This document provides an overview of the structure of dentin. It discusses the formation of dentin through odontoblast activity and mineralization. It describes the composition and structural components of dentin, including dentinal tubules, peritubular dentin, intertubular dentin, and different types of dentin such as primary, secondary, and tertiary dentin. The document also covers topics like patterns of mineralization, vascular and nerve supply of dentin, physical and chemical properties, and age-related changes in dentin structure.

1. STRUCTURE OF
DENTIN
P R E S E N T E D B Y
D R . A B H I S E K G U R I A
D E P T. O F C O N S E R V AT I V E D E N T I S T R Y A N D E N D O D O N T I C S

2. Contents
 Introduction
 History
 Dentinogenesis
 Formation of organic matrix
 Mineralization
 Odontoblast
 Odontoblastic process
 Odontoblastic biology
 Pre-odontoblasts
 Secretory odontoblasts
 Transitional odontoblasts
 Aged odontoblasts
 Matrix proteins influence mineralization

3.  PATTERNS OF MINERALIZATION
 Globular pattern
 Linear patter
 Vascular supply
 Nerve supply
 Physical & chemical properties
 Chemical composition
 Organic component
 Inorganic component
 Structural components
 Primary curvatures
 Secondary curvatures
 Peri-odontoblastic space
 Lamina limitans
 Peritubular dentin
 Intertubular dentin

4.  Predentin
 Primary dentin
 Secondary dentin
 Tertiary dentin
 Reactionary dentin
 Reparative dentin
 Interglobular dentin
 Granular layer
 Dentinoenamel junction
 Cementodentinal junction
 Enamel spindle
 Incremental lines
 Incremental lines ofVon Ebner
 Lines of Schreger
 Contour line of Owen
 Neonetal line

5.  Dentinal fluid
 Dentin permeability
 Age changes
• DEAD TRACTS
• DENTIN SCLEROSIS
• EBURNATED DENTIN
• Clinical considerations
 Hypersensitivity
 Direct neural stimulation theory
 Transduction theory
 Hydrodynamic theory
 Modulation theory
 Pulp dentin complex
 Dentinal caries

6.  Infected and AffectedDentin
 Remaining dentin thickness
 Cavity preparation
 Operative Instrumentation
 Pulp protection
 Vital pulp therapy
 Indirect pulp capping
 Direct pulp capping
 Bonding to Dentin
 Dentin in Endodontics
 Apexification & apexogenesis
 Smear layer

7.  Developemental anomalies
 Dentinogenesis imperfect
 Dentin dysplasia
 Regional odontodysplasia
 Dense in dente
 Tetracyclin staining
 Conclusion
 Referances

8. INTRODUCTION
 Second layer of the tooth
 Structure that provides the bulk and general form of
the tooth
 determines the shape of the crown, including the cusps
and ridges
 closely resembles bone
 Said to be a living tissue

9. HISTORY
• 1771 – John Hunter → hard tissue.
• 1775 – Anton VonLeeuwenhoek: Described tubularstructures.
• 1837 -Purkinje and Retzius explained about DentinalTubules.
• Cuvien gave the name “Ivory” to Dentin
• 1867 – Neuman gave the term Neuman’s sheath
• 1891 – VonEbner gave the term – Ebner’s growth lines or
Imbrication lines .
• 1906 – VonKorff gave the term – Korff’s fibres

10. DENTINOGENESIS

11. STAGES
1. Synthesis Of Organic matrix
2. Subsequent Mineralization.
• Carried out by- ODONTOBLASTS

12. ODONTOBLASTS
• Cells Of Pulp, Mesenchymal in origin.
• Lie along Dental papilla- Adjacent to
IEE.
• Tall columnar cells- length 25-40 µm,
diameter 4-7 µm,
• Development- Initiated by epigenetic
influence of various signalling
molecules produced by Ameloblasts.

13. ODONTOBLASTIC PROCESSES
 Cytoplasmic extensions of the odontoblasts
 Extend into the dentinal tubules
 largest in diameter near the pulp and taper
further into dentin
 The odontoblast cell bodies are approx. 7µm
in diameter & 40µm in length

14. ODONTOBLASTIC PROCESSES

15. ODONTOBLAST BIOLOGY
• PRE-ODONTOBLASTS
• SECRETORY ODONTOBLASTS
• TRANSITIONAL ODONTOBLASTS
• AGED ODONTOBLASTS

17. FORMATION OF PRIMARY DENTIN

18. The Cells of IEE become taller and
start differentiating into
Ameloblasts
Reversal of polarity – early bell
stage
Induce differentiation of odontoblast
Odontoblastic process developes and start
depositing collagen matrix – predentin
Ameloblasts to start depositing Enamel matrix

19. DEPOSITION OF COLLAGEN MATRIX
INITIALLY:
• Large dia Type III Collagen
• VON KORFF’S FIBRES
-Cork Screw Shaped
-Perpendicular to DEJ
-Argyrophillic in nature.
LATER
• smaller Fibrils- perpendicular to
Tubules
• parallel To DEJ.

20. Odontoblast migrates twards the pulp
Odontoblast Process- (TOME’S FIBRES)-
Tubular nature is established.
MINERALIZATION Begins once matrix is
about 5µ thick.

21. CALCIFICATION OF MATRIX- initiated by
small crystallites within MatrixVesicles
MATRIX VESICLES contain Alkaline
Phosphatase -↑ concentration of phosphates →
combine with Calcium →Hydroxyapatite Crystals
Crystals- grow rapidly, rupture the matrix
vesicles
Spread -clusters of crystallites → fuse with
adjacent clusters to form a continuous layer of
mineralized matrix

22. Matrix Proteins Influence Mineralization
• DPP- binds to ca, controls growth of H.A crystals
• 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.

23. PATTERNS OF MINERALIZATION
GLOBULAR(CALCOSPHERIC) pattern :
• Deposition of HA crystals in several discrete areas of matrix at any
one time.
• Continued crystal growth → globular masses → enlarge →
fuse → single layer of calcified mass.
• MANTLE DENTIN
INTERGLOBULAR DENTINRADIAL CRYSTALGROWTH

24. LINEAR pattern
• when the rate of dentin formation occurs
slowly
• mineralization front appears more uniform –
Circumpulpal Dentin

25. ROOT DENTIN FORMATION
• Begins once Enamel& Dentin
formation reaches the future CEJ.
• Initiated by Cells of HERS which
induce odontoblast
differentiation.
• Collagen fibres- parallel to CDJ.
• Less mineralized, less no. of
Tubules.

26. VASCULAR SUPPLY
• Provided by the Capillaries found in the subodontoblastic
layer of the pulp.
• Migrate between odontoblasts, and later - Regress.

27. INNERVATION OF DENTIN
• Numerous Nerve Endings
in Predentin and Inner Dentin.
• Closely Associated with Odontoblast Process.
• Arise from myelinated nerve fibers of Dental
Pulp- (Aδ fibres) Reach Brain via Trigeminal N.

28. PHYSICALANDMECHANICAL PROPERTIES
PROPERTY VALUE
• 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

29. CHEMICAL COMPOSITION
BY VOLUME
45%
22%
33%
BY WEIGHT
20%
15%
65%
INORGANIC ORGANIC WATER

30. 1. ORGANIC COMPONENTS
• Collagen – 82% ,
• MAINLYTYPE I and some Type III and V.
• Non Collagenous Matrix Proteins- 18%
-Phosphoproteins- DPP(Phosphoryn), Gla-Protein.
-Glycoproteins- Dentin Sialoprotein,Osteonectin,
Osteocalcin
- Proteoglycans- Chondroitin SO4 (seen mainly in Predentin)

31. • Enzymes- Acid Phosphatase, Alkaline Phosphatase.
• Lipids- phospholipids, glycolipids etc. in traces.
 Growth factors:
• Bone morphogenetic proteins (BMP)
• Insulin like growth factors (IGFs)
• Transforming growth factors β (TGF- β

32. 2. INORGANIC COMPONENTS
32
• Calcium Hydroxyapatite: Ca10(PO4)6(OH)2
• Thin plate like crystals, shorter than enamel.
• 3.5 nm thick, 100 nm long.
• Salts- calcium carbonate, sulphate, phosphate
• Trace Elements- Cu, Fe, F, Zn

33. STRUCTURALCOMPONENTS
• Odontoblast
Process
• Dentinal Tubules
• Non mineralized
matrix- Predentin
• Mineralized matrix-
Peritubular and
Intertubular Dentin.

34. DENTINAL TUBULES
• From pulp to DEJ
• resembles an S shape
• Ratio btwn outer and inner
surfaces of dentine is about 5:1
• Smaller branches- canaliculi -pathways
of exchange
• More tubules per unit area in the
crown than in the root

35. A. - 50,000 to 90,000 / sqmm
pulpal surface
B. - 30,000 to 35,000/sqmm
middle dentine
C. - 10,000 to 25,000/sqmm
peripheral dentine
Tubule density/ unit area - ↑ toward pulp.
No. of Tubules / unit area – crown> root.

36. PRIMARY CURVATURES
CROWN ROOT
• Tubules exhibit Sigmoid curvatures-More prominent in
crown.
• Least pronounced at cusp tips, incisal edges

37. SECONDARY CURVATURES
At Increased Magnification- Secondary Curvatures.

38. PERI-ODONTOBLASTIC SPACE
• Potential space between tubule wall and od. Process.
• Contents - nerves, collagen fibrils, plasma proteins,
glycoproteins and mitochondria.

39. Lamina Limitans
• Organic sheath or membrane lining the Dentinal tubules
• seen in EM sections.

40. PREDENTIN
 Located adjacent to the pulp tissues
 2-6µm, depending on the activity of
odontoblasts
 First formed dentin and is not
mineralized
• Stains less intensely

42. PERITUBULAR DENTIN
•PERILUMINAL/ INTRATUBULAR DENTIN
• Immediately surrounds the dentinal tubules
• Collar - ↑ Calcified Matrix
• ↓ collagen fibrils, ↑ sulfated proteoglycans.
• 40% more mineralized than ITD.
• Hardness of H. A. crystals-250 KHN
(Kinney Et al- 1996)
• Thickness- 0.75µm- 0.4µm
• Lost in decalcified Sections

43. INTERTUBULAR DENTIN
• Main Body Of Dentin.
• 10 SecretoryProduct.
• Less mineralized
• Hardness -52KHN
• (Kinney et al 1996)
• The fibrils exhibit crossbanding at
64µm intervals

44. Dentinal
Tubule
Peritubular
Dentin
Intertubular
Dentin

45. INTERGLOBULAR DENTIN
• Unmineralized islands- due to
failure of fusion of mineral
globules .
• In Circumpulpal Dentin
• Subjacent to pits and fissures.
• Tubules pass uninterrupted.
• Vitamin ‘D’ deficiency or
Hypophosphatasia

46. TYPES OF DENTIN
• Primary dentin
– Mantle
– Circumpulpal
• Secondary dentin
• Tertiary dentin
• Reparative dentin
• Reactionary dentin

47. MANTLE CIRCUMPULPAL
LOCATION Below DEJ B/n Mantle Dentin
and Predentin.
THICKNESS 20 µ 68nm
MINERALIZATION ↓ ↑
DEFECTS ↓ ↑
COLLAGEN FIBRES Larger- 0.1-0.2µ
perpendicular to
the DEJ
Smaller- 0.02- 0.05µ
parallel to the DEJ.
Closely packed.
47
PRIMARY DENTIN
(Prior ToRoot Completion)

48. PRIMARY DENTIN

49. MANTLE DENTIN
• First layer of primary dentin
• under polarised light, mantle
dentin (RED Band) can be
differentiated from the
Circumpulpal dentin (Purple
with black dentinal tubules)
 due to difference in collagen
fibres in mantle dentin

50. CIRCUMPULPAL DENTIN
 After mantle dentin has been deposited
 Major part of primary and secondary dentin
 mineralised through calcospherites in the mineralisation
front between predentin and mineralizing dentin

51. SECONDARY DENTIN
• after root completion
• Narrow band- bordering the pulp
• Deposited 1µ/day.
• Fewer tubules
• Bending of tubules at the 10 & 2°
Dentin interface.
• greater amounts at roof of pulp
chamber- protecting the pulp horns.
51

52. TERTIARYDENTIN
• Localized At pulp – in response to noxious
stimuli
Also known as:
Reactive Dentin,
Reparative Dentin,
Irritation Dentin,
Replacement Dentin,
Adventitious Dentin,
Defense Dentin
No continuity with 10 or 20 Dentin so
there is ↓ Dentin permeability.
Quality Depends on :
• Intensity of stimulus.
• Vitality of pulp.

53. TERTIARYDENTIN
REACTIONARY DENTIN REPARATIVE DENTIN
STIMULUS FOR
FORMATION
MILD AGGRESSIVE
FORMATIVE CELLS SURVIVING POST MITOTIC
ODONTOBLASTS
NEW ODONTOBLAST- LIKE
CELLS FROM
PROGENITORS
STRUCTURE PHYSIOLOGIC DENTIN
CHANGE IN DIRECTIONOF
NEW DENTINALTUBULES
HETEROGENOUS:
-TUBULAR (ORGANISED)
OSTEODENTIN
FIBRODENTIN
(DISORG)
50
SMITH ET AL (1994)

54. REACTIONARY DENTIN REPARATIVE DENTIN
Rate of deposition= 2.8-3 µ/day

55. GRANULAR LAYER OF TOMES
• In Root Dentin
• Increases in amt. from CEJ to
Apex.
• Looping /coalescing of
Dent. Tubules.
• Hypomineralized areas.

56. ENAMEL SPINDLES
• Odontoblast processes sometimes extend into the Enamel.
• Length is about 10- 40 m
• near Incisal edges &
cusp tips
• Dark in ground sections
• Hypomineralized
• Spread of Caries from Enamel to Dentin.

57. INCREMENTAL LINES OFVON
EBNER/ IMBRICATION LINES
• Fine striations- perpendicular to
tubules.
• Daily rhythmic deposition
• 4-8µ apart in crown, closer in
root.
• 5 DAY INCREMENT- 20µm

58. LINES OF SCHREGER
Congruence Of PRIMARY CURVATURES of Dentinal tubules.

59. CONTOUR LINES OF OWEN
• “Co-incidence of 2o
curvatures”
• ACCENTUATED
INCREMENTALLINES
• Disturbance in matrix formation
• Hypomineralized areas.
• Periods of illness/ inadequate
nutrition.
GROUND SECTION

60. NEONATALLINE
• Accentuated Incremental line
• Primary teeth, permanent first
molars.
• Zone of hypo calcification
• Reflects abrupt change in
environment- At Birth.
• Dentin formed Before birth-Better
Quality

61. DENTINOENAMEL JUNCTION
• First hard Tissue Interface to
develop
• Scalloped- with convexity towards
Dentin.
• Scalloping greatest in Cuspal area
→Occlusal stress more
• Branching of Od. Process here →
sensitivity.

62. DENTINO-CEMENTAL
JUNCTION
• FirmAttachment
• Smooth in Permanent teeth,
scalloped in 1o.
• Intermediate Zone- Hyaline layer Of
Hopewell Smith- Cements the
cementum to Dentin.
• Product Of HERS
• Apical Constriction- Termination of
Instrumentation. 45

63. DENTINAL FLUID
( Dentin Lymph)
• Occupies space b/n dentinal tubule and od. Process.
• Ultrafiltrate- pulp Capillaries
• Ca content is 2-3 times higher than in plasma.
• Tissue pressure of pulp- 14 cm of H2O,
• (Ciucchi et al 1995) pressure gradient -tends to flow outwards
slowly

64. • Exposure of Tubules - Outward movement →
dehydrating the surface-rapid flow of fluid -
sensitivity.
• Slow outward flow of fluid (0.02 nl/sec/mm to
1-1.5.microlitre/sec/mm for nerves to begin
firing.
• Acts as barrier for microbes and toxins .

65. Dentin Permeability
• 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.

66. MORE PERMEABLE LESS PERMEABLE
DENTIN NEAR PULP HORNS DENTIN FURTHER AWAY
AXIAL WALLSOF CLASS
II CAVITY
PULPAL FLOOR OF CLASS II
CAVITY
CORONAL DENTIN ROOT DENTIN
NORMAL DENTIN SCLEROTIC DENTIN

67. AGE AND FUNCTIONAL
CHANGES
• Deadtracts
• Dentinsclerosis
• Eburnateddentin

68. DEAD TRACTS
• Empty Tubules Filled with air.
• Due to → Degeneration of
odontoblastic process
• Black in transmitted light, WHITE
IN REFLECTED LIGHT.
• Older Teeth - Areas of narrow
pulp horns. ↓ sensitivity.

69. SCLEROTIC DENTIN
• Presence of irritating stimuli → Deposition of Apatite
Crystals & Collagen in Dentinal Tubules.
• Blocking of tubules- Defensive reaction.
• Filled with H. A - Obliteration of Lumen- Peritubular
Dentin.
• Refractive indices are equalized- Transparent
• Elderly people – Mostly in Roots

70. • Also seen- slowly
progressing Caries.
• Reduced Permeability
• Prolonged pulp vitality
• Resistant to Caries
• Forensic Odontology: One
of the criteria for age
determination using
Gustafson’s method.SCLEROTIC DENTIN

72. EBURNATED DENTIN
• Exposed portion of reactive sclerotic Dentin.
• Slow caries has destroyed overlying tooth structure
• hard , darkened , cleanable surface.
• Resistant to further cariesAttack.

73. CLINICAL CONSIDERATIONS
Hypersensitivity
Pulp dentin complex
Dentinal caries
Infected and AffectedDentin
Remaining dentin thickness
Cavity preparation
Operative Instrumentation
Pulp protection
Vital pulp therapy
Bonding to Dentin
Endodontics
Smear layer

74. Hypersensitivity
• Unusual symptom of Pulp- Dentin Complex.
• It is a condition characterized by short , sharp pain arising
from exposed dentin in response to stimuli typically thermal
, evaporative , tactile, osmotic or chemical and which cannot
be ascribed to any other form of dental defect or pathology .
( Holland et al 1997)
• Sharp Pain- easily localized.
• Etiology-
Exposure of Dentinal tubules
loss of enamel
loss of cementum

75. Direct neural
stimulation
Transduction
theory
Hydrodynamic
theory
Modulation
theory

76. DIRECT NEURALSTIMULATION
• By Scott Stella in 1963
• Nerve endings in Tubules are
Directly Activated by External
Stimuli
• This view rests on the
assumption that - Nerve fibres
Extend to DEJ.

77. • Drawbacks:
• No nerve endings in dentinal tubules
• Topical application of local anaesthetic agents do
not abolish sensitivity

78. TRANSDUCTION THEORY
• By Thomas 1994
• Odontoblastic Processes are
primary structures excited by
stimulus.
• Transmit impulse to Nerve
Endings
• Supported by evidence that
odontoblasts → Neural Crest
Origin
Drawbacks:
• No synaptic Contacts or vesicles -
b/n odontoblasts and axons.

79. HYDRODYNAMIC THEORY
• Gysi (1900), Brannstrom
• Various stimuli heat, cold, airblast
dessication or mechanical or osmotic
pressure affect fluid movement in the
dentinal tubules.
• Activating the Free Nerve Endings
Associated with Odontoblast and its
Process
• Act as Mechanoreceptors-
Sensation is felt as pain.

80. • Nerve impulses in the pulp are modulated through the
liberation of polypeptides from the odontoblasts, when
injured.
• Alter permeability of the odontoblastic cell membrane
through hyperpolarisation,
• So that pulp neurons are more prone to discharge upon
receipt of subsequent stimuli
MODULATION THEORY

81. • Management - Block The Dentinal Tubules!!!
• Desensitising toothpastes-
• AgNo3, SrCl2, fluorides, BondingAgents, lasers etc.

82. Suggestion for patients
• Avoid gingival recession due to plaque deposition by
practicing good oral hygiene
• Avoid using large amount of dentifrice
• Avoid hard bristled tooth brushes
• Avoid brushing with excessive pressure
• Avoid excessive flossing or incorrect use
• Avoid picking at gums

83. Pulp dentin complex
• Orbans(1980) stated that “The pulp lives for the dentin
and the dentin lives by the grace of the pulp. Few
marriages in nature are marked by a greater
interrelationship. Thus it is with the pulp and the four
functions that it serves: namely, the formation and the
nutrition of dentin and the innervation and defense of the
tooth.”
• Based on this Nanci (2005) has stated that the pulp and dentin
can no longer be studied as two separate entities but must be
viewed as the pulp-dentin complex.

84. Dentinal caries
• Zone1: Zone of fatty degeneration (from pulp)
• Zone2: DENTINAL sclerosis
• Zone3- Dentin decalcification
• Zone4: Decomposed dentin.

86. Remaining dentin thickness
• From base of the cavity to roof of pulp
• Methods of measurement
• Radiographic method
• CBCT
• Electrical resistance
• Prepometer
RDT influence treatment outcome
• 1 mm of residual root dentine following post preparation is claimed to
reduce the risk of root fracture
• Pulpal toxicity of certain materials (eg zinc oxide eugenol) reduces with
increasing dentine thickness

87. • Bond strength of resin-based adhesive systems reduces as
the dentine thickness reduces.
• Hydraulic conductance of radicular dentine decreases with
increasing distance from the pulp
• Heat-induced pulpal injury following curing with light-
emitting diode units or from burs during caries removal is
more likely with reduced dentine thickness.

88. • Minimal effects are transmitted to the pulp if RDT is 2mm or
more.
• For an amalgam restoration 1- 2 mm is preferred.
• For a non metallic 0.5 – 1mm of dentin or liner / base is
sufficient.
• Approximately a 20 fold increase is seen from extending a
cavity preparation that is 3 mm from the pulp to 0.5 mm
• An acid etchant can increase permeability by 4- 5 folds as
tubule apertures are enlarged.

90. “Cavity Preparation”
• Cavity Floor → Dentin
• Dentin is RESILIENT → Absorbs and
Resists Forces of Mastication and
Deformation – Grips the restorative
material.
• Grooves, coves, pins etc -completely in
Dentin.

91. Operative Instrumentation
• To prevent damage to the odontoblasts
AVOID-
Excessive Cutting
Heat Generation
Continuous Drying
USE :
 Air- Water Coolant.
 Sharp hand Instruments
 Tungsten Carbide Burs to Cut vital
Dentin

92. Pulp protection
• Irritants from Restorative materials-
pulp damage
• Need for pulp protection
1. Mechanical protection
2. Barrier to chemical components
3. Thermal protection
4. Galvanic protection
5. Adequate seal at interface
71

93. 1) THERMALAGENTS
• Degree of heat produced depends on instrument
type, speed of rotation , cavity depth, effectiveness
of cooling.
• Metal restorations without insulating base and liner
& heat produced by setting cements irritate pulp by
dehydration of dentinal tubule.

94. 2) CHEMICALAGENTS:
• Alcohol &chloroform
• produce thermal irritation by evaporation and dehydrate
dentinal tubules
• Hydrogen peroxide
• may travel through dentinal tubules into the pulp producing
emboli and perhaps even arresting circulation.
• Dentin conditioning agents:
• widens the tubule increasing permeability.

95. • ACID LIQUID COMPONENTS OF CEMENTS:
• Initial acidity of zinc phosphate, silicate , zinc polycarboxylateand
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
impulse.

96. • Thermal Protection- Bases below
Restoration
• Base: materials that are used to
replace missing dentin or to block
out undercuts in preparation for
indirect restorations.
• Chemical Protection- Cavity sealers,
liners

97. • Sealers : materials that provide protective coating to
the walls of the prepared cavity.
• Eg: cavity varnish, resin bonding agent
• Liners: these are cement coating of minimal
thickness, which serve as a physical barrier to
bacteria
• Eg: calcium hydroxide, GIC

98. “Vital pulp therapy”
• The reparative Dentin Formation can be stimulated by
cavity lining materials (such as Calcium hydroxide).
• Direct Indirect pulp capping
• Indirect pulp capping
• THE DENTINAL BRIDGE repair tissue that forms
across the pulpal wound.

99. INDIRECT PULP CAPPING
• Definition
• A procedure wherein the deepest layer of the remaining
affected carious dentin is covered with a layer of
biocompatible material in order to prevent pulpal exposure
and further trauma to pulp.
• Performed as single or two-step approach.

101. DIRECT PULP CAPPING
• DEFINITION :
• A procedure in which the exposed vital pulp is covered with
a protective dressing or base placed directly over the site of
exposure in an attempt to preserve the pulpal vitality.

102. INDICATIONS
• Iatrogenic mechanical exposure of pulp in an asymptomatic
vital tooth
• Small carious exposures in an asymptomatic permanent
tooth with an incomplete root formation.
• Radiographically no thickening of PDL space and no
evidence of peri-radicular lesion.

103. CONTRAINDICATIONS
• Large carious exposures in symptomatic permanent
tooth
Materials used
• Calcium hydroxide
• Theracal
• MTA
• Biodentin

104. CALCIUM HYDROXIDE
• Pulpdent paste and Dycal
HEALING WITH CALCIUM HYDROXIDE
• Zone of obliteration
• Zone of coagulation necrosis
• Zone of dentin bridge formation
• Line of demarcation

105. “Bonding to Dentin”
• Adhesion to Dentin… A CHALLENGE!!
• Due to - ↑organic content, tubular
nature and presence of Fluid.
• Further complicated by “Smear
Layer”
• It decreases dentinal permeability-
but interferes with bonding
SMEAR
LAYER

106. • 1949, Dr. Hagger, a Swiss chemist used first dental adhesive
“cavity seal”
Generations of bonding agent
• 1st gen - 1956
• Use glycerol-phosphoric acid & dimethacrylate (NPG GMA)
• Reduce bond strength
• 2nd gen - 1970
• formation of ionic bond between calcium and chlorophosphate
groups
• Still fail to remove smear layer

107. • 3rd gen- Late 1970s
• Acid etching
• 4th gen -1980s
• Total etch tech
• Etchant, primer, bonding agent
• Technique sensitive
• All bond 2, 3, scotchbond multipurpose
• 5th gen - 1990s
• 1 bottle system (primer + adhesive)
• Excite, all bond plus, clearfill new bond

108. 6th gen- early 2000s
• “self-etching primers”,
• 1 step 2 bottle (etchant& primer + adhesive)
• Lower bond strength
• Clearfil ac, g bond, adper scotchbond ac
7th gen- early 2005
• one-bottle self-etching system
• Reduced long term strength
• One coat 7.0, xeno iv, adper easy one
8th gen- 2010
• voco America introduced voco futurabond DC,
contains nano fillers

109. “Endodontics”
• 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”

110. APEXIFICATION
• Definition : Its defined as a method to induce a calcific
barrier across an open apex of an immature, pulpless
tooth.
Objective
• formation of an apical “calcific barrier” against which
obturation can be achieved.
Apexogenesis
• Refers to a vital pulp therapy procedure to encourage
physiological development and formation of root apex

111. 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]
• Has a potential to provide a media for recurrent caries
and bacterial irritation of the pulp
• 2–5 lm thick

112. Methods of removal of smear layer
• Chelating agent EDTA
• Weak acid i.E. (10 % citric acid)
• Thorough canal rinsing with 3 to 5 % NAOCL.
• Ultrasonic removal with 1% Naocl
• Laser removal (ne:yag, er:yag, co2 laser)

113. DEVELOPMENTALDEFECTS

114. Dentinogenesis Imperfecta
• Anomaly of Mesodermal Portion of the
Odontogenic Apparatus.
 CLASSIFICATION:
 (ACC. TO SHIELDS)
 TYPE I- Assoc with. O.I.
Type II – Not Assoc with O.I
Type III- Brandy wine Type.

115. TYPE I TYPE II TYPE III
CLINICAL
FEATURES
• Tulip Shaped teeth,
Bluish- grey-
Yellow/Brown
Translucent. Enamel
• Chips away→ Exposed
dentin, rapid attrition.
Amber appearance,
Excessive wear,
Multiple pulp
Exposures.
RADIOGRAPHIC
FEATURES
Partial/complete
obliteration of pulp
chamber , root canals
Shell teeth- Normal
Enamel, Thin Dentin,
Huge pulp Chambers,
shortroots.

116. TREATMENT
• first ascertain which type he/she is dealing with.
• Severe cases of DI type 1
• 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.

117. • Patients not exhibiting enamel fracturing and rapid
wear crown placement and routine restorative
techniques may be used.
• Bonding of veneers may be used to improve
the esthetics.
• In more severe cases, where there is significant
enamel fracturing and rapid dental wear, the
treatment of choice is full coverage crowns.

118. • However in case of D.I III with thin root are not good cases
for full coverage because of cervical fractures.
• Occlusal wear with loss of vertical dimension –
Metal castings
Newer composites.

119. Dentin Dysplasia (Root less teeth)
Rare Dental Anomaly.
Normal Enamel, Atypical
Dentin, Abnormal Pulp
Morphology
CLASSIFICATION:
(Acc. ToWHITKOP)
-TYPE I- RADICULAR
-TYPE II – CORONAL

120. TYPE I(RADICULAR) TYPE II (CORONAL)
CLINICAL FEATURES
Normal Morphology,
Amber Translucency.
Extreme Mobility and
Premature Exfoliation
Primary- yellow
/brown- grey.
Permanent – normal.
RADIOGRAPHIC
FEATURES
Deciduous - pulp
chambers completely
obliterated, short conical
roots.
Permanent– crescent
shaped pulp chambers-
Difficulty in locating
canal orifices.
Deciduous – pulp
chambers obliterated
Permanent -
“thistle tube” appearance

121. Regional Odontodysplasia
• Maxillary Anteriors
• CLINICAL FEATURES:
• delay or failure of eruption,
irregular shape.
• RADIOGRAPHIC FEATURES:
“Ghost Teeth.”

122. Treatment:
• No treatment required
• Meticulous oral hygiene
• Extraction / Endodontic treatment
• Prosthetic rehabilitation

123. 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 chamber
• Endodontic Treatment Difficult-
abnormal Anatomy.

124. Tetracycline Pigmentation
• Yellow- Brown/grey
Discoloration.
• Fluoresce Bright Yellow
under U.V light.
• Deposited along Incremental
lines of Dentin and to lesser
Extent in Enamel.

125. CONCLUSION…!!!
 Although dentin and pulp have different structures, once they
are formed, they react to stimuli as a functional unit.
 Exposure of dentin through attrition, caries or trauma produces
profound pulpal reactions that tend to reduce permeability and
stimulate formation of additional dentin.

126. REFERENCES
1. Orbans oral histology and embryology – 12th edition
2. Ten Cate’s Oral Histology- Development, structure and Function- Antonio Nanci-
Sixth Edition.
3. Pathways of the pulp- Cohen. Hargreaves- Ninth Edition.
4. Shafer’s Textbook of Oral Pathology- Shafer, Hine, Levy-5th
Edition.
5. Oral and Maxillofacial Pathology- Neville-3rd Edition.
6. The art and science of Operative dentistry- Theodore Sturdevant- 4th Edition.
7. An Atlas and Textbook of Oral Anatomy and Histology- Berkovitz.
8. Tooth Wear and sensitivity Clinical Advances in restorative
Dentistry-Martin Addy, Graham Embery, W Michael Edgar

127. THANK YOU!!!!