This document discusses the biological considerations of operative dentistry related to enamel, dentin, and the dentinoenamel junction. It provides details on the structure, composition, properties and clinical significance of enamel and dentin. Key points include that enamel is the hardest substance in the body but has no self-repair ability. Dentin lines the inner walls of teeth and contains tubules that connect to the pulp and determine permeability. The dentinoenamel junction is a critical area that provides strength between the two tissues.

1. BIOLOGICAL
CONSIDERATION
IN OPERATIVE
DENTISTRY
SARANG SURESH HOTCHANDANI
Dentist @ BibiAseefa Dental College, SMBBMU.
Larkana, Sindh, Pakistan

2. Contents •Enamel
•Dentine
•Pulp
•Gingiva 2

3. ENAMEL
3

4. Enamel
Functions
• Provide the shape & hard,
outer covering for teeth.
• Protect underlying dentine &
pulp.
• Esthetics provided by
enamel’s color & form. 4

5. Enamel • When enamel is exposed to an oral
environment of occlusal, chemical and
bacterial challenges, its crystalline
mineral makeup and rigidity is
damaged from acid demineralization,
attrition & fracture.
• Repair or replacement of enamel can
only be accomplished through dental
therapy.
5

6. Enamel
Permeability
• Inorganic hydroxyapatite
– 96% by weight
– More than 86% by volume
• Small volume of organic matrix
• Water
– 4 – 12 % by volume
– Water is contained in network of micro pores, which
open into external surface of oral cavity in inter-
crystalline spaces of enamel.
– This network provides connection b/w oral cavity &
dentinal fluid & pulp interstitial space.
6

7. Enamel
Permeability
• Enamel is semipermeable
– That’s why various fluids, pigments, ions, LMW
substances acid demineralization, remineralization,
fluoride uptake & vital bleaching is possible in enamel.
• CLINICAL POINT
– When teeth become dehydrated from;
• Nocturnal mouth breathing during sleep OR
• Rubber dam isolation
– Then enamel appears chalky & lighter in color, it is
reversible when enamel become wet again.
– That’s why shade matching should be
determined with full spectrum of light
before isolation with rubber dam.
7

8. Effects of
Aging on
Permeability
of Enamel
• Color (hue) is increased or
intensified
• Following things in enamel
decreases with aging.
– Acid solubility of enamel
– Pore volume
– Water content
– Permeability
8

9. Clinical
Appearance
& Defects
• Key diagnostic signs on enamel
includes;
– color changes,
– white spots,
– plaque,
– crake,
– craze lines,
– demineralization,
– erosion/abrasion,
– attrition,
– restoration margin integrity.
9

10. Color • Enamel translucency (clearness) is directly proportional
to degree of mineralization.
• COLOR OF ENAMEL DEPENDS UPON;
– Thickness of enamel
• 2.5 mm at cusp tips & 2.0 mm at incisal edges
• Thickness decreases below deep occlusal fissures and
tapers to become very thin in the cervical area near CEJ
• Young anterior teeth have translucent grey or slightly
bluish hue (shade/color) near the incisal edge
• Yellow – orange shade predominates cervical because of
thin enamel present from which color of underlying
dentine is visible.
– Color of underlying dentine
10

11. Color • In about 10% of teeth, a gap b/w enamel &
cementum in cervical area is present
which exposes vital and highly sensitive
dentine.
• Natural color of enamel can be altered by;
– Anomalies of development & mineralization
– Extrinsic stains
– Antibiotic therapy
– Excessive fluoride
– Dental caries
• White spot lesion 11

12. White Spot
Lesion
• It is early caries lesion characterized by
subsurface enamel porosity result from
demineralization caused by few streptococci
mutans within biofilm.
• Clinically appear as milky white opacity after
air drying of enamel.
• When this subsurface demineralization
reaches DEJ, this white spot opacity become
visible not only with air drying but also when
it is we with saliva. 12

13. White Spot
Lesion
• Early fissure caries lesions are difficult to be visualized
on bitewing radiographs but can be assessed by
visually examining discoloration enamel around pits &
fissures.
• It takes 4 to 5 years for this white spot lesion
demineralization to progress through enamel.
• When the caries involves dentine, the clinical sign
which indicate dentine involvement is;
– Blue or grey shade of enamel
• Invasive restorative procedures should only be
considered when;
– Caries is extended to dentine confirmed by above
mentioned clinical sign of discoloration
– Enamel is cavited into dentine
– Caries is visualized on radiographs
• If these above mentioned conditions are not present
preventive measures can be applied.
13

14. Cavitation
• Smooth surface enamel caries lesion when
seen in two dimensions, as in radiographs, it
appears triangular with the base of triangle at
the enamel surface.While in three-dimension
view, smooth surface lesion is cone shaped
with base at enamel surface and apex of cone
at DEJ.
• The shape of pit and fissure enamel caries is
complex, because it occurs simultaneously at
confluence of two or more cuspal lobes.
– In two dimension, fissure caries has also triangular
shape with base towards & parallel to DEJ and apex
in pit or fissure.
14

15. Cavitation
• Unless, preventive measures or
remineralization reverse the
process of demineralization, the
dentine is compromised and can
no longer support the enamel
which result in development of
cavity.
– Untreated cavity will lead to;
• Compromise crown & strength of
tooth.
• Jeopardize the vitality of pulp due to
active proliferation of bacteria.
15

16. Enamel
Wear
• Enamel is as hard as steel.
– Knoop hardness number of enamel is 343
– Knoop hardness number of dentine is 68
• Wear of enamel occur because of following reasons;
– Attrition
– Frictional contact against opposing enamel or restorative
material
– Bruxism
– Erosion
– Malocclusion
– Age
– Other parafunctional habits
– Hard diet
– Compromised occlusal function
• In preparing tooth for restoration, outline form should
have designed in such a way that the margins of
restorative material avoid critical high stress areas of
occlusal contacts.
16

17. Enamel
Wear
• Normal physiologic wear rate
for enamel is 15 – 29
micrometer per year.
• Tooth wear causes loss of
vertical dimension of tooth
structure.
– This can be counteracted by
active tooth eruption & apical
cementogenesis.
17

18. Enamel
Faults &
Fissures
• Faults as named below are defects
of enamel surface which
contribute to the accumulation
and retention of plaque.
– Perikymata (parallel ridges formed
by cyclic deposition of enamel)
– Pitting defects (formed by
termination of enamel rods)
– Hypoplastic areas
– Linear defects or craze line 18

19. Enamel
Faults &
Fissures
• Fissure is formed by incomplete fusion of
lobes of cuspal enamel in the tooth.
– Fissures provide the protected niche for acidogenic
bacteria and the nutrients they require for caries
development.
• Caries lesions are 5 times more to occur on
occlusal fissures than on the facial or lingual
fissures.
– Caries lesions are 2.5 times more to occur on facial
or lingual fissures than on proximal surfaces.
• Resin fissure sealant is effective preventive
method for this caries.
19

20. Enamel
Cracks
• A cracked tooth that is
symptomatic or involves dentine
requires following treatment;
– Crown
– Splinting
20

21. Rod &
Interrod
Crystal
Structure
• The carbonated component in the
hydroxyapatite crystal;
– Produce destabilizing effect on the crystal
– Most susceptible to demineralization and
the first to be solubilized.
• in the presence of fluoride, enamel
crystals are replaced with Fluorapatite
or fluorohydroxyapatite which is
relatively insoluble.
21

22. Rod &
Interrod
Crystal
Structure
• Ameloblasts cytoplasmic extension named
tomes’ process;
– Secret enamel protein matrix
– Initiate the mineralization
– Orient the enamel crystal
• After orientation of enamel crystals two
structural units of enamel are formed;
– Cylindrical enamel rods
– Inter rod enamel
• The matrix protein enamelin and water forms
the envelop of crystal.
22

23. Rod &
Interrod
Crystal
Structure
• Enamel rods and inter rod enamel
differs only in orientation of crystals.
– Inter rod crystals are perpendicular to
enamel rod crystals.
– Crystals in the enamel rods are parallel to
long axis of rods, while rods are
perpendicular to enamel surface.
• Enamel rods are separated by rods sheaths
which is composed of organic material.
• Hydroxyapatite crystal is hexagonal in
shape with cross sectional dimension
of;
– 30 x 60 nanometer
23

24. Hunter –
Schreger bands
These are alternative light and
dark bands in the enamel seen
under magnification in cut or
fractured sections of tooth
structure.
This occurs because of variation
of light reflection from the bands
of the enamel crystals that are
oriented in different directions.
24

25. Enamel &
Acid
Etching
• Initially, acid etchant removes about 10
micros – meter of surface enamel which does
not contain any rod structure.
• After removal of this, rods & inter – rods of
enamel are exposed.
– Dissolution of this rod & inter – rod creates macro –
porosity.
• The acid etched enamel surface has high
surface energy so that resin flows into and
polymerize within the resin tags into pores up
to depth of 20 micrometers.
25

26. How Micro
porosity is
Created in
Enamel
Etching???
• As you know crystals in the enamel rod
run parallel to length of enamel rods &
enamel rods always run perpendicular to
tooth surface
– So, the rods which are present in that wall
which is perpendicular to tooth surface will
expose the sides of rods & their crystals
during acid etching & while those rods
which are present in that wall which is
parallel to surface will expose the
transverse section or face of crystals and
create micro – porosities in the core of
these rods.
26

27. How Micro
porosity is
Created in
Enamel
Etching???
• In these micro – porosities micro tags
are formed.
– It is these mini tags which are formed within
individual crystal core contribute the bond
strength in enamel – resin bond.
• There are about 30,000 – 40,000 enamel rods
per millimeter of enamel and etching increases
the surface area 10 – 20 folds
• That’s why beveling is done in
composite restoration to expose the
face of rods and increase the bonding.
27

28. Enamel
Strength &
Resilience
• Enamel demineralization is much
slower than dentine because,
apatite crystals in enamel are 10
times larger than dentine crystals.
• Enamel rods are in spiral shaped
at cusp tips.
– If the enamel were uniformly
crystalline, it would shatter with
occlusal function.
28

29. DENTINE
29

30. Dentine
Functions
• Provide color & elastic foundation for
enamel.
• Form bulk of the tooth.
• Provide strength & durability to crown
of tooth.
• Protective barrier & chamber for the
vital pulp tissues.
• Does not have any vasculature or
innervation.
• Respond to external thermal, chemical
or mechanical stimuli 30

31. Dentino
Enamel
Junction
(DEJ)
• It is a transitional area
demarcating the junction of
enamel & dentine.
• The width/ thickness of DEJ range
from 2 – 15 micrometers.
– Width of DEJ is different in different
locations of teeth.
31

32. Dentino
Enamel
Junction
(DEJ)
• DEJ is scalloped with wave – like
crests pointing outward toward
enamel.
– This scalloping provides the strength b/w
enamel & dentine.
– Scalloping is larger in posterior teeth.
• The part of dentine which is present in DEJ
is soft & is mantle layer of dentine.
– This layer of dentine is called as SOFT ZONE.
– This soft zone provides cushioning soft layer b/w
enamel & dentine.
32

33. Dentine
Support
• Maximum bite force is 738 N (166lb)
• Resistance to tooth fracture is compromised with
increasing depth and/or width of cavity.
• Endodontically treated tooth retain only 1/3 of the
fracture resistance of normal intact tooth.
• In MOD coronal stiffness decrease more than 60%
of normal tooth.
• So, try to conserve the tooth structure during
preparation. 33

34. Morphology
of Dentine
• Dentine is composed of small, thin
apatite flakes of crystals embedded in a
collagen matrix.
– Thickness of apatite crystals near DEJ is 3.5
mm while, near pulp they are approx. 2 mm
in thickness.
– usually, these crystals are randomly
oriented but they are parallel to each other
at cusps.
• Matrix formation & mineralization is
controlled by odontoblasts.
34

35. Morphology
of Dentine
• Thickness of dentine from pulp
chamber to DEJ is about 3.0 to 3.5
mm.
• Diameter of dentinal tubule
– 2.5 micrometers near pulp
– 0.8 micrometers near DEJ
• Tubules comprise 10% of dentinal
volume. 35

36. Morphology
of Dentine
• Dentinal tubules follow “S –
shaped” curve in axial areas of
teeth while;
– Dentinal tubules are straight in the
occlusal areas & root areas.
• Odontoblastic process extends
within dentinal tubule to about
1/3rd of dentinal thickness.
36

37. Morphology
of Dentine
• Dentine is;
– 45% - 50% inorganic apatite
– 30% organic matrix
– 25% water
– Pale yellow in color
– Harder than bone
• Dentine is of two types;
– Inter-tubular dentine
• Forms bulk of dentine
– Peritubular dentine
• Present only in lining of tubule walls
37

38. Dentine
Permeability
• When external covering of teeth; enamel &
cementum is removed due to following mentioned
reasons, the exposed dentinal tubules become
conduits b/w the pulp and external oral
environment.
– Cavity preparation
– Root planning
– Caries
– Trauma
– Abrasion
– Erosion
• Exposure of dentinal tubules is compensated by
smear layer.
– Removal of smear layer leads to;
• Increased permeability of dentinal tubules.
• Outward flow of dentinal fluid.
38

39. Dentine
Permeability
• Outward flow of dentinal fluid occurs in response
to following effects which are caused by injury to
dentine during above mentioned process.
– Pulpal vasodilation
– Increased pulpal blood flow
– Increased interstitial fluid pressure
• In vitro studies shown that outward flow of
dentinal fluid decreases the inward permeability
of toxic substances by 50% - 60%.
– Also, during outward flow, dentinal fluid also contains
albumin & other immunoglobulins which provide
immune response to bacteria and prevent their inward
flow to pulp.
39

40. Dentine
Permeability
• Prevention of inward permeability can
also be achieved by;
– Blockage of dentinal tubules.
• Another method of preventing inward
diffusion of exogenous products in
exposed pulp is presence of greater
amount of remaining dentine thickness
(RDT)
– Remaining dentine thickness represents
small dentinal tubule diameter and greater
tubules length. 40

41. Dentinal
Tubule
Diameter &
Dentine
Permeability
• Small constricted diameter prevents the
movement of exogenous products
• Functional diameter of dentinal tubule is
much smaller than the anatomic diameter.
And bacteria are unable to pass through
this functional diameter of tubule.
• Anatomic diameter; overall lumen of dentinal
tubule.
• Functional diameter; dentinal tubule is filled with
cellular, collagenous and mineral particles, so
empty space which is left after these materials is
functional diameter of tubule.
41

42. Dentinal
Tubule
Diameter &
Dentine
Permeability
• The coronal occlusal dentine (pulpal
floor of cavity) is less permeable than
dentine around pulp horn or axial
surface.
• In restored teeth diffusion of toxic
material through dentinal tubules can
occur via a process of micro leakage.
– Micro leakage occurs due to;
• Polymerization shrinkage
• Condensation gaps around restorative material.
• Differences in thermal expansions.
42

43. Dentinal
Tubule
Diameter &
Dentine
Permeability
• This micro leakage can lead to;
– Marginal staining
– Sensitivity
– Chronic pulpitis
• Without treatment loss of tooth structure can
occur.
– If the stimuli are moderate and slow then defensive
reactions of dentine occur as mentioned below.
• Hyper mineralization or sclerosis of dentinal
tubules.
• Formation of tertiary dentine
43

44. Dentinal
Substrates
• Variation in the form & composition of
dentine occurs throughout the life of
tooth.Which result from;
– Natural developmental or aging process
– External factors;
• Caries, injury, wear etc.
• Reason for studying this dentinal tissue
variation;
– To evaluate the long – term success of
dental procedures or therapies.
44

45. Dentinal
Substrates
45

46. Primary &
Secondary
Physiologic
Dentine
• Dentine which is formed from before
physiologic apexification of maturation
of tooth is called as primary dentine.
– Mantle dentine; it is primary dentine near
DEJ.
• It is 150 micrometers thick
• 4% less mineralized than circumpulpal dentine.
• Unlike circumpulpal dentine, collagen fibers in
this dentine are arranged perpendicular to DEJ
– Circumpulpal dentine; primary bulk dentine
except mantle dentine, which surround the
pulp chamber and canal.
• It is formed at a rate of 4 – 8 micrometers per
day and after apex closure, its formation
declines and secondary dentine begin to form.
46

47. Primary &
Secondary
Physiologic
Dentine
• Secondary dentine is laid gradually and
asymmetrically and leads to;
– Decrease in dimension of pulp chamber & canal.
• Occluso – gingival decrease in dimension is more
frequent.
• With reduction in size of pulp chamber & root,
the risk of pulp exposure is decreased with
aging.
• That’s why always evaluate radiographically
size of pulpal tissue in relation to size or
location of caries in order to assess the need
for indirect or direct pulp exposure.
47

48. Outer
Dentine
• It is the dentine which is present in the periphery
near DEJ.
• Dentinal tubules in this are far apart and have
narrow lumen due to continued & excessive
deposition of peri – tubular & inter – tubular
dentine.
• Number of tubules in outer dentine is approx.
20,000 tubules/mm2.
– Diameter of lumen in outer dentine about 0.8
micrometers.
– This lumen constitutes about 4% surface area in outer
dentine.
48

49. Dentine
Dentin near the DEJ (outer)
and near the pulp (inner) are
compared to show relative
differences in intertubular
and peritubular dentin and in
lumen spacing and volume.
49

50. Outer
Dentine
• Dentinal tubule also has got interconnecting branches
in outer dentine.
• So, the reason for learning this is that; cavity
preparation or caries lesions which are confined to outer
dentine do not directly damage the odontoblastic process
because odontoblastic process extends no farther than
the inner 3rd of adult dentine.
• Cavity preparation or lesions in outer dentine with
remaining dentine thickness of about 2 mm or more
provides sufficient physiologic barrier to protect the pulp.
– However, there is an exception in case of crown
preparation.
• Although crown preparation if occurring in near outer dentine
can damage the pulp due to heat generated without cooling.
50

51. Inner
Dentine
• It is dentine near pulp
• Thickness of Predentine; 20 micrometers.
– It consists of newly secreted organic matrix which is
waiting to be mineralized.
• Number of tubules in inner dentine are
approx. 58,000/mm2. And contain
odontoblastic process.
• So try to carefully prepare tooth to avoid
damage to odontoblastic process
51

52. Inner
Dentine
• Tubule diameter are about 2.5 – 3.0 micrometers.
– Peritubular dentine is very small or absent in inner dentine.
– Tubules are very close in inner dentine as shown in above pic.
– Area occupied by inter – tubular dentine is about 12%
– Tubule lumen constitute about 80% of surface area in inner
dentine.
• Inner dentine is about 22x times more permeable &
cause wetness after tooth preparation than outer
dentine.
• Fluid in tubule is extension of fluid from pulp and has
pressure of about 5 – 20 mmHg.
– So deeper the cavity more the wetness. ;)
52

53. Carious
Dentine
• Progressive destructive changes in
non – intervened caries process;
– Subsurface demineralization
– Dentinal demineralization
– Cavitation
– Infection of demineralized dentine
– Dentine matrix dissolution
– Pulp necrosis
53

54. Carious
Dentine
• Initial response of dentine in an incipient, non –
Cavitated enamel;
– Very initially, Hyper mineralization of peritubular
dentine which are subjacent to those enamel rods which
have been dissolved due to acid.
• Increased permeability of these rods stimulate this
response from dentine.
– Demineralization of dentine result when acid reach at
DEJ.
• Demineralization in dentine is more rapid because of;
– Tubular network
• High surface to volume ratio of hydroxyapatite
crystals embedded into collagen. 54

55. Carious
Dentine
• Clinically affected dentine is
distinguished from normal dentine
by;
• Decreased hardness
• Yellow – brown discoloration
– Discoloration is due to acid effect on organic
matrix or exogenous staining.
• However, at this stage dentine lesion
is sterile because of intact enamel.
– This type of lesion can be arrested with
plaque control or other non – invasive
preventive therapy. 55

56. Carious
Dentine
• When the enamel surface become
Cavitated, a pathologic cycle of tooth
destruction, infection and tubular invasion
of dentine structure occurs.
– Demineralization of peritubular walls and
intertubular crystals occurs.
– Proteolytic destruction of collagen of dentine.
• Infected dentine is soft, readily excavated,
wet & generally light yellow to orange
color.
– Below this infected dentine, lies affected
dentine which contain intact dentine matrix and
is invaded by a very few microorganisms. 56

57. Carious
Dentine
• Bacterial fill and demineralize the lumens of
tubules peripherally, but dissolved minerals
repercipitate at deeper levels stimulate the
sclerosis of dentine below caries.
• Reparative dentine with irregular tubules
forms a final obstruction against caries
bacteria and their metabolites.
• After cavitation and dentinal infection,
restorative treatment is necessary to remove
the infected dentine and restore the integrity
of coronal surface. 57

58. Carious
Dentine
Bacterial fill and demineralize the lumens of tubules
peripherally, but dissolved minerals repercipitate at
deeper levels stimulate the sclerosis of dentine below
caries.
Reparative dentine with irregular tubules forms a final
obstruction against caries bacteria and their
metabolites.
After cavitation and dentinal infection, restorative
treatment is necessary to remove the infected
dentine and restore the integrity of coronal surface.
58

59. Altered
Dentine
• Alteration in dentine morphology occurs due to;
– Aging process
– Localized defensive and repair responses to injury from
caries, trauma etc.
• Hard tissue defensive and repair responses, which
restrict the tubular diffusion of noxious agents.
– Dentinal tubule hyper mineralization
– Sclerosis
– Tertiary dentine formation
• Pulpal defensive and repair responses;
– Activation of odontoblastic and sub odontoblastic cells.
– Proliferation of vascular & neural tissues
– Initiation of immune response & inflammation. 59

60. Sclerotic
Dentine
• It is characterized by blockage of the tubules with
whitelockit crystals and by a denatured collagen
network.
• Usually form in Non-carious lesions of tooth;
– Abrasion
– Attrition
– Erosion
– Occlusal stress
• Exposed dentine in non-carious lesion appear;
– Deep yellow in color
– Transparent glossy surface
– Sensitive to touch
• Sclerosis occur in those tubules which are exposed
due to non – carious lesions.
60

61. Hyper
Mineralized
Dentine
• Secondary dentine produced
throughout life of teeth cause increase
in thickness of peritubular walls
subsequently narrowing of dentinal
tubules, resulting decreased
permeability.
• Secondary dentine in physiologic
condition deposits very slowly, but the
process accelerated during injury to
tooth. 61

62. Hyper
Mineralized
Dentine
• During acidic environment, minerals are released
into acid which gets supersaturated with mineral
crystals, if the buffering of acid occur then these
minerals repercipitate in tubules and mineralize it
and block the diffusion of noxious products.
• The combination of peritubular wall thickness and
intra – tubular crystals creates a zone of hyper
mineralized dentine beneath carious dentine or
exposed dentine.
• Sclerosis and hyper mineralization of dentine
depends on;
– Rate of caries lesion
– Age 62

63. Tertiary
Dentine
• It is newly formed dentine which is
formed at pulpal dentine interface
and provide the pulpal seal against
noxious diffusion through dentinal
tubules.
• There are two types of tertiary
dentine;
– Reactionary tertiary dentine
– Reparative tertiary dentine
63

64. Reactionary
Tertiary
Dentine
• It is formed in low grade damage to enamel.
– Incipient caries
– NonCavitated lesion
• Formed from already present odontoblasts.
• It may tubular or atubular
– It is tubular in mild slow progressing caries lesion
and also resemble with natural secondary dentine.
• In this dentine, tubules are continuous with
natural already present secondary dentine. 64

65. Reparative
Tertiary
Dentine
• It is formed from newly formed odontoblast
like cells generated from stem cell of pulp.
• The formation of these new odontoblast like
cells take about 20 – 40 days.
• The tubules in the reparative dentine is less
regular (atubular) and not continuous with
those of overlying already present secondary
dentine.
• Matrix formed during reparative dentine
formation is called as interface dentine.
65

66. Tertiary
Dentine
• Both of these reparative or reactionary dentine can form below
the same caries lesion.
• However, this type of defense system depends on;
– Increased vascularity
– Immune response
– Inflammation
• Now question arises, from where signals for these responses
arrives.
– Any trauma to dentine pulp complex from caries or restorative
treatment leads to release of growth factors & molecular signals
which are embedded in the dentine or pulp and in result these factors
stimulate the stem cells to produce these defense responses.
– Example of factors;
• Bone morphogenetic factor
• Transforming growth factor beta
• Etc.
66

67. Dentine
Sensitivity
• Dentine does not have blood or nerve
supply.
– Only in about 20% tubules in which nerve fiber
from pulp are penetrating not more than few
microns.
• The odontoblastic process also does not
extend beyond the inner dentine.
• Cell membranes, cell bodies, & process of
odontoblastic cells are also
nonconductive. 67

68. Dentine
Sensitivity
• There is no any synaptic
connection b/w odontoblast cells
and terminal branches of pulp
nerves.
• When anesthesia is applied on
dentine still pain occurs. Or when
odontoblastic layer is disrupted,
pain still occurs.
68

69. Mechanism
of Dentine
Sensitivity
• Theory is given based on capillary flow
dynamic of fluid filled dentinal tubules.
• According to this theory, outward flow
dentinal fluid caused by various stimuli
displaces the odontoblasts which touch
the terminal branches of nerves in the
pulp and this touching generates action
potential in these nerves.
69

70. Treatment
of Dentine
Sensitivity
• So, this sensitivity can be removed by
blocking the dentinal tubules so that
fluid movement does not occur.This
blockage can be accomplished by;
– Oxalates, strontium chloride which are
present in tooth pastes.
– Other materials which reduce dentine
sensitivity;
• Potassium nitrate
• Resin glutaraldehyde
• Fluoride varnish
– Resin bonding agents
70

71. DENTAL PULP
71

72. Dental Pulp • It is viscous C.T of collagen fibers & organic
ground substance supporting the vital
cellular, vascular & nerve structure of tooth.
• Composed of;
– 75% water
– 25% organic material
• No collateral vessels and space for expansion
during inflammation.
• Blood is supplied only through apical
foramina 72

73. Functions of
Dental Pulp
• Formative (dentinogenesis)
– Primary, secondary & tertiary dentine
• Nutritive
– Vascular supply and ground substance for maintenance of cells
of organic matrix.
• Sensory
– Nociception/ pain sensation
• Protective
– Inflammation, antigenic, neurogenic & dentinogenic response to
injury.
– Homeostasis & clearance of noxious substances through vascular
& lymphatic system.
73

74. Morphology of
Dental Pulp
Pulpal histology.
Odontoblast cell layer contain
immunocompetent dendritic cells,
cell-free zone contains both nerve
and capillary plexuses,
cell-rich zone contains fibroblasts
and undifferentiated cells, and
pulp core.
74

75. Dental Pulp
core of the pulp is ground substance,
which contain pulpal cells, blood
vessels & nerves of pulp.
In the pulp, collagen fibers are not
organized but they are dispersed here
& there.
Proportion of collagen increases with
age.
75

76. Pulpal Cells
(odontoblasts)
• Present on outer periphery of pulp.
• They produce & adapt the dentine matrix.
– Provide active transport of calcium ions.
• They synthesize collagenous, non-collagenous protein
& various growth factors and signaling molecules.
• When they are active; they become large and columnar.
While during inactive stage, they become small &
flattened.
• These odontoblasts are interconnected by tight or
gapped junction. 76

77. Pulpal Cells
(Fibroblasts)
• Most numerous pulpal cells.
– Produce, maintain and remodel pulp
matrix and collagen.
– Present mostly in cell rich zone.
• Immunocompetent cells
– They include macrophages, lymphocytes
& dendritic cells.
– Function as host defense 77

78. Vascular
System of
Pulp
• The presence of lymphatic system in the normal pulp
is controversial;
– Some say that lymphatic vessels are not present in healthy
pulp but they develop during pulpal inflammation.
– While, some say that interstitial fluid of pulp is drained via
non endothelialized interstitial channels and exit the tooth
through apical foramina.
• The equilibrium b/w diffusion & clearance of products
may be temporarily ceased by use of long acting
anesthetic agents containing vasoconstrictors.
– However, no permanent changes in the pulp occur due to
ischemia because low respiratory requirements of pulp.
78

79. Vascular
System of
Pulp
• During inflammation, blood flow &
capillary permeability is increased.
– This capillary permeability leads to edema &
increase in the interstitial fluid pressure.
– However, this edema & increased interstitial
fluid pressure is confined to inflamed area only
because of presence of following features in
pulp;
• Numerous arterioles
• Reverse flow loops of vessels
• Arteriole –Venules anastomosis/shunts
79

80. Vascular
System of
Pulp
• This pulpal inflammation, (increased
fluid pressures) causes outward flow
of dentin tubular fluid.
• The pulpal inflammation also induce
hyperalgesia (increased sensitivity
due to lowering of threshold of pulpal
nerves)
80

81. Pulpal
Innervation
• Pain does not affect the vitality of pulp but it is the
inflammation which affect the vitality of pulp.
– You can say pulp is non-vital on the basis of presence of
pain in tooth.
• Primary innervation of pulp is from Sensory
(afferent) axons whose cells bodies lie in trigeminal
ganglion.
• Sympathetic (efferent) axons with nuclei in
cervical sympathetic ganglion are also present.
– Produce vasoconstriction on activation
81

82. Pulpal
Innervation
• Most sensory interdental nerves are A delta or
unmyelinatedC fibers.
• About 13% nerves in the premolar are myelinated A nerves.
– A delta conduction velocity 13.0 m/second.
– Have low sensitization threshold (they are easily stimulated on
very low stimuli)
– Pain of A delta; sharp & intense thunderbolt.
• About 78% of axons in premolar are small unmyelinated C
fibers.
– Conduction velocity of C fibers; 0.5 – 1.o m/second.
– They have high threshold and are activated by a level of stimuli
capable of creating tissue destruction just like high temperature
or pulpitis.
82

83. Pulpal
Innervation
• C fibers are not affected by tissue hypoxia
– So, pain may persist in anesthetized, infected
or even non-vital tooth.
– That’s why pain in non-vital, infected or
anesthetized tooth is due to stimulation of C
fibers.
• Sensation from C fibers; diffuse burning or
throbbing pain & difficult to locate.
83

84. Restorative
Dentistry &
Pulpal
Health
• With all restorative procedure, try to maintain thick residual
dentine thickness (RDT) to decrease the chances of pulpal
irritation or injury.
• Water coolant and intermittent rotary instrument contact
with tooth structure during crown preparation is essential to
avoid histopathologic damage of pulp.
• Materials utilized in treatment and restoration of dental tissue
can have direct effect on pulp tissues;
– With reduced RDT, the permeability of dentine increases, and
resulting more freely movement of materials from the restorative
materials.
– Some materials can damage the pulp due to high temperatures
from their exothermic reactions.
• Methacrylate based crowns
• Tooth bleaching 84

85. Age
Changes of
Tooth
• Reduced blood supply
• Small pulp chamber
• Decreased number of pulpal cells
– Lower ratio of pulp cells to collagen fibers
• Loss and degeneration of myelinated nerves,
• Decreased neuropeptides
• Loss of water from ground substance
• Increased intra pulpal mineralization (denticles)
• Decreased sensitivity due to;
– Sclerosis
– Tertiary dentine formation. 85

86. GINGIVA
86

87. Gingiva • Both the width and thickness of
gingival tissue should be
evaluated before placement of
restorations that will extend
subgingivally. In compromised
areas muco-gingival therapy
should be considered.
87

88. Biological
Width
• Dento – gingival junction; It is combination of two gingival
tissue (junctional epithelium & it’s ConnectiveTissue)
• Stabilize & seal the gingiva around the tooth.
• Biologic Width; it is vertical dimension (width) of Dento –
gingival unit.
• Dento – gingival complex; biologic width plus the sulcus
depth.
• Clinical attachment level; the distance from CEJ to the tip of
probe when the probe is in the sulcus.
88

89. Biological
Width
• Biologic width and dento-gingival complex.
Note that the gingival crown Cavosurface
margin is ideally no more than ½ mm into the
sulcus.The tip of the periodontal probe has
been pushed through the DEJ (junctional
epithelium and connective tissue attachment)
to the osseous crest (bone sounding).
• Violation of biologic width will lead to;
– Chronic inflammation
– Loss of attachment
– Bone resorption
– Gingival recession
89

90. Biological
Width
• Restorations should not be placed more than 0.5
mm below the gingival margin.
• Margins of restoration in sub gingival areas
should be parallel to cemento enamel junction in
all surfaces.
• If the vertical dimension of gingival complex is less
than 3.0 mm, this can be treated by;
• Muco gingival flap
• Osseous resection (crown lengthening)
90

91. Defective
Restoration
&
Periodontal
Health
• Poor quality of restoration impairs
the periodontal health.
– Marginal opening (marginal
discrepancy)
– Marginal roughness
– Overhanging.
– Over contoured axial surface
– Traumatic occlusion
– Defective inter proximal contacts
91

92. Defective
Restoration
&
Periodontal
Health
• Ideally, marginal discrepancy for cast
metal restoration should be less than 10
micrometers.While, marginal discrepancy
for ceramic restoration should be less than
50 micrometers.
– Marginal discrepancy can be increased by;
• Thick cement
• Faulty tooth preparation
– Effects of increased marginal discrepancy;
• Increased gingival problems
• Bone loss
• Biofilm retention
• Rough interface 92

93. Defective
Restoration
&
Periodontal
Health
• Effects of overhanging
restoration;
– Bone loss
– Attachment loss
– Increased pocket depth
– Increased gingival inflammation
• The large the size of overhang,
more the destruction of
periodontium. 93

94. THE END
Summit’s Fundamentals of Operative Dentistry
A Contemporary Approach
(4th Edition)
94