Dentin

This presentation introduces one to dentin and its significance in operative dentistry.

1. CONTENTS INTRODUCTION DENTINO-PULPAL COMPLEX HISTORY DENTINOGENESIS COMPOSITION PROPERTIES OF DENTIN HISTOLOGY OF DENTIN FUNCTION OF DENTIN CLINICAL SIGNIFICANCE AGE AND FUNCTIONAL CHANGES DEVELOPMENTAL ANOMALIES CONCLUSION REFERENCES

2. INTRODUCTION Most Voluminous Mineralized Connective Tissue Of Tooth Hard Portion Of Dentino-Pulpal Complex Dentin = Vital Tissue with Living Protoplasm

3. DENTINO-PULPAL COMPLEX

4. The dental pulp and dentin functions as a unit. Odontoblasts are located in the periphery of the pulp tissue with extensions into the inner part of the dentin. Dentin would not exist unless produced by odontoblasts and dental pulp is dependant on the dentin for protection(alongwith enamel). Likewise, integrated dynamics of the pulp-dentin complex imply that impacts on the dentin may affect the pulpal component and that disturbances in the pulpal will in turn affect the quantity and quality of dentin produced.

5. ODONTOBLASTS The odontoblasts line the entire pulpal aspect of the predentin. The odontoblasts are tall columnar cells or sometimes somewhat cuboidal in shape (especially in the root). The nucleus is oval, has one or two nucleoli. The cytoplasm of the cell body contains numerous organelles rough surfaced endoplasmic reticulum (arranged in longitudinally running cisternae) a well developed Golgi apparatus, Mitochondria, Vesicles. Vacuoles, Electron bodies, Microtubules and fibrils. The odontoblasts cells bodies are approximately 7 micrometre in diameter & 40 micrometre in length.

6. ODONTOBLASTIC PROCESS The odontoblast processes are the cytoplasmic extensions of the odontoblasts. The odontoblasts cells reside in the peripheral pulp at the pulp-predentin border and their processes extend in to the dentinal tubules . The processes are largest in diameter near the pulp (3 to 4 mm) and taper into the dentin. The odontoblast processes divide near the dentino enamel junction and may indeed extend in to enamel in the “ enamel spindles ”

7. HISTORY

8. The biological structure of dentin has been investigated since time of: 1) Anton Van Leeuwenhock : Explained the tubular structure of dentin. 2) Von Purkinje and Retrices : Explained abt. dentinal tubules. 3) John Hunter : Specified it as hard tissue 4) Cuvien : coined the term IVORY for dentin

9. Numerous structural elements of dentin carry the name of well-known histologists of 19 th century: 1) Owen: Contour lines of Owen (1840) 2) Von Ebner: Ebner’s growth lines (1891) 3) Neumann: Neumann’s sheath (1863) 4) John Tomes: Tomes granular layer (1838) Tomes process (1856) 5) Von Korff: Korff’s fibers (1906)

10. DENTINOGENESIS

11. Dentin is formed by cells called odontoblasts that differentiates from ectomesenchymal cells of dental papilla following an organizing influence that emanates from inner dental epithelium. Dental papilla is the formative organ of dentin and eventually becomes the pulp of the teeth, a change in terminology generally associated with the moment dentin formation begins.

12. Dentinogenesis is composed of three stages i.e. 1) CYTODIFFERENTIATION 2) MATRIX FORMATION 3) MINERALIZATION

13. CYTODIFFERENTIATION * This takes place during the BELL STAGE. * In this stage, the cells from the papillae sac differentiates to produce odontoblasts under the influence of the Inner dental epithelium starting at the cuspal or incisal region. * The cells become cylindrical in shape and are sometimes referred as Preodontoblasts . * The no. of organelles markedly increases with the cell becoming tall and columnar located at end farthest from basement membrane of Inner dental epithelia. These cells are known as Odontoblast.

14. * Concomitant with the formation of predentin at cuspal and incisal, continued differentiation of new odontoblasts takes place further apic- -ally in dental papilla. * After the crown is fully formed, the rate of dentin slows down markedly(2-3yrs post- -natal) until root formation starts i.e. similar to cytodifferentiation in crown.

15. MATRIX FORMATION * The odontoblasts exhibits all the characterstics of matrix-producing cells i.e. an abundance of RER, a well developed Golgi apparatus, mitochondria and secretory granules. * Pro-collagen is synthesized by RER, transferr- -ed to Golgi apparatus and finally, secreted by secretory granules. * The collagen, glycoprotein and proteoglycan complexes constitutes the organic matrix of dentin prior to mineralization, two layer in pre- -dentin may be differentiated.

16. * The fibers involved in the formation of the initial predentin are argyrophilic and k/a VON KROFF’S FIBERS. * VON KROFF’S FIBERS are the first fibers that signifies the first formed dentin. Due to the argyrophilic rxn, it was long believ- -ed that bundles of collagen formed among the odontoblasts. * Recently EM studies revealed that the staining is of ground substance among the cells and not collagen.

17. * As the matrix formation continues, the odontoblastic process lenghtens, as does the dentinal tubule. * Initially, 4µ of daily increments are added. This continues until the crown is formed and the teeth move into occlusion. After this time a daily incremental deposit of 1µ takes place.

18. MINERALIZATION * Basically, it occurs by globular calcification. * Earliest crystal deposition takes place in the form of very fine plates of hydroxyapatite on the surface of collagen fibrils in the ground substance. * The crystals are laid down within the fibrils themselves with the crystals that are associated with collagen being in orderly manner( long axis parallel to fibrils long axis) and in rows conforming to 64nm striation pattern within the globular islands of mineraliz- -ation .

19. * The crystal deposition appears to take place readily from common centers in so-called Spherulite form. * The peritubular region becomes highly minera- -lization at a very early stage. The ultimate crystal size remains very small about 3mm in thickness and 100nm in length * The hydroxyapatite crystal of dentin resembles bone and cementum. They are 300 times smaller than enamel crystals.

20. COMPOSITION COMPOSITION

21. COMPOSITION PERCENTAGE CONTENT INORGANIC 70%(by weight) 45%(by volume) CALCIUM HYDROXYAPATITE ORGANIC 20%(by weight) 33%(by volume) 1)TYPE I COLLAGEN (minor type III and IV) 2) MINOR FRACTION a) Lipids b) Non-collagenous matrix protein WATER 10%(by weight) 22%(by volume)

22. COMPOSITION(contd.) COLLAGEN TYPE I The Scaffold that accommodates a large portion(56%) of minerals in the holes and pores of fibrils

23. COMPOSITION(contd.) NON COLLAGENOUS MATRIX PROTEIN • Regulates Mineral Deposition and can act as Promoter or Inhibitor. • Pack the space between Collagen fibrils and accumulates along the periphery of dentinal tubules. (Peritubular Dentin)

24. COMPOSITION(contd.) IMP. NON COLLAGENOUS MATRIX PROTEINS 1) Dentin Sialophosphoprotein 2) Dentin Matrix Protein 1 3) Osteonectin(SPARC) 4) Osteocalcin 5) Osteopontin 6) Bone Sialoprotein 7) Matrix Extracellular Phosphoglycoprotein

25. PROPERTIES OF DENTIN

26. S.No. PROPERTY EXPLAINATION SIGNIFICANCE 1 COLOR DARKER THAN ENAMEL (Light yellow in young adult and Dark yellow in elderly) EBURNATED DENTIN 2 THICKNESS MAXIMAL 1) Cuspal height 2) Incisal edge MINIMAL Cervical areas 1)Thickness increases with age. 2) 3-3.5 mm in Coronal aspect. 3 HARDNESS 1/5 th of Enamel (High Compressive strength and low Tensile strength) MOE= 1670000 Psi (more flexibility hence shows Cushion Effect)

27. HISTOLOGY OF DENTIN

28. 1) DENTINAL TUBULES CORONAL RADICULAR DENTIN DENTIN (Also seen at incisal edge and cuspal tip)

29. The dentinal tubules follow a Gentle ‘S’ shaped curve in crown and is straighter in incisal edges, cusps and root areas. Its perpendicular to CEJ and DEJ. They have lateral branches throughout dentin k/a CANALICULI or MICROTUBULES . No. and Diameter of dentinal tubules NUMBER DIAMETER(in µ) PULP 45000-65000 2-3 DEJ 15000-20000 0.5-0.9

30. 2) PREDENTIN

31. First formed dentin i.e. not mineralized. 10-30 µm zone of unmineralized zone between Odontoblasts and Mineralized dentin. This layer of dentin lies very close pulp tissue i.e. just next to CELL BODIES OF ODONTOBLASTS .

32. 3) PERITUBULAR AND INTERGLOBULAR DENTIN

33. PERITUBULAR DENTIN • Dentin lining the Dentinal Tubules • More mineralized than Intertubular dentin. INTERTUBULAR DENTIN • Dentin i.e. present between the tubules and is less mineralized compared to Peritubular dentin. • It determines ELASTICITY of dental matrix

34. 4) 1º,2º AND 3º DENTIN

35. PRIMARY DENTINE SECONDARY DENTINE TERTIARY DENTINE DEFINITION Dentine formed before root completion Formed after root completion Formed in response to external stimuli TYPE OF CELLS 1º Odontoblasts 1º Odontoblasts 2º Odontoblasts or undiff. Mesenchymal cells of pulp LOCATION All areas of dentine Not uniform (roof and floor of pulp ) Localized in areas of ext. stimuli ORIENTATION OF TUBULES Regular Irregular Atubular RATE OF FORMATION Rapid Slow Rapid (1.5-3.5 µm/day) PERMEABILITY More Less Least

36. 5) SCLEROTIC DENTIN

37. CAUSE 1) Aging patients 2) Mild irritation(Eg. Slowly advancing caries) HISTOLOGICAL CHANGES Increased deposition of calcified materials from enamel to pulp leading to widening of PERITUBULAR DENTIN. CLINICAL SIGNIFICANCE Area becomes HARDER,DENSER,LESS SENSITIVE and MORE PROTECTIVE against irritation.

38. TYPES OF SCLEROTIC DENTIN 1) PHYSIOLOGICAL SCLEROTIC DENTIN Sclerotic dentin due to aging. 2) REACTIVE SCLEROTIC DENTIN Sclerotic dentin due to irritants. 3) EBURNATED DENTIN Type of Reactive Sclerotic dentin i.e. formed due to destruction by slow carious process or mild chronic irritation leading to HARD , DARKENED CLEANABLE on outward portion of Reactive dentin.

39. 6) DEAD TRACTS

40. Severe Stimulation to Dentin leads to Destruction and Disintegration of Odontoblasts and Odontoblastic Process. The Dentin Tubules are empty and filled with air.(often surrounded by Sclerotic Dentin) Appears Black in Ground Sections. Commonly seen in areas of narrow Pulpal Horns due to Odontoblastic crowding.

41. 7) INTERGLOBULAR DENTIN Interglobular Dentin = Hypomineralization due to Vit. D deficiency

42. 8) TOMES GRANULAR LAYER

43. 9) INCREMENTAL GROWTH LINES

44. Also known as Incremental lines of Von Ebner. Growth lines that is seen in ground section of dentin parallel to the dentinal tubules. These lines represents the rest phase in dentin deposition with dentin deposition rate of 6 µ/day in crown to 3.5 µ/day in roots

45. 10) OSTEODENTIN Seen in tertiary dentin due to entrapment of odontoblast cells in the dentin. Since it appears like bones so k/a OSTEODENTIN.

46. FUNCTION OF DENTIN

47. 1) Provide Strength to the tooth. 2) Offers Protection to the pulp. 3) Provides Flexibility to the tooth. 4) Affects Color of the enamel. 5) Defensive in action.

48. CLINICAL SIGNIFICANCE

49. 1) HYPERSENSITIVITY Dentinal hypersensitivity is the term used to describe clinical condition of an exaggerated response to an exogenous stimuli. Dental hypersensitivity is defined as “sharp, short pain arising from exposed dentin in response to stimuli typically thermal, chemical, tactile or osmotic and which cannot be ascribed to any other form of dental defect or pathology.”(Holland et al,1997)

50. Theories of Dentinal Hypersensitivity are 1) Transducer Theory * The theory assumed that odontoblast extends to the periphery and its membrane comes in close apposition to the nerve endings in the pulp and so transmit excitation. * Thomas,1984 indicated that process of odontoblasts are restricted to the inner third of the dentinal tubules.

51. 2) Neural Theory * The neural theory attributes to activation of the nerve endings in the tubules which conducts the stimuli along the parent 1º afferent nerve fibers in the pulp into the dental nerve branch. * According to this theory, nerve is located throughout the thickness of the dentin, but this was not found so in ground sections.

52. 3) Hydrodynamic Theory * Put forth by Brannstrom,1962. * According to this theory, hypersensitivity is due to displacement of the fluids in the dentinal tubules. * Mathews et al,1994 noted that stimuli such as cold causes fluids to flow away from the pulp, produces more rapid and greater pulp nerve responses than those such as heat, which causes inward flow of fluid.

53. * When exposed dentin is dehydrated using air blasts, it causes outward fluid movt. and stimulates the mechanoreceptor to cause pain. * When overexposed to such stimuli, dentinal plugs are formed that protect the pulp from further such stimuli.

54. Etiology of hypersensitivity * Main etiology is exposure of the dentinal tubules due to either of the two causes i.e. loss of covering enamel or loss of gingival attachment. * Loss of gingival attachment is the most common cause of dentinal hypersensitivity. Various factors causing gingival attachment loss are as follows: 1) Inadequate attached gingiva 2) Improper brushing technique 3) Periodontal surgery

55. 4) Overzealous tooth cleaning 5) Oral habits 6) Recession secondary to diseases such as NUG, Periodontitis, Herpetic gingivo- -stomatitis 7) Crown preparation * Once the dentinal tubules are exposed there are process to maintain its patency i.e. 1) Poor plaque control 2) Enamel wear 3) Improper oral hygiene technique 4) Cervical erosion 5) Exposure to acids

56. Management of Hypersensitivity 1) Desensitizing by occlusion of dentinal tubules a) formation of smear layer by burnishing with orangewood sticks. b) Use of topical agents such as i) Calcium hydroxide ii) Calcium phosphate paste iii) Silver nitrate iv) Strontium chloride v) Flouride vi) Potassium oxalate vii) Varnish viii) Ionophoresis

57. c) Placement of restoration i) GIC ii) Composite cements d) Uses of lasers( carbon dioxide, Nd:YAG, Er:YAG, He:Ne) 2) Desensitization by blocking pulpal sensory nerves E.g.. Potassium nitrate in pastes in which potassium ions passes via tubules and desensitizes the nerves.

58. 2) PULP PROTECTION The cells of exposed dentin should be insulated against bacterial toxins, strong drugs and undue operative procedures. When 1mm of dentin is exposed, 30000 living cells are exposed. Hence, its advisable to provide thermal and chemical protection. The protocol is defined by the concept of REMAINING DENTIN THICKNESS(RDT) .

59. RDT > 2mm (SHALLOW) RDT (0.5-2mm) MODERATE RDT < 0.5mm DEEP SILVER AMALGAM VARNISH BASE OF ZnPolyF and GIC Ca HYDROXIDE WITH BASE GLASS IONOMER CEMENT NOT REQUIRED NOT REQUIRED CALCIUM HYDROXIDE LINER COMPOSITE DBA DBA CALCIUM HYDOXIDE + GIC + DBA CAST GOLD NOT REQUIRED BASE CALCIUM HYDROXIDE + BASE

60. 3) DENTINAL CARIES The rapid penetration and spread of caries is attributed to its low Calcium content and dentinal tubule system . The enamel may be undermined at DEJ but due to dentinal tubules, a passage is formed for bacteria. The electron microscopy of carious dentin shows 5 distinct histological zones.

61. ZONE 1 : NORMAL DENTIN Deepest area is normal dentin which has tubules with odontoblastic process that are smooth and no crystals in the lumens. The inter tubular dentin has normal cross banded collagen and normal dense apatite crystals. No bacteria in the tubules. Stimulation of dentin (e.g. :by osmotic gradient, a bur, a dragging instrument or air blow) produces a sharp pain. 

62. ZONE 2 : SUBTRANSPARENT DENTIN Zone of demineralization of the intertubular dentin and initial formation of very fine crystals in the tubule lumen at the advancing front. Odontoblastic process damage is evident. No bacteria are found in this zone. Stimulation of dentin produces pain. Dentin is capable of remineralization

63. ZONE 3 : TRANSPARENT DENTIN This dentin is softer than normal dentin and shows further loss of mineral from the inter tubular dentin and many large crystals in the lumen of the tubules. Stimulation produces pain. Intact collagen can serve as a template for the remineralization of the inter tubular dentin and thus this region is capable of self repair , provided the pulp remains vital.

64. ZONE 4: TURBID DENTIN Zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules which are filled with bacteria. There is very little mineral present and the collagen is irreversibly denatured. Dentin in this zone will not self repair .This zone cannot be remineralized and must be removed before restoration.

65. ZONE 5 : INFECTED DENTIN Outer most decomposed dentin that is teeming with bacteria. No recognizable structure to the dentin and collagen ,and minerals are absent. Removal of infected dentin is essential to sound, successful restorative procedure as well as prevention of spreading of infections.

66. It is also important to understand the concept of Affected and Effected dentin AFFECTED DENTIN EFFECTED DENTIN 1. SOFT DEMINERALIZED DENTIN INVADED BY BACTERIA. DENTIN IS DEMINERALIZED BUT NOT INVADED BY BACTERIA. 2. SOFT LEATHERY SURFACE WHICH IS EASILY REMOVED. SOFT SURFACE BUT NOT EASILY REMOVED. 3. IRREVERSIBLE DEGRADATION OF DENTIN. UNINTERRUPTED COLLAGEN CROSS LINKAGE. 4. CANT BE REMINERALIZED. CAN BE REMINERALIZED. 5. CARIES STAINING DRUGS STAINS IT. CARIES DRUGS CANT STAIN IT.

67. 4) CAVITY FLOOR Cavity’s pulpal floor must lie in dentin. Due to low Modulus of Elasticity of Dentin(compared to Enamel) it acts as a resilient base below the restoration and so are able to absorb the masticatory forces without fracture.

68. 5) OPERATIVE PROCEDURES Undue trauma from operative procedures can damage the pulp. PRESSURE Air driven cutting instrument can dislodge the odontoblast and aspiration within the dentinal tubule which could be an important factor of inflamed pulp. HEAT PRODUCTION due to rotation of the rotary instruments is important damaging factor. If temperature is elevated by 11ºF, destructive rxn. will occur even in a normal and vital periodontal organ.

69. SPEED : If speed is b/w 3000-30,000 rpm without coolant, then, pulpal damage will occur. Dull and worn out instrument leads to increased vibration and reduced cutting efficiency leading to rise in heat. VIBRATION : Vibration leads to damage to pulp and higher vibration leads to development of cracks in dentin and enamel.

70. 6) SMEAR LAYER Presence of smear layer was first demonstrated by BOYDE et al,1963. Smear layer is the debris smeared on the surface of enamel and dentin by cutting of tooth. Cameron(1983) and Mader(1984) examined smear layer under EM and concluded that it’s amorphous, irregular and granular in appearance and consist of 2 layers i.e. 1) Superficial and loosely attached to underlying dentin. 2) Deeper layer consisting of dental plugs in dentinal tubules

71. Smear layer is composed of both Inorganic and Organic component . 1) The organic portion is comprised of microbes, heat coagulated proteins, necrotic pulp tissue, odontoblastic process, saliva and blood cells. 2)The inorganic component of smear layer is comprised of the tooth debris. Significance of Smear layer 1) Interferes with bonding of GIC and composites. 2) Bacteria laden mass whose toxic product may migrate to pulp.

72. Imp. Agent responsible for removal of smear layer are: 1) 6% Citric acid for 60s 2) Polyacrylic acid for 5s 3) EDTA 4) Maleic acid

73. 7) ETCHING OF DENTIN In 1955, S. Buonocore developed the technique of acid etching for bonding of restoration to enamel. But etching of tooth was done far before it though unknowingly. ( Soderholm JKM. Dental Adhesives how it started and Later evolved. J Adhes Dent 2007;9:227-230) 1) In Pre-Columbian era, the Mayans used to cement their inlays to the tooth surface by acidic cements . 2) Also dentists have been using several acidic cements for centuries in which acid was found in the cement even after setting which etches the dentin surface to produce rougher surface for good adhesion. Hence, its difficult to decide who discovered ACID ETCHING: the Mayans or Buonocore.

74. But at that time, it was confined to enamel and dentin was not etched. In 1979, Fusayama used 37% orthophosphoric acid and showed Dentin etching doesn’t damage the pulp In 1982, Nakabayashi discovered formation of HYBRID LAYER OF RESIN INFILTRATED DENTIN. Around 1990’s, ETCHING OF DENTIN became a common practice.

75. Significance of acid etching 1) Removal of smear layer and plugs 2) Opening dentinal tubules and deminer- -alize Peri-and intertubular dentin, thus increasing dentin permeability ( Pashley DIL, Carvahlo RM. Dentin permeability and dentin adhesion. J Dent 1997;25: 355-72)

76. Depth range of decalcifications by acid etching varies from 2-4µ and depends on the following factors: 1) Etchant pH 2) Etchant type 3) Etchant concentration 4) Etchant viscosity 5) Application time Perdigao J, Lambreehts P, Van Meerbeek B, Tome AR, Vanherle G, Lopes AB. Morphological field emission-SEM study of the effects of six phosphoric acid etching agents on human dentin. Dent Mater 1996;12:262-71

77. Even though, acid etching promotes profound changes in chemical composition and physical properties of the dental matrix, it is widely used in restorative dentistry. Frankenberger R, Lobbaner U, Roggendorf MJ, Naumann M, Taschner M. Selective enamel etching reconsidered : better than etch and rinse and self etch? J Adhes Dent 2008; 10: 339-334

78. 8) BONDING AGENT Bonding agents are an integral part of restorative dentistry. The enamel bonding agent failed when employed for dentin. This can be attributed to following causes: 1) Complex surface of the dentin with lesser calcium content. 2) Remaining water of about 10% that oozes

79. out of dentinal tubules exposed due to tooth preparation contaminates the field. 3) Presence of smear layer. 4) Controversy regarding etching of dentinal surface. 5) Biological sensitivity of dentin. 6) Low organic material surface energy. Hence an effort was done to develop that shows bonding to dentin

80. GENERATION IMPORTANT FEATURES EXAMPLE 1 ST GENERATION Very weak bond 2 ND GENERATION Weak bond (1-10MPa) with main component HEMA or Bis-GMA. No consideration given to shrinkage or smear layer. Scotchbond , Bondlite 3 RD GENERATION Modification or removal of smear layer for improvement in bond strength. Scotchbond II, Gluma, Prisma, Universal Bond 2/3 4 TH GENERATION Adoption of total etch tech. for complete removal of smear layer. Three step bonding. Scotchbond multipurpose, All bond 2, Optibond FL 5 TH GENERATION Same principle as 4 th generation with self etching primer or self priming adhesive. Self etching primer(Clearfil SE bond) Self priming adhesives(Prime n Bond NT) 6 TH GENERATION Self etching adhesives, two bottle systems mixed before application Prompt L-Pop, Xeno IV 7 TH GENERATION Single bottle adhesives I-Bond ,G-Bond, Xeno V

81. 9) DENTINO-ENAMEL JUNCTION The DEJ is a scalloped junction between enamel and dentin. SCALLOPED NATURE OF DEJ 1) If DEJ is flat, tensile strength act at DEJ over continuous areas would push the two areas apart , thus leading to delamination. 2) In scalloped DEJ, the net compression towards the DEJ was consistently higher than net tension away from it. As a consequence, at DEJ, enamel and dentin are pushed towards one another during mastication . ( Shimizu D, Macho GA. Functional significance of microstructural detail of primate dentino-enamel junction: a possible example of exaption. J Hum Evol 2007;52(1):103-11 )

82. 10) DENTINO-CEMENTAL JUNCTION The dentino-cemental junction is of special concern as it forms the apical constriction. Apical constriction is the narrowest diameter upto which Biomechanical preparation and Obturation is done. Its usually 0.5-1.0 mm short of apical foramen.

83. 11) IPC/DPC Indirect Pulp Capping Reparative dentin can be stimulated by cavity lining material since dentin is produced throughout life. * Deep penetrating lesions is treated by partial removal of effected dentin and leaving the affected dentin intact. After this, we leave a calcium hydroxide liner. Then dressing is done for minimum three weeks. * The liner stimulates the odontoblasts to form new dentin along the pulpal surface.

84. Direct Pulp Capping Direct pulp capping can be done to stimulate reparative dentin young, non inflamed pulps to secrete reparative dentin.

85. AGE AND FUNCTIONAL CHANGES

86. VITALITY OF DENTIN Since the odontoblast and its process are an integral part of the dentin. There is no doubt that dentin is a vital tissue. Again, if vitality is understood to be the capacity of the tissue to react to physiologic and pathologic stimuli dentin must be considered a vital tissue. Dentin is laid down through out life, although after the teeth have erupted and have been functioning for a short time, Dentinogenesis slows, and further dentin formation is at a much slower rate. As peritubular diameter increases tubule caliber is diminished. Pathologic effects of dental caries, abrasion, attrition etc cause changes in dentin. With age, tubule closure progress pulp ward and may affect tubules of greater diameter too)

87. DEAD TRACTS When a ground section of tooth is observed by transmitted light, sclerotic dentin appears light, but other parts of the dentin frequently appear as dark bands. These areas are called “dead tracts” and represents groups of empty air filled dentinal tubules. They appear black in transmitted and white in reflected light. These dead tracts mainly appears due to loss of odontoblastic processes as a result of caries, attrition, abrasion, cavity preparation or erosion Their degeneration is often observed in the area of narrow pulpal horns because of crowding of odontoblasts. Dentin areas characterized by degenerated odontoblasts processes give rise to dead tracts. These areas decreased sensitivity and appear to a greater extent in older teeth

88. SCLEROTIC OR TRANSPARENT DENTIN In cases of caries, attrition, abrasion, erosion or cavity preparation, sufficient stimuli are generated to cause collagen fibers and apatite crystals to begin appearing in the dentinal tubules, especially in older individuals. In such cases blocking of the tubules is considered a defensive reaction of dentin. The calcified tubular space assumes a different refractive index becoming transparent. This calcified predentin and process of tubule is called sclerotic or transparent dentin. It is filled with a fine meshwork of crystals and the mineral density is greater in this area.   It appears transparent or light in transmitted light and dark in reflected light. It is more frequently found in root and slowly progressive caries as well as cervical areas of older teeth with cervical cementum exposure and may prolong vitality

89. DEVELOPMENTAL ANOMALIES

90. DENTINOGENESIS IMPERFECTA REGIONAL ODONTODYSPLASIA DENTINAL DYSPLASIA

91. DENTINOGENSIS IMPERFECTA # WHAT IS IT? Dentinogenesis imperfecta is an AUTOSOMAL DOMINANT trait seen due to mutation in DSPP. Characteristic feature of the condition is OBLITEARTION OF DENTINAL PULP

92. # CLASSIFICATION 1) Dentinogenesis Imperfecta Type I  Dentinogenesis imperfecta with osteogenesis imperfecta.  Error in Collagen type I synthesis 2) Dentinogenesis Imperfecta Type II  Not associated with osteogenesis imperfecta  Opalescent Teeth 3) Dentinogenesis Imperfecta Type III  Associated with Opalescent teeth but with quite varied clinical manifestation.  Also k/a BRANDYWINE TYPE

93. # CLINICAL FEATURE  Mostly they share a lot of common clinical features i.e.  Also k/a Tulip or Bell shaped teeth (excessive cervical constriction) S.No. PROPERTIES EXPLANATION 1 Color Yellowish brown to bluish grey (due to abnormal dentin) 2 Enamel Though quite normal but fractures quite easily(abnormal dentin and lack of scalloping at DEJ) 3 Roots Shortened and Blunt 4 Susceptibilities to caries Slight resistant due to loss of contact

94. Type I is different from Type II as it is associated with Osteogenesis Imperfecta. Type III D.I presents with some extra features compared to Type I and II i.e. 1) Multiple pulp exposures 2) Periapical radiolucency 3) Variant radiological feature.

95. # RADIOLOGICAL FEATURE 1) Type I and II D.I. a) Opaque pulpal chamber and canal b) Bell shaped or Tulip shaped teeth c) Short and blunt roots 2) Type III D.I. Extremely large pulpal chambers and canals with very thin dentin, so k/a SHELL TEETH

96. # TREATMENT  No specific treatment  Use of full crowns for aesthetics

97. REGIONAL ODONTODYSPLASIA # WHAT IS IT? Anomaly of teeth that involves all the hard tissue i.e. enamel, dentin and cementum. Unknown etiology with the most popular being local vascular defect.

98. # CLINICAL FEATURE  SITE Maxillary teeth are more commonly affected. Central > Lateral > Cuspid Incisors Incisors  SYMPTOM a) Delayed or no eruption is observed b) Features of teeth i) Short root ii) Large pupal chambers and canals with open apical foramina iii) Increase fractures due to poor mineral- -ization. iv) Irregular shape with mottled appearance

99. # RADIOLOGICAL FEATURES Marked reduction of radio-opacity of enamel and dentin with increase in pulpal volume, so k/a GHOST TEETH # TREATMENT Extraction and replacement with prosthesis

100. DENTIN DYSPLASIA (Rushton,1939) # INTRODUCTION  Autosomal dominant disorder which manifests with normal enamel, atypical dentin and abnormal pulp morphology.  Witkop classified it into two type i.e. a) Radicular Dentin Dysplasia (Type I dentin dysplasia) b) Coronal Dentin Dysplasia ( Type II dentin dysplasia)

101. # CLINICAL AND RADIOLOGICAL FEATURE FEATURE RADICULAR DENTIN DYSPLASIA CORONAL DENTIN DYSPLASIA CLINICAL Both types of dentition are involved. Look normal in appearance though have AMBER color appearance. Short roots. Delayed eruptions. Both type of dentition are involved. 1º dentition shows yellowish-brown to bluish- grey color. 2º dentition shows normal picture. RADIOLOGICAL Obliterated pulp chamber Periapical radiolucency Short, conical and blunt roots Crescent shaped pulpal remnant in some 2º dentition. 1º dentition Obliterated pulp chamber. b) 2º dentition Abnormally large pulp chamber with pulp stone.

102. # TREATMENT No treatment

103. CONCLUSION

104. The Dentino-Pulpal complex is a very important partnership. What happens to one, affects the other. Hence, it is quite important to understand the dentin in order to attain success in the field of conservative dentistry and endodontics.

105. IMPORTANT FACTS XENO V is an important 7 th generation Dentin Bonding agent. Important liners seen under the composite resins in deep carious lesion( RDT<0.5mm ) are Light Cure GIC followed by Type I GIC due to their short setting time. Affected dentin comprises of the INFECTED ZONE(Zone 5) and the TURBID ZONE(Zone 6).

106. Effected dentin comprises of SUBTRANSPARENT DENTIN (Zone 2) and TRANSPARENT DENTIN (Zone 3). Apical gauging is a very important procedure as it gives a good approximation of canal diameter in the most important apical 3-5mm of the root canal. For e.g. if apical diameter of an root canal is 0.4mm then its not advisable to instrument this canal to less than 40 K-File. Hence, it acts as a guide.

107. REFERENCES

108. Nanci Antonio. Tencate’s Oral Histology. 6 th ed. USA: Mosby; 2003. O Heymann Harald, J Swift Edward, V Ritter Andre. Sturdevant’s Art and Science of Operative Dentistry. 1 st ed. New Delhi: Elsevier; 2013. Garg Nisha, Garg Amit. Textbook of Operative Dentistry. 2 nd ed. New Delhi: Jaypee; 2013. A Regezi Joseph, J Sciubba James, C K Jordan Richard. Oral Pathology. 5 th ed. Delhi: Elsevier; 2009. Shafer, Hine, Levy. Shafer’s Textbook of Oral Pathology. 6 th ed. Delhi: Elsevier; 2009.

109. THANK YOU

110. THANK YOU