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![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.](https://image.slidesharecdn.com/dentin-150125010616-conversion-gate02/85/Dentin-92-320.jpg)
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Dentin
- 1. 1 GOOD MORNING!!! DR.RINKU SHANKLESHA DEPARTMENTOF CONSERVATIVE DENISTRY AND ENDODONTICS. KVGDC, SULLIA
- 2.
- 3. CONTENTS Introduction History Development (Dentinogenesis) Physical Properties Chemical Composition Structure of Dentin Types Of Dentin Age and functional changes Innervation of Dentin Clinical considerations Developmental anomalies conclusion 3
- 4. HISTORY • 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 4
- 5. DENTINOGENESIS • Process ofDentin formation. • Dentin-First Formed Dental Hard Tissue –crown and roots • -Formation of Dentin Precedes Enamel • Late Bell stage. • Future cusp tips, Proceeds Apically. 5 LATE BELL STAGE
- 6. STAGES • Formation OfDentin- similar to bone and Cementum. 1. Synthesis Of Organic matrix 2. Subsequent Mineralization. Carried out by- ODONTOBLASTS 6
- 7. ODONTOBLASTS • Cells OfPulp. • Derived - Dorsal Cranial Neural Crest, 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. • 7
- 8. 8 ODONTOBLAST BIOLOGY 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
- 9. 9 AGED ODONTOBLASTS: Reductionin length and cytoplasmic Organelles, increase in number and size of lysosomes and phagosomes, decreased secretory capacity, degenerate with age.
- 10. FORMATION OF PRIMARY DENTIN BeforeDentinogenesis-There 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. 10
- 11. 11 They induce thedifferentiation of odontoblasts, with reversal of polarity. Odontoblasts Develop variable no. of small processes at the formative end- start depositing Collagen matrix- Predentin. This induces the Ameloblasts to start depositing Enamel matrix.
- 12. 12 INITIALLY: large diaType 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
- 13. 13 A Single ProminentProcess- Odontoblast Process- (TOME’S FIBRES)- Tubular nature Is established. The rate of matrix production - about- 4- 8µ/day for Primary Dentin. And secondary dentin -1µ/day As more matrix is formed- the Odontoblast Migrates centripetally, towards the pulp. MINERALIZATION Begins once matrix is about 5µ thick.
- 14. 14 Various Matrix ProteinsInfluence 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. CALCIFICATION OF MATRIX- initiated by small crystallites within MatrixVesicles, budded from odontoblasts.
- 15. 15 Crystals- grow rapidly,rupture the matrix vesicles Spread -clusters of crystallites → fuse with adjacent clusters to form a continuous layer of mineralized matrix Initially- on the surface of the collagen fibrils and ground substance, later within the fibrils- aligned with collagen. . MATRIX VESICLES contain Alkaline Phosphatase -↑ concentration of phosphates → combine with Calcium →Hydroxyapatite Crystals.
- 16. PATTERNS OF MINERALIZATION •GLOBULAR(CALCOSPHERIC) :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- matrix vesicles. 16 RADIAL CRYSTAL GROWTH INTERGLOBULAR DENTIN
- 17. 17 LINEAR PATTERN LINEAR :When the rate of Dentin formation occurs Slowly -Mineralization front appears more Uniform – CIRCUMPULPAL DENTIN
- 18. 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. • Complete- 18mths after eruption-Primary 2-3 yrs -Permanent Teeth 18
- 19. VASCULAR SUPPLY • Providedby the Capillaries found in the subodontoblastic layer of the pulp. • Migrate between odontoblasts, and later - Regress. 19
- 20. PHYSICALAND MECHANICAL PROPERTIES PROPERTY VALUE COLOURPALE 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
- 21. CHEMICAL COMPOSITION 21 BY VOLUME 45% 22% 33% BYWEIGHT 20% 15% 65% INORGANIC ORGANIC WATER
- 22. ORGANIC COMPONENTS • 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. 22
- 23. INORGANIC COMPONENTS • CalciumHydroxyapatite: CA10(PO4)6(OH)2 • Thin plate like crystals, shorter than enamel. • 3.5 nm thick, 100 nm long. • Salts- calcium carbonate, sulphate, phosphate etc. • Trace Elements- Cu, Fe, F, Zn 23
- 24. STRUCTURAL COMPONENTS • Odontoblast Process •Dentinal Tubules • Non mineralized matrix- Predentin • Mineralized matrix- Peritubular and Intertubular Dentin. 24
- 25. DENTINAL TUBULES • MostStriking 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 exchange • 1-2µ apart. 25
- 26. CROWN ROOT PRIMARY CURVATURES 26 Tubulesexhibit Sigmoid curvatures-More prominent in crown. Least pronounced at cusp tips, incisal edges
- 27. SECONDARY CURVATURES 27 At IncreasedMagnification- Secondary Curvatures.
- 28. 28 A. - 50,000to 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 - ↑es toward pulp. No. of Tubules / unit area – crown> root.
- 29. PERIODONTOBLASTIC SPACE • Potentialspace between tubule wall and od. Process. • Contents - nerves, collagen fibrils, plasma proteins, glycoproteins and mitochondria. • Surface Area Tubule lumina - 1% at DEJ, 22 % at Pulp(PASCHLEY-1996) 29
- 30. Lamina Limitans 30 • Organicsheath or membrane lining the Dentinal tubules • seen in EM sections.
- 31. DENTINAL FLUID ( DentinLymph) • 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
- 32. • Slow outwardflow of fluid (0.02nl//sec/mm -1- 1.5.microlitre/sec/mm for nerves to begin firing. 32 •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)
- 33. PREDENTIN • First FormedDentin. • A layer of Un Mineralized Matrix • Thickness- 50 µ, 2-6µm wide • Collagen and Non-collagenous matrix proteins. • Gradually Mineralizes. • Thickness Remains Constant. • Stains less intensely 33 PREDENTIN
- 34. PERITUBULAR DENTIN PERILUMINAL/INTRATUBULAR DENTIN. • Dentinthat 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
- 35. INTERTUBULAR DENTIN • MainBody Of Dentin. • 10 Secretory Product. • Less mineralized • Hardness of H. A crystals -52KHN (Kinney et al 1996) 35
- 36.
- 37. INTERGLOBULAR DENTIN • Unmineralizedislands 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 Hypophosphatasia 37
- 38. INCREMENTAL LINES OFVON EBNER/ IMBRICATION LINES • Fine striations- perpendicular to tubules. • Daily rhythmic deposition of Dentin- • 4-8µ apart in crown, closer in root. • 5 DAY INCREMENT-20µm 38
- 39. LINES OF SCHREGER 39 CongruenceOf PRIMARY CURVATURES of Dentinal tubules.
- 40. CONTOUR LINES OFOWEN • “Co-incidence of 2o curvatures” • ACCENTUATED INCREMENTAL LINES • Disturbance in matrix formation • Hypomineralized areas. • Periods of illness/ inadequate nutrition. 40 GROUND SECTION
- 41. NEONATAL LINE • AccentuatedIncremental line • Primary teeth, permanent first molars. • Zone of hypo calcification • Reflects abrupt change in environment- At Birth. • Dentin formed Before birth -Better Quality 41 ENAMEL DENTIN
- 42. GRANULAR LAYER OFTOMES • Granular zone- • Ground sections- Root Dentin in transmitted light. • Increases in amt. from CEJ to Apex. • Looping /coalescing of Dent. Tubules. • Hypomineralized areas. 42
- 43. DENTINOENAMEL JUNCTION • Firsthard Tissue Interface To Develop • Scalloped- with convexity towards Dentin. • Scalloping greatest in Cuspal area →Occlusal stress more • Branching of Od. Process here → ↑ed sensitivity. 43
- 44. ENAMEL SPINDLES • Odontoblastprocesses 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. 44
- 45. DENTINO-CEMENTAL JUNCTION • 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. 45
- 46. TYPES OF DENTIN •Primary dentin – Mantle – Circumpulpal • Secondary dentin • Tertiary dentin 46
- 47. PRIMARY DENTIN MANTLE CIRCUMPULPAL LOCATIONBelow DEJ B/n Mantle Dentin and Predentin. THICKNESS 20 µ 68mm 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 (Prior To Root Completion)
- 48. SECONDARY DENTIN • Developsafter 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 pulp horns. 48
- 49. TERTIARY DENTIN • Localizedformation of Dentin At pulp –Dentin Border in response to noxious stimuli- Caries, Trauma Attrition , Cavity Prep. Etc. Also known as: Reactive Dentin, Reparative Dentin, Irritation Dentin, Replacement Dentin, Adventitious Dentin, Defense Dentin 49 No continuity with 10 or 20 Dentin so there is ↓ Dentin permeability. Quality Depends on : •Intensity of stimulus. •Vitality of pulp.
- 50. TERTIARY DENTIN REACTIONARY DENTINREPARATIVE DENTIN STIMULUS FOR FORMATION MILD AGGRESSIVE FORMATIVE CELLS SURVIVING POST MITOTIC ODONTOBLASTS NEW ODONTOBLAST- LIKE CELLS FROM PROGENITORS STRUCTURE PHYSIOLOGIC DENTIN CHANGE IN DIRECTION OF NEW DENTINAL TUBULES HETEROGENOUS: -TUBULAR (ORGANISED) OSTEODENTIN FIBRODENTIN (DISORG) 50 SMITH ET AL (1994)
- 51. 51 REPARATIVE DENTINREACTIONARY DENTIN Theavg. daily rate of reparative dentin formation is about 2.8-3 µ/day- acc to Stanley in 1996.
- 52.
- 53. AGE AND FUNCTIONAL CHANGES •DEAD TRACTS • DENTIN SCLEROSIS • REPARATIVE DENTIN 53
- 54. DEAD TRACTS • RepresentEmpty Tubules Filled with air. • 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
- 55. SCLEROTIC DENTIN • Presenceof irritating stimuli -Caries, Attrition, Erosion, Cavity Preparation → 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 55
- 56. • 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. 56 SCLEROTIC DENTIN
- 57. EBURNATED DENTIN • Exposedportion of reactive sclerotic Dentin. • Slow caries has destroyed overlying tooth structure . • hard , darkened , cleanable surface. • Resistant to further caries Attack. 57
- 58. REPARATIVE DENTIN • Formedin response to trauma, chronic irritation etc. • Provides protection to the underlying pulp- by Decreasing dentin permeability. 58
- 59. INNERVATION OF DENTIN •Numerous Nerve Endings in Predentin and Inner Dentin. • 100-150µm from pulp. • % of tubules innerveted Near Pulp Horns –(40%) • ↓ near CEJ- 1% • Closely Associated with Odontoblast Process. • Arise from myelinated nerve fibers of Dental Pulp- (Aδ fibres) Reach Brain via Trigeminal N. 59
- 60. 60 PAIN TRANSMISSION THROUGH DENTIN •DIRECT NEURAL STMULATION • TRANSDUCTION THEORY • HYDRODYNAMIC THEORY
- 61. DIRECT NEURAL STIMULATION •It was proposed 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. • Not accepted 61
- 62. TRANSDUCTION THEORY • OdontoblasticProcesses are primary structures excited by stimulus. • Transmit impulse to Nerve Endings • Supported by evidence that odontoblasts → Neural Crest Origin • Discarded -No synaptic Contacts or vesicles - b/n odontoblasts and axons. 62
- 63. HYDRODYNAMIC THEORY • Mostpopular Theory • Gysi (1900), Brannstrom • Various stimuli such as Heat, Cold, Air, Mechanical Pressure →Movement of Fluid Within Tubule ↓ • Activating the Free Nerve Endings Associated with Odontoblast and its Process • Act as Mechanoreceptors- Sensation is felt as pain. 63
- 64.
- 65. “Hypersensitivity” • Unusual symptomof 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
- 66. Dentin Permeability • HighlyPermeable- 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
- 67. 67 MORE PERMEABLE LESSPERMEABLE DENTIN NEAR PULP HORNS DENTIN FURTHER AWAY AXIAL WALLS OF CLASS II CAVITY PULPAL FLOOR OF CLASS II CAVITY CORONAL DENTIN ROOT DENTIN NORMAL DENTIN SCLEROTIC DENTIN
- 69.
- 70. “Exposure of DentinalTubules” • Tooth wear, fractures, caries, cavity cutting procedures etc. lead to exposure of Dentinal tubules. • 1 mm of Exposed Dentin → Damage to 30,000 living odontoblasts. • Exposed Tubules- Should not be insulted!! • Sealed- Bonding agents, varnishes or Restorations. 70
- 71. Pulp protection • Irritantsfrom Restorative Materials- Pulpal Damage • Thermal Protection- Bases below Restoration • Chemical Protection- Cavity liners and varnishes 71
- 72. Dentinal Caries • TubularNature of Dentin→ Rapid spread of Caries Through Dentin. • Lateral spread along DEJ→ Undermined Enamel. 72 ZONE 1 – Normal dentin ZONE 2 – Sub transparent ZONE 3 – Transparent dentin ZONE 4 – Turbid dentin ZONE 5 – Infected dentin
- 73. INFECTED DENTIN AFFECTEDDENTIN SOFTENED AND CONTAMINATED WITH BACTERIA SOFTENED , DEMINERALISED BUT NOT YET INVADED BY BACTERIA CONTAINS IRREVERSIBLY DENATURED COLLAGEN – STAINED BY CARIES DETECTING DYE . CONTAINS REVERSIBLY DENATURED COLLAGEN REQUIRES REMOVAL DOES NOT REQUIRE REMOVAL Infected and Affected Dentin 73
- 74. Operative Instrumentation • AVOID- ExcessiveCutting Heat Generation Continuous Drying – dislodgement - aspiration into tubules. • USE : Air- Water Coolant. Sharp hand Instruments- most suitable Tungsten Carbide Burs to Cut vital Dentin.- Less Heat generation. 74 Dentin- Treated with care during op. instrumentation to prevent damage to the odontoblasts
- 75. “Cavity Preparation” • CavityFloor → Dentin • Dentin is RESILIENT → Absorbs and Resists Forces of Mastication and Deformation – Grips the rest. material. • Grooves, coves, pins etc -completely in Dentin. 75
- 76. “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. 76
- 77. “Bonding to Dentin” •Adhesion to Dentin… A CHALLENGE!! • Due to - ↑organic content, tubular nature and presence of Fluid. • Further complicated by “Smear Layer”- abraded dentin surfaces- denatured collagen, HA crystals, debris.(1-4µm thick) • It decreases dentinal permeability- but interferes with bonding – should be removed. 77 SMEAR LAYER
- 78. • Steps inBonding: - Conditioning - Priming - Application of Bonding Agent Hybrid Layer Composed of collagen, Bonding Agent and Resin 78
- 79. “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” 79
- 80.
- 81. Dentinogenesis Imperfecta Anomaly ofMesodermal 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. 81
- 82. TYPE I TYPEII 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, short roots.
- 83. TREATMENT • In patientwith 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.
- 84. • Patients notexhibiting enamel fracturing and rapid wear crown placement androutine restorative techniques may be used. • Bonding of veneers may be used to improve the esthetics.
- 85. • In moresevere 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 cervical fractures. • Occlusal wear with loss of vertical dimension – Metal castings Newer composites.
- 86. Dentin Dysplasia (Rootless teeth) Rare Dental Anomaly. Normal Enamel, Atypical Dentin, Abnormal Pulp Morphology CLASSIFICATION: (Acc. To WHITKOP) -TYPE I- RADICULAR -TYPE II – CORONAL 86
- 87. TYPE I(RADICULAR) TYPEII (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 87
- 88. Regional Odontodysplasia • MaxillaryAnteriors • CLINICAL FEATURES: delay or failure of eruption, irregular shape. • RADIOGRAPHIC FEATURES: “Ghost Teeth.” 88
- 89. Treatment: • No treatmentrequired • Meticulous oral hygiene • Extraction / Endodontic treatment • Prosthetic rehabilitation
- 90. 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. 90
- 91. 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. 91
- 92. RESPONSE OF DENTINTO 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.
- 93. • Reduces sensitivityand 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.
- 94. 2) Restorative procedurescan affect the permeability of remaining dentin • 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 is sufficient.
- 95. • Approximately a20 fold increase in permeability is seen from extending a cavity preparation that is 3 mm from the pulp to 0.5 mm • 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.
- 96. 3) THERMAL AGENTS: •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.
- 97. 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 permeability.
- 98. • The acidshould 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.
- 99. • ACID LIQUIDCOMPONENTS 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 • Antibacterial • Anodyne effect through desensitization and blockage of pain impulse. • ZOE is found to be the most effective sealing agent
- 100. 5. RESTORATIVE MATERIALS: Arestoration 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 .
- 101.
- 102. REFERENCES • Orbans’ OralHistology and Embryology-G.S Kumar – Twelfth Edition • 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 Edition. • Oral and Maxillofacial Pathology- Neville-3rd Edition. • The art and science of Operative dentistry- Theodore Sturdevant- 4th Edition. • 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 102
- 103. THAN K YOU THANK U You canneither win nor lose if you don't run the race - David Bowie
Editor's Notes
- #4 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.
- #6 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.
- #7 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.
- #8 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.
- #9 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.
- #13 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.
- #14 The secondary dentin is laid down at a much slower rate of about 1 µ/day.
- #16 H. A. crystals of dentin = cementum & bone. They are 33 times smaller than the enamel crystals.
- #17 :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.
- #18 In a linear pattern- the crystals are deposited along and within the collagen fibres- forming a more uniform pattern.
- #19 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.
- #21 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.
- #22 .
- #23 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.
- #25 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.
- #26 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.
- #28 Minute curvatures are present along the entire length of the dentinal tubules.they are sinusoidal in shape.
- #30 The presence of collagen fibres reduces the permeability of dentin.
- #34 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.
- #35 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.
- #36 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.
- #38 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.
- #40 .
- #41 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.
- #42 It is an seen in. it is which that occurs at birth. The.
- #44 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.
- #46 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
- #48 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.
- #51 Smith et al have classified tertiary dntin into reactive or reparatve
- #53 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.
- #55 reparative dentin formed seals of the dentinal fluid.Initial step of fomation of sclerotic dentin
- #56 Stimuli may induce not only reparative formation but also additnal protective mechanism
- #58 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. .
- #60 The percentage of tubules innervated is about 40% near the pulp horns and decreases to 1% at or below the CEJ
- #61 Each of these theories has supportive factors as well as information that is non supportive in regard to the mechanism of conduction through dentin.
- #62 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.
- #64 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.
- #65 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-
- #66 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
- #67 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.
- #71 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.
- #73 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
- #75 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
- #78 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 .
- #80 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.
- #88 It is a rare dental anomaly characterized by normal enamel, atypical dentine with abnormal pulp morphology. Witkop classified into following types
- #89 Unusual anomaly -Localized areaThin Enamel and Dentin, Large Pulp Chamber.
- #102 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.