SlideShare utilise les cookies pour améliorer les fonctionnalités et les performances, et également pour vous montrer des publicités pertinentes. Si vous continuez à naviguer sur ce site, vous acceptez l’utilisation de cookies. Consultez nos Conditions d’utilisation et notre Politique de confidentialité.
SlideShare utilise les cookies pour améliorer les fonctionnalités et les performances, et également pour vous montrer des publicités pertinentes. Si vous continuez à naviguer sur ce site, vous acceptez l’utilisation de cookies. Consultez notre Politique de confidentialité et nos Conditions d’utilisation pour en savoir plus.
Dentin forms the bulk of the tooth structure-it is a mineralized connective tissue that borders the enamel and cementum and encloses the pulp. A thorough understanding of the basic str and biology of the dentin is essential for a success in clinical dentistry.
Dentin is the first formed dental hard tissue, thus it determines the shape of the crown and roots. The formation of dentin precedes the formation of enamel.Differentiation of epithelial and mesenchymal cells into amelo and odonto begins in late bell. Dentinogenesis begins in the late bell stage of tooth development and at the site of the future cusp tips, from where it proceeds apically.
THE FORMATION OF DENTIN TAKES PLACE in two stages. The synthesis of organic matrix and its subsequent mineralization. This process is carried out by specialised cells known as odontoblasts. Before we start with the formation of dentin, lets see briefly about the odontoblasts.
Odontoblasts are the cells of the pulp. They are derived from the dorsal cranial neural crest, and are thus mesenchymal in origin. They lie along the dental papilla adjacent to the Inner Enamel ep. The development of odontoblasts is initiated under the epigenetic influence of various signaling molecules- mainly Transforming growth factor β produced by the developing ameloblasts.. This is seen in the early bell stage of tooth development.
The odontoblasts develop from the ectomesenchymal cells of the dental papilla- these are typical undifferentiated flattened cells with a large central nucleus, sparse cytoplasm and few cell organelles. These cells under the influence of the developing inner enamel epithelium differentiate to form preodotoblasts and then odontoblasts. Preodonoblasts are small ovoid cells with a high nucleus to cytoplasmic ratio and poorly developed organelles. These increase in height and become cylindrical to form secretory odontoblasts. These are mature cells which are 40 µm length , 4-7 µm diameter, having a large nucleus and abundant RER, golgi apparatus, mitochondria and secretory granules.
The collagen fibres initially deposited are at right angles to the Dej, later however, the smaller fibrils deposited are laid down perpendicular to the dentinal tubules and parallel to the dej. The Larger fibres initially laid down are known as VON Kroff’s Fibres. They are cork screw shaped and fan out from the odontoblasts towards the DEJ. These are Argyrophillic in nature ie stain Black with silver.
The secondary dentin is laid down at a much slower rate of about 1 µ/day.
H. A. crystals of dentin = cementum & bone. They are 33 times smaller than the enamel crystals.
:Deposition of HA crystals in several discrete areas of matrix at any one time. With continued With continued crystal growth, the globular masses are formed which enlarge and fuse to form single calcified mass . This is seen in mantle dentine where matrix vesicles are formed and the mineralization foci grow & coalesce. With continued crystal growth occurs, globular masses are formed these enlarge and fuse to form a single calcified mass, thus the pattern of Crystal deposition is radial. areas where the globules do not fuse are hypomineralized and known as interglobular dentin.
In a linear pattern- the crystals are deposited along and within the collagen fibres- forming a more uniform pattern.
The formation of root dentin is initiated by the cells of he HERS once the enamel and dentin formation have reached the future CEJ. The HERS consists of IEE and OEE. It induces the dental paplila cells to lay down dentin.
DENTIN is pale yellow to white in color and the color darkens with age and pathology, thus carious dentin is darker in color. Dentin is resilient as compared to the brittle enamel, is provides stability to the overlying enamel preventing fracture. The hardness of Dent is 68KHN. dentin is softer than enamel, but harder than bone or cementum, it is and is more susceptible to shearing forces. It can be cut using hand instruments. Dentin thus can be deformed and aids in better gripping of the restoration in the prepared cavity. This occurs when dentin regains its original position while the rest. Mat. Remains rigid thereby completely obliterating any space in cavity preparation.
The organic phase of dentin in which mineral crystals are embedded is often referrd to as the organic matrix. Phosphoryn is a highly phosphorylated phosphoprotein involved in extracellular mineralization. It is unique to dentin and makes up half of the non collagenous matrix. and is not found in any other mesenchymal cell lines.
Dentin is a tubular structure composed of dentinal tubules. The basic structural components of the dentin include the odontoblast process- which is responsible for its synthesis and maintenance, a non mineralized matrix-the predentin, whch lies next to the odontogenic zone- and mineralized matrix includes peritubular and intertubular dentin.
These are the most striking feature of dentin. And extend from the pulp to the DEJ. The size of the dentinal tubules varies with location- it is about 3-4µ at the pulp and about 1µ at near the DEJ.The tubules have smaller branches known as canaliculi extending at right angles. These are about 1µm in dia, 2µm in length.
Minute curvatures are present along the entire length of the dentinal tubules.they are sinusoidal in shape.
The presence of collagen fibres reduces the permeability of dentin.
Predentn is the first formed dentin Matrix. It is laid down by the odontoblasts as a layer of unmineralised matrix having a thickness of about0-50 microns. It is composed of both collagen and non collagenous matrix proteins like choindroitin sulphate, phosphoproteins etc. as the formation of dentin continues, the predentin gradually mineralises to form dentin. The thickness of the predentin layer remains constant as a new layer is formed circumpulpally. It is easy to identify in h/e sections as it stains less intensely than mineralized dentin.
Peritubular dentin is also known as Periluminal or intratubular dentin. It forms the walls of the Dentinal tubules and surround s them like a collar. It is 40 % more mineralized than inter tubular dentin and has a hardness of 52KHN. tHe thickness of peritubular dentin varies from ).75 microns at the dentin ssurface to about 4 microns near the pulp., thus the dentinal tubules become wider nearer the pulp, leading to increased sensitivity.
Intertubular dentin is the dentin present between the dentinal tubules. It forms the main body of dentin and is the the primary secretory product of the odontoblasts. Interubular dentin has a greater organic content as compared to peritubular dentin.
Dentin mineralization follows a globular pattern, when these globules fail to colasce, the give rise to certain unmineralized areas within the dentin. This is known as interglobular dentin. It is found in the circumpulpal dentin below the mantle dentin, subjacent to pits and fissures. The amount of interglobular dentin increases in cases od Vt. D deficiency or in Hypopophatasia.
When 2° curvatures of tubules become coincident – optical effect so produced →contour lines of Owen. Rare in primary dentine . Hypomineralised areas – disturbance in matrix formation ? Illness/inadequate nutrition.
It is an seen in. it is which that occurs at birth. The.
The Dentinoenamel Junction Is scalloped in nature. The convexities of The Scallops are toward the dentin. The round. This provides a firm hold of the enamel cap onto the dentin. At times, the dentinal tubules pass across DEJ and enter the Enamel. These are known as enamel spindles.
Peripheral to Granular layer of Tomes is 10 µm less mineralized layer Hyaline layer of Hopewell Smith which is now known to be a product of Hertwig epithelial root sheath. In the apical portion the DCJ forms the apical constriction . Which is of special concern in endodontics – termination of instrumentation
Primary Dentin s the dentin laid down rapidly during tooth development, before the formation of the apical foramen. It is of two types- mantle Dentin and Circumpupal dentin. Mantle dentin is located below the Dej and is about 20 microns thick, circumpulpal dentin on the other hand is located beween the mantle dentin and the predentin. It forms the bulk of the tooth and is about 68 mm in thickness. Mante dentin is less minerlised and also has less no. of defects as compared o circumpulpal dentin. The collagen fibres of mantle dentin are larger is 0.1-0.2µ in diameter and they are oriented perpendicular to the DEJ. Those of circumpulpal dentin are smaller- about 0.02-0.05 microns in diameter and parallel to the DEJ.
Smith et al have classified tertiary dntin into reactive or reparatve
Reparative dentin can histologically be seen as having more twisted tubules than normal dentin. There might be fewer tubules, Dentin forming cells may also be included in the intercellular matrix- this is known as ostodentin. He tubules may be irregularly arranged or A combination of osteodentin and tubular dentin may also be seen.
reparative dentin formed seals of the dentinal fluid.Initial step of fomation of sclerotic dentin
Stimuli may induce not only reparative formation but also additnal protective mechanism
Refers to the exposed portion of reactive sclerotic dentine , where the slow caries has destroyed the formerly overlying tooth structure , leaving a hard , darkened , cleanable surface. Resistant to further caries Attack. .
The percentage of tubules innervated is about 40% near the pulp horns and decreases to 1% at or below the CEJ
Each of these theories has supportive factors as well as information that is non supportive in regard to the mechanism of conduction through dentin.
Stella and Fuentes in 1963 claimed to have seen nerve fibres near the DEJ through an optical miroscope. However, this was not confirmed by various ulit states that nerve fibres extend into the outer dentin till the DEJ. The nociceptive stimuli are picked up at or below the DEJ and carried to the pulp via nerve ending activation and then directly without synapse to the descending nucleus of the trigeminal system. trastructural studies.
Support is demonstraed when histamine or substance p is placed on cut dentin- no nociception is recorded. However, when aconitine a substance that excites cutaneous mechanoreceptors is used- activation of receptors in the dentinal tubule occurs.
Dentinal tubules act as small capillary tubes through which fluid movement occurs. Stimuli which remove the fluid from the tubule like dehydration- cause an outward flow of fluid-
Hypersensitivity is an unusual symptom of the pulp dentin complex. Characterized by a sharp pain which is easily localizable. It is mostly caused by the exposure of dentinal tubules due to attrition, erosion etc. or due to loss of cementum or covering gingiva. concept that alteration in the fluid and cellular contents of dentinal tubules causes stimulation of free nerve endings in contact with these cells
Dentin is a permeable tissue due to its tubular nature. The permeability can be broadly decided into trans dentinal- where there is movement of substances through the entire thickness of dentin via the deninal tubules and Intradentinal- ie movement of exogenous substances into the intertubular dentin – this is seen mainly during bonding. This leads too passage of irritants towards the pulp. Decreased Dentin thickness leads to increased permeability, thus dentinal tubules have to be sealed during restorative procedures to prevent pulpal irritation.
Dentin may be exposed due to physiologic Exposed Tubules should be sealed with non irritating, insulating substancesal changes such as tooth wear, dentinal fractures, cavity cutting proced Exposed Dentin- Should not be insulted by toxins, undue operative trauma , or irritating restorative materials. ures etc.
This is due in part to the spaces in Dej due to en. Tufts and spindles and due to the open and branched dentinal tubules
Dentine must be treated with great care during restorative procedures to prevent damage to odontoblasts. Air – water spray to be used with high speed hand pieces to avoid heat generation Continuous drying causes dislodgement of odontoblasts from periphery of the pulp and their aspiration within the dentinal tubule. Tungsten carbide burs should be used to cut dentin instead of diamond point as it causes less heat generation
Adhesion to dentin remains still as a challenge because of its composition as the dentin contains substantial amount of organic material and water and also because of its tubular nature and the presence of smear layer. Formed when dentine is cut or abraded Consists of denatured collagen , HA crystals , debris →1-4 µm thick Advantages : ↓ dentine permeability to toxins , bacteria and oral fluids
↓ Low viscosity monomers diffuse into this region to form resin – dentine interdiffusion zone . ↓ On polymerisation – HYBRID LAYER of resin reinforced dentine is formed .
A method finding increasing favor, and one that inadvertently happens more often than not, is the apical dentin chip plug, against which other materials are then compacted. It provides A “biologic seal” rather than a mechanochemical seal.
It is a rare dental anomaly characterized by normal enamel, atypical dentine with abnormal pulp morphology. Witkop classified into following types
Unusual anomaly -Localized areaThin Enamel and Dentin, Large Pulp Chamber.
I’d like to conclude by saying that dentin forms an integral part of the tooth str. It has a regenerative potential and is a vital tissue provides support to the overlying enamel and protection to the underlying pulp. Thus we as clinicians should respect the dentin and do it no harm- intentional or unintentional.
DEPARTMENT OF CONSERVATIVE DENISTRY
Structure of Dentin
Types Of Dentin
Age and functional changes
Innervation of Dentin
• 1771 – John Hunter →hard tissue.
• 1775 – Anton Von Leeuwenhoek: Described tubular structures.
• 1837 -Purkinje and Retzius explained about Dentinal Tubules.
• Cuvien gave the name “Ivory” to Dentin
• 1867 – Neuman gave the term Neuman’s sheath
• 1891 – Von Ebner gave the term – Ebner’s growth lines or
Imbrication lines .
• 1906 – Von Korff gave the term – Korff’s fibres
• Process of Dentin
• Dentin-First Formed Dental
Hard Tissue –crown and
• -Formation of Dentin
• Late Bell stage.
• Future cusp tips, Proceeds
LATE BELL STAGE
• Formation Of Dentin- similar to bone and
1. Synthesis Of Organic matrix
2. Subsequent Mineralization.
Carried out by- ODONTOBLASTS
• Cells Of Pulp.
• Derived - Dorsal Cranial Neural Crest,
Mesenchymal in origin.
• Lie along Dental papilla- Adjacent to
• Tall columnar cells- length 25-40 µm ,
diameter 4-7 µm,
• Development- Initiated by epigenetic
influence of various signalling
molecules produced by Ameloblasts.
ECTOMESENCHYMAL CELLS- Undifferentiated, Flattened
Cells with a large Central Nucleus, Sparse Cytoplasm.
PRE-ODONTOBLASTS - small, ovoid cells with a high
nuc :cyt ratio poorly developed organelles.
SECRETORY ODONTOBLASTS. : Tall columnar cells , 40
µm length , 4-7 µm diameter, Large nucleus – with upto 4 nucleoli,
Abundant RER, Golgi apparatus, mitochondria ,secretory
granules- near the process.
TRANSITIONAL ODONTOBLASTS: Narrower, fewer
organelles, autophagic vacuoles
AGED ODONTOBLASTS: Reduction in length and cytoplasmic
Organelles, increase in number and size of lysosomes and
phagosomes, decreased secretory capacity, degenerate with age.
FORMATION OF PRIMARY
exists an acellular zone b/n the
IEE and Dental Papilla cells -
ground substance laid down by
the subodontoblastic cells.
The Cells of IEE become taller
and start differentiating into
Ameloblasts-polarity of cell
reverses.- Early Bell Stage.
They induce the differentiation of
odontoblasts, with reversal of
Odontoblasts Develop variable no.
of small processes at the formative
end- start depositing Collagen
This induces the Ameloblasts to
start depositing Enamel matrix.
INITIALLY: large dia Type III
Collagen - 0.1- 0.2µ
VON KORFF’S FIBRES
-Cork Screw Shaped
-Perpendicular to DEJ
-Argyrophillic in nature.
LATER- smaller Fibrils-
perpendicular to Tubules,
parallel To DEJ.
DEPOSITION OF COLLAGEN MATRIX
A Single Prominent Process- Odontoblast
Process- (TOME’S FIBRES)- Tubular nature Is
The rate of matrix production - about- 4-
8µ/day for Primary Dentin. And secondary
As more matrix is formed- the Odontoblast
Migrates centripetally, towards the pulp.
MINERALIZATION Begins once matrix is
about 5µ thick.
Various Matrix Proteins Influence Mineralization:
• DPP- Binds to Ca, Controls Growth of H.A
• Osteonectin- Inhibits growth of H.A crystals,
promotes their Binding to Collagen
• Gla-proteins, Phospholipids- Act as nucleators
to concentrate calcium.
• Proteoglycans- inhibit premature mineralization
seen in predentin.
CALCIFICATION OF MATRIX- initiated by
small crystallites within MatrixVesicles, budded from
Crystals- grow rapidly, rupture the matrix vesicles
Spread -clusters of crystallites → fuse with
adjacent clusters to form a continuous layer of
Initially- on the surface of the collagen fibrils and
ground substance, later within the fibrils- aligned
MATRIX VESICLES contain Alkaline Phosphatase
-↑ concentration of phosphates → combine with
Calcium →Hydroxyapatite Crystals.
PATTERNS OF MINERALIZATION
• GLOBULAR(CALCOSPHERIC) :Deposition of HA
crystals in several discrete areas of matrix at any one
• Continued crystal growth → globular masses →
enlarge → fuse → single layer of calcified mass.
• MANTLE DENTIN- matrix vesicles.
RADIAL CRYSTAL GROWTH INTERGLOBULAR DENTIN
LINEAR : When the rate of Dentin
formation occurs Slowly -Mineralization
front appears more Uniform –
ROOT DENTIN FORMATION
• Begins once Enamel& Dentin
formation reaches the future
• Initiated by Cells of HERS-
which induce odontoblast
• Collagen fibres- parallel to CDJ.
• Less mineralized, less no. of
• Complete- 18mths after
2-3 yrs -Permanent Teeth 18
• Provided by the Capillaries found in the subodontoblastic
layer of the pulp.
• Migrate between odontoblasts, and later - Regress.
COLOUR PALE YELLOW- WHITE
THICKNESS 3 - 10mm
MODULUS OF ELASTICITY 15-20GPA
HARDNESS 68 KHN
CARIOUS DENTIN 25 KHN
SCLEROTIC DENTIN 80 KHN
COMPRESSIVE STRENGTH 266 MPa
TENSILE STRENGTH 50 Mpa
PROPORTIONAL LIMIT 148 MPa
RADIOOPACITY LESS THAN ENAMEL 20
INORGANIC ORGANIC WATER
• Collagen – 82% , MAINLY TYPE I and some amount of Type
III and V.
• Non Collagenous Matrix Proteins- 18%
-Phosphoproteins- DPP(Phosphoryn), Gla-Protein.
-Glycoproteins- Dentin Sialoprotein,Osteonectin, Osteocalcin,
(Seen in mineralized matrix)
- Proteoglycans- Chondroitin SO4 (seen mainly in Predentin)
• Enzymes- Acid Phosphatase, Alkaline Phosphatase.
• Lipids- phospholipids, glycolipids etc. in traces.
• Dentinal Tubules
• Non mineralized
• Mineralized matrix-
• Most Striking Feature.
• From pulp to DEJ
• Occupy 1% superficial and 30%
volume of Deep Dentin.
• Size- varies with location.3-4µm near
pulp,1µ near the DEJ (ratio,5:1))
• Smaller branches- canaliculi (1µm in
dia, 2µm in length)-pathways of
• 1-2µ apart.
Tubules exhibit Sigmoid curvatures-More prominent
Least pronounced at cusp tips, incisal edges
At Increased Magnification- Secondary Curvatures.
A. - 50,000 to 90,000 / sqmm
B. - 30,000 to 35,000/sqmm
C. - 10,000 to 25,000/sqmm
Tubule density/ unit area - ↑es toward pulp.
No. of Tubules / unit area – crown> root.
• Potential space between tubule wall and od.
• Contents - nerves, collagen fibrils, plasma
proteins, glycoproteins and mitochondria.
• Surface Area Tubule lumina - 1% at DEJ, 22 %
• Organic sheath or membrane lining the Dentinal
• seen in EM sections.
( Dentin Lymph)
• Occupies space b/n dentinal tubule and od. Process.
• Ultrafiltrate- pulp Capillaries
• Composition is similar to that of plasma..Ca content in
dentinal fluid of predentin is 2-3 times higher than in plasma.
• Tissue pressure of pulp- 14 cm of H2O, (10.3mm Hg).
(Ciucchi et al 1995) pressure gradient exists between pulp and
oral cavity -tends to flow outwards slowly
• Exposure of Tubules- tooth fracture or cavity prep.-Outward
movement → tiny droplets.-dehydrating the surface-rapid flow
of fluid-sensitivity. 31
• Slow outward flow of fluid (0.02nl//sec/mm -1-
1.5.microlitre/sec/mm for nerves to begin firing.
•Acts as barrier for microbes and toxins .
•Hydraulic transfer and relief of stresses in Dentin-
through the Periodontium and Enamel.
•Non vital Teeth- More brittle. (Carter et al 1983)
• First Formed Dentin.
• A layer of Un Mineralized Matrix
• Thickness- 50 µ, 2-6µm wide
• Collagen and Non-collagenous
• Gradually Mineralizes.
• Thickness Remains Constant.
• Stains less intensely 33
• Dentin that immediately surrounds the dentinal tubules
• Collar - ↑ Calcified Matrix – surrounds Dentinal tubules.
• ↓ collagen fibrils, ↑ sulfated proteoglycans.
• 40% more mineralized than ITD.
• Hardness of H. A. crystals-250 KHN
(Kinney Et al- 1996)
• Thickness-0.75µm- .4µm
• Lost in decalcified Sections, 34
• Main Body Of Dentin.
• 10 Secretory Product.
• Less mineralized
• Hardness of H. A
(Kinney et al 1996)
• Unmineralized islands within the
Dentin- formed due to failure of
fusion of mineral globules .
• In Circumpulpal Dentin- just
below Mantle Dentin,
• Subjacent to pits and fissures.
• Tubules pass uninterrupted.
• Vitamin ‘D’ deficiency or
INCREMENTAL LINES OF VON
EBNER/ IMBRICATION LINES
• Fine striations- perpendicular to
• Daily rhythmic deposition of
• 4-8µ apart in crown, closer in root.
• 5 DAY INCREMENT-20µm
LINES OF SCHREGER
Congruence Of PRIMARY CURVATURES of Dentinal tubules.
CONTOUR LINES OF OWEN
• “Co-incidence of 2o
• Disturbance in matrix
• Hypomineralized areas.
• Periods of illness/
• Accentuated Incremental
• Primary teeth, permanent
• Zone of hypo calcification
• Reflects abrupt change in
environment- At Birth.
• Dentin formed Before birth
GRANULAR LAYER OF TOMES
• Granular zone-
• Ground sections- Root
Dentin in transmitted
• Increases in amt. from
CEJ to Apex.
• Looping /coalescing of
• Hypomineralized areas.
• First hard Tissue Interface
• Scalloped- with convexity
• Scalloping greatest in
Cuspal area →Occlusal
• Branching of Od. Process
here → ↑ed sensitivity.
• Odontoblast processes sometimes extend into the Enamel.
• Length is about 10—40 m
• Seen near Incisal edges
& cusp tips
• Appear dark
in ground sections
• Hypomineralized Areas
• Responsible for the Spread of Caries from Enamel to Dentin.
• Firm Attachment
• Smooth in Permanent teeth,
scalloped in 1o.
• Intermediate Zone- Hyaline layer
Of Hopewell Smith- Cements the
cementum to Dentin.
• Product Of HERS
• Endodontics- Apical Constriction
Termination of Instrumentation.
LOCATION Below DEJ B/n Mantle Dentin
THICKNESS 20 µ 68mm
MINERALIZATION ↓ ↑
DEFECTS ↓ ↑
COLLAGEN FIBRES Larger- 0.1-0.2µ
Smaller- 0.02- 0.05µ
parallel to the DEJ.
(Prior To Root Completion)
• Develops after root completion
• Narrow band- bordering the pulp
• Deposited more slowly- 1µ/day.
• Fewer tubules
• Bending of tubules at the 10 &
2° Dentin interface.
• Formed in greater amts.- roof of
pulp chamber- protecting the
• Localized formation of Dentin At pulp –Dentin
Border in response to noxious stimuli- Caries,
Trauma Attrition , Cavity Prep. Etc.
Also known as:
Defense Dentin 49
No continuity with 10 or 20
Dentin so there is ↓ Dentin
Quality Depends on :
•Intensity of stimulus.
•Vitality of pulp.
REACTIONARY DENTIN REPARATIVE DENTIN
FORMATIVE CELLS SURVIVING POST MITOTIC
NEW ODONTOBLAST- LIKE
STRUCTURE PHYSIOLOGIC DENTIN
CHANGE IN DIRECTION OF
NEW DENTINAL TUBULES
SMITH ET AL (1994)
REPARATIVE DENTINREACTIONARY DENTIN
The avg. daily rate of reparative dentin formation is about 2.8-3 µ/day-
acc to Stanley in 1996.
AGE AND FUNCTIONAL
• DEAD TRACTS
• DENTIN SCLEROSIS
• REPARATIVE DENTIN
• Represent Empty Tubules Filled
• Due to → Degeneration of
odontoblastic process (caries,
erosion, attrition etc.)
• Ground Sections
• Black in transmitted light, WHITE
IN REFLECTED LIGHT.
• Older Teeth-Areas of narrow
pulp horns. ↓ sensitivity. 54
• Presence of irritating stimuli -Caries, Attrition, Erosion, Cavity
Preparation → Deposition of Apatite Crystals & Collagen in
• Blocking of tubules- Defensive reaction.
• Filled with H. A - Obliteration of Lumen- Peritubular Dentin.
• Refractive indices are equalized- Transparent
• Elderly people – Mostly in Roots
• Also seen- slowly
• Reduced Permeability
• Prolonged pulp vitality
• Resistant to Caries
• Forensic Odontology:One of
the criteria for age
• Exposed portion of reactive sclerotic Dentin.
• Slow caries has destroyed overlying tooth
• hard , darkened , cleanable surface.
• Resistant to further caries Attack.
• Formed in response to
• Provides protection to
the underlying pulp- by
INNERVATION OF DENTIN
• Numerous Nerve Endings in
Predentin and Inner Dentin.
• 100-150µm from pulp.
• % of tubules innerveted Near Pulp
• ↓ near CEJ- 1%
• Closely Associated with Odontoblast
• Arise from myelinated nerve fibers of
Dental Pulp- (Aδ fibres) Reach Brain
via Trigeminal N.
PAIN TRANSMISSION THROUGH
• DIRECT NEURAL STMULATION
• TRANSDUCTION THEORY
• HYDRODYNAMIC THEORY
DIRECT NEURAL STIMULATION
• It was proposed by Scott
Stella in 1963
• Nerve endings in Tubules
are Directly Activated by
• This view rests on the
assumption that Nerve
fibres Extend to DEJ.
• Not accepted
• Odontoblastic Processes are
primary structures excited by
• Transmit impulse to Nerve
• Supported by evidence that
odontoblasts → Neural Crest
• Discarded -No synaptic Contacts
or vesicles - b/n odontoblasts and
• Most popular Theory
• Gysi (1900), Brannstrom
• Various stimuli such as Heat,
Cold, Air, Mechanical
of Fluid Within Tubule
• Activating the Free Nerve
Endings Associated with
Odontoblast and its Process
• Act as Mechanoreceptors-
Sensation is felt as pain.
• Unusual symptom of Pulp- Dentin Complex.
• Sharp Pain- easily localized.
• Etiology- Exposure of Dentinal tubules
loss of enamel- Attrition, abrasion, erosion etc.
loss of cementum- scaling and RP, Gingival Recession
• Best Explained by the Hydrodynamic Theory.
• Management - Block The Dentinal Tubules!!!
• Desensitising toothpastes-AgNo3, SrCl2, fluorides, Bonding Agents,
lasers etc. 65
• Highly Permeable- Tubular Nature
• TRANS DENTINAL- Movement-Through
entire thickness of Dentin- via tubules.
• INTRADENTINAL- Movement of
exogenous subst. into intertubular Dentin.-
seen during bonding.leading to passage of
irritants towards pulp.
• ↓Dentin thickness -↑Dentin permeability.
MORE PERMEABLE LESS PERMEABLE
DENTIN NEAR PULP
DENTIN FURTHER AWAY
AXIAL WALLS OF
CLASS II CAVITY
PULPAL FLOOR OF CLASS
CORONAL DENTIN ROOT DENTIN
NORMAL DENTIN SCLEROTIC DENTIN
“Exposure of Dentinal Tubules”
• Tooth wear, fractures, caries,
cavity cutting procedures etc.
lead to exposure of Dentinal tubules.
• 1 mm of Exposed Dentin → Damage to 30,000 living
• Exposed Tubules- Should not be insulted!!
• Sealed- Bonding agents, varnishes or Restorations.
• Irritants from Restorative
Materials- Pulpal Damage
• Thermal Protection- Bases
• Chemical Protection- Cavity
liners and varnishes
• Tubular Nature of Dentin→ Rapid spread of Caries
• Lateral spread along DEJ→ Undermined Enamel.
ZONE 1 – Normal dentin
ZONE 2 – Sub transparent
ZONE 3 – Transparent dentin
ZONE 4 – Turbid dentin
ZONE 5 – Infected dentin
INFECTED DENTIN AFFECTED DENTIN
DEMINERALISED BUT NOT
YET INVADED BY
DENATURED COLLAGEN –
STAINED BY CARIES
DETECTING DYE .
REQUIRES REMOVAL DOES NOT REQUIRE
Infected and Affected Dentin
Continuous Drying – dislodgement -
aspiration into tubules.
• USE :
Air- Water Coolant.
Sharp hand Instruments- most
Tungsten Carbide Burs to Cut vital
Dentin.- Less Heat generation.
Dentin- Treated with care during op. instrumentation
to prevent damage to the odontoblasts
• Cavity Floor → Dentin
• Dentin is RESILIENT → Absorbs and Resists
Forces of Mastication and Deformation – Grips the
• Grooves, coves, pins etc -completely in Dentin.
“Vital pulp therapy”
• The reparative Dentin Formation can be stimulated by
cavity lining materials (such as Calcium hydroxide).
• Includes Direct and Indirect pulp capping
• Results in formation of reparative dentin .
• THE DENTINAL BRIDGE repair tissue that forms
across the pulpal wound.
• Sign of successful healing.
“Bonding to Dentin”
• Adhesion to Dentin… A
• Due to - ↑organic content, tubular
nature and presence of Fluid.
• Further complicated by “Smear
Layer”- abraded dentin surfaces-
denatured collagen, HA crystals,
• It decreases dentinal permeability-
but interferes with bonding – should
• Steps in Bonding:
- Application of Bonding Agent
Hybrid Layer Composed of collagen, Bonding
Agent and Resin
• Secondary & Tertiary Dentin →obliteration of Pulp Chamber
& Root Canals.
• Endodontic treatment → Difficult.
• Periapical surgery- Root Resection- closer to 90o
to minimize no. of exposed tubules.
• Apical Dentin Chip Plug- Dentinal Chips compacted at apex
during Obturation- provides a “biologic seal”
Anomaly of Mesodermal Portion of the
(ACC. TO SHIELDS)
TYPE I- Assoc with. O.I.
Type II – Not Assoc with O.I
Type III- Brandy wine Type.
TYPE I TYPE II TYPE III
Tulip Shaped teeth, Bluish-
Translucent. Enamel Chips
away→ Exposed dentin,
obliteration of pulp
chamber , root canals
Shell teeth- Normal
Enamel, Thin Dentin,
Huge pulp Chambers,
• In patient with DI, one must first ascertain which type
he/she are dealing with.
• Severe cases of DI type 1 associated Osteogenesis
imperfecta can present significant medical
management problems. Careful review of the patient's
medical history will provide clues as to the severity of
bone fragility based on the number of previous
fractures and which bones were involved.
• Patients not exhibiting enamel fracturing and
rapid wear crown placement androutine
restorative techniques may be used.
• Bonding of veneers may be used to improve
• In more severe cases, where there is significant
enamel fracturing and rapid dental wear, the treatment
of choice is full coverage crowns.
However in case of D.I III with thin
root are not good cases for full coverage because of
• Occlusal wear with loss of vertical dimension –
Dentin Dysplasia (Root less teeth)
Rare Dental Anomaly.
Normal Enamel, Atypical
Dentin, Abnormal Pulp
(Acc. To WHITKOP)
-TYPE I- RADICULAR
-TYPE II – CORONAL
TYPE I(RADICULAR) TYPE II (CORONAL)
CLINICAL FEATURES Normal Morphology,
Extreme Mobility and
Primary- yellow /brown-
Permanent – normal.
Deciduous - pulp
obliterated, short conical
Permanent – crescent
shaped pulp chambers-
Difficulty in locating
Deciduous – pulp
“thistle tube” appearance
Dens in Dente
• Dentin & enamel forming
tissue invaginate the whole
length of a tooth.
• Radiographically- “tooth
within a tooth.”
• Food lodges in the cavity to
cause caries which rapidly
penetrates the distorted pulp
• Endodontic Treatment
Difficult- abnormal Anatomy.
• Yellow- Brown/grey
• Fluoresce Bright
Yellow under U.V
• Deposited along
Incremental lines of
Dentin and to lesser
Extent in Enamel.
RESPONSE OF DENTIN TO RESTORATIVE
PROCEDURE AND MATERIALS
1) SMEAR LAYER:
The smear layer is an amorphous , relatively smooth layer of
microcrystalline debris with a featureless surface that cannot
be seen with the naked eye [ Pashley DH 1984]
The cutting of dentin during cavity preparation produces
microcrystalline grinding debris that coats the dentin and
clogs the orifices of the dentinal tubules. This layer of debris
is termed as smear layer.
• Reduces sensitivity and permeability
• Interferes with the apposition or adhesion of dental
materials to dentin
• Has a potential to provide a media for recurrent caries
and bacterial irritation of the pulp
Methods of removal of smear layer from root canals
before obturation is the alternative use of a chelating
agent(disodium ethylenediamine tetra acetic acid EDTA)
or weak acid i.e. (10 % citric acid) followed by thorough
canal rinsing with 3 to 5 % NaOCl.
2) Restorative procedures can affect the permeability of
• Minimal effects are transmitted to the pulp if the remaining dentin
thickness is 2mm or more.
• For an amalgam restoration in a deep tooth preparation a total of
1- 2 mm of underlying dentin is preferred.
• For a non metallic restoration which has better insulating
properties than a metallic one, 0.5 – 1mm of dentin or liner / base
• Approximately a 20 fold increase in permeability is seen from
extending a cavity preparation that is 3 mm from the pulp to
• An acid etchant can increase the permeability by 4- 5 folds as
tubule apertures are enlarged.
• Loss of coronal enamel or cervical cementum exposes dentin
and can produce hyperalgesic response.
• Cementation and impression procedures exert tubular pressure
which results in odontoblastic displacement.
3) THERMAL AGENTS:
• Degree of heat produced depends on instrument
type, speed of rotation , cavity depth, effectiveness
• Metal restorations without insulating base and liner
& heat produced by setting cements irritate pulp by
dehydration of dentinal tubule.
4) CHEMICAL AGENTS:
• Sterilization and disinfecting chemicals applied to the dentin
produce odontoblastic injury
• Alcohol &chloroform produce thermal irritation by evaporation
and dehydrate dentinal tubules
• Hydrogen peroxide may travel through dentinal tubules of deep
cavity preparations and into the pulp producing emboli and
perhaps even arresting circulation.
• Dentin conditioning agents: classic acid etchant used on dentin de
mineralize Peritubular dentin which widens the tubule increasing
• The acid should be passively applied for short periods 5-15 secs
• This technique leaves behind smear plugs in tubule apertures
• The intact collagen framework interacts with hydrophilic priming
agents which penetrate through the remnant smear layer and into
the Intertubular dentin and fills the spaces left by the dissolved
apatite crystals. This allows acrylic monomers to form an
interpenetrating network around dentin collagen. Once
polymerized , this layer produces what Nakabayashi (1992)
referred to as HYBRID ZONE( Interdiffusion zone or
Interpenetration zone) 0.1 to 5 um deep.
• ACID LIQUID COMPONENTS OF CEMENTS: Initial
acidity of zinc phosphate, silicate , zinc polycarboxylate and
glass ionomer cements produce pulpal irritation.
• ACRLIC MONOMER: Produces shrinkage and is unable to
seal effectively produces pulpal irritation
• EUGENOL: Anti inflammatory activity through the inhibition
of prostaglandin synthesis
• Anodyne effect through desensitization and blockage of pain
• ZOE is found to be the most effective sealing agent
5. RESTORATIVE MATERIALS:
A restoration placed in a cavity preparation can develop
contraction gaps between the restoration and the cavity wall.
This gap then fills with fluid from the outflow of tubules or saliva
from external surface. An environment is created for bacterial
growth and failure of restoration .
• Orbans’ Oral Histology and Embryology-G.S Kumar – Twelfth
• Ten Cate’s Oral Histology- Development, structure and Function-
Antonio Nanci- Sixth Edition.
• Pathways of the pulp- Cohen. Hargreaves- Ninth Edition.
• Shafer’s Textbook of Oral Pathology- Shafer, Hine, Levy-5th
• Oral and Maxillofacial Pathology- Neville-3rd Edition.
• The art and science of Operative dentistry- Theodore Sturdevant- 4th
• An Atlas and Textbook of Oral Anatomy and Histology- Berkovitz.
• Tooth Wear and sensitivity Clinical Advances in restorative
Dentistry-Martin Addy, Graham Embery, W Michael Edgar
You can neither win nor lose if you don't run the race
- David Bowie