Dentin

 INTRODUCTION
 DENTINO-PULPAL COMPLEX
 HISTORY
 DENTINOGENESIS
 COMPOSITION
 PROPERTIES OF DENTIN
 HISTOLOGY OF DENTIN
 FUNCTION OF DENTIN
 CLINICAL SIGNIFICANCE
 AGE AND FUNCTIONAL CHANGES
 DEVELOPMENTAL ANOMALIES
 CONCLUSION
 REFERENCES

INTRODUCTION
 Most Voluminous Mineralized
Connective Tissue Of Tooth
 Hard Portion Of Dentino-Pulpal
Complex
 Dentin = Vital Tissue with Living
Protoplasm

 The dental pulp and dentin functions as a unit.
 Odontoblasts are located in the periphery of the
pulp tissue with extensions into the inner part of
the dentin.
 Dentin would not exist unless produced by
odontoblasts and dental pulp is dependant
on the dentin for protection(alongwith enamel).
 Likewise, integrated dynamics of the pulp-
dentin complex imply that impacts on the dentin
may affect the pulpal component and that
disturbances in the pulpal will in turn affect the
quantity and quality of dentin produced.

ODONTOBLASTS
 The odontoblasts line the entire pulpal aspect of the
predentin.
 The odontoblasts are tall columnar cells or
sometimes somewhat cuboidal in shape (especially
in the root).
 The nucleus is oval, has one or two nucleoli. The
cytoplasm of the cell body contains numerous
organelles rough surfaced endoplasmic reticulum
(arranged in longitudinally running cisternae) a well
developed Golgi apparatus, Mitochondria, Vesicles.
Vacuoles, Electron bodies, Microtubules and fibrils.
 The odontoblasts cells bodies are approximately 7
micrometre in diameter & 40 micrometre in length.

ODONTOBLASTIC
PROCESS
 The odontoblast processes are the
cytoplasmic extensions of the
odontoblasts. The odontoblasts cells reside
in the peripheral pulp at the pulp-predentin
border and their processes extend in to the
dentinal tubules .
 The processes are largest in diameter near
the pulp (3 to 4 mm) and taper into the
dentin. The odontoblast processes divide
near the dentino enamel junction and may
indeed extend in to enamel in the “enamel
spindles”

 The biological structure of dentin has been
investigated since time of:
1) Anton Van Leeuwenhock : Explained the
tubular structure of dentin.
2) Von Purkinje and Retrices : Explained abt.
dentinal tubules.
3) John Hunter : Specified it as hard tissue
4) Cuvien : coined the term IVORY for dentin

 Numerous structural elements of dentin carry
the name of well-known histologists of 19th
century:
1) Owen: Contour lines of Owen (1840)
2) Von Ebner: Ebner’s growth lines (1891)
3) Neumann: Neumann’s sheath (1863)
4) John Tomes: Tomes granular layer (1838)
Tomes process (1856)
5) Von Korff: Korff’s fibers (1906)

 Dentin is formed by cells called odontoblasts
that differentiates from ectomesenchymal
cells of dental papilla following an organizing
influence that emanates from inner dental
epithelium.
 Dental papilla is the formative organ of dentin
and eventually becomes the pulp of the teeth,
a change in terminology generally associated
with the moment dentin formation begins.

Dentinogenesis is composed of three stages
i.e.
1) CYTODIFFERENTIATION
2) MATRIX FORMATION
3) MINERALIZATION

 CYTODIFFERENTIATION
* This takes place during the BELL STAGE.
* In this stage, the cells from the papillae sac
differentiates to produce odontoblasts under
the influence of the Inner dental epithelium
starting at the cuspal or incisal region.
* The cells become cylindrical in shape and
are sometimes referred as Preodontoblasts.
* The no. of organelles markedly increases
with the cell becoming tall and columnar
located at end farthest from basement
membrane of Inner dental epithelia. These cells
are known as Odontoblast.

* Concomitant with the formation of predentin
at cuspal and incisal, continued differentiation
of new odontoblasts takes place further apic-
-ally in dental papilla.
* After the crown is fully formed, the rate of
dentin slows down markedly(2-3yrs post-
-natal) until root formation starts i.e. similar
to cytodifferentiation in crown.

 MATRIX FORMATION
* The odontoblasts exhibits all the characterstics
of matrix-producing cells i.e. an abundance
of RER, a well developed Golgi apparatus,
mitochondria and secretory granules.
* Pro-collagen is synthesized by RER, transferr-
-ed to Golgi apparatus and finally, secreted by
secretory granules.
* The collagen, glycoprotein and proteoglycan
complexes constitutes the organic matrix of
dentin prior to mineralization, two layer in pre-
-dentin may be differentiated.

* The fibers involved in the formation of the
initial predentin are argyrophilic and k/a
VON KROFF’S FIBERS.
* VON KROFF’S FIBERS are the first fibers
that signifies the first formed dentin. Due
to the argyrophilic rxn, it was long believ-
-ed that bundles of collagen formed
among the odontoblasts.
* Recently EM studies revealed that the
staining is of ground substance among the
cells and not collagen.

* As the matrix formation continues, the
odontoblastic process lenghtens, as does
the dentinal tubule.
* Initially, 4µ of daily increments are added.
This continues until the crown is formed
and the teeth move into occlusion. After
this time a daily incremental deposit of 1µ
takes place.

 MINERALIZATION
* Basically, it occurs by globular calcification.
* Earliest crystal deposition takes place in the
form of very fine plates of hydroxyapatite on
the surface of collagen fibrils in the ground
substance.
* The crystals are laid down within the fibrils
themselves with the crystals that are
associated with collagen being in orderly
manner( long axis parallel to fibrils long axis)
and in rows conforming to 64nm striation
pattern within the globular islands of mineraliz-
-ation .

* The crystal deposition appears to take place
readily from common centers in so-called
Spherulite form.
* The peritubular region becomes highly minera-
-lization at a very early stage. The ultimate
crystal size remains very small about 3mm
in thickness and 100nm in length
* The hydroxyapatite crystal of dentin resembles
bone and cementum. They are 300 times
smaller than enamel crystals.

COMPOSITION PERCENTAGE CONTENT
INORGANIC 70%(by weight)
45%(by volume)
CALCIUM HYDROXYAPATITE
ORGANIC 20%(by weight)
33%(by volume)
1)TYPE I COLLAGEN
(minor type III and IV)
2) MINOR FRACTION
a) Lipids
b) Non-collagenous matrix
protein
WATER 10%(by weight)
22%(by volume)

COMPOSITION(contd.)
COLLAGEN TYPE I
The Scaffold that accommodates a
large portion(56%) of minerals in
the holes and pores of fibrils

COMPOSITION(contd.)
NON COLLAGENOUS MATRIX PROTEIN
• Regulates Mineral Deposition and
can act as Promoter or Inhibitor.
• Pack the space between Collagen
fibrils and accumulates along the
periphery of dentinal tubules.
(Peritubular Dentin)

COMPOSITION(contd.)
IMP. NON COLLAGENOUS MATRIX
PROTEINS
1) Dentin Sialophosphoprotein
2) Dentin Matrix Protein 1
3) Osteonectin(SPARC)
4) Osteocalcin
5) Osteopontin
6) Bone Sialoprotein
7) Matrix Extracellular Phosphoglycoprotein

S.No. PROPERTY EXPLAINATION SIGNIFICANCE
1 COLOR DARKER THAN ENAMEL
(Light yellow in young
adult and Dark yellow
in elderly)
EBURNATED
DENTIN
2 THICKNESS MAXIMAL
1) Cuspal height
2) Incisal edge
MINIMAL
Cervical areas
1)Thickness
increases with age.
2) 3-3.5 mm in
Coronal aspect.
3 HARDNESS 1/5th of Enamel
(High Compressive
strength and low Tensile
strength)
MOE= 1670000 Psi
(more flexibility hence
shows Cushion
Effect)

1) DENTINAL TUBULES
CORONAL RADICULAR
DENTIN DENTIN
(Also seen at incisal edge
and cuspal tip)

 The dentinal tubules follow a Gentle ‘S’
shaped curve in crown and is straighter in
incisal edges, cusps and root areas.
 Its perpendicular to CEJ and DEJ.
 They have lateral branches throughout dentin
k/a CANALICULI or MICROTUBULES.
 No. and Diameter of dentinal tubules
NUMBER DIAMETER(in µ)
PULP 45000-65000 2-3
DEJ 15000-20000 0.5-0.9

 First formed dentin i.e. not mineralized.
 10-30 µm zone of unmineralized zone
between Odontoblasts and Mineralized
dentin.
 This layer of dentin lies very close pulp
tissue i.e. just next to CELL BODIES
OF ODONTOBLASTS .

3) PERITUBULAR AND
INTERGLOBULAR
DENTIN

 PERITUBULAR DENTIN
• Dentin lining the Dentinal Tubules
• More mineralized than Intertubular
dentin.
 INTERTUBULAR DENTIN
• Dentin i.e. present between the tubules
and is less mineralized compared to
Peritubular dentin.
• It determines ELASTICITY of dental
matrix

PRIMARY
DENTINE
SECONDARY
DENTINE
TERTIARY
DENTINE
DEFINITION Dentine formed
before root
completion
Formed after root
completion
Formed in response
to external stimuli
TYPE OF CELLS 1º Odontoblasts 1º Odontoblasts 2º Odontoblasts
or
undiff. Mesenchymal
cells of pulp
LOCATION All areas of dentine Not uniform
(roof and floor of
pulp )
Localized in areas of
ext. stimuli
ORIENTATION OF
TUBULES
Regular Irregular Atubular
RATE OF
FORMATION
Rapid Slow Rapid
(1.5-3.5 µm/day)
PERMEABILITY More Less Least

 CAUSE
1) Aging patients
2) Mild irritation(Eg. Slowly advancing
caries)
 HISTOLOGICAL CHANGES
Increased deposition of calcified
materials from enamel to pulp leading
to widening of PERITUBULAR DENTIN.
 CLINICAL SIGNIFICANCE
Area becomes HARDER,DENSER,LESS
SENSITIVE and MORE PROTECTIVE
against irritation.

 TYPES OF SCLEROTIC DENTIN
1)PHYSIOLOGICAL SCLEROTIC DENTIN
Sclerotic dentin due to aging.
2)REACTIVE SCLEROTIC DENTIN
Sclerotic dentin due to irritants.
3)EBURNATED DENTIN
Type of Reactive Sclerotic dentin
i.e. formed due to destruction by
slow carious process or mild chronic
irritation leading to HARD ,
DARKENED CLEANABLE on outward
portion of Reactive dentin.

 Severe Stimulation to Dentin leads to
Destruction and Disintegration of Odontoblasts
and Odontoblastic Process.
 The Dentin Tubules are empty and filled with
air.(often surrounded by Sclerotic Dentin)
 Appears Black in Ground Sections.
 Commonly seen in areas of narrow Pulpal
Horns due to Odontoblastic crowding.

7) INTERGLOBULAR
DENTIN
Interglobular Dentin = Hypomineralization
due to Vit. D deficiency

 Also known as Incremental lines of Von
Ebner.
 Growth lines that is seen in ground section
of dentin parallel to the dentinal tubules.
 These lines represents the rest phase in
dentin deposition with dentin deposition
rate of 6 µ/day in crown to 3.5 µ/day in
roots

10) OSTEODENTIN
 Seen in tertiary dentin due to entrapment of
odontoblast cells in the dentin. Since it
appears like bones so k/a OSTEODENTIN.

1) HYPERSENSITIVITY
 Dentinal hypersensitivity is the term used to
describe clinical condition of an exaggerated
response to an exogenous stimuli.
 Dental hypersensitivity is defined as “sharp,
short pain arising from exposed dentin in
response to stimuli typically thermal, chemical,
tactile or osmotic and which cannot be ascribed
to any other form of dental defect or
pathology.”(Holland et al,1997)

 Theories of Dentinal Hypersensitivity are
1) Transducer Theory
* The theory assumed that odontoblast
extends to the periphery and its
membrane comes in close apposition
to the nerve endings in the pulp and so
transmit excitation.
* Thomas,1984 indicated that process of
odontoblasts are restricted to the inner
third of the dentinal tubules.

2) Neural Theory
* The neural theory attributes to activation
of the nerve endings in the tubules which
conducts the stimuli along the parent 1º
afferent nerve fibers in the pulp into the
dental nerve branch.
* According to this theory, nerve is located
throughout the thickness of the dentin, but
this was not found so in ground sections.

3) Hydrodynamic Theory
* Put forth by Brannstrom,1962.
* According to this theory, hypersensitivity
is due to displacement of the fluids in the
dentinal tubules.
* Mathews et al,1994 noted that stimuli such
as cold causes fluids to flow away from the
pulp, produces more rapid and greater pulp
nerve responses than those such as heat,
which causes inward flow of fluid.

* When exposed dentin is dehydrated using
air blasts, it causes outward fluid movt. and
stimulates the mechanoreceptor to cause
pain.
* When overexposed to such stimuli, dentinal
plugs are formed that protect the pulp from
further such stimuli.

 Etiology of hypersensitivity
* Main etiology is exposure of the dentinal tubules
due to either of the two causes i.e. loss of
covering enamel or loss of gingival attachment.
* Loss of gingival attachment is the most common
cause of dentinal hypersensitivity.
Various factors causing
gingival attachment loss are as follows:
1) Inadequate attached gingiva
2) Improper brushing technique
3) Periodontal surgery

4) Overzealous tooth cleaning
5) Oral habits
6) Recession secondary to diseases such
as NUG, Periodontitis, Herpetic gingivo-
-stomatitis
7) Crown preparation
* Once the dentinal tubules are exposed there are
process to maintain its patency i.e.
1) Poor plaque control
2) Enamel wear
3) Improper oral hygiene technique
4) Cervical erosion
5) Exposure to acids

 Management of Hypersensitivity
1) Desensitizing by occlusion of dentinal tubules
a) formation of smear layer by burnishing with
orangewood sticks.
b) Use of topical agents such as
i) Calcium hydroxide
ii) Calcium phosphate paste
iii) Silver nitrate
iv) Strontium chloride
v) Flouride
vi) Potassium oxalate
vii) Varnish
viii) Ionophoresis

c) Placement of restoration
i) GIC
ii) Composite cements
d) Uses of lasers( carbon dioxide, Nd:YAG,
Er:YAG, He:Ne)
2) Desensitization by blocking pulpal sensory
nerves
E.g.. Potassium nitrate in pastes in which
potassium ions passes via tubules and
desensitizes the nerves.

2) PULP PROTECTION
 The cells of exposed dentin should be
insulated against bacterial toxins, strong
drugs and undue operative procedures.
 When 1mm of dentin is exposed, 30000
living cells are exposed. Hence, its
advisable to provide thermal and chemical
protection.
 The protocol is defined by the concept of
REMAINING DENTIN THICKNESS(RDT).

RDT > 2mm
(SHALLOW)
RDT (0.5-2mm)
MODERATE
RDT < 0.5mm
DEEP
SILVER
AMALGAM
VARNISH BASE OF ZnPolyF
and GIC
Ca HYDROXIDE
WITH BASE
GLASS IONOMER
CEMENT
NOT REQUIRED NOT REQUIRED CALCIUM
HYDROXIDE
LINER
COMPOSITE DBA DBA CALCIUM
HYDOXIDE + GIC
+ DBA
CAST GOLD NOT REQUIRED BASE CALCIUM
HYDROXIDE +
BASE

3) DENTINAL CARIES
 The rapid penetration and spread of
caries is attributed to its low Calcium
content and dentinal tubule system.
 The enamel may be undermined at DEJ
but due to dentinal tubules, a passage is
formed for bacteria.
 The electron microscopy of carious
dentin shows 5 distinct histological
zones.

ZONE 1 : NORMAL DENTIN
 Deepest area is normal dentin which has
tubules with odontoblastic process that are
smooth and no crystals in the lumens.
 The inter tubular dentin has normal cross
banded collagen and normal dense apatite
crystals.
 No bacteria in the tubules.
 Stimulation of dentin (e.g. :by osmotic
gradient, a bur, a dragging instrument or air
blow) produces a sharp pain.

ZONE 2 : SUBTRANSPARENT
DENTIN
 Zone of demineralization of the intertubular
dentin and initial formation of very fine crystals in
the tubule lumen at the advancing front.
 Odontoblastic process damage is evident.
 No bacteria are found in this zone.
 Stimulation of dentin produces pain.
 Dentin is capable of remineralization

ZONE 3 : TRANSPARENT DENTIN
 This dentin is softer than normal dentin and
shows further loss of mineral from the inter
tubular dentin and many large crystals in the
lumen of the tubules.
 Stimulation produces pain.
 Intact collagen can serve as a template for
the remineralization of the inter tubular
dentin and thus this region is capable of self
repair , provided the pulp remains vital.

ZONE 4: TURBID DENTIN
 Zone of bacterial invasion and is marked by
widening and distortion of the dentinal
tubules which are filled with bacteria.
 There is very little mineral present and the
collagen is irreversibly denatured.
 Dentin in this zone will not self repair .This
zone cannot be remineralized and must be
removed before restoration.

ZONE 5 : INFECTED DENTIN
 Outer most decomposed dentin that is
teeming with bacteria.
 No recognizable structure to the dentin
and collagen ,and minerals are absent.
 Removal of infected dentin is essential to
sound, successful restorative procedure
as well as prevention of spreading of
infections.

 It is also important to understand the concept
of Affected and Effected dentin
AFFECTED DENTIN EFFECTED DENTIN
1. SOFT DEMINERALIZED
DENTIN INVADED BY
BACTERIA.
DENTIN IS DEMINERALIZED
BUT NOT INVADED BY
BACTERIA.
2. SOFT LEATHERY SURFACE
WHICH IS EASILY REMOVED.
SOFT SURFACE BUT NOT
EASILY REMOVED.
3. IRREVERSIBLE
DEGRADATION OF DENTIN.
UNINTERRUPTED COLLAGEN
CROSS LINKAGE.
4. CANT BE REMINERALIZED. CAN BE REMINERALIZED.
5. CARIES STAINING DRUGS
STAINS IT.
CARIES DRUGS CANT STAIN IT.

4) CAVITY FLOOR
 Cavity’s pulpal floor must lie in dentin.
 Due to low Modulus of Elasticity of
Dentin(compared to Enamel) it acts as a
resilient base below the restoration and
so are able to absorb the masticatory
forces without fracture.

5) OPERATIVE
PROCEDURES
 Undue trauma from operative procedures can
damage the pulp.
 PRESSURE Air driven cutting instrument can
dislodge the odontoblast and aspiration within
the dentinal tubule which could be an important
factor of inflamed pulp.
 HEAT PRODUCTION due to rotation of the
rotary instruments is important damaging
factor. If temperature is elevated by 11ºF,
destructive rxn. will occur even in a normal and
vital periodontal organ.

 SPEED : If speed is b/w 3000-30,000 rpm
without coolant, then, pulpal damage will
occur.
 Dull and worn out instrument leads to
increased vibration and reduced cutting
efficiency leading to rise in heat.
 VIBRATION : Vibration leads to damage to
pulp and higher vibration leads to
development of cracks in dentin and
enamel.

6) SMEAR LAYER
 Presence of smear layer was first demonstrated by
BOYDE et al,1963.
 Smear layer is the debris smeared on the surface of
enamel and dentin by cutting of tooth.
 Cameron(1983) and Mader(1984) examined smear
layer under EM and concluded that it’s amorphous,
irregular and granular in appearance and consist of
2 layers i.e.
1) Superficial and loosely attached to underlying
dentin.
2) Deeper layer consisting of dental plugs in
dentinal tubules

 Smear layer is composed of both Inorganic and
Organic component .
1) The organic portion is comprised of
microbes, heat coagulated proteins, necrotic pulp
tissue, odontoblastic process, saliva and blood
cells.
2)The inorganic component of smear layer is
comprised of the tooth debris.
 Significance of Smear layer
1) Interferes with bonding of GIC and
composites.
2) Bacteria laden mass whose toxic product
may migrate to pulp.

 Imp. Agent responsible for removal of smear
layer are:
1) 6% Citric acid for 60s
2) Polyacrylic acid for 5s
3) EDTA
4) Maleic acid

7) ETCHING OF DENTIN
 In 1955, S. Buonocore developed the technique of acid
etching for bonding of restoration to enamel.
But etching of tooth was done far before it though
unknowingly.( Soderholm JKM. Dental Adhesives how it
started and Later evolved. J Adhes Dent 2007;9:227-230)
1) In Pre-Columbian era, the Mayans used to cement their
inlays to the tooth surface by acidic cements .
2) Also dentists have been using several acidic cements for
centuries in which acid was found in the cement even after
setting which etches the dentin surface to produce rougher
surface for good adhesion.
Hence, its difficult to decide who discovered ACID ETCHING:
the Mayans or Buonocore.

 But at that time, it was confined to enamel
and dentin was not etched.
 In 1979, Fusayama used 37%
orthophosphoric acid and showed Dentin
etching doesn’t damage the pulp
 In 1982, Nakabayashi discovered formation
of HYBRID LAYER OF RESIN INFILTRATED
DENTIN.
 Around 1990’s, ETCHING OF DENTIN
became a common practice.

 Significance of acid etching
1) Removal of smear layer and plugs
2) Opening dentinal tubules and deminer-
-alize Peri-and intertubular dentin, thus
increasing dentin permeability( Pashley
DIL, Carvahlo RM. Dentin permeability
and dentin adhesion. J Dent 1997;25:
355-72)

 Depth range of decalcifications by acid etching
varies from 2-4µ and depends on the following
factors:
1) Etchant pH
2) Etchant type
3) Etchant concentration
4) Etchant viscosity
5) Application time
Perdigao J, Lambreehts P, Van Meerbeek B,
Tome AR, Vanherle G, Lopes AB. Morphological
field emission-SEM study of the effects of six
phosphoric acid etching agents on human dentin.
Dent Mater 1996;12:262-71

 Even though, acid etching promotes profound
changes in chemical composition and
physical properties of the dental matrix, it is
widely used in restorative dentistry.
Frankenberger R, Lobbaner U, Roggendorf MJ,
Naumann M, Taschner M. Selective enamel
etching reconsidered : better than etch and
rinse and self etch? J Adhes Dent 2008; 10:
339-334

8) BONDING AGENT
 Bonding agents are an integral part of
restorative dentistry.
 The enamel bonding agent failed when
employed for dentin. This can be attributed to
following causes:
1) Complex surface of the dentin with lesser
calcium content.
2) Remaining water of about 10% that oozes

out of dentinal tubules exposed due to
tooth preparation contaminates the
field.
3) Presence of smear layer.
4) Controversy regarding etching of
dentinal surface.
5) Biological sensitivity of dentin.
6) Low organic material surface energy.
 Hence an effort was done to develop that
shows bonding to dentin

GENERATION IMPORTANT FEATURES EXAMPLE
1ST
GENERATION
Very weak bond
2ND
GENERATION
Weak bond(1-10MPa) with main
component HEMA or Bis-GMA. No
consideration given to shrinkage or
smear layer.
Scotchbond, Bondlite
3RD
GENERATION
Modification or removal of smear layer
for improvement in bond strength.
Scotchbond II, Gluma,
Prisma, Universal Bond
2/3
4TH
GENERATION
Adoption of total etch tech. for
complete removal of smear layer.
Three step bonding.
Scotchbond multipurpose,
All bond 2, Optibond FL
5TH
GENERATION
Same principle as 4th generation with
self etching primer or self priming
adhesive.
Self etching primer(Clearfil
SE bond)
Self priming
adhesives(Prime n Bond
NT)
6TH
GENERATION
Self etching adhesives, two bottle
systems mixed before application
Prompt L-Pop, Xeno IV
7TH
GENERATION
Single bottle adhesives I-Bond ,G-Bond, Xeno V

9) DENTINO-ENAMEL
JUNCTION The DEJ is a scalloped junction between
enamel and dentin.
 SCALLOPED NATURE OF DEJ
1) If DEJ is flat, tensile strength act at DEJ over
continuous areas would push the two areas apart ,
thus leading to delamination.
2) In scalloped DEJ, the net compression towards
the DEJ was consistently higher than net tension
away from it. As a consequence, at DEJ, enamel and
dentin are pushed towards one another during
mastication .
( Shimizu D, Macho GA. Functional significance of
microstructural detail of primate dentino-enamel
junction: a possible example of exaption. J Hum Evol
2007;52(1):103-11)

10) DENTINO-CEMENTAL
JUNCTION
 The dentino-cemental junction is of special
concern as it forms the apical constriction.
 Apical constriction is the narrowest diameter
upto which Biomechanical preparation and
Obturation is done.
 Its usually 0.5-1.0 mm short of apical foramen.

11) IPC/DPC
 Indirect Pulp Capping
Reparative dentin can be stimulated by
cavity lining material since dentin is
produced throughout life.
* Deep penetrating lesions is treated by
partial removal of effected dentin and
leaving the affected dentin intact. After
this, we leave a calcium hydroxide liner.
Then dressing is done for minimum three
weeks.
* The liner stimulates the odontoblasts to form
new dentin along the pulpal surface.

 Direct Pulp Capping
Direct pulp capping can be done to stimulate
reparative dentin young, non inflamed pulps
to secrete reparative dentin.

VITALITY OF DENTIN
 Since the odontoblast and its process are an integral
part of the dentin. There is no doubt that dentin is a
vital tissue.
 Again, if vitality is understood to be the capacity of the
tissue to react to physiologic and pathologic stimuli
dentin must be considered a vital tissue.
 Dentin is laid down through out life, although after the
teeth have erupted and have been functioning for a
short time, Dentinogenesis slows, and further dentin
formation is at a much slower rate.
 As peritubular diameter increases tubule caliber is
diminished. Pathologic effects of dental caries,
abrasion, attrition etc cause changes in dentin. With
age, tubule closure progress pulp ward and may affect
tubules of greater diameter too)

DEAD TRACTS
 When a ground section of tooth is observed by
transmitted light, sclerotic dentin appears light, but other
parts of the dentin frequently appear as dark bands.
These areas are called “dead tracts” and represents
groups of empty air filled dentinal tubules.
 They appear black in transmitted and white in reflected
light.
 These dead tracts mainly appears due to loss of
odontoblastic processes 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 odontoblasts
processes give rise to dead tracts. These areas
decreased sensitivity and appear to a greater extent in
older teeth

SCLEROTIC OR TRANSPARENT 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, especially in older individuals.
 In such cases blocking of the tubules is considered a
defensive reaction of dentin. The calcified tubular space
assumes a different refractive index becoming
transparent. This calcified predentin and process of
tubule is called sclerotic or transparent dentin.
 It is filled with a fine meshwork of crystals and the mineral
density is greater in this area.
 It appears transparent or light in transmitted light and dark
in reflected light. It is more frequently found in root and
slowly progressive caries as well as cervical areas of
older teeth with cervical cementum exposure and may
prolong vitality

1) DENTINOGENESIS IMPERFECTA
2) REGIONAL ODONTODYSPLASIA
3) DENTINAL DYSPLASIA

DENTINOGENSIS
IMPERFECTA
# WHAT IS IT?
Dentinogenesis imperfecta is an
AUTOSOMAL DOMINANT trait seen
due to mutation in DSPP.
Characteristic feature of the condition is
OBLITEARTION OF DENTINAL PULP

# CLASSIFICATION
1) Dentinogenesis Imperfecta Type I
 Dentinogenesis imperfecta with
osteogenesis imperfecta.
 Error in Collagen type I synthesis
2) Dentinogenesis Imperfecta Type II
 Not associated with osteogenesis
imperfecta
 Opalescent Teeth
3) Dentinogenesis Imperfecta Type III
 Associated with Opalescent teeth but
with quite varied clinical manifestation.
 Also k/a BRANDYWINE TYPE

# CLINICAL FEATURE
 Mostly they share a lot of common clinical features i.e.
 Also k/a Tulip or Bell shaped teeth(excessive cervical
constriction)
S.N
o.
PROPER
TIES
EXPLANATION
1 Color Yellowish brown to bluish grey
(due to abnormal dentin)
2 Enamel Though quite normal but fractures
quite easily(abnormal dentin and lack
of scalloping at DEJ)
3 Roots Shortened and Blunt
4 Susceptibilities
to caries
Slight resistant due to loss of contact

 Type I is different from Type II as it is
associated with Osteogenesis
Imperfecta.
 Type III D.I presents with some extra
features compared to Type I and II i.e.
1) Multiple pulp exposures
2) Periapical radiolucency
3) Variant radiological feature.

# RADIOLOGICAL FEATURE
1) Type I and II D.I.
a) Opaque pulpal chamber and canal
b) Bell shaped or Tulip shaped teeth
c) Short and blunt roots
2) Type III D.I.
Extremely large pulpal chambers and
canals with very thin dentin, so k/a
SHELL TEETH

# TREATMENT
 No specific treatment
 Use of full crowns for aesthetics

REGIONAL
ODONTODYSPLASIA
# WHAT IS IT?
Anomaly of teeth that involves all the hard
tissue i.e. enamel, dentin and cementum.
Unknown etiology with the most popular
being local vascular defect.

# CLINICAL FEATURE
 SITE
Maxillary teeth are more commonly
affected.
Central > Lateral > Cuspid
Incisors Incisors
 SYMPTOM
a) Delayed or no eruption is observed
b) Features of teeth
i) Short root
ii) Large pupal chambers and canals with
open apical foramina
iii) Increase fractures due to poor mineral-
-ization.
iv) Irregular shape with mottled appearance

# RADIOLOGICAL FEATURES
Marked reduction of radio-opacity of
enamel and dentin with increase in
pulpal volume, so k/a GHOST TEETH
# TREATMENT
Extraction and replacement with
prosthesis

DENTIN DYSPLASIA
(Rushton,1939)
# INTRODUCTION
 Autosomal dominant disorder which
manifests with normal enamel, atypical
dentin and abnormal pulp morphology.
 Witkop classified it into two type i.e.
a) Radicular Dentin Dysplasia
(Type I dentin dysplasia)
b) Coronal Dentin Dysplasia
( Type II dentin dysplasia)

# CLINICAL AND RADIOLOGICAL FEATURE
FEATURE RADICULAR DENTIN
DYSPLASIA
CORONAL DENTIN
DYSPLASIA
CLINICAL a) Both types of dentition are
involved.
b) Look normal in
appearance though have
AMBER color appearance.
c) Short roots.
d) Delayed eruptions.
a) Both type of dentition are
involved.
b) 1º dentition shows
yellowish-brown to bluish-
grey color.
c) 2º dentition shows normal
picture.
RADIOLOGICAL a) Obliterated pulp chamber
b) Periapical radiolucency
c) Short, conical and blunt
roots
d) Crescent shaped pulpal
remnant in some 2º
dentition.
a) 1º dentition
Obliterated pulp chamber.
b) 2º dentition
Abnormally large pulp
chamber with pulp stone.

 The Dentino-Pulpal complex is a very
important partnership. What happens to
one, affects the other.
 Hence, it is quite important to
understand the dentin in order to attain
success in the field of conservative
dentistry and endodontics.

IMPORTANT FACTS
 XENO V is an important 7th generation Dentin
Bonding agent.
 Important liners seen under the composite
resins in deep carious lesion(RDT<0.5mm) are
Light Cure GIC followed by Type I GIC due to
their short setting time.
 Affected dentin comprises of the INFECTED
ZONE(Zone 5) and the TURBID ZONE(Zone
6).

 Effected dentin comprises of SUBTRANSPARENT
DENTIN (Zone 2) and TRANSPARENT DENTIN
(Zone 3).
 Apical gauging is a very important procedure as it
gives a good approximation of canal diameter in
the most important apical 3-5mm of the root canal.
For e.g. if apical diameter of an root canal is
0.4mm then its not advisable to instrument this
canal to less than 40 K-File. Hence, it acts as a
guide.

 Nanci Antonio. Tencate’s Oral Histology. 6th ed. USA: Mosby; 2003.
 O Heymann Harald, J Swift Edward, V Ritter Andre. Sturdevant’s Art
and Science of Operative Dentistry. 1st ed. New Delhi: Elsevier; 2013.
 Garg Nisha, Garg Amit. Textbook of Operative Dentistry. 2nd ed. New
Delhi: Jaypee; 2013.
 A Regezi Joseph, J Sciubba James, C K Jordan Richard. Oral
Pathology. 5th ed. Delhi: Elsevier; 2009.
 Shafer, Hine, Levy. Shafer’s Textbook of Oral Pathology. 6th ed. Delhi:
Elsevier; 2009.

Dentin

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