Dentin with emphasis on applied physiology and pathology
- 1. Presented by Dr Nadeem Aashiq 1st year Mds Department of Conservative and Endodontics
- 2. •Introduction • Physical properties • Composition • Structure of Dentin Dentinal tubules Peritubular dentin Intertubular dentin Predentin Dentino enamel junctiom Odontoblastic processes
- 3. Primary dentin Secondary dentin Tertiary dentin Interglobular dentin Granular layer •Innervation of Dentin •Age and functional changes in Dentin •Dentinal fluid •Clinical considerations •Developmental disturbances •References
- 4. Introduction Second layer of the tooth. Structure that provides the bulk and general form of the tooth Since it begins to form slightly before the enamel, it determines the shape of the crown, including the cusps and ridges and also the number and size of the roots.
- 5. Physically and chemically, it closely resembles bone Said to be a living tissue since the tubules present in it contains processes of specialized cells, the odontoblasts. Main morphologic difference between bone and dentin is that some of the osteoblasts that form bone marrow are enclosed within its matrix substance as osteocytes, whereas the dentin contains only the processes of the cells that form it.
- 6. Physical Properties Color Light yellowish in color becomes darker with age Consistency Elastic and resilient Harder than bone but softer than enamel Tensile strength : 40mpa Compressive strength : 266mpa
- 7. Composition 20% organic matter 5% water 75% inorganic material
- 8. The organic matrix of dentin is collagenous The principle inorganic component of dentin is hydroxyapatite crystals .The high mineral content of dentin makes it harder than bone and cementum but softer than enamel Lower content of mineral salts in dentin renders it more radiolucent than enamel. Provides resilience to the crown which is necessary to withstand the forces of mastication.
- 9. Organic substances: Type I collagenous fibrils Type V collagenous fibrils (minor) Non collagenous proteins: •Dentin phosphoprotien (DPP) •Dentin matrix protein 1 (DMP1) •Dentin sialoprotein (DSP) •Bone sialoprotein (BSP) •Osteopontin, Osteocalcin Proteoglycans Phospholipids Growth factors: •Bone morphogenetic proteins (BMP) •Insulin like growth factors (IGFs) •Transforming growth factors β (TGF- β)
- 10. Inorganic substances: Calcium hydroxy appatite crystals. Type I collagen is the principal type of collagen found in dentine Inorganic crystals are plate shaped and much smaller than hydroxyl apatite crystals in enamel Dentin also contains small amount of sulphates, phosphates and carbonates.
- 11. STRUCTURE OF DENTIN The dentinal matrix of collagen fibres are arranged in a network. As dentin calcifies, the HA crystals mask the collagen fibres The bodies of odontoblasts are arranged in a layer on the pulpal surface of the dentin and only their cytoplasmic processes are included in the tubules in the mineralised matrix
- 12. Each cell gives rise to one process which traverses the predentin & calcified dentin within one tubule and terminates in a branching network to the DEJ or CDJ
- 13. DENTINAL TUBULES The course of the dentinal tubules follow a gentle curve in the crown where it resembles an S shape Starts at right angles at the pulpal surface, the first convexity of this doubly curved course is directed towards the apex of the tooth These tubules end perpendicular to the DEJ & CDJ
- 14. It is almost straight near the root tip and along the incisal edges and cusps. Dentin thickness ranges from 3-10mm or more. Ratio between outer and inner surfaces of dentin is about 5:1. No. of tubules per square millimeter varies from 15000 at the DEJ to 65000 at the pulp – density and diameter increases with depth. There are more tubules per unit area in the crown than in the root
- 16. Clinical significance of dentinal tubules Dentinal tubules are filled with dentinal fluid (a transudate of plasma). When enamel or cementum is removed during tooth preparation, the external seal of dentin is lost, allowing tubular fluid to move towards the cut surface.
- 17. PERITUBULAR DENTIN The dentin that immediately surrounds the dentinal tubules is termed peritubular dentin Highly mineralized than intertubular dentin Twice as thick in outer dentin(approx. 0.75μm) than inner dentin(approx. 0.4μm) Calcified tubule wall has an inner organic lining termed the Lamina Limitans which is high in glucosaminoglycans (GAG)
- 18. Clinical significance of peritubular dentin The increased stiffness of peritubular dentin can increasese stresses around tubules and thus affects crack propagation. Peritubular dentin serve to control calcuim binding and crystal growth.
- 19. INTERTUBULAR DENTIN Located between the dentinal tubules or more specifically between the zones of peritubular dentin One half of its volume is organic matrix, specifically collagen fibres The fibrils range from 0.5-0.2μm in diameter and exhibit crossbanding at 64μm intervals HA crystals are formed along the fibres with their long axis oriented parallel to the collagen fibres. Well mineralised , Provide tensile strength to dentin.
- 21. PREDENTIN Located adjacent to the pulp tissues 2-6μm, depending on the activity of odontoblasts First formed dentin and is not mineralised The collagen fibres undergo mineralization at the predentin- dentin junction , the predentin then becomes dentin and a new layer of predentin forms circumpulpally.
- 22. Significance of predentin Predentin, the unmineralized organic matrix is important in maintaining the integrity of dentin.
- 23. DENTINO ENAMEL JUNCTION The DEJ is a complex and critical structure uniting these two dissimilar calcified tissues and acts to prevent the propogation of cracks from enamel into dentin. The DEJ has a three level structure, 25-100 μm scallops with their convexities directed toward the dentin and concavities toward the enamel.
- 25. Clinical Significance of DEJ Any trauma, caries, attrition or abrasion beyond DEJ leads to dentin surface exposed ,the continuing deposition of secondary dentin throughout life takes place. The development of tertiary dentin in response to caries or restorative procedures can lead to reduction in size obliteration of the pulp chamber and root canals. When the canals are small and hard to locate, effective treatment becomes difficult and prognosis is poor
- 26. ODONTOBLASTIC PROCESSES Cytoplasmic extensions of the odontoblasts The odontoblasts reside in the peripheral pulp at the pulp-predentin border and their processes extend into the dentinal tubules The processes are largest in diameter near thepulp and taper further into dentin The odontoblast cell bodies are approximately 7μm in diameter & 40μm in length
- 28. Clinical significance of odontoblasts located in the outermost layer of dental pulp form a natural barrier between mineralized tissues, dentin, and soft tissues, dental pulp of the vital tooth, and they first recognize caries- related pathogens and sense external irritations. In the presence of severe exogenous stimuli, such as the expansion of caries lesions and pulpal exposure to the oral cavity by trauma or cavity preparation, odontoblasts are destroyed, and DPSC might differentiate into odontoblast‐like cells to form reparative dentin.
- 29. PRIMARY DENTIN Dentin that is formed prior to eruption of a tooth(before root completion) Classified as Orthodentin, the tubular form of dentin lacking of cells found in teeth of all dentate mammals Secreted at a relatively higher rate Constitutes major part of the dentin in the tooth. TWO TYPES: MANTLE AND CIRCUMPULPAL
- 30. MANTLE DENTIN: Mantle dentin is the first formed dentin in the crown underlying the DEJ Regular in structure less mineralised and provides cushioning effect to the tooth It is the outer or most peripheral part of the primary dentin and is about 150μm thick Ground section of tooth viewed in polarized light A – Enamel B – Dentin C – Mantle dentin
- 31. CIRCUMPULPAL DENTIN: Circumpupal dentin forms the remaining primary dentin or the bulk of the tooth The collagen fibrils are much smaller in diameter and are more closely packed together Slightly more mineral content than in mantle dentin A- Odontoblasts B- Predentin C- Pulp D-Circumpulpal dentin
- 32. SECONDARY DENTIN Formed after root completion Narrow band of dentin bordering the pulp Contains fewer tubules than primary dentin There is usually a bend in the tubules at primary and secondary dentin interface Appears in greater amounts on the roof and floor of the pulp where it protects the pulp from exposure in older teeth
- 33. TERTIARY DENTIN Also known as: Reactive Dentin, Reparative Dentin, Irritation Dentin, Replacement Dentin, Adventitious Dentin, Defense Dentin. By pathologic process or operative procedures, the odontoblastic processes are exposed or cut, the odontoblasts die or survive, depending on the extend of injury If they survive, dentin that is produced is called reactionary or regenerated dentin Demineralized section showing loss of continuity of: B-Tertiary dentin compared to A- Normal dentin
- 34. Killed odontoblasts are replaced by the migration of undifferentiated cells arising in the deeper layers of the pulp to the dentin interface. This newly differentiated odontoblasts then begin deposition of reparative dentin to seal off the zone of injury as a healing process initiated by the pulp, Resulting in resolution of the inflammatory process and removal of dead cells This type dentin produced by a new generation of odontoblast-like cells in response to appropriate stimulus after the death of original odontoblasts is called Reparative dentin This reparative dentin has fewer and more twisted tubules than normal dentin
- 35. Histological difference between reactionary and reparative dentin is that reactionary dentin is deficient in acid proteins so it doesn’t stain. Reactionary dentin appears as either osteodentin type or orthodentin type Reparative dentin has structure-less mineralization as in bone.
- 36. INTERGLOBULAR DENTIN Sometimes mineralization of dentin begins in small globular areas that fail to fuse into a homogenous mass. This results in zones of hypomineralisation between the globules. These zones are called interglobular dentin. Forms in crowns of teeth in the circumpulpal dentin just below the mantle dentin Seen in dental anomlies (hypophosphatasia) A- Interglobular dentin
- 37. GRANULAR LAYER There is a zone adjacent to the cementum that appears granular known as Tome’s granular layer It slightly increases in amount from the CEJ to the root apex Caused by coalescing and looping of the terminal portions of the dentinal tubules
- 38. INNERVATION OF DENTIN Nerve fibres were shown to accompany 30-70% of the odontoblastic process and these are referred to as intratubular nerves These nerves and their terminals are found in close association with the odontoblasts process within the tubules.
- 39. Theories of pain transmission through dentin Direct neural stimulation Odontoblast receptor theory Hydrodynamic theory
- 40. DIRECT NEURAL STIMULATION This theory postulates that direct mechanical stimulation of Exposed nerve endings at the dentinoenamel junction is responsible for dentinal hypersentivity. The shortcoming of this theory is that there is insufficient evidence to prove that the outer dentin is most prone to be sensitive is well innervated. Topical application of local anaesthetic agents do not abolish sensitivity Hence this theory is not accepted
- 41. Odontoblast receptor theory This theory proposes that the odontoblasts themselves act as neural receptors and relay the signal to the nerve terminals. the major shortcoming of this theory is that there is no evidence to demonstrate synapses between odontoblasts and nerve terminals.
- 42. HYDRODYNAMIC THEORY Most accepted theory Proposed by Brannstrom This postulates that the dentin tubules, which are open and wide, contain fluid various stimuli i.e thermal, tactile, chemical, or osmotic changes displaces the fluid in the dentinal tubules in either an inwardly or outwardly direction. The movement of this liquid stimulates the odontoblatic processes, and the subsequent mechanical disturbances stimulates the baroreceptors that lead to neural discharges. This neural pulpal activation is percieved as pain by the patient.
- 43. AGE AND FUNCTIONAL CHANGES IN DENTIN Vitality of dentin Odontoblasts and its processes are an integral part of dentin and so vitality is understood to be the capacity of the tissue to react to physiologic and pathologic stimuli ,dentin must be considered a vital tissue. Dentinogenesis is a process that continues 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 slower rate. This is secondary dentin Pathologic changes in dentin such as dental caries, abrasion, attrition or the cutting of dentin in operative procedures cause changes in dentin. They are the dead tracts, sclerosis and the addition of reparative dentin.
- 44. DEAD TRACTS When dentin is damaged odontoblastic processes die or retract leaving empty dentinal tubules under transmitted light these tubules appear black when viewed under microscope these are called dead tracts. Degeneration is often observed in areas of narrow pulp horns because of crowding of odontoblasts
- 45. These degenerated empty areas demonstrate decreased sensitivity Seen to a greater extend in older teeth Dead tracts are probably the initial step in the formation of sclerotic dentin
- 47. Sclerotic or transparent dentin Sclerotic dentin describes dentinal tubules that have become occluded with calcified material When this occurs in several tubules in the same area the dentin assumes a glassy appearance and becomes translucent Increases with age and is most common in the apical third of root and in the crown midway between the DEJ and surface of the pulp Because sclerosis reduces the permeability of dentin,it may help to prolong pulp vitality
- 48. DENTINAL FLUID Free fluid occupies 1% of superficial dentin and 22% of total volume of deep dentin Ultrafiltrate of blood from pulp capillaries Contains plasma proteins Serve as a sink from which injurious agents can diffuse into the pulp producing inflammatory response Also serve as a vehicle for egress of bacteria from a necrotic pulp into periradicular tissue.
- 50. DENTIN HYPERSENSITIVITY According to Clark, 1885) Dentin hypersensitivity can be described as an adverse reaction or pain in one or more teeth resulting from either a thermal mechanism or chemical stimulus. (According to Grossman, 1935) It is a commonly sensitive or painful response of exposed dentin to an irritation. Prevalence rate- 8.7 to 30 % of adult population.
- 51. It has been stated in the literature that DH develops in two phases: lesion localization and lesion initiation Lesion localization occurs by loss of protective covering over the dentin, thereby exposing it to external environment. It includes loss of enamel via attrition, abrasion, erosion or abfraction. Another cause for lesion localization is gingival recession which can be due to toothbrush abrasion, pocket reduction surgery, tooth preparation for crown, excessive flossing or secondary to periodontal diseases. As stated earlier, not all exposed dentine is sensitive. For DH to occur, the lesion localization has to be initiated. It occurs after the protective covering of smear layer is removed, leading to exposure and opening of dentinal tubules.
- 52. MANAGEMENT OF HYPERSENSITIVITY • Nerve desensitization Potassium nitrate • Protein precipitation Gluteraldehyde Silver nitrate Zinc chloride • Occluding dentinal tubules Sodium fluoride Stannous fluoride Strontium chloride Potassium oxalate Calcium carbonate Dentin adhesives Dentin bonding agents Composites Glass ionomers Crown placement lasers
- 53. Dentin and Restorative Treatments It is well accepted that dentin is the best insulator for the pulp. Dentin must be treated with great care during restorative procedures to minimize damage to the odontoblasts and pulp. Air water spary should be used whenever cutting with high speed handpieces to avoid heat bulidup. The dentin should not be dehydrated by compressed air blasts.it should always maintain its normal fluid content.
- 54. Protection also is provided by judicious use of liners, bases ,dentin-bonding agents, and non toxic restorative materials. Restorations must seals the preparation adequately to avoid micro leakage and bacterial penetration. It is best to conserve as much sound tooth structure as possible and therefore the Remaining Dentin Thickness is the single most important factor in deciding the technique and materials of choice during restorative procedures
- 55. Based on the RDT the following pulp protective agent is placed before the final restorative material
- 56. SMEAR LAYER AND SMEAR PLUGS Smear Layer term most often used to describe the grinding debris left on dentin by cavity preparation. This smear layer is only a few micrometres thick and is composed of denatured collagen, hydroxyapatite, and other cutting debris. The smear layer serves as a natural bandage over the cut dentinal surface because it occludes many of the dentinal tubules with debris called smear plugs.
- 57. The smear layer is a good protective barrier, it has a realtively weak attachment to the dentin and is subject to dissolution by acids.
- 58. Dentin Etching and Bonding Buonocore first brought about the concept of acid etching the tooth surface for better bonding Although acid etched enamel showed great results, etched dentin which was air dried did not have positive results Nakabayashi et al in 1982 published a paper on how etched dentin lost its mineral content and that only the collagenous matrix remained.
- 59. This solubilized phase when infiltrated with resin formed a layer that was neither dentin nor resin and was hence called as the ‘Hybrid Layer’ Bonding of resin to dentin using ‘total etch technique’ (Generation IV & V are based on this philosophy)
- 60. Scanning electron micrograph of etched dentin showing etched collagen fibers Etched dentin showing exposed collagen fibers
- 61. MOIST VERSUS DRY DENTIN SURFACES Moist dentin- A glistening appearance without accumulation of water In early 1990’s, Kanca developed the wet or moist bonding technique Most new adhesives utilize the ‘wet bonding technique’. The ‘wet bonding’ has repeatedly shown enhanced bond strengths as water preserves the porosity of collagen network available for monomer interdiffusion
- 62. Excessive drying of tooth preparation can cause odontoblasts to be aspirated in the dentinal tubules
- 63. VITAL PULP THERAPY The reparative Dentin Formation can be stimulated by cavity lining materials (such as Calcium hydroxide) Materials like MTA Biodentine - can be used as a substitute to dentin(capable of inducing reactionary dentin by stimulating odontoblastic activity and repairative dentin by induction of cell differentiation ) Includes Direct and Indirect pulp capping • Results in formation of reparative dentin .
- 64. ENDODONTICS AND DENTIN The continuing deposition of secondary dentin through out life & development of tertiary dentin in response to caries & restorative procedures can lead to a reduction in size & effectively cause obliteration of pulp chambers & root canals. Thus, making effective endodontic treatment difficult. Residual dentin thickness indicates the mechanical limits of instrumentation and canal preparation. Atleast 1mm of dentin should remain in all root aspects along its entire length after all intracanal procedures are done.
- 65. Ellis classification (Tooth fractures) Ellis Class I Enamel fracture: This level of injury includes crown fractures that extend through the enamel only. These teeth are usually non tender and without visible color change but have rough edges. Ellis Class II Enamel and dentin fracture without pulp exposure: Injuries in this category are fractures that involve the enamel as well as the dentin layer. These teeth are typically tender to the touch and to air exposure. A yellow layer of dentin may be visible on examination
- 66. Ellis Class III Crown fracture with pulp exposure: These fractures involve the enamel, dentin, and pulp layers. These teeth are tender (similar to those in the Ellis II category) and have a visible area of pink, red, or even blood at the center of the tooth. Ellis Class IV Traumatized tooth that has become non-vital with or without loss of tooth structure. Ellis Class V Luxation: The effect on the tooth that tends to dislocate the tooth from the alveolus. Teeth loss due to trauma. Ellis Class VI Fracture of root with or without loss of crown structure.
- 67. Ellis Class VII Displacement of a tooth without the fracture of crown or root. Ellis Class VIII Fracture of the crown en masse and its replacement. Ellis Class IX Fracture of deciduous teeth
- 69. TREATMENT OF CLASS II ELLIS Simple restorations
- 70. Bevels are angulations which is made by 2 surfaces of a prepared tooth which is other than 90 degrees. They are created to increase the retention and to prevent marginal leakage They are given at various angulations depending upon the type of material used for restoration and the purpose the material serves BEVELS:
- 74. Developmental disturbances Dentinogenesis imperfecta Dentin dysplasia Regional odontodysplasia Dentin hypocalcification
- 75. Dentinogenesis imperfecta Dentinogenesis imperfecta is an autosomal dominant condition affecting both deciduous and permanent dentition Affected teeth are gray to yellowish brown and have broad crowns with constriction of cervical area resulting in a ‘tulip’ shape Radiographically teeth appear solid lacking pulp chambers and root canals Enamel is easily broken leading to exposure of dentin that undergoes accelerated attrition
- 77. Radiographic appearance Partial/complete obliteration of pulp chamber , root canals Shell teeth- Normal Enamel, Thin Dentin, short roots
- 78. Treatment Prevention of loss of enamel & subsequent loss of dentin. Cast metal crowns on posterior teeth & porcelain jacket crown on anterior teeth are usually preferred
- 80. DENTIN DYSPLASIA It is characterized by normal enamel but atypical dentin formation with abnormal pulp morphology. ETIOLOGY- Hereditary disease transmitted as an autosomal dominant trait. CLASSIFICATION: (Acc. ToWHITKOP) – TYPE I- RADICULAR TYPE II – CORONAL
- 81. Type I – (Radicular Dentin Dysplasia Both dentitions are affected & crowns appear clinically normal. Teeth exhibit mobility & are exfoliated prematurely. Roots are short, blunt, conical or malformed. Root canals are completely obliterated.
- 82. Type – II (Coronal Dentin Dysplasia) Deciduous teeth have yellow, brown or bluish grey opalescent appearance. Pulp chambers of deciduous teeth are obliterated. Typical ‘Thistle tube’ appearance is seen in almost all teeth.
- 83. Radiological features Periapical radiolucencies, absence of pulp chambers, canals & defective root formation Retarded root formation, obliteration of pulp chamber & apical radiolucencies
- 84. TREATMENT- No treatment Prognosis depends upon occurrence of periapical lesions necessitating tooth extractions
- 85. Regional Odontodysplasia Usually seen in Maxillary and Mandibular Anteriors CLINICAL FEATURES: unusually large pulp chambers with thin layers of enamel and dentin are evident.delay or failure of eruption, irregular shape RADIOGRAPHIC FEATURES: “Ghost Teeth
- 86. TREATMENT No treatment required • Meticulous oral hygiene • Extraction / Endodontic treatment • Prosthetic rehabilitation
- 87. Normal dentin is calcified by deposition of calcium salts in the organic matrix in the form of globules,which increase in size by peripheral deposition of salts until all the globules are finally united into a homogenous structure Failure of union of many of these globules results in dentin hypocalcification There is no alteration in clinical appearence Dentin hypocalcification
- 88. DENS IN DENTE Dentin & enamel forming tissue invaginate the whole length of a tooth. Arises due to localised external pressure, focalgrowth retardation,focal growth stimulation in certain areas of tooth bud Pear shaped invagination Radiographically- “tooth within a tooth
- 90. REFERENCES Orbans’ Oral Histology and Embryology-G.S Kumar Pathways of the pulp- Cohen. Hargreaves- eleventh Edition. Shafer’s Textbook of Oral Pathology- Shafer, The art and science of Operative dentistry- Theodore Sturdevant- 5th Edition.
- 91. THANK YOU