DENTIN

GUIDED BY - DR SHUBHASHINI. N
PRESENTED BY - KRITHIKA. D
CONTENTS:

 Introduction
 History
 Stages of tooth development
 Physical properties and chemical properties
 Structure -
Dentinal tubules
Peritubular dentin
Intertubular dentin
Predentin
Odontoblast process
 Dentin-enamel junction (DEJ)
 Cemento-dentinal junvtion (CDJ)
Contents:
 Types of Dentin
Primary dentin
Secondary dentin
Tertiary dentin
 Incremental lines
 Interglobular dentin
 Granular layer
 Innervation of dentin
 Permeability of dentin and dentinal fluid
 Age and functional changes in dentin
 Developmental disturbances
 Clinical considerations
 New study facts and evoluton
INTRODUCTION
 Second layer of the tooth structure that provides the
bulk and general form of the tooth
 Since it begins to form slightly before the enamel,
it determines the shape of the crown, including the cusps
and ridges and also the number and size of the roots
 Dentin physically and chemically, closely resembles bone
 Said to be a living tissue since the tubules present in it contains
processes of specialized cells, the odontoblasts
 Main morphologic difference between bone and dentin is that
some of the osteoblasts exists on the surface of the bone and
when one of the cells become enclosed within its matrix, it is called osteocyte
HISTORY

 1771: John hunter- hard tissue

 1775: Anton Von Leeuwenhoek- described tubular structures
 1837: Purkinje and Retzius- explained about dentinal tubules
 1867: Neuman gave the term Newman’s sheath
 1891: Von Ebner gave the term Ebner’s growth lines or Imbrication lines
 1906: Von Korff gave the term Korff’s fibres
STAGES OF TOOTH DEVELOPMENT
LAMINA STAGE

 First morphologic sign of tooth development

 Visible at approximately 6th week of human gestation

 At this stage, basal cells of oral ectoderm proliferates

into underlying ectomesenchyme → primary epithelial
band
 Lingual process → Dental lamina Buccal process →
Vestibular lamina
 Distal extension of dental lamina → perm molars
BUD STAGE
 Primordia of enamel organ

 Dental lamina proliferate → tooth

bud

 Condensation of ectomesenchyme
→ Dental papilla

 Ectomesenchyme sur these two →

Dental sac
CAP STAGE
 The tooth bud assumes the shape of a cap


 Ectodermal compartment is called enamel organ

 Cuboidal cells → periphery of the dental organ →

Outer enamel epithelium

 Columnar cells that border the dental papilla →

Inner enamel epithelium

 Star shaped cells in center → Stellate reticulum

 Dental papilla cells proliferate and capillary buds

form
EARLY BELL STAGE
 Dental organ assumes the shape of a bell as cells
continue to divide but at differential rates

 Squamous cells → Stratum intermedium → ↑ ALP +

glycogen deposits

 Inner epithelium → diff into ameloblasts

 Dental papilla → peripheral cells diff into odontoblast

 Stellate reticulum collapses - nutrient capillaries

closer

 OEE- folds and capillary loops from dental sac

ADVANCED BELL STAGE
 Mineralization and root formation

 Predentin by odontoblast
 Enamel by Ameloblast

 Cervical portion of enamel → IEE+OEE→ HERS

( Hertwigs epithelial root sheath )

 Dental sac → diff into periodontal fibres →

embedded in cementum and alveolar bone
 DENTINOGENESIS

TGF, IGF n BMP in IEE Odontoblastic differentiation from

released peripheral dental papilla cells
Collagen matrix formation
phase

Chondroitin sulphate, Odontoblast takes Mineralization phase

fibronectin, laminin up Ca from tissue
fluids Matrix vesicle- alkaline phosphatase-↑ PO4-
with Ca forms apatite
DPP- key protein in min- binds to Ca n
transport it to min front
osteonectin- binding of apatite to collagen
Gla protien + phospholipids → seeds/nucleation sites Globular islands of mineralization
begins at center and grows radially

HA crystals- 300 times smaller than

in enamel
 As cell recedes- matrix continues-
cell process lengthens- enclosed in
Dentinal tubule
 4 um/day till eruption n occlusion
 Early dentin- korff’s fibres
 Radicular dentin- slower, less min
PHYSICAL PROPERTIES
Colour :
 Young age – light yellowish
 With advancing age – becomes darker
( reparative dentin )
 Clinical sig : Shade selection

Consistency :
 Visco-elastic and resilient
 Harder than bone but softer than
enamel
 Clinical sig : less tendency to fracture
than enamel
Ideal requirement of a restorative material is to have properties close to
properties of tooth structure

 Ideal requirement of restorative RESTORATIVE MOE COMP TEN

material is to have properties close MATERIAL Gpa STR STR
to the properties of tooth
structure. AMALGUM (LOW Cu) 20 343 60
Mpa Mpa

COMPOSITE RESIN 15-20 350- 75-90

(HYBRID) 400

TYPE 2 GIC 7.3 196- 18-26

250
A comparison of nanohardness of A comparison of elastic moduli of
dental tissues and a range of dental dental tissues and a range of dental
restorative materials restorative
COMPOSITION :

 35% organic matter and water  65% inorganic materia

 The organic matrix of dentin is  The principle inorganic component

collagenous embedded in ground of the dentin is hydroxyapatite
substance of mucopolysaccharides crystals

 It provides resiliency to the crown  Hardness more than bone and

which is necessary to withstand the cementum but less than enamel
forces of mastication
 ORGANIC SUBSTANCE
Non collagenous proteins:
• Dentin phosphoprotien (DPP) Growth factors:
• Dentin matrix protein 1 (DMP1)
Collagenous protiens: • Dentin sialoprotein (DSP) Bone morphogenic
Type I collagen fibrils and • Bone sialoprotein (BSP) protein(BMP)
Type V collagen fibrils (minor) • Osteopontin, Osteocalcin Insulin like growth factor(IGF)
• Proteoglycans Phospholipids
Transforming growth factor B
INORGANIC SUBSTANCE
 Hydroxyapatite 3Ca3 (PO4 )2 . Ca (OH)2
 Also contains small amounts of phosphates, carbonates and sulphates.
 Distint difference wrt enamel-
 Crystals are almost 300 times smaller
 In the process of decalcification the organic constituents can be retained and
still maintains shape of dentin ( unlike enamel)
 DENTINAL TUBULES
 course → gentle curve in the crown → resembles an S ( sigmoid course) in shape

 Primary curvatures - Starts at right angles at the pulpal surface, the first convexity directed towards the apex of
the tooth. These tubules end perpendicular to the DEJ & CDJ Secondary curvatures – rest of the length exhibits
regular s shaped curvatures

 Dentin thickness → 3-10mm or more ( tubules are longer) ,Ratio btw outer and inner surfaces of dentin is about
5:1

 No. of tubules per square millimeter varies from 15000 at the DEJ to 65000

at the pulp - density and diameter increases with depth

Terminal branches of dentinal tubules

 At the DEJ, dentinal tubules branch → increased

density of dentinal tubules in C-S of dentin in this region.
 Branching is more profuse in root dentin than coronal dentin
 Root tip, incisal edges and cusp tips- tubules almost straight
 Near pulp- closely spaced
larger diameter
 Near DEJ- widely spaced
narrower diameter

o Clinical sig- Hypersensitity, Post op sensitivity-marginal leakage,

component of Hybrid layer in dentin bonding
PERITUBULAR DENTIN
 The dentin that immediately surrounds the dentinal
tubules is termed peritubular dentin ( except in
dentin near pulp)
 Constricts dentinal tubules to a diameter of 1µm near
DEJ
 Highly mineralised than intertubular dentin
 Twice as thick in outer dentin(approx. 0.75um) than
inner dentin(approx. 0.4um)
 Calcified tubule wall has an inner organic lining
termed the Lamina Limitans

 Clinical sig : etching of cavity floor opens up tubules

because of decalcification of peritubular dentin
INTERTUBULAR DENTIN
 Located between the zones of
peritubular dentin (forms main
body of dentin)
 The fibrils diameter 0.2-0.5 um
crossbanding at 64um intervals.
 HA crystals oriented parallel to
the collagen fibres

 Clinical sig- One half of its volume

is organic matrix, specifically
collagen fibres (hence retained
even after decalcification)
PREDENTIN
 First formed dentin and is not mineralised
 Located adjacent to the pulp tissues 2-6µm
wide, depending on extent of activity of
odontoblasts
 Un-mineralized
 As collagen fibres undergo mineralization at the
predentin-dentin junc, predentin becomes
dentin and a new layer of predentin forms
circumpulpally

 Clinical sig- faster progression of caries

ODONTOBLASTIC PROCESS
 Are cytoplasmic extensions of the odontoblasts into
dentinal tubules
 The processes are largest in diameter near the pulp and
taper further into dentin.
 The odontoblast cell bodies are approximately 7um in
diameter & 40um in length
 life span = age of the tooth
 some processes traverse entire thickeness of dentin
 some maybe shortened process in tubules that are
narrow and obliterated by mineral deposit.
DENTINO-ENAMEL JUNCTION

 The DEJ is a complex and critical structure

uniting these two dissimilar calcified
tissues.
 Shallow depressions of dentin- rounded
projections of enamel
 Scalloping are more pronounced in
occlusal areas – higher masticatory stress

 Clinical sig- transfer stress from enamel to

dentin
CEMENTO-DENTINAL JUNCTION

 Relatively smooth surface in perm tooth

 scalloped in decideous teeth
 wide zone- collagen, GAG, water
 Redistribute occlusal load to alveolar bone

 Clinical sig- Older patients-obturation

terminate 1mm above AF
PRIMARY DENTIN
 Dentin that is formed prior to eruption of
a tooth (before root completion)
 Classified as Orthodentin- the tubular form
of dentin lacking of cells
 found in teeth of all dentate mammals
 Secreted at a relatively higher rate
 Constitutes major part of the dentin in the
tooth
 TWO TYPES: MANTLE AND CIRCUMPULPAL
DENTIN
MANTLE DENTIN CIRCUMPULPAL DENTIN

Mantle dentin is the first formed dentin in Circumpupal dentin forms the remaining
the crown underlying the DE primary dentin or the bulk of the tooth

It is the outer or most peripheral part of the found below mantle dentin
primary dentin and is about 20 цm thick

larger diameter collagen fibres known as Von The collagen fibrils are much smaller in
Korff’s fibres ( silver stained ) diameter and are more closely packed
together

fewer defects defects maybe found more than mantle

dentin

less mineralised and provides cushioning Slightly more mineral content than in mantle
effect to the tooth dentin

globular mineralization globular or linear pattern of

mineralization(linear more uniform)
 A → pulp
B → ameloblasts
C → enamel
D → artifactual space

E → dentin
F → reticular fibers
G → odontoblasts
H → D-E junction

VON KORFF’S FIBRES

SECONDARY DENTIN
 Called Regular seccondary dentin → regular arrangement of
dentinal tubules
 Not in response to external stimuli
 Formed after root completion
 Narrow band of dentin bordering the pulp
 Similar to primary dentin except for fewer tubules
 There is usually a bend in the tubules where primary and
secondary dentin interface
 Formed slower than primary dentin and not formed uniformly

 Clinical sig- Appears in greater amounts on the roof and floor

of the pulp where it protects the pulp from exposure in older
teeth
TERTIARY DENTIN
 Also known as: Reparative, Reactionary, Regenerated dentin
or irregular secondary dentin
 Healing process initiated by the pulp ( TGF-ß and BMP)
 Localized formation of dentin at Pulp -Dentin border in
response to
noxious stimuli- Caries, Trauma, Attrition, Cavity Prep
 Bacteria, or their toxins, chemical subs from restorative
materials, migrate down tubules to pulp → stimulate pulpal
response
 Odontoblast process exposed or cut → survive or die
(intensity)
 If they survive → reparative dentin is formed
 if they die → replaced by migration of undifferentiated cells
from cell-rich zone of pulp → newly differentiated
odontoblasts lay down reparative dentin
 Fewer and more twisted tubules than normal dentin (glob
dentin and incr lines)
 Osteodentin → cells trapped in intercellular subs → rapidly
progressing caries
 There is ↓ Dentin permeability
Quality Depends on: intensity of stimulus and Vitality of pulp

 Clinical sig- Pulp capping procedures

INCREMENTAL LINES

 The incremental lines of Von Ebner or Imbrication lines appear as

fine lines or striations in dentin
 These lines reflect the daily rhythmic, recurrent deposition of
dentin matrix
 Run at right angles to the dentinal tubules.
 20 um apart → represent 5 day interval
 Daily increment decreases once tooth reaches functional occlusion
 Some of these incremental lines are accentuated
because of disturbances in the matrix and
remineralization process.
 Such lines are known as Contour lines of Owen
 These lines represent hypocalcified bands
 In the deciduous teeth and in the first permanent
molars, the prenatal and postnatal dentin is
separated by an accentuated contour line, this is
termed the Neonatal line
INTERGLOBULAR DENTIN

 Sometimes mineralization of dentin begins in small globular areas

that fail to fuse into a homogenous mass.
 This results in zones of hypomineralisation btw the globules.
 These zones are called interglobular dentin.
 Forms in crowns of teeth in the circumpulpal dentin just below the
mantle dentin
 Dentinal tubules pass uninterrupted→ defect in mineralization not matrix
formation
 Black in transmitted light
 Incidence :-

 Crown- cervical > middle 3rd >

coronal 3rd
 Root- cervical 3rd > middle 3rd

 Clinical sig- pathway for

propogation of caries
TOME’S GRANULAR LAYER

 In transmitted light→ zone adj to cementum appears

granular
 It slightly increases in amount from the CEJ to the
root apex
 Odontoblasts turn on themselves during early dentin
formation→ coalescing and looping of terminal
portions of dentinal tubules
 Remains unmineralized like interglobular dentin

 Clinical sig- pathway for propogation of caries

INNERVATION OF DENTIN
Nerve fibres 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 predentin and inner dentin

 Found in coronal zone especially in pulp horns

Nerve endings are packed with small vesicles

filled with neurotransmitter
THEORIES
 Direct neural stimulation
 Transduction theory
 Modulation theory
 "Gate" control / Vibration theory
 Hydrodynamic theory
DIRECT NEURAL STIMULATION

 According to which nerves in the

dentin get stimulated.
 Drawbacks: The nerves in dentinal
tubules are not commonly seen and
even if they are present, they do not
extend beyond the inner dentin
 Topical application of local
anaesthetic agents do not abolish
sensitivity ; Hence this theory is not
accepted
ODONTOBLAST TRANSDUCTION THEORY

 According to which the odontoblasts

process is the primary structure excited
by the stimulus and that the impulse is
transmitted to the nerve endings in the
inner dentin ( Synapse like complex)
 Drawbacks: Since there are no
neurotransmitter vesicles in the
odontoblast process to facilitate the
synapse or synaptic specialization
 odontoblast extend only 1/3rd to half
thickness of dentin
 MODULATION THEORY
 Upon irritation → odontoblast may become injured →
release a variety of neurotransmitting agents, vasoactive and
pain producing amines and protein → modulate the nerve
fiber action potentials by raising neuronal cyclic AMP levels

GATE CONTROL THEORY

 Melzack & Wall in 1965
 Transmission of impulses to the brain are modulated by
spinal-gating system.
 Large (A-beta) fibres inhibit transmission and small (A-delta
& C) fibres facilitate it. 
 When activity of spinal cord transmission cells exceed a
threshold, pain is percieved
 FLUID HYDRODYNAMIC THEORY
Brannstorm 1963
 Most popular and accepted theory
 According to which various stimuli →heat, cold, air blast
desiccation, or mechanical pressure→affect fluid movement
in dentinal tubule
 Fluid movement either inward or outwards→mechanical
disturbance of odontoblast process→nerve ending acts as
mechanoreceptor→pain
 Intradental myelinated A-β and some A-δfibres are thought
to respond to stimuli
 Sensitive teeth having many more (eight times) and wider
(two times) tubules at the buccal cervical area compared
to non-sensitive teeth
 odontoblasts express mechano-
and/or thermosensitive transient
receptor potential ion channels
(TRPV1, TRPV2, TRPV3, TRPV4,
TRPM3, KCa and TREK-1)
 These are likely to sense heat
and/or cold or movements of
dentinal fluid within tubules
 → Dental pain and odontoblasts:
facts and hypotheses. J Orofac
Pain. 2010;24:335–349. [PubMed]
PERMEABILITY OF DENTIN
 Dentinal tubules become occluded by growth of peritubular dentin or
reprecipitation of minerals from demineralized areas of dental caries
 Outward flow of fluid and odontoblast process acts as barrier for entry of
bacteria and their toxins

Outer dentin Inner dentin close to pulp

↓ ↓
tubular occlusion, smear layer, lack number and diameter of tubules
of communication btw primary and more
reparative dentin ↓
↓ increases permeability
reduced permeability ↓
↓ more sensitivity
lesser sensitivity
DENTINAL FLUID

 Free fluid occupies 1% of superficial dentin and 22% of

total volume of deep dentin
 Ultraflitrate of blood from pulp capillaries
 Contains plasma proteins
 Serve as a sink from which injurious agents can difuse into
the pulp producing inflammatory response
 Also serve as a vehicle for ingress of bacteria from a
necrotic pulp into periradicular tissue
AGE AND FUNCTIONAL CHANGES
Vitality of dentin
 Odontoblasts and its processes are an integral part of dentin
 And so vitality is understood to be the capacity of the tissue to react to
physiologic and pathologic stimuli, dentin must be considered a vital tissue
 Dentinogenesis is a process that continues 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 slower rate.
This is secondary dentin.
 Pathologic changes in dentin such as dental caries, abrasion, attrition or the
cutting of dentin in operative procedures cause changes in dentin. They are
the dead tracts, sclerosis and the addition of reparative dentin.
DEAD TRACTS AND BLIND TRACTS

 In dried ground sections of normal dentin the odontoblast processes

disintegrate, and the empty tubules are filled with air. They appear black in
transmitted and white in reflected light
 In teeth with vital pulp→as a result of caries, attrition, abrasion, cavity
preparation, or erosion
 With time, these dead tracts can become completely filled in mineral. This
region is called blind tracts and appears white in sections of ground tooth.
 The dentin in blind tracts is called sclerotic dentin

 Clinical sig - decreased sensitivity due to occlusion of tubules and appear to a

greater extent in older teeth
A - dead tracts
B - interlobular dentin
C - primary curvatures
SCLEROTIC DENTIN

 Presence of irritating stimuli -Caries, Attrition,

Erosion, Cavity Preparation - deposition of Apatite
Crystals & Collagen in dentinal Tubules
 protective changes in the existing dentin
 prevalent in older individuals especially in the
root dentin
 also called transperant dentin→refractive indices
of dentin becomes equalized

 Clinical sig - reduce permeability of dentin and

prolong pulp vitality
DEVELOPMANTAL DISTURBANCES
DENTINOGENESIS IMPERFECTA

Anomaly of mesodermal portion of the odontogenic apparatus.

 TYPE I -Assoc with. O.I
 TYPE II -Not Assoc with O.I
 TYPE III -Brandy wine Type
CLINICAL FEATURES
 Tulip Shaped teeth, Bluish-grey- Yellow/Brown Translucent.
 Enamel chips away exposed dentin → rapid attrition.
 Amber appearance, excessive wear, multiple pulp Exposures.
REPARATIVE DENTIN

 If the dentin forms as a reaction to an irritant

(trauma or dental caries) to protect the pulp,
it is called reparative/re
active/tertiary/irregular secondary dentin.
 The tertiary shows irregularity in the number,
size, and arrangement of tubules-the
irregularity increases with the rapidity of
formation.
 RADIOGRAPHIC FEATURES
 Partial/complete obliteration of pulp chamber, root canals
 Shell teeth- Normal enamel, thin Dentin, short root

TREATMENT
 In patient with DI, one must first be certain which type
he/she are dealing with.
 Severe cases of DI type 1 associated Osteogenesis imperfecta
can present significant medical management problems.
Careful review of the patient's medical history will provide
clues as to the severity of bone fragility based on the number
of previous fractures and which bones were involved.
 Patients not exhibiting enamel fracturing and rapid wear →
less severe cases → bleaching to treat dicoloration Upper left and right central incisor after the
reconstruction of labial surface with direct
 Bonding of veneers may be used to improve the esthetics for
composite labial veneers
anteriors
 In more severe cases, where there
is significant enamel fracturing and
rapid dental wear, the treatment
of choice is full coverage crowns.

 Dentinogenesis imperfecta : a
challenge for root canal treatment-
case report
CMP → thin dentinal walls
pulp chamber and root canal were totally
obliterated → perforation and canal
deviation resulted
DENTIN DYSPLASIA(ROOTLSS TEETH)
 Rare dental anomaly
 Normal Enamel, Atypical Dentin, Abnormal Pulp
Morphology

CLASSIFICATION: (Acc. To WHITKOP)

 TYPE I- RADICULAR
 TYPE I- CORONAL

CLINICAL FEATURES
Normal Morphology, Amber Translucency. Extreme
Mobility and
Premature Exfoliation Primary- yellow /brown- grey. A case of dentin dysplasia type I in a
12-year-old Iranian boy
 RADIOGRAPHIC FEATURES
 Deciduous - pulp chambers completely obliterated,
short conical roots.
 Permanent- crescentshaped pulp chambers-Difficulty
in locating canal orifices.Permanent "thistletube"
appearance

HISTOLOGIC FEATURES:
 Calcified/ atubular dentin
 Lava flowing around boulders pattern is seen
 Amorphous forms and cascades of dentin
 TREATMENT

 Effective oral hygiene, caries preventive procedures

 primary dentition - space maintainers
 Stainless steel crowns
 teeth with pulp necrosis and peri-apical abscess - Extraction
 Follow-up and routine conservative treatment
 peri-apical surgery and retrograde filling, which is recommended in teeth
with long roots
 Since these patients usually have early exfoliation of the teeth and,
consequently, maxillomandibular bony atrophy, treatment with a
combination of onlay bone grafting and a sinus lift technique to
accomplish implant placement can be used successfully
Dentin dysplasia type I: a challenge for treatment with dental
implants - case report -2007

preoperative panoramic radiographs showing

initial clinical situation.
features of dentin dysplasia type I.
 postoperative panoramic radiographs after
implant setting and bone augmentation.

Alveolar ridge augmentation

of the maxilla (above) and
the mandible (below) using
autogenous bone grafts from
the iliac crest.

postoperative clinical situation after

completion of the implant treatment.
 REGIONAL ODONTODYSPLASIA

 The condition is characterized by deficient and

abnormal formation of both dentin and enamel
 Not hereditary
 Usually seen in Maxillary Anteriors

Multiple discolored hypoplastic teeth

CLINICAL FEATURES: along with multiple unerupted teeth
 unusually large pulp chambers with thin layers of in right maxillary segment
enamel and dentin are evident, Delay or failure of
eruption, irregular shape.

RADIOGRAPHIC FEATURES:
"Ghost Teeth."
 HISTOLOGIC FEATURES:
 Reduction in amount of dentin
 Widening of pre-dentin layer
 Presence of large interglobular dentin
 Iregular tubular pattern of dentin

TREATMENT
 Multidisciplinary approach
 Meticulous oral hygiene
 Most of the cases extraction
 Followed by esthetic and Prosthetic rehabilitation
 DENS IN DENTE
 Dentin & enamel forming tissue invaginate the whole length of a tooth.
 Arises due to localised external pressure, focal growth retardation,focal
growth stimulation in certain areas of tooth bud
 Pear shaped invagination

RADIOGRAFICAL FEATURES-
 "tooth within a tooth" appearance

 Food lodges in the cavity to cause caries which rapidly penetrates the
distorted pulp chamber
 Endodontic Treatment Difficult- abnormal Anatomy
CINICAL CONSIDERATION OF DENTIN
EXPOSURE OF DENTINAL TUBULES
 Tooth wear; attrition, abrasion, erosion and abfraction, fractures, caries,
cavity cutting procedures etc. lead to exposure of Dentinal tubules.
 1-2 mm of exposed dentin damages→ upto 30,000 living odontoblasts.
 bacterial toxins, strong drugs, undue operative trauma, unnecessary thermal
changes, or irritating re- storative materials can insult cells of exposed dentin
 It is advisable to seal exposed dentin surface with non irritating, insulating
substance ( varnishes, bonding agents or restorations)
DENTIN HYPERSENSITIVITY
 Short, sharp pain → exposed dentine in response to stimuli→ thermal,
evaporative, tactile, osmotic or chemical

Etiology-
 Enamel loss - Attrition, Abrasion, Erosion, Abfraction.
 premature occlusion, Orthodontic tooth movement
 Improper instrumentation, Enamel and cementum do not meet at the CEJ
 Gingival recession cause: Tooth brushing, ANUG and ANUP, Self- inflicted
injury, Periodontal disease, Periodontal surgical and non-surgical procedures,
dehiscence / fenestrations.
 THEORIES OF DENTINAL HYPERSENSITIVITY
 Direct neural stimulation theory
 Gate control theory
 Transduction theory
 Hydrodynamic theory

TREATMENT
Removing etiologic factors and preventing DH
 Overenthusiastic brushers
 Periodontal treated patients
 Bulimics
 People with xerostomia
 High-acid food/drink consumers
 Older people exhibiting gingival recession
 Chewing ‘smokeless’ or ‘snuff’ tobacco
AT HOME IN OFFICE
Desensitizing toothpastes, Agents that alter neural response Agents that block dentinal tubules
mouthwashes and chewing gums potassium salts (potassium nitrate) Flourides-
containing - 2 forms-aqueous solution and Sodium fluoride 2 % , stanous
adhesive gel flouride, APF
 potassium salts such as Fluorides and fluoro-silicates with
potassium chloride, potassium MOA→ number of potassium ions iontophoresis
citrate, and potassium nitrate decrease when they enter dentinal
 sodium flouride tubules and decrease the Oxalates- Potassium oxalate
 calcium phosphate excitability of nerves that transmit
complexes(CCP_ACP) pain Varnishes- Flouride varnish
 calcium carbonate
 8% arginine Lazer therapy- GaALAS Adhesive resins- varnishes,
laser,Nd:YAG laser, Er:YAG laser bonding agents, and repairing
MOA→ and CO2 laser resin composites
 blocking axionic action of intra-
dental nerve fibres→decreases MOA→1. Occlusion through Bioglass
excitability coagulation of the proteins of the
 remineralizing the exposed fluid inside the dentinal tubules Portland cement- silicate cement
tubules 2. Occlusion of tubules through
partial sub-melting
Remin agents- CCP-ACP, GC Tooth
3. Discharging of internal tubular
Mousse
nerve
DENTAL CARIES

 Due to increased permeability of dentin by tubules,it acts as

a pathway for various kinds of micro organisms
 Rapid spread of caries through Dentin
 ZONE 1- Fatty degeneration of odontoblast
 ZONE 2- Dentinal Sclerosis
 ZONE 3- Decalcification
 ZONE 4- Bacterial invasion
 ZONE 5- Decomposed dentin

TREATMENT- excavation and restoration with appropriate

restorative material depending on extent of caries
INFECTED DENTIN AND AFFECTED DENTIN
CAVITY PREPARATION
 Cavity floor is in dentin in most cases
 Dentin is RESILIENT absorbs and resists forces of mastication and deformation

OPERATIVE INSTRUMENTATION
 AVOID-Excessive cutting heat generation, Continuous drying
 USE: Air- Water Coolant, Sharp hand Instruments- most suitable
 Tungsten Carbide Burs to Cut vital Dentin →Less Heat generation.
Frictional heat generated

DENTINand
evaporation DESCICATION
expansion ofAND ASPIRATED
the tissue fluid inODONTOBLASTS
dentin

Teeth
 loss reduction
of tissue fluid atwithout water
the surface coolantdentin
of exposed → heatandtrauma→ desiccation of the
dentin
an and aspiration
outwardcapillary flow of odonto- blasts into the dentinal tubules.
 Also occurs following prolonged application of an air blast
 Aspirated odontoblast → autolysis within 24 hr →reparative dentin formation in
1 to 3 months
BEVELS
PULP PROTECTION

 Irritants from Restorative Materials → Pulpal Damage

 Thermal Protection- Bases below Restoration

 Chemical Protection- Cavity liners and varnishes

VITAL PULP THERAPY
 The Reparative dentin formation can be stimulated → cavity lining materials
such as Calcium hydroxide
 Materials like MTA, Biodentine can be used as a substitute to dentin(capable
of inducing reactionary dentin by stimulating odontoblastic activity and
repairative dentin by induction of cell differentian)
 Includes Direct and Indirect pulp capping techniques
 DENTINAL BRIDGE repair tissue forms across the pulpal wound
REPARATIVE DENTIN AND REACTIONARY
DENTIN

Clinical sig : main MOA in pulp capping procedures

REMAINING DENTIN THICKNESS
INTERNAL RESORPTION

 Also called Pink Tooth of Mummery

 Begins centrally within the tooth → inflammatory hyperplasia of pulp
 associated with carious exposure and pulpal infection
 CLINICAL FEATURES : Pink hued area on crown of tooth
 HISTOLOGY : Presence of osteoclasts, odontoclasts → Odontoclastoma
 TREATMENT : If perforation has not occured - RCT
 If perforation has occured - extraction
RESTORATIVE MATERIAL

 A restoration placed in a cavity preparation can develop contraction gaps

between the restoration and the cavity wall.
 This gap then fills with fluid from the outflow of tubules or saliva from
external surface → MICROLEAKAGE
 An environment is created for bacterial growth and failure of restoration →
SECONDARY CARIES
SMEAR LAYER AND SMEAR PLUG
 Smear Layer term most often used to describe the grinding debris left on
dentin by cavity preparation
 Cutting debris when forced into dentinal tubules, it forms plugs known as
smear plugs
 Smear layer 1-3 um Smear plug : 40 um
 Significance - Lowers the permeability of dentin surface and occludes it
 Disadvantage: prevents the adhesion of restorative materials in the dentin
DENTIN CONDITIONING
 Classic acid etchant → de-mineralize PERITUBULAR DENTIN → widens the
tubule increasing permeability.
 Conditioning - cleaning, structural alteration, and increasing the adhesiveness
of the substrate
 The acid should be passively applied for short periods 5-15 sec
 This technique leaves behind smear plugs in tubule apertures
 The intact collagen framework interacts with priming agents which penetrate
through the remnant hydrophilic smear layer and into the Intertubular dentin
and fills the spaces left by the dissolved apatite crystals.
 This allows acrylic monomers to form an interpenetrating network around
dentin collagen
BONDING ON DENTIN

 Adhesive resin of the dentin

bonding agent micromechanically
interlocks within the inter tubular
dentin and surrounding collagen
fibers
 Hybrid layer also called Resin-
Dentin interdiffusion zone is
formed in following manner:
 ETCHING
Removes smear layer PRIMER ADHESIVE RESIN
exposes collagen fibres penetrates collagen along with primer
dissolves intertubular network forms resin microtags
dentin
 B. Adhesive resin (blue) bonded to smear
A. Smear layer-covered human dentin layer (no-etch bonding systems). When
stressed to failure, the split occurs at the
smear layer (black gap), indicating that it
was the weak link when using the no-etch
technique.
FUSAYAMA’S TOTAL ETCH CONCEPT

After etching,
If the surface is dried, the fibrils collapse
upon themselves, decreasing the size of
interfibrillar spaces that are necessary for
resin uptake.(Pashley et al.5)
stiffness of normal dentin- 19000 Mpa
stiffness of acid ecthed dentin- 1 Mpa
Wet bonding technique: The water used
in wet bonding or in primers re-expands
the collapsed matrix when the total-etch
technique is coupled with wet bonding,
preparing it for resin uptake (Kanca 1991)
Technique sensitive - Possible complication

“over-wet” phenomenon (especially in proximal boxes). When single bottle primer/

adhesives are applied, the solvent may diffuse into the water, instead of vice versa, forcing
adhesive monomers to undergo phase changes, resulting in blisters and resin globules.
These blisters may compress when the restoration is under occlusal function, forcing
dentinal fluid toward the pulp and causing postoperative sensitivity
single-bottle, 2-step, total-etch, wet-bonding technique
Combined primer and Adhesive
Applied twice →1. to remove excess water and monomer
pennetration →2. excess solvent to redissolve resin globules and
leaves more homogenous film
NEW CONCEPT OF RETAINING SMEAR LAYER

Acidic monomers dissolved → 30% to 40% hydroxyethyl methacrylate (HEMA, a very water-
soluble priming monomer) →new formulation →self-etching and self-priming adhesive →
etch through smear layers into the underlying dentin

Smear layer incorporated into hybrid layer → smear plug retained → reduced post op
sensitivity → higher bond strength (thinner hybrid layer)
ELLIES CLASSIFICATION OF FRACTURE
TREATMENT:

Class 1 - bond to tooth if fragment available, restore with composite resin

depending on extent + location of fracture
Class 2 - bond to tooth if fragment available, provisional treatment with glass
ionomer or permanent restoration using a bonding agent + composite resin
Class 3 - open apex → preserve pulp vitality- pulp capping or partial pulpotomy
closed apex → root canal treatment
Class 4 - same as for class 3
ENDODONTICS

 Secondary& Tertiary Dentin → obliteration of Pulp Chamber & Root Canals →

Endodontic treatment → Difficult
 Complex Endodontic biofilms → dentinal walls of root canal → proper
instrumentation and irrigation
 Smear layer → removed with chelating agents like EDTA → facilitate
penetration of sealer
 Apical Dentin Chip Plug → Dentinal Chips compacted at apex during
Obturation → provides a “biologic seal” → prevents over obturation
ENDODONTIC SURGERY

 Foremost cause of endodontic treatment faillure

→ persistence of microbial infection
 Bacteria harboured → isthmuses, dentinal tubules
and apical ramifications → may evade
disinfectants
 Complex anatomy of apical-third of Root canal
→ Accessary canals, apical delta
 All isthmus must be found, prepared and filled
during surgery
Material Advantage Disadvantage
Zinc oxide Eugenol is released have Cannot regenerate
eugenol cements effects cementum and
on healing has limited antibacterial
effect
Glass ionomer marginal adaptation is sensitive to moisture
cements better with light during
cured GIC initial set which increases
Resin modified GICs – less solubility and reduces
sensitive to moisture bond strength

Composites Can give very good seals Blood contamination can

in vitro reduce
(next best after MTA – but bond strength and
very good increase
moisture control needed) leakage.
MTA Good seal, biocompatible Takes almost four hours
Capacity to stimulate to set
hard tissue formation –
cementum laid down
adjacent to MTA