNMEZ2
CLASSIFICATION OF DENTAL ADHESIVES
Development of Dentin Bonding Systems from Past to Present- Review article Mağrur
KAZAK1, Nazmiye DÖNMEZ2
DENTIN ETCHING
• Etchants are strong acids which are used to remove smear layers and open tubules, increase retention of resin
sealant and promote mechanical retention.
• Dentin etching is more technique sensitive than enamel etching because of complexity of dentin structure. Unlike
enamel , dentin is living tissue, consisting of 50% (volume%)of hydroxyapatite, 30% organic material,
20%fluid.Acid etching removes hydroxyapatite almost completely from several microns of sound dentin ,
exposing a microporous network of collagen suspened in water.
• Application of acid to dentin results in partial or total removal of the smear layer and demineralization of the
underlying dentin.
• Acids demineralize intertubular and peritubular dentin, open the dentin tubules, and expose a dense collagen
fibrils , increasing the microporosity of the intertubular dentin .
• Dentin is demineralized by up to approximately 7.5 µm depending on the type of acid, application time, and
concentration.
• 37% phosphoric acid is used for etching
• Other materials used as etchants are maleic acid, tartaric acid, citric acid, EDTA, acidic monomers, polyacrylic
acid, hydrochloric acid, nitric acid and hydrofluoric acid
STURDEVANT’S ART AND SCIENCE OF OPERATIVE DENTISTRY / ANDRÉ V. RITTER, EDWARD J. SWIFT,
JR., HAROLD O. HEYMANN, V. GOPIKRISHNA - A SOUTH ASIA ED -
PRIMER ?????
DENTIN
HYDROPHILIC
COMPOSITE
HYDROBHOBIC
DENTIN BONDING
• Bonding to enamel is a relatively simple process, whereas bonding to dentin presents a much greater challenge.
• Several factors account for this difference between enamel and dentin bonding
• Dentin contains a substantial proportion of water and organic material, primarily type I collagen.
• Dentin is an intrinsically hydrated tissue, penetrated by a maze of fluid-filled tubules.
• Movement of fluid from the pulp to the DEJ is a result of a slight but constant pulpal pressure . Pulpal pressure
has a magnitude of 25–30 mmHg
• Dentinal tubules enclose cellular extensions from the odontoblasts and are in direct communication with the
pulp.
• Adhesion can be affected by the remaining dentin thickness after tooth preparation. Bond strengths are
generally less in deep dentin than in superficial dentin
• Dentin is in close proximity to pulp , so different chemicals used for etching and dentin bonding may irritate
the pulp
STURDEVANT’S ART AND SCIENCE OF OPERATIVE DENTISTRY / ANDRÉ V. RITTER, EDWARD J. SWIFT,
JR., HAROLD O. HEYMANN, V. GOPIKRISHNA - A SOUTH ASIA ED -
ADHESION ENHANCING AGENT
• The primer molecules are bipolar and contain two different functional groups. Of these, the hydrophilic one
interacts with moist dentin, while the hydrophobic one interacts with adhesives. Primers are binding-
enhancing materials that dissolve in solvents such as water, ethanol, or acetone.
• The primer containing the HEMA monomer is applied to the surface of the enamel/dentin, where the
surface conditions have been changed, in order to increase the surface energy due to its wettability.
• The primer is applied to the dentin surface with a microbrush until a bright surface is obtained in two or
more layers according to the case after the roughening stage with acid, and dried with air for 5-10 seconds.
• During the drying process, care is taken to fully vaporize the solvents (acetone, ethanol) in the adhesive
content.The primer prepares the surface for adhesive bonding by altering the sequences of collagen fibrils,
and then helps make the penetration of the monomer more effective.
• The primer, which passes through the residual smear base in the acidified dentin tissue, is replaced by
water on the dentin surface due to the volatile property of acetone and/or ethanol and fills the nano-
cavities left by hydroxyapatite crystals that melt between the collagen fibrils.
DEVELOPMENT OF DENTIN BONDING SYSTEMS FROM PAST TO PRESENT-

REVIEW ARTICLE MAĞRUR KAZAK1, NAZMIYE DÖNMEZ2
SMEAR LAYER
•Whenever tooth structure is prepared with a bur or other instrument, residual organic and inorganic components form
a ‘smear layer’ of debris on the surface.
•The smear layer fills the orifices of dentin tubules, forming ‘smear plugs’ and decreases dentin permeability by
nearly 90%
The composition of the smear layer is basically hydroxyapatite and altered denatured collagen.
The superficial smear layer: loosely attached to underlying dentin upto depth of 1-5 microns
Smear plugs : They occlude the dentinal tubules and may extend upto a depth of 10 microns.
Clinical significance :-
- Removal of the smear layer and smear plugs with acidic solutions results in an increase of the
fluid flow onto the exposed dentin surface.
- This fluid can interfere with adhesion because hydrophobic resins do not adhere to hydrophilic
substrates, even if resin tags are formed in the dentin tubules
STURDEVANTS ART AND SCIENCE OF OPERATIVE DENTISTRY
DENTIN BONDING AGENTS
CLASSIFICATION OF MODERN DENTIN BONDING
AGENTS
Based on their interaction with smear

layer proposed by Van Meerbeek
Smear layer modifying DBA
e.g. - ProBond
Smear layer removing DBA [total etch or

etch and rinse adhesives]
e.g. – scotch bond multipurpose ,
singlebond
Smear layer dissolving DBA [self etch

adhesives]
e.g. – prompt-L-pop
Glass ionomer based adhesives

e.g. – Fuji Bond LC
CLINICAL OPERATIVE DENTISTRY PRINCIPLES AND PRACTICE RAMYA RAGHU RAGHU SRINIVASAN-2ND EDITION
HYBRID LAYER/ RESIN-DENTIN
INTERDIFFUSION / INTERDIFFUSION ZONE
•The distinct zone between the bulk adhesive and nondemineralized
dentin (i.e.,) consisting of 50%collagen matrix and 50%resin is termed as
hybrid layer.
•Hybrid layer is formed when an adhesive resin penetrates a de-
mineralized or acid etched dentin surface infiltrates the visible collagen
fibrils .
•Infiltration of demineralized collagen fibers with resin and formation of
hybrid layer results in Successful bonding.
•The superiority of the hybrid layer that is formed decides the strength of
resin-dentin interface.
CONTEMPORARY DENTIN BONDING AGENTS-A REVIEW NANDINI PUGAL ET AL

Three characteristics are necessary for the formation of hybrid layers
a. The aggressive acid expose collagen below the hybrid layer and leaves a zone of weak dentin that leads
to long term degradation
b. The bonding resin must include monomers with both hydrophilic and hydrophobic groups that can
penetrate the dentin and combine with that.
c. The catalyst present here should allow polymerization process in the presence of oxygen and water

ZONES OF HYBRID LAYER
1. Top zone: It consists of loosely arranged collagen fibrils with inter-fibrillary spaces filled with the
adhesive resin
2. Mid-zone: This consists of collagen fibrils infiltrated with resin with residual hydroxyapatite crystals
between collagen
3. Bottom zone: it shows an abrupt transition to the underlying unaltered dentin with partially de-
mineralized dentin containing hydroxyapatite crystals enveloped by adhesive resin.
•The resin monomers are not able to fully infiltrate the de-mineralized dentin, only a part of de-mineralized
dentin remains susceptible to hydrolytic degradation.
•The remaining water gets entrapped in the hybrid layer and deteriorates the bond strength.
•The hydrophilic monomers act as a semi permeable membrane which allows the movement of water,
classically known as “water tree” phenomenon.
•This exposes bothCONTEMPORARY
resin and DENTINexposed collagen
BONDING AGENTS-A REVIEW NANDINIfibers
PUGAL ET ALto degradation by hydrolysis .

REVERSE HYBRID LAYER
•Hybrid layer is surrounded by more inorganic material.
•The hybrid layer degrades coincidently with decreasing bond strength which contributes to the
ageing of dentin bond integrity.
•This is caused by the activation of MMP’s (matrix metalloproteiase) which denature the collagen
in the hybrid layer.

CLINICAL CONSIDERATION DURING BONDING
•Complete drying of dentin after completion of the
acid-etching procedure is not clinically recommended
as vital dentin is inherently wet.Drying the dentin
surface with air would cause the dentinal collagen to
collapse which would prevent the monomers from
penetrating the nanochannels formed by dissolution of
hydroxyapatite crystals between collagen fibres.
•Studies showed that the excess water after rinsing the
etching gel can be removed with one of the following
methods without adversely affecting bond strengths:
• damp cotton pellet, • high-volume suction, •
disposable brush or • laboratory tissue paper
DEVELOPMENTAL DEFECTS OF DENTIN
1. Dentinogenesis imperfecta
2. Dentin dysplasia
3. Dentin hypocalcificaion
4. Dens in dent
5. Regional odontodysplasia
DENTINOGENESIS IMPERFECTA

•Dentinogenesis imperfecta is an autosomal dominant condition affecting both deciduous and
permanent teeth which originaties during the histodifferentiation stage of tooth development.
•This anomaly involves a defect of predentin matrix that results in amorphic, disorganized, and
atubular circumpulpal dentin.
• Witkop reported a prevalence of 1 in 8000 in a survey of 96,000 Michigan children.
MCDONALD’S AND AVERY’S DENTISTRY FOR THE CHILD AND ADOLESCENT 11TH EDITION
CLINICAL PRESENTATION
•Clinically teeth appears reddish-brown to blue-gray opalescent color.
• Soon after the primary dentition is complete, enamel is worn and often breaks away from
the incisal edges of anterior teeth and the occlusal surfaces of posterior teeth.
• The exposed soft dentin abrades rapidly, occasionally to the extent that the smooth,
polished dentin surface is continuous with the gingival tissue.
•Multiple root fractures are often seen, particularly in older patients.
•Crowns of the permanent teeth often seem to be of better quality and have less destruction.
•Broad crowns with constriction of the cervical area resulting in a “tulip ” shape
•Radiographically, slender roots and bulbous crowns present ; as well as pulp chamber is
large initially which undergoes obliteration later.
•Caused by mutation in the DSPP gene, encoding dentin phosphoprotein and dentin sialoprotein.
•The gene maps to chromosome number 4 .
•It is distinct from osteogenesis imperfecta with opalescent teeth, and affects only the teeth
•There is no increased frequency of bone fractures in this disorder
•The teeth are blue-grey or amber brown.
SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 8TH EDITION

CLASSIFICATION
Shield’s classification
Type I: occurs without
osteogenesis imperfecta
Type II: associated with
osteogensis imperfecta
Type III: Bradywine type
Radiographic appearance:
•The teeth have bulbous crowns,
•Roots that are narrower than normal
•Pulp chambers and root canals are smaller than normal or completely
obliterated.
•The enamel may split readily from the dentin when subjected to
occlusal stress

DENTINOGENESIS
IMPERFECTA II
•Dentinogenesis imperfecta II is caused by mutation in the DSPP gene
(gene map locus 4q21.3), encoding dentin phosphoprotein and
dentin sialoprotein .
•The crowns of the deciduous and permanent teeth wear rapidly after
eruption and multiple pulp exposures may occur.
•The dentin is amber and smooth.
•Zhang et al. (2001) studied a Chinese family with dentinogenesis
imperfecta Shields type II. Affected members in three generations
showed discoloration and severe attrition of their teeth, with
obliterated pulp chambers.

•Occurs with osteogenesis imperfecta.
•An inherited defect in collagen formation results in
osteoporotic brittle bones, bowing of the limbs,
bitemporal bossing, and blue sclera.
•Primary teeth tend to be more severely affected than
permanent teeth.
MEDINAZ.COM
• Radiographic appearance
• In deciduous dentition-very large pulp chambers and root canals
• In permanent teeth-pulpal spaces are either smaller than normal or
completely obliterated.
• MacDougall et al stated that the manifestations of DGI-2 can differ from

those of DGI-1 by the presence of multiple pulp exposures, normal
nonmineralized pulp chambers and canals and a general appearance of' shell
teeth'.
• They illustrated the amber discolouration of the teeth, attrition and fractured
enamel, as well as the classic 'shell teeth' appearance on radiographs.

DENTINOGENESIS IMPERFECTA TYPE III
•Dentinogenesis Imperfecta(DGI-III) is quite similar to the previous two.
•It is quite rare and has only been found in the Brandywine population in Maryland, USA.
• The clinical features are varies and the new teeth show multiple pulp revelations.

HISTOLOGICAL FEATURES
• It is purely a mesodermal disturbance.
• Enamel is normal except for its peculiar shade, which is due the dentinal
disturbance.
• The dentin is composed of irregular tubules, often with large areas of uncalcified
matrix.
• The Pulp chamber is usually almost obliterated by the continued deposition of
dentin.
• The tubules tend to be larger in diameter and thus less numerous than normal in a
given volume of dentin.
• In some areas there may be complete absence of tubules

TREATMENT
Aim :To prevent loss of enamel and dentin through attrition .Chances of
providing optimal treatment decrease as the patient ages,
thus demonstrating the need for early diagnosis
• Mild to moderate cases :
Routine restorative procedures eg- composties
• Severe cases
Primary teeth-Stainless steel crown(posterior teeth)
Stainless crown with open face composite (anterior teeth)
Permanent tooth porcelain fused metal crowns
• Partial appliances which exert stress on the teeth used with caution because the roots are easily fractured
• Experience has further shown that fillings are not usually permanent because of the softness of the dentin

DENTIN DYSPLASIA
•Dentin dysplasia is a rare disturbance of dentin formation characterized by normal enamel but
atypical dentin formation with abnormal pulpal morphology.
•It is autosomal dominant.
•The first description of the disease was by Ballschmiede, who in 1920 reported the spontaneous
exfoliation of multiple teeth in seven children of one family and called this phenomenon
'rootless teeth'.
•In 1973, Shields and associates proposed a classification based on characteristic patterns of
dentinal dysplasia.
SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 8THEDITION

CLASSIFICATION
1) Shields classification
type I (dentin dysplasia)
type II (anomalous dysplasia of dentin)
2) Witkop classification
Type I-radicular dentin dysplasia
Type II-coronal dentin dysplasia

TYPE-I RADICULAR DENTIN DYSPLASIA
•Inherited as an autosomal dominant trait.
•Both dentitions are affected.
•Normal eruption pattern, although delayed eruption has been
reported in a few cases.
•Teeth exhibit extreme mobility and are commonly exfoliated
prematurely or after minor trauma due abnormally short roots.

Clinical and stereomicroscopic observations of normal and DD-I affected
teeth. a A deciduous tooth affected by DD-I and (b) a permanent tooth from the
subject affected by DD-I. Examples of a (c) normal permanent tooth and (d) a
permanent tooth affected by DD-I
DENTIN DYSPLASIA TYPE I—NOVEL FINDINGS IN DECIDUOUS AND PERMANENT TEETH

BMC ORAL HEALTH VOLUME
• The root canals and pulp chambers are absent .
•Teeth may be slightly opalescent and blue or brown.
•Radiographically, the roots are short and may be more pointed than normal.
•Periapical radiolucency may be present at the apices of affected teeth.
•Investigation:- dentin dysplasia type I associated with extreme microdontia and aberrant crown
morphology disclosed homozygosity for a splice-site mutation in the SMOC2 gene.
RADIOGRAPHIC FEATURES :-
- In both dentitions, the roots are short, blunt, conical
- Deciduous teeth-pulp chambers and root canals are usually
completely obliterated,
- Permanent dentition-crescent shaped pulpal remnant seen in
the pulp chamber.
- This obliteration in the permanent teeth commonly occurs
pre-eruptively.

HISTOLOGY :- Normal dentinal tubule formation appears to be blocked so new dentin forms
around obstacles and takes on the characteristic appearance described as 'lava flowing around
boulders’

TYPE-II CORONAL DENTIN DYSPLASIA
•Dentin dysplasia type II is inherited as an autosomal
dominant trait in which the primary dentition appears
opalescent and radiographically shows obliterated
pulp chambers similar to those in dentinogenesis
imperfecta.
•However, dentin dysplasia type II has distinctive
feature - the permanent dentition has normal color
and radiographically exhibits a thistle tube pulp
configuration with pulp stones.
•Dean et al. hypothesized that these conditions may be
due to different alleles of the same gene. Investigation
represented that the dentin dysplasia type II gene
overlaps the likely location of the gene for Shields
type II dentinogenesis imperfecta.
Clinical features:-
•Both dentitions are affected.
•Deciduous teeth-yellow, brown, or bluish-grey opalescent appearance
•Permanent teeth-clinical appearance is normal.

Histologic features
•Deciduous teeth -amorphous and atubular dentin in the radicular portion , coronal dentin is
normal.
•Permanent teeth -normal coronal dentin, but the pulp has multiple pulp stones or denticles

Radiographic features :-
Deciduous teeth - pulp chamber obliterated
Permanent teeth - an abnormally large pulp chamber in
the coronal portion of the tooth , described as 'thistle-
tube' in shape, and radiopaque foci resembling pulp
stones may be found.
Treatment :
There is no treatment for the disease, and its prognosis
depends upon the occurrence of periapical lesion if
periapical lesion present then tooth extraction should be
done.

SUMMARY
lassification Dentin dysplasia type I Dentin dysplasia type II
Incidence 1 in 100 000. Unknown—thought to be lower
than DD type I.
Clinical presentation Normal but can vary in •Normal crown colour, shape and
appearance with brown/yellow height.
opacities present.
Radiographic presentation •Partial or complete obliteration •Pulp chambers described as

of the pulp. ‘thistle tube’; enlarged pulp
•Roots are shorter (absent in chambers with thin root canals.
severe cases), merged with an •Pulp stones are common.
apical conical aspect, with sharp
construction.
•Periapical radiolucencies are
frequent without any other
associated pathology.
Causative genes Genetically heterogeneous DSPP.

including SSUH2, VPS4B, SMOC2.
Dentin dysplasia Type I: A rare case report
Intraoral photograph showing Ellis Class II fracture with respect to 11 and 21 with
normal color, texture and shape of teeth
JOURNAL OF ORAL MAXILLOFACIAL PATHOLOGY 2019
Journal of oral maxillofacial pathology 2019
DENTIN HYPOCALCIFICATION
•Normal dentin is calcified by deposition of calcium salts in the
organic matrix in the form of globules, which increase in size by
further peripheral deposition of salts until all the globules are
finally united into a homogeneous structure.
•In dentinal hypocalcification there is failure of union of many of
these globules, leaving interglobular areas of uncalcified matrix.
•Hypocalcified dentin is softer than well-calcified dentin.
•Conditions like parathyroid deficiency or rickets, could produce
hypocalcification

DENS IN DENT (Dens lnvaginatus, Dilated Composite
Odontome)
•It is a developmental variation which arise as a result of an invagination in the
surface of tooth crown before calcification has occurred
•Etiology -an increased localized external pressure, focal growth retardation and
focal growth stimulation in certain areas of the tooth bud.

•Most frequently affected teeth is Permanent maxillary lateral incisors,
•The maxillary central incisors and posterior teeth are sometimes involved
•It appears to represent an accentuation in the development of the lingual pit
•The condition is frequently bilateral.
•Radicular variety of 'dens in dente' occurs due to the radicular invagination, usually results from
an in folding of Hertwig’s epithelial root sheath and takes its origin within the root after
development is complete

CLASSIFICATION
•The first classification of invaginated teeth was published by Hallett in
1953. However, commonly used classification proposed by Oehlers in
1957 includes the following 3 types according to the depth of the
invagination
•Type I: Invagination confined inside the crown, not extending beyond

the cemento-enamel junction (CEJ).
•Type II: Invagination extending beyond the CEJ; it may or may not
communicate with the pulp and not reach the periradicular tissue.

• Type IIIA: The invagination extends through the root and
communicates laterally with the periodontal ligament space
through a pseudo-foramen.
• Type IIIB: The invagination extends through the root and
communicates with the periodontal ligament at the apical
foramen.

Radiographic features
•It is recognized as a pear-shaped invagination of enamel and dentin with a
narrow constriction at the opening on the surface of the tooth and closely
approximating the pulp in its depth
•Gives tooth within the tooth appearance

Treatment :
1) Prophylactic or preventive sealing of the invagination
2) Root canal treatment
3) Endodontic apical surgery
4) Intentional replantation
5) Extraction

REGIONAL ODONTODYSPLASIA (GHOST TEETH)
•Unusual dental anomaly in which one or several teeth in a localized area are affected in an
unusual manner.
TEETH INVOLVED:
•Most frequently maxillary teeth than mandibular.
•Maxillary and mandibular permanent central incisor, lateral incisor and cuspid being the most
common.
•Deciduous teeth may also be involved.

ETIOLOGY
Somatic mutation or due a latent virus residing in the
odontogenic epithelium, which subsequently becomes active
during development of tooth.
Local vascular defects may be involved in pathogenesis.
Clinical Features:-
The teeth affected by odontodysplasia exhibit either a delay or a
total failure in eruption.
Shape is altered,very irregular in appearance,with defective
mineralization.

Radiographic Features:-
•Characteristic feature-marked reduction in
radiodensity so that the teeth assume a GHOST
APPEARANCE
•Enamel and the dentin appear very thin
•Pulp chamber is exceedingly large

Histologic Features:-
•Marked reduction in the amount of dentin, the widening of the predentin layer, the presence of
large areas of interglobular dentin and an irregular tubular pattern of dentin.

Treatment
Because of the poor cosmetic appearance of these teeth, extraction followed by restoration by a
prosthetic appliance is usually indicated

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DENTIN

BY DR. SHREYA POKIYA {PG-|}

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

•Collagenous fibrils embedded in •Consist hydroxyapatite

•Principle collagen fibres is type-1 •Formula of cell : 3Ca3(PO4)2. Ca(OH)2

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

Phosphpo- Growth factors

Chondroitin sulfates Dentin sialoproteins IGFs

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

orban's oral histology & embryology 14th edition

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

• Enclosed by highly mineralized wall- peritubular dentin

• Lateral branches – along its course

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

- Intertubular -Globular dentin

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ESSENTIALS OF ORAL HISTOLOGY AND EMBRYOLOGY , CLINICAL APPROACH BY JAMES K. AVERY

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE,’S ORAL HISTOLOGY 9TH EDITION

inner enamel epithelium reverse polarity

ectomesenchymal cells rapidly enlarge and elongate to become preodontoblasts

Volume of cytoplasm increases to accommodate protein-synthesizing organelles to convert preodontoblasts

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

THE NEWER GENES INVOLVED:

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION

ORBAN'S ORAL HISTOLOGY & EMBRYOLOGY 14TH EDITION

TEN CATE’S ORAL HISTOLOGY 9TH EDITION