with clinical considerations related endodontics and conservative

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.

49. Clinical considerations

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

76. Clinical appearance

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