Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Dentin

15,874 views

Published on

Published in: Education
  • Be the first to comment

Dentin

  1. 1. 1 GOOD MORNING!!! DR.RINKU SHANKLESHA DEPARTMENT OF CONSERVATIVE DENISTRY AND ENDODONTICS. KVGDC, SULLIA
  2. 2. Dentin 1
  3. 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. 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. 5. DENTINOGENESIS • Process of Dentin 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. 6. STAGES • Formation Of Dentin- similar to bone and Cementum. 1. Synthesis Of Organic matrix 2. Subsequent Mineralization. Carried out by- ODONTOBLASTS 6
  7. 7. ODONTOBLASTS • Cells Of Pulp. • 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. 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. 9 AGED ODONTOBLASTS: Reduction in length and cytoplasmic Organelles, increase in number and size of lysosomes and phagosomes, decreased secretory capacity, degenerate with age.
  10. 10. FORMATION OF PRIMARY DENTIN Before Dentinogenesis-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. 11 They induce the differentiation 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. 12 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
  13. 13. 13 A Single Prominent Process- 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. 14 Various 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. CALCIFICATION OF MATRIX- initiated by small crystallites within MatrixVesicles, budded from odontoblasts.
  15. 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. 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. 17 LINEAR PATTERN LINEAR : When the rate of Dentin formation occurs Slowly -Mineralization front appears more Uniform – CIRCUMPULPAL DENTIN
  18. 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. 19. VASCULAR SUPPLY • Provided by the Capillaries found in the subodontoblastic layer of the pulp. • Migrate between odontoblasts, and later - Regress. 19
  20. 20. PHYSICALAND MECHANICAL 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 20
  21. 21. CHEMICAL COMPOSITION 21 BY VOLUME 45% 22% 33% BY WEIGHT 20% 15% 65% INORGANIC ORGANIC WATER
  22. 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. 23. INORGANIC COMPONENTS • 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 etc. • Trace Elements- Cu, Fe, F, Zn 23
  24. 24. STRUCTURAL COMPONENTS • Odontoblast Process • Dentinal Tubules • Non mineralized matrix- Predentin • Mineralized matrix- Peritubular and Intertubular Dentin. 24
  25. 25. DENTINAL TUBULES • 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 exchange • 1-2µ apart. 25
  26. 26. CROWN ROOT PRIMARY CURVATURES 26 Tubules exhibit Sigmoid curvatures-More prominent in crown. Least pronounced at cusp tips, incisal edges
  27. 27. SECONDARY CURVATURES 27 At Increased Magnification- Secondary Curvatures.
  28. 28. 28 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 - ↑es toward pulp. No. of Tubules / unit area – crown> root.
  29. 29. PERIODONTOBLASTIC SPACE • Potential space 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. 30. Lamina Limitans 30 • Organic sheath or membrane lining the Dentinal tubules • seen in EM sections.
  31. 31. DENTINAL FLUID ( 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
  32. 32. • Slow outward flow 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. 33. PREDENTIN • First Formed Dentin. • 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. 34. PERITUBULAR DENTIN PERILUMINAL/INTRATUBULAR DENTIN. • 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
  35. 35. INTERTUBULAR DENTIN • Main Body Of Dentin. • 10 Secretory Product. • Less mineralized • Hardness of H. A crystals -52KHN (Kinney et al 1996) 35
  36. 36. Dentinal Tubule Peritubular Dentin Intertubular Dentin 36
  37. 37. INTERGLOBULAR DENTIN • 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 Hypophosphatasia 37
  38. 38. INCREMENTAL LINES OF VON 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. 39. LINES OF SCHREGER 39 Congruence Of PRIMARY CURVATURES of Dentinal tubules.
  40. 40. CONTOUR LINES OF OWEN • “Co-incidence of 2o curvatures” • ACCENTUATED INCREMENTAL LINES • Disturbance in matrix formation • Hypomineralized areas. • Periods of illness/ inadequate nutrition. 40 GROUND SECTION
  41. 41. NEONATAL LINE • 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 41 ENAMEL DENTIN
  42. 42. GRANULAR LAYER OF TOMES • 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. 43. 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 → ↑ed sensitivity. 43
  44. 44. ENAMEL SPINDLES • 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. 44
  45. 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. 46. TYPES OF DENTIN • Primary dentin – Mantle – Circumpulpal • Secondary dentin • Tertiary dentin 46
  47. 47. PRIMARY DENTIN MANTLE CIRCUMPULPAL LOCATION Below 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. 48. SECONDARY DENTIN • 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 pulp horns. 48
  49. 49. TERTIARY DENTIN • Localized formation 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. 50. TERTIARY DENTIN 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 DIRECTION OF NEW DENTINAL TUBULES HETEROGENOUS: -TUBULAR (ORGANISED) OSTEODENTIN FIBRODENTIN (DISORG) 50 SMITH ET AL (1994)
  51. 51. 51 REPARATIVE DENTINREACTIONARY DENTIN The avg. daily rate of reparative dentin formation is about 2.8-3 µ/day- acc to Stanley in 1996.
  52. 52. REPARATIVE DENTIN 52
  53. 53. AGE AND FUNCTIONAL CHANGES • DEAD TRACTS • DENTIN SCLEROSIS • REPARATIVE DENTIN 53
  54. 54. DEAD TRACTS • Represent Empty 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. 55. SCLEROTIC DENTIN • Presence of 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. 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. 57. EBURNATED DENTIN • Exposed portion of reactive sclerotic Dentin. • Slow caries has destroyed overlying tooth structure . • hard , darkened , cleanable surface. • Resistant to further caries Attack. 57
  58. 58. REPARATIVE DENTIN • Formed in response to trauma, chronic irritation etc. • Provides protection to the underlying pulp- by Decreasing dentin permeability. 58
  59. 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. 60 PAIN TRANSMISSION THROUGH DENTIN • DIRECT NEURAL STMULATION • TRANSDUCTION THEORY • HYDRODYNAMIC THEORY
  61. 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. 62. TRANSDUCTION THEORY • Odontoblastic Processes 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. 63. HYDRODYNAMIC THEORY • Most popular 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. 64. 64
  65. 65. “Hypersensitivity” • 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
  66. 66. 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
  67. 67. 67 MORE PERMEABLE LESS PERMEABLE 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
  68. 68. CLINICAL CONSIDERATIONS 69
  69. 69. “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 odontoblasts. • Exposed Tubules- Should not be insulted!! • Sealed- Bonding agents, varnishes or Restorations. 70
  70. 70. Pulp protection • Irritants from Restorative Materials- Pulpal Damage • Thermal Protection- Bases below Restoration • Chemical Protection- Cavity liners and varnishes 71
  71. 71. Dentinal Caries • Tubular Nature 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
  72. 72. INFECTED DENTIN AFFECTED DENTIN 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
  73. 73. Operative Instrumentation • AVOID- Excessive Cutting 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
  74. 74. “Cavity Preparation” • Cavity Floor → Dentin • Dentin is RESILIENT → Absorbs and Resists Forces of Mastication and Deformation – Grips the rest. material. • Grooves, coves, pins etc -completely in Dentin. 75
  75. 75. “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
  76. 76. “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
  77. 77. • Steps in Bonding: - Conditioning - Priming - Application of Bonding Agent Hybrid Layer Composed of collagen, Bonding Agent and Resin 78
  78. 78. “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
  79. 79. DEVELOPMENTAL DEFECTS 80
  80. 80. 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. 81
  81. 81. 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, short roots.
  82. 82. TREATMENT • 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.
  83. 83. • Patients not exhibiting enamel fracturing and rapid wear crown placement androutine restorative techniques may be used. • Bonding of veneers may be used to improve the esthetics.
  84. 84. • 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 cervical fractures. • Occlusal wear with loss of vertical dimension – Metal castings Newer composites.
  85. 85. Dentin Dysplasia (Root less teeth)  Rare Dental Anomaly.  Normal Enamel, Atypical Dentin, Abnormal Pulp Morphology  CLASSIFICATION: (Acc. To WHITKOP) -TYPE I- RADICULAR -TYPE II – CORONAL 86
  86. 86. 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 87
  87. 87. Regional Odontodysplasia • Maxillary Anteriors • CLINICAL FEATURES: delay or failure of eruption, irregular shape. • RADIOGRAPHIC FEATURES: “Ghost Teeth.” 88
  88. 88. Treatment: • No treatment required • Meticulous oral hygiene • Extraction / Endodontic treatment • Prosthetic rehabilitation
  89. 89. 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
  90. 90. 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
  91. 91. 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.
  92. 92. • 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.
  93. 93. 2) Restorative procedures can 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.
  94. 94. • Approximately a 20 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.
  95. 95. 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.
  96. 96. 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.
  97. 97. • 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.
  98. 98. • 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 • Antibacterial • Anodyne effect through desensitization and blockage of pain impulse. • ZOE is found to be the most effective sealing agent
  99. 99. 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 .
  100. 100. CONCLUSION…!!!
  101. 101. REFERENCES • Orbans’ Oral Histology 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
  102. 102. THAN K YOU THANK U You can neither win nor lose if you don't run the race - David Bowie

×