PULPAL RESPONSE OF DENTAL MATERIALS

1. PULPAL RESPONSE OF
DENTAL MATERIALS

2. CONTENTS
• DENTAL PULP
• PULPAL REACTIONS TO CARIES
• PULPAL REACTIONS TO DESENSITIZING AGENTS
• PULPAL NERVE FIBERS
• PULPAL REACTIONS TO LOCAL ANAESTHETICS
• PULPAL REACTIONS TO RESTORATIVE PROCEDURES
• PULPAL REACTIONS TO RESTORATIVE MATERIALS
• DIRECT PULP CAPPING PROCEDURES
• THE USE OF HEMOSTATIC AGENTS AND DISINFECTANTS ON DIRECT PULP EXPOSURES
• PULPAL REACTIONS TO LASER PROCEDURES
• PULPAL REACTIONS TO VITAL BLEACHING TECHNIQUES
• REFERENCES
2

3. DENTAL PULP
• Dental pulp can be defined as a richly
vascularized and innervated connective
tissue of mesodermal origin enclosed by
dentin with communications to the
periodontal ligament (Orbans)
3

4. MORPPHOLOGICAL ZONES OF PULP 4

5. • Located immediately subjacent to the predentin.
• Composed of the cell bodies of odontoblasts, capillaries,
nerve fibres, dendritic cells
• Coronal pulp contains more cells than the radicular pulp
ODONTOBLASTIC LAYER 5

6. • Narrow zone - 40µm in width.
• Relatively free of cells and hence called cell free layer of Weil.
• It is traversed by blood capillaries, unmyelinated nerve fibers and the slender
cytoplasmic process of fibroblasts.
• The presence or absence of cell poor zone depends on functional status of the
pulp.
Cell free zone 6

7. •Fibroblast,Undifferentiated mesenchymal cells ,defence cells (macrophages and
lymphocytes),blood capillaries, and nerves.
• High density of fibroblast.
• More prominent in coronal pulp.
•This zone is a source of cells that differentiate into secondary (replacement ) odontoblast on
injury to primary odontoblast.
Cell rich zone
7

8. OD – odontoblastic layer
CFZ- cell free zone
CRZ- cell rich zone
8

9.  The pulp proper is the central mass
of the pulp
 It consists of loose connective
tissue and contains the larger blood
vessels and nerves.
 The most prominent cell in this
zone is the fibroblast.
PULP PROPER
9

10. 10
Exposure to dental
caries
A prevalent
chronic infectious
disease
The scarcity of
collateral
circulation
Injury and
complicate its
regeneration
 A rich neurovascular supply
 The treatment of dental caries

11. PULPAL REACTIONS TO CARIES 11

12. PROTECTIVE PULPAL REACTIONS
 A decrease in dentin permeability
 Tertiary dentin formation
 Inflammatory and immune reactions.
12

13. DENTIN SCLEROSIS
• the first defense to caries - dentin sclerosis.
• increased deposition of intratubular dentin and the direct
deposition of mineral crystals into the narrowed dentin tubules to
decrease dentin permeability
• A combination of increased deposition of intratubular dentin
and tubule occlusion by precipitated crystals
13

14. 14

15. • Bacterial proteolytic enzymes, toxins, and metabolic by-products
have been thought to initiate pulpal reactions, yet the buffering
capacity of dentin and dentinal fluid likely attenuate these
deleterious effects.
• This protective function is significantly reduced when the
remaining dentin thickness is minimal..
15

16. • In initial-to-moderate lesions, current evidence suggests that
acidic by-products of the carious process act indirectly by
degrading the dentin matrix and thereby liberating bioactive
molecules previously sequestered during dentinogenesis.
• Once liberated, these molecules again assume their role in dentin
formation, this time stimulatory for tertiary dentinogenesis
16

17. TERTIARY DENTIN FORMATION
• demineralized dentin matrix implanted at the site of pulpal
exposure can induce dentinogenesis.
• a longer period than does that of sclerotic dentin
17

18. DENTINOGENESIS IN VITRO
Heparin-binding
growth factor
transforming
growth factor
(TGF)-β1, TGF-
β3
insulin-like
growth factors I
and II
platelet-derived
growth factor
bone
morphogenetic
protein-2 (BMP-
2)
angiogenic
growth factors
18

19. Its resultant character is highly dependent on the stimulus.
• IN MILD CARIOUS LESION
• Mild stimuli - activate resident quiescent odontoblasts whereupon they elaborate
the organic matrix of dentin.
• reactionary dentin
• can be observed beneath the noncavitated enamel lesion.
19

20. • In aggressive lesions
• The carious process may prove cytocidal to subjacent odontoblasts
• The organization and composition of the resultant matrix are a direct reflection of
the differentiation state of the secretory cells.
• This accounts for the heterogeneity of reparative dentin, where the morphology can
range from organized tubular dentin to more disorganized irregular fibrodentin.
20

21. 21

22. INFLAMMATORY AND IMMUNE REACTIONS
• The pulpal immune response provides humoral and cellular challenges to
invading pathogens.
• In the progressing carious lesion, the host immune response increases in
intensity as the infection advances.
• It has been shown that titers of t-helper cells, B-lineage cells, neutrophils,
and macrophages are directly proportional to lesion depth in human teeth.
22

23. • The disintegration of large amounts of dentin, however, is not necessary to
elicit a pulpal immune response
• This is supported by the observation that a pulpal inflammatory response can
be seen beneath noncavitated lesions and noncoalesced pits and fissures.
23

24. • The early inflammatory response to caries is characterized by the focal
accumulation of chronic inflammatory cells
• This is mediated initially by odontoblasts and later by dendritic cells.
• Pathogen detection in general is accomplished via specific receptors called
pattern recognition receptors (PRRs).
24

25. • As the carious lesion progresses, the density of the chronic inflammatory
infiltrate as well as that of dendritic cells in the odontoblast region
increases.
• With caries progression they aggregate initially in the pulp and
subodontoblastic regions, then extend into the odontoblast layer, and
eventually migrate into the entrance to tubules beside the odontoblast
process
25

26. • Pulpal exposure in primary and immature
permanent teeth can lead to a proliferative
response or hyperplastic pulpitis.
• Exuberant inflammatory tissue proliferates through
the exposure and forms a “pulp polyp”
• Conventional root canal therapy or progressive
vital pulp therapy is indicated.
26

27. NEUROGENIC MEDIATORS
• Neurogenic mediators are involved in the pulpal response to
irritants and, like immune components, they can mediate
pathology as well as the healing response
27

28. External
stimulation of
dentin
proinflammatory
neuropeptides
from pulpal
afferent nerves
• . Substance P (SP),
calcitonin gene–
related peptide
(CGRP), neurokinin A
(NKA), neurokinin Y,
and vasoactive
intestinal peptide
vasodilation and
increased
vascular
permeability
• increase in
tissue
pressure that
can progress
to necrosis
28

29. SUBSTANCE P
Substance P's most well-known function is as a neurotransmitter and a
modulator of pain perception by altering cellular signaling pathways.
 Additionally, substance P plays a role in gastrointestinal functioning,
memory processing, angiogenesis, vasodilation, and cell growth and
proliferation.
29

30. • Free nerve endings (C-fibers) in the skin contain nociceptors and
thermoreceptors that sense pain and temperature, respectively.
• The pain signal from the free nerve ending travels along small,
unmyelinated axons to synapse in the spinal cord.
• Contained in the presynaptic axon terminal are vesicles containing
substance P and glutamate, which are released into the synaptic cleft of the
dorsal horn.
30

31. • The hypothesis is that substance P helps sensitize the postsynaptic neurons
to glutamate, aiding in the transmission of pain signals to the
somatosensory area of the brain.
• SP acts as a chemotactic and stimulatory agent for macrophages and T
lymphocytes. The result of this stimulation is increased production of
arachidonic acid metabolites, stimulation of lymphocytic mitosis, and
production of cytokines
31

32. • CGRP has been shown to stimulate the production of bone
morphogenic protein by human pulpal cells - tertiary
dentinogenesis.
• Substance P appears to increase in the dental pulp and
periodontal ligament as a result of acutely induced occlusal
trauma - the pain associated with concussion traumatic injury
32

33. PULPAL REACTIONS TO DESENSITISING AGENTS
• Dentin hypersensitivity is characterized by
brief sharp pain arising from exposed
dentin in response to stimuli, typically
thermal, evaporative, tactile, osmotic, or
chemical, that cannot be ascribed to any
other form of dental defect or pathosis.
• Facial root surfaces in canines, premolars,
and molars are particularly affected,
especially in areas of periodontal
attachment loss
33

34. MAY BE RELATED TO
EXCESSIVE ABRASION DURING TOOTH
BRUSHING
PERIODONTAL DISEASES
EROSION FROM DIETARY OR GASTRIC
ACIDS
34

35. DUE TO …..
the lack of protection by cementum
loss of smear layer by acidic dietary
fluids
the hydrodynamic movement of fluid
in dentinal tubules
35

36. TREATMENT
• The application of neural modulating agents such as potassium
nitrate
• tubule blocking agents such as strontium chloride, oxalates or
dentin bonding agents
36

37. • calcium sodium phosphosilicate bioactive glass (SootheRx,
NovaMin Technology Inc., Alachua, FL)
• a combination of a calcium oxalate and an acid-etched bonding
material to seal the dentinal tubules (BisBlock, Bisco Inc.,
Schaumberg, IL).
37

38. • However, one study found that BisBlock and two other products—
Seal&Protect (Dentsply Professional, York, Pennsylvania) and Vivasens
(Ivoclar Vivadent AG, Schaan, Liechtenstein)—were effective compared
to placebo several weeks after treatment
• In the long term, the development of smear layer, such as from tooth
brushing, dentin sclerosis, reactionary dentin, and the blockage of
tubules with large endogenous macro molecules, is all thought to
reduce the problem
• Pamir T, Dalgar H, Onal B: Clinical evaluation of three desensitizing agents in relieving dentin
hypersensitivity, Oper Dent 32:544, 2007
38

39. • A practice-based, randomized clinical trial compared the effectiveness
of non-desensitizing toothpaste (Colgate Cavity Protection Regular,
Colgate-Palmolive, New York, New York), desensitizing toothpaste
(Colgate Sensitive Fresh Stripe, Colgate-Palmolive), and a professionally
applied desensitizing agent (Seal & Protect).
• The findings showed a significant reduction of dentin hypersensitivity in
the desensitizing therapies compared to the non-desensitizing group that
was a much more significant reduction in the professionally applied
desensitizing agent over a 6-month period
Gibson M, Sharif MO, Smith A, et al: A practice-based randomised controlled trial of the efficacy of three
interventions to reduce dentinal hypersensitivity, J Dent 41:668, 2013
39

40. the dental pulp
is enclosed in a
rigid chamber
An intact pulpal blood flow is
critical
supplied by few
arterioles
through the
apical foramina
cannot benefit
from collateral
circulation
benefit from
volumetric
changes that
compensate for
changes in
blood flow in
other soft
tissues
reduction in blood flow -
reducing the clearance of
large molecular weight toxins
or waste products
40

41. PULPAL NERVE FIBERS 41

42. • Approx 80% nerves of pulp-C fibres
• Rest-A Delta fibres
• Nerve trunk composed of myelinated A delta in the periphery and unmyelinated
C fibres in the center
42

43. Impulses travel from C or A
delta nerve
endings,through Plexus of
Raschkow to the nerve trunk
in central zone of the pulp
the nerve trunk
nerve trunk joins the
maxillary or mandibular
division of trigeminal nerve
exit the tooth through
apical foramen
the pons, thalamus, finally
to cortex intercepted as
pain
43

44. C fibres A delta fibres
• Unmyelinated
• Diameter-0.3-1.2µm
• Conduction velocity-0.4-
2m/s
• Conduction-slow
• Dull, poorly localised
throbbing pain
• Myelinated
• Diameter-2-5µm
• Conduction velocity-6-
30m/s
• Conduction –fast
• Short, well localised ,
sharp, pricking pain

45. PULPAL REACTIONS TO LOCAL ANASESTHETICS
• Local anaesthesia is the loss of sensation in an area of the body
caused by an inhibition of the peripheral nerve conduction or a
depression of excitation in nerve endings .
• . Local anesthetics work by binding to voltage-gated Na+ channels
in nerves, therefore block sodium transportation and nerve
conduction
45

46. • Local anaesthesia mainly causes autophagy and cell death in the
pulp cells.
• Autophagy is a catabolic process involving the degradation of
unnecessary or aberrant cellular components through hydrolysis of
lysosomes.
• It therefore controls the turnover of organelles and proteins
within cells, and of cells within organisms.
46

47. VASOCONSTRICTORS
• Vasoconstrictors are added to local anesthetics
• enhance the duration of anesthesia.
• negative impact on the health of the pulp
• they reduce blood flow, particularly if the pulp is inflamed
preoperatively
47

48. 48

49. • vasoconstrictors in local anesthetics do reduce pulpal blood flow
in experimental animals when administered by infiltration and
nerve block
• more severe with periodontal ligament injections.
49

50. • subjects were given infiltration of different local anesthetics with
or without epinephrine at a concentration of 1:100,000 and the
pulpal blood flow was measured by laser Doppler flowmetry.
• In groups that received the epinephrine, there were consistently
significant reductions in pulpal blood flow, even if the infiltration
was palatal to maxillary premolars
• Musselwhite JM, Klitzman B, Maixner W, Burkes EJ Jr: Laser Doppler flowmetry: a clinical test of
pulpal vitality, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 84:411, 1997
50

51. • When inferior alveolar nerve block injections of lidocaine and
1:100,000 or 1:80,000 epinephrine were administered
• The reduction in pulpal blood flow with epinephrine infiltration
was more than the reduction in gingival blood flow and did not
return to baseline values after 1 hour of injection.
51

52. intraosseous injection of Depo-Medrol™ (a
corticosteroid) in patients with symptomatic
irreversible pulpitis causes a significant reduction
of prostaglandin E2 in the pulp 1 day after
administration
significant permeation into the pulpal tissues.
Isett J, Reader A, Gallatin E, et al: Effect of an intraosseous injection of depo-medrol on pulpal concentrations of PGE2 and
IL-8 in untreated irreversible pulpitis, J Endod 29:268, 2003.
52

53. • local anesthesia with vasoconstrictors may compromise the inflamed
pulp’s ability to recover from inflammation,
• severely inflamed
• the tooth is subjected to extensive restorative procedures
• the anesthetic is delivered via a periodontal ligament or an intraosseous route.
53

54. PULPAL REACTIONS TO TOOTH PREPARATION
• Tooth cavity preparation caused increase of PBF
significantly.
• Strong vasodilatation effect in the dental pulp
• The complex interactions occurring within the pulp
between the dental nerves and pulp vessels,
mediated by neurovascular regulators
54

55. 55
Tooth
preparation
The release of a
significant
amount of
substance p-like
or bradykinin-
like substances)
Excite c-fibers,
can trigger the
release of
neuropeptides

56. • 48 Patients
hospital in
Hong Kong
• preoperatively vital pulps treated
with single-unit MC crowns
• 14 year observation period
122 teeth
• bridge abutments
• 15.6 year observation period
77 teeth
56
Cheung GS, Lai SC, Ng RP: Fate of vital pulps beneath a metal-ceramic crown or a
bridge retainer, Int Endod J 38:521, 2005.

57. Pulpal necrosis
had occurred in
15.6% of the
teeth treated
with single-unit
crowns
32.5% of the
pulps in the
bridge retainer
groups had
become necrotic
54.5% of anterior
abutment teeth
examined
57

58. Remaining Dentinal Thickness
• The RDT from the depth of cavity preparation to the pulp is the single
important factor in protecting the pulp.
• No material that can be placed in a tooth provides better protection for
the pulp than dentin.
58

59. 59
A 0.5-mm thickness reduces the
effect of toxins by 75%.
A 1.0-mm thickness reduces
the effect of toxins by 90%.
A 2.0-mm thickness or more
lead to a little pulpal reaction.

60. • The greatest impact on the pulp occurs when the RDT is no more
than 0.25 to 0.30 mm.
• Conservation of remaining tooth structure is more important to
pulpal health than is replacement of lost tooth structure.
60

61. Factors affecting the effects of dental
procedures on the pulp
• The Degree of Inflammation of the Pulp Preoperatively
• The Amount of Physical Irritation Caused by the Procedure
• The Proximity of the Restorative Procedures to the Dental Pulp
and the Surface Area of Dentin Exposed
• The Permeability of Dentin and the Odontoblastic Layer Between
the Area Being Restored and the Pulp
• The Age of the Patient
61

62. The Degree of Inflammation of the Pulp
Preoperatively 62
The more severe the pulp is
inflamed, the less will be its ability
to respond to further irritation,

63. • Cox CF, Bergenholtz G, Fitzgerald M, et al: Capping of the dental pulp mechanically exposed to the oral microflora: a 5 week observation of wound healing in the monkey, J Oral Pathol 11:327, 1982
63
• A study that evaluated the response of the pulp to
capping procedures as a function of duration of
exposure
• the pulp responds favorably to exposures for up to 24
hours after exposure
• not as favorably after longer periods of exposure to
the oral environment

64. The Amount of Physical Irritation Caused by
the Procedure
• Heat
• Desiccation
• Biologic and Chemical irritation
• vibration
64

65. HEAT
an intrapulpal temperature rise of 10° C
causes irreversible pulp pathosis in 15%
a 20° C rise caused pulp abscess
formation in 60% of teeth
65
studies documented burns or severe inflammation in the
pulp when cavity or crown preparations were performed
without coolants
Zach L, Cohen G: Pulp response to externally applied heat, Oral Surg Oral Med Oral Pathol
19:515, 1965.

66. 66
Heat increase in rat pulp
tissue to 42° C in vitro
raised heat shock protein-70,
which is known to be tissue
protective, and caused
changes in alkaline
phosphatase and gap junction
proteins that were reversed to
normalcy a few hours later.
 heat applied in deep cavity preparations,
prepared atraumatically in human teeth
caused histologic changes that were
dependent on the proximity of the heat
source to the pulp.
 a loss of odontoblasts or their aspiration
into the dentinal tubules.
 In cases where the cavity floor was less
than 0.5 mm from the pulp, areas of
coagulation necrosis could be seen,
although the patients remained
asymptomatic for the 1-month duration
of the study
Amano T, Muramatsu T, Amemiya K, et al: Responses of rat pulp cells to heat stress in vitro, J Dent Res
85:432, 2006.

67. • Cavity and crown preparations include a number of other irritating
stimuli such as desiccation, severance of odontoblastic processes,
vibration, and smearing of bacterial irritants onto the surface of
dentin.
• The transient increase in temperature to levels relevant to
modern dental procedures on its own may not be the culprit in
inducing pulpal changes.
• The synergistic application of excessive heat with other irritation
factors and its proximity to the pulp may induce pathologic
changes.
67

68. Desiccation
cause aspiration of odontoblastic nuclei into dentinal tubules and
pulpal inflammation
 30 seconds of continuous air drying of class V cavities in human
molars with uninflamed pulp caused significant displacement of
odontoblastic nuclei, pulp inflammation, and even areas of
necrosis related to the areas that were dried.
68

69.  The effects of desiccation are transient in that within 7 to 30
days there is autolysis of the aspirated cells and formation of
reactionary dentin.
The pulp in cases with aspirated odontoblasts, following
desiccation for 1 minute, was not sensitive to clinical scraping
with an explorer.
69

70. BIOLOGIC AND CHEMICAL IRRITATION
• Despite the elimination of visible caries during cavity
preparation, the cavity floor is undoubtedly left with some
contamination by caries bacteria.
• Although the rubber dam should be used with any cavity
preparation to prevent cavity contamination with salivary
microorganisms, the use of water coolants allows the cavity to be
contaminated with bacteria from water lines.
70

71. • Concerns about residual cavity contamination prompted some to use
cavity disinfection with caustic chemicals.
• Chemicals such as hydrogen peroxide, sodium hypochlorite, or calcium
hydroxide solutions
• An earlier study showed that the amounts of residual bacteria following
adequate restoration are not significant. Once dentin is exposed, there
is a constant outward flow of dentinal fluid that minimizes the inward
flow of any noxious agents. This may aid in the reduction of irritation
from residual microbial factors in dentinal tubules.
71

72. • the application of etching agents, especially strong acids, in the
form of total dentin etch, particularly if capping of exposed pulp
is performed.
• If the cavity is relatively superficial and is adequately sealed with
a restorative resin, then etching of dentin is probably not
detrimental to the pulp
• the narrow diameter of dentinal tubules
• low density in peripheral dentin.
72

73. • In fact, one study documented that histologic evidence of
bacteria in human cavities restored with composite was
significantly less if the cavity had been etched with phosphoric
acid than if it were etched with 17% EDTA or nonetched.
• Murray PE, Smyth TW, About I, et al: The effect of etching on bacterial microleakage of an adhesive composite restoration, J Dent
30:29, 2002.
73

74. • Self-etching formulations have become popular because they
eliminate the separate etching step involved in total-etch
procedures.
• Some have speculated that the bonding of self etching systems
may be poorer than total-etch systems because of the weaker
acidity of the acidic primers of self-etching systems when
compared to that of total-etch systems
74

75. • unpolymerized monomer and polymerization shrinkage.
Higher concentrations of monomeric resin components were
shown to exert an inhibitory effect on T lymphocytes and spleen
cells, and monocytes/macrophages in vitro..
Shrinkage during polymerization of composites may induce
internal stresses on dentin and create voids that allow
microleakage. Shrinkage of resins is estimated to range from 0.6%
to 1.4%, and should be minimized during placement by
incremental curing and possibly starting the restoration with
flowable resins.
75

76. 76

77. The Proximity of the Restorative Procedures to the
Dental Pulp and the Surface Area of Dentin
Exposed
• The diameter and density of dentinal tubules increase closer to
the pulp .
• Based on the dentinal tubule density at the DEJ (about
65,000/mm2 ) and the pulp (about 15,000/mm2 ) it was estimated
that the area occupied by tubule lumina at the DEJ was 1% of the
total surface area at the DEJ and 22% at the pulp.
• Pulpal inflammation in response to restorative procedures
increases with the reduction in RDT
77

78. • Reduction in the permeability of RDT.
• Due to rapid deposition of reactionary dentin
• The migration of large proteins into the tubules
• The diminution of tubule diameter as dentin becomes more sclerotic.
78

79. Using a primate model, it was shown that the basic rate of secondary dentin
deposition was about 0.8 µm/day and that this rate increased to an average of
2.9 µm/day following restorative procedures.
 Interestingly, in this study dentin deposition was also more rapid next to
shallow cavities than deep cavities
 However, another study showed that total reactionary dentin deposited was
thicker in deeper and wider cavities
regular and irregular secondary dentin in monkey teeth, Oral Surg Oral Med Oral Pathol 54:232, 1982.
79

80. • a crown preparation exposes more dentinal tubules to microbial or chemical
irritation.
• During crown fabrication, there are added irritation factors such as length of time of
the preparation, impression techniques, and the imperfect adaptation of temporary
restorations, causing microleakage during the temporization period.
• some providers may be inclined to reduce the coolant during crown preparation steps
such as finalizing the finishing lines. However, crown preparations without coolants
have been shown to dramatically reduce pulpal blood flow in an animal model
80

81. The Permeability of Dentin and the Odontoblastic
Layer Between the Area Being Restored and the
Pulp
• Permeability depends on factors such as the location within the same tooth, the
age of the patient, and the presence of pathologic conditions such as dental
caries
• The permeability of dentin depends on the collective sum of the permeability of
individual tubules at a particular site in the tooth.
• The tubular diameter increases from about 0.6 to 0.8 µm close to the DEJ to
about 3 µm at the pulp.
81

82. • With age the width of peritubular dentin increases, causing a
reduction in tubular lumen or sclerosis.
• Caries causes demineralization in superficial dentin, which is
associated with remineralization and the formation of caries
crystals within the tubules of inner undemineralized dentin.
• This causes a decrease in permeability in dentin subjacent to the
carious lesion and could be considered a protective mechanism, as
it may delay the progress of the carious lesion
82

83. The Age of the Patient
• Resting pulpal blood flow (PBF), as well as the changes in PBF in
response to cold application, will decrease with age.
• Age may also be associated with reduction in pulpal
neuropeptides.
• However, studies show no differences between young and old pulp
in the regenerative capacity of odontoblast-like cells and in the
presence of cells positive for class II major histocompatibility
complex, heat shock protein 25, or nestin, when subjected to
cavity preparation.
83

84. PULPAL REACTIONS TO RESTORATIVE
MATERIALS
• relate directly to the permeability of the associated dentin.
• The most important variable in dentin permeability to restorative
materials is the thickness of dentin between the floor of the
cavity preparation and the pulp.
84

85. Liners, Varnishes, and Nonresin Cements
• Calcium hydroxide cavity liners come in many forms, typically as
pastes with a very alkaline pH (>12).
• The high pH of calcium hydroxide in suspension leads to extreme
cytotoxicity in screening tests
85

86. 86
The initial response after exposing pulp tissue
to these highly alkaline aqueous pulp-capping
agents is necrosis to a depth of 1 mm or more
Shortly after necrosis occurs, neutrophils
infiltrate into the subnecrotic zone
After 5 to 8 weeks, only a slight inflammatory
response remains. Within weeks to months,
however, the necrotic zone undergoes
dystrophic calcification, which appears to be
a stimulus for dentin bridge formation

87. Resin containing calcium hydroxide
• calcium hydroxide compounds become less irritating
• stimulate dentin bridge formation more quickly than the Ca(OH)2
suspension alone.
• no zone of necrosis, and reparative dentin is laid down adjacent
to the liner
• This indicates that replacement odontoblasts form the dentin
bridge in contact with the liner.
87

88. • Recent evidence suggests that calcium hydroxide placed on
residual dentin in a tooth preparation may also have a stimulating
effect on dentin remineralization through the solubilization of
noncollagenous proteins, including growth factors such as
transforming growth factor-beta-1 (TGF-β1), and
glycosaminoglycans from the dentin
88

89. DENTAL CEMENTS
ZINC PHOSPHATE
• Zinc phosphate has been widely used as a cement for seating
castings and fixing orthodontic bands, and as a thermal insulating
base under metallic dental restorations,
89

90. • zinc phosphate cement elicits strong-to-moderate cytotoxic reactions that decrease with
time. Leaching of zinc ions and a low pH may explain these effects.
• Focal necrosis, observed in implantation tests with zinc phosphate cements injected into
rat pulp, confirms the cytotoxic effects of this cement when it contacts pulp tissue
90

91. In usage tests in deep cavity preparations, moderate-to-severe localized pulpal damage is produced
within 3 days, probably because of the initial low pH (4.2 at 3 minutes). However, the pH of the set
cement approaches neutrality after 48 hours
. By 5 to 8 weeks, only mild chronic inflammation is present, and reparative dentin has usually
formed. Because of the initially painful and damaging effects on the pulp by this cement when
placed in deep cavities
91
The placement of a protective layer of
of a dentin-bonding agent, ZOE, varnish, or calcium
hydroxide, is recommended in preparations with minimal
remaining dentin covering the pulp

92. • ZINC POLYACRYLATE CEMENTS
(POLYCARBOXYLATE CEMENTS)
• developed as biocompatible and cements chemically adhesive to
tooth structure.
• In short-term tissue culture tests, cytotoxicity of freshly set and
completely set cements has correlated with both the release of
zinc and fluoride ions into the culture medium and with a reduced
pH
92

93. • Some researchers suggest that this cytotoxicity is an artifact of
tissue culture because the phosphate buffers in the culture
medium facilitate zinc ion leaching from the cement.
• Supporting this theory, cell growth inhibition can be reversed if
EDTA, which chelates zinc, is added to the culture medium.
Furthermore, inhibition of cells decreases as the cement sets.
93

94. • The polymer component of the cement may also be of concern,
because concentrations of polyacrylic acid above 1% appear to be
cytotoxic in tissue culture tests.
94

95. • Polyacrylate cements evoke a pulpal response similar to that
caused by ZOE, with a slight-to-moderate response after 3 days
and only mild, chronic inflammation after 5 weeks.
• Reparative dentin formation is minimal with these cements, and
thus they are recommended only in cavities with intact dentin in
the floors of the cavity preparations
95

96. ZINC OXIDE EUGENOL
• In vitro, eugenol from ZOE fixes cells, depresses cell respiration,
and reduces nerve transmission with direct contact.
• The effects of eugenol are dose dependent and diffusion through
dentin dilutes eugenol by several orders of magnitude.
96

97. • The concentration of eugenol in the cavity preparations just
below the ZOE has been reported to be 10−2 M (bactericidal), the
concentration on the pulpal side of the dentin may be 10−4 M or
less.
• This lower concentration reportedly suppresses nerve transmission
and inhibits synthesis of prostaglandins and leukotrienes
(antiinflammatory).
97

98. • Cavity preparations in primate teeth (usage tests), ZOE caused
only a slight-to moderate inflammatory reaction within the first
week.
• This was reduced to a mild, chronic inflammatory reaction, with
some reparative dentin formation (within 5 to 8 weeks), when
cavities were deep.
• For this reason, it has been used as a negative control substance
for comparison with restorative procedures in usage tests.
98

99. OBTUNDANT EFFECT
• Kozam et al observed that eugenol irreversibly blocked the
conduction of action potentials in the frog sciatic nerve.
• Brodin and Rded tested the effect of eugenol and ZOE cement on
compound action potentials in the phrenic nerve. At low
concentrations eugenol inhibited nerve activity in the reversible
manner like a local anesthetic. After exposure to high
concentrations of eugenol, nerve conduction was irreversibly
blocked, indicating a neurotoxic effect.
99

100. • It may be argued that sedation of the pulp is undesirable because
it merely masks the symptoms of pulpal inflammation. According
to our contemporary view of inflammation, sensory nerve fibers
and their function are known to play an important role in the
generation of the inflammatory response.
100

101. • Sensory nerves in the dental pulp contain vasoactive peptides such
as substance P, calcitonin gene-related peptide, and others.
• These vasoactive peptides are capable of causing vasodilation and
an increase in tissue pressure in the dental pulp .
• Stimulation of the inferior alveolar nerve causes a similar increase
in pulpal blood flow (PBF).
101

102. • The evidence strongly suggests that direct pulp capping with
eugenol-containing materials should be avoided if long-term
maintenance of pulp vitality is to be achieved.
• Direct placement of a eugenol-soaked pellet over a vital exposure
should be done when an endodontic procedure can be performed
within a few days.
102

103. OBTUNDANT EFFECT
• An agent or drug that has the property of reducing or relieving
pain.
• help the pulp to relax after trauma from tooth preparation.
103

104. GIC
• Glass ionomer has been used as a cement (luting agent), liner,
base, and restorative material.
• Lightcured ionomer systems use HEMA or other monomers or
oligomers as additives or as pendant chains on the polyacrylic acid
main chain
104

105. pulpal biocompatibility of glass ionomer materials
weak acidic nature of the polyacrylic acid
high molecular weight
105

106. 106
when the
material is
placed over an
existing dentin
surface.
an initial
inflammatory
reaction
natural tooth
repair

107. Amalgam and Casting Alloys
• Biocompatibility of amalgam as a dental restorative material is
thought to be determined largely by the corrosion products
released while in service.
• Amalgam is a complex metallic material composed of multiple
phases, and its corrosion, in turn, depends on the type of
amalgam, whether it contains the tin-mercury γ2 phase, and its
composition.
107

108. • In usage tests, the response of the pulp to amalgam in shallow
cavities or in deeper but lined cavities is minimal, and amalgam
rarely causes irreversible damage to the pulp.
• pain results from using amalgams in deep, unlined cavity
preparations (0.5 mm or less remaining dentin), with an
inflammatory response occurring after 3 days.
108

109. cavities with less than 0.5 to 1.0 mm
• the transfer of hot and cold stimuli,
primarily from food and drink, through
the amalgam may be substantial
• margins of newly placed amalgam
restorations show significant
microleakage
109

110. Cast alloys
• used for single restorations, fixed partial dentures, ceramic-metal
crowns, and removable partial dentures.
• The gold content in these alloys ranges from 0 wt% to 85 wt%.
• These alloys contain several other noble and nonnoble metals that
may have an adverse effect on cells if they are released from the
alloys.
110

111. DIRECT FILLING GOLD 111
the trauma of
cavity
preparation
to forces of
condensation
to microleakage
to the high
thermal
conductivity of
the filling
to a combination

112. CERAMIC
• The tricalcium phosphate ceramic was biologically well tolerated.
It had a low irritational potential.
• It stimulated reparative dentinogenesis around the particles.
• A major problem with the ceramic, however, was the difficulty in
applying it so that it would remain confined over the pulp
exposure.
112

113. ACID ETCHING
• In contemporary practice, most chemical irritation during
restorative procedures results from the application of etching
agents, especially strong acids, in the form of total dentin etch,
particularly if capping of exposed pulp is performed.
113

114. • If the cavity is relatively superficial and is adequately sealed with a restorative
resin, then etching of dentin is probably not detrimental to the pulp because of
the narrow diameter of dentinal tubules and their low density in peripheral
dentin.
• In fact, one study documented that histologic evidence of bacteria in human
cavities restored with composite was significantly less if the cavity had been
etched with phosphoric acid than if it were etched with 17% EDTA or nonetched.
114

115. • study showed that pulpal response to the selfetching adhesive,
Xeno III, was minimally different from the total-etch adhesive,
Prime & Bond NT. Sixteen of 40 cases (40%) showed varying
degrees of pulpal inflammatory activity; 45% cases of the Prime &
Bond NT group and 35% cases of the Xeno III exhibited pulpal
inflammation. Prime & Bond NT and Xeno III groups detected
stainable bacteria in 45% and 40% of specimens, respectively.
115

116. BONDING AGENTS
• Many of these reagents are cytotoxic to cells in vitro if tested alone..
• Longer-term in vitro studies suggest, however, that components of the bonding
agents may penetrate up to 0.5 mm of dentin and cause significant suppression
of cellular metabolism for up to 4 weeks after application. This suggests that
residual unbound constituents may cause adverse reactions.
116

117. • Hydroxyethyl methacrylate (HEMA), a hydrophilic resin contained in several
bonding systems, is at least 100 times less cytotoxic in tissue culture than
bisphenol A-glycidyl methacrylate (Bis-GMA).
• Studies using long-term in vitro systems have shown, however, that adverse
effects of resins occur at much lower concentrations (by a factor of 100 or
more) when exposure times are increased to 4 to 6 weeks.
117

118. • Many cytotoxic effects of resin components are reduced
significantly by the presence of a dentin barrier.
• . What effect HEMA may then have on the pulp cells in situ is not
known, but HEMA has been shown to stimulate the expression of
growth factors in mouse odontoblast like cells.
118

119. • studies have also shown that the release of matrix
metalloproteinases (MMPs) from dentin by virtue of its interaction
with the acid components in dentin adhesives may cause
degradation of the adhesive bond by enzymatic action on the
exposed collagen within the hybrid layer.
119

120. RESIN
• Some of the components of resin restorations are released at
cytotoxic levels after polymerization is completed, leading to
chronic stimulation and a resultant prolonged inflammatory
response.
• Furthermore, even subtoxic concentrations of certain agents are
capable of eliciting allergic reactions in humans.
120

121. • In vitro, freshly set chemically cured and light-cured resins often
cause moderate cytotoxic reactions in cultured cells over 24 to 72
hours of exposure, although several newer systems seem to have
minimal toxicity.
• The cytotoxicity is significantly reduced 24 to 48 hours after
setting and by the presence of a dentin barrier
121

122. • Evidence indicates that the light-cured resins are less cytotoxic
than chemically cured systems, but this effect is highly dependent
on the curing efficiency of the light and the type of resin system.
122

123. 123
The pulpal inflammatory
response to chemically
and light-activated resin
composites was low to
moderate after 3 days
an increase in
reparative dentin 5 to 8
weeks

124. LIGHT CURING
• Tooth exposure to light-curing units (LCUs) is one of the routine
conditions in restorative dentistry most highly associated with PT
increase, which can widely vary from 1.5 ◦C to 23.2 ◦C, probably
depending on the differential experimental settings in different
studies
• In addition to the heat produced by the LCU, the polymerization
of the composite induces an exothermic reaction that has been
discussed as a cause of tissue damage.
124

125. • Additionally, a proportional relationship has been established
between the temperature rise from the exothermic reaction and
the amount of composite resin applied. Therefore, the possibility
of pulpal damage caused by temperature rise should be considered
when using light-cured bulk-fill materials in very deep cavities.
125

126. • Resin doesn’t penetrate at all or
debond from it
• Large space
MICROLEAKAGE
• Resin doesn’t completely penetrate
the collagen fibril
• Small space exist between dentinal
tubule and external tooth surface
NANOLEAKAGE
126

127. 127

128. MICROLEAKAGE
• There is evidence that restorative materials may not adequately
bond to or seal enamel or dentin.
• In this case, bacteria, food debris, or saliva may be drawn into
the gap between the restoration and the tooth by capillary action.
128

129. Various dental restorative materials irritated pulp tissue in animal
tests
The products of microleakage, not the restorative materials,
caused the irritation
Bacteria present under restorations and in dentinal tubules might
be responsible for pulpal irritation
Bacteria or bacterial products such as lipopolysaccharides could
cause pulp irritation within hours of being applied to dentin
129

130. • Finally, a classic animal study shed light on the roles of restorative
materials and microleakage on pulpal irritation.
• Amalgam, composite, zinc phosphate cement, and silicate cement
were used as restorative materials in class 5 cavity preparations in
monkey teeth. The materials were placed directly on pulp tissues.
130

131. • Half of the restorations were surface sealed with ZOE cement.
Although some irritation was evident in all restorations at 7 days,
after 21 days, the sealed restorations showed less pulpal irritation
than those not sealed, presumably because microleakage had been
eliminated
131

132. NANOLEAKAGE
• Nanoleakage refers to the leakage of saliva, bacteria, or material
components through the interface between a material and tooth
structure.
• dentin bonding, and may occur between mineralized dentin and a
bonded material in the very small spaces of demineralized
collagen matrix into which the bonded material did not penetrate.
• nanoleakage can occur even when the overall bond between the
material and dentin is intact.
132

133. DIRECT PULP CAPPING
• Direct pulp capping involves the placement of a biocompatible
agent on healthy tissue that has been inadvertently exposed from
caries excavation or traumatic injury.
INGLE
133

134. Mechanism of dentin bridge formation
• Dentin bridge -a repair tissue that is formed across the pulpal wound.
• Cells responsible for bridge formation
fibroblasts, progenitor cells, perivascular cells,
bioactive molecules-calcitonin gene related peptide
growth factors-TGF 6,BMP 2,4,6
• Rate of reparative dentin formation =1.4m/day
134

135. CALCIUM HYDROXIDE
• stimulation of dentinal bridge formation subsequent to
microscopic or gross pulpal exposure.
• The low-grade pulpal irritation that it induces is important for
dentinal bridge formation in exposures.
135

136. • The degree of inflammation is dependent on the preparation of calcium
hydroxide used.
• Aqueous suspensions of calcium hydroxide applied to exposed pulps
cause superficial necrosis of pulpal tissue followed by lowgrade
inflammatory changes.
• Within 30 days the tissue subjacent to the necrotic zone has reorganized
and resumed normal architecture.
136

137. • The irritation potential of calcium hydroxide across intact dentin
is dependent on factors such as the remaining dentin thickness
and permeability.
• Application of calcium hydroxide to intact dentin appears to
induce sclerosis by promoting crystal precipitation within the
tubules accompanied by reductions in permeability.
137

138. • Numerous authors have demonstrated that dentin matrix proteins
like TGF-β1 and adrenomedullin are liberated by both calcium
hydroxide and mineral trioxide aggregate.
• Once liberated they are able to facilitate hard tissue formation
again.
138

139. HISTOLOGY OF HEALING AFTER CH PULP CAPPING
1. Zone of obliteration:
• completely deranged and distorted because of the caustic effect of the drug.
• This zone consists of debris, dentinal fragments, hemorrhage, blood clot, blood
pigment, and particles of calcium hydroxide.
• Schoder and Granath explained that this zone of obliteration was due to the
• chemical injury due to a high concentration of hydroxyl ions
• The high pressure of the medicament application.
139

140. Zone of coagulation necrosis:
Schroder’s layer of ‘firm necrosis’ and Stanley’s ‘mummified zone’.
• The tissue together with its plasma proteins within the zone of obliteration takes the
brunt of the calcium hydroxide chemical thrust.
• A weaker chemical effect reaches the subjacent, more apical tissues and results in a zone
of coagulation necrosis and thrombosis
• This zone of coagulation necrosis ranges from 0.3-0.7 mm thickness.
140

141. Zone of demarcation:
• A line of demarcation develops between the deepest level of the
zone of coagulation necrosis and the subjacent vital pulp tissue.
• Glass and Zander believed that this line resulted from
• the reaction of the calcium hydroxide with the tissue protein to form
proteinate globules.
141

142. THE DENSE ZONE(EARLY STAGE OF BRIDGE FORMATION)
• Immediately subjacent to the line of demarcation proliferation of
mesenchymal cells occur
• Within 2-3 days after the injury, connective tissue fibres accumulate
• At first they are disorganised, consisting of both fine and coarse fibres
lying parallel to the applied medicament
• The increase in collagen formation becomes apparent at 3- 7 days
142

143. • The number of fibroblast, mesenchymal cells multiply sufficiently to present a modified
cell rich layer
• The cells within this layer gradually differentiate into preodontoblast and columnar
shaped odontoblasts.
• By 7 days the matrix thickens and becomes more differentiated
• The replication of odontoblasts favoured over fibroblast because of basic environment
143

144. CALICIFICATION OF THE BRIDGE
• A mineralized barrier or dentin bridge is usually produced following the application of
Ca(OH)2.
• Necrotic zone is formed adjacent to the material and the dentin bridge is formed between
this necrotic layer and underlying vital pulp
• Calcification occurs soon after the predentin has developed
• The stage of tubular predentin formation may be reached in 2 weeks
• After 1-3 month the barrier consists of more coronal layer of irregular osteodentin like tissue
with cellular inclusions and the pulpal part consists of predentin lined with odontoblasts
144

145. • With this high Ph CH, bridge formation occurs at the line of demarcation
• Over a period of time the coagulated necrotic tissue above the line of demarcation
degenerates
• In case of lower PH such as dycal the necrotic zone similarly formed, but is resorbed prior
to the dentin bridge which then forms to be directly against the capping material
• Dentinal bridge formed by high PH materials are histologically similar to those produced by
lower PH material but are easier to distinguish on a radiograph because of the space B/W
the bridge and Ca(OH)2
145

146. 146

147. • While the formation of a dentin bridge has been believed to be the key for the clinical success of direct
pulp-capping,it has been reported that 89% of dentin bridges formed by calcium hydroxide cement
contained tunnel defects.
• These tunnel defects that form in the heterogeneous dentin bridge not only fail to provide a permanent
barrier, but also fail to provide a long-term biological seal against bacterial infection.
• Another disadvantage of calcium hydroxide is dissolution.
• This may lead to the formation of a dead space and microleakage
147

148. DIRECT PULP CAPPING WITH MINERAL
TRIOXIDE AGGREGATE
• Prospective animal studies and human case reports have evaluated
the ability of MTA to allow for the formation of a reparative dentin
bridge and maintain continued pulp vitality.
148

149. • When placed in contact with dentin, these materials may cause
the release of these bioactive molecules, which then serve as
signaling agents to recruit undifferentiated cells to the wound
site.
• These cells may then differentiate to odontoblastlike cells that
begin the process of dentin bridge formation
149

150. • pulp cells exposed to MTA undergo proliferation and migration,
followed by differentiation to odontoblast-like cells.
• MTA-derived products can stimulate osteoblast-like cells and
fibroblasts to express proteins, such as osteonectin, osteocalcin,
and osteopontin, which are involved with extracellular matrix
formation and mineralization.
150

151. MTA-PULP CAPPING –
• CARIOUS PULP EXPOSURE
• 40 PT AGED 7 – 45 YR DIAGNOSED WITH REVERSIBLE PULPITIS
• Caries removed using caries detection dye & sodium hypochlorite for
hemostasis
• 2 visit to allow MTA to set up and to confirm pulp sensibility to pulp test
• success determined radiographically
• outcomes measured over a period of upto 9 yr postoperatively
• Success – 97 %
Bogen G, Kim JS, Bakland LK: Direct pulp capping with mineral trioxide aggregate: an observational study, J Am
Dent Assoc 139:305; quiz 305, 2008
151

152. • In another clinical study in which dentists and students
participated in the treatment, pulp capping of carious pulp
exposures was compared between MTA and calcium hydroxide.
• At follow-up, 122 cases of patients with a mean age of 40 years
were available.
• The success with MTA was 78% and that with calcium hydroxide
was 60%, a difference that was statistically significant
Mente J, Geletneky B, Ohle M, et al: Mineral trioxide aggregate or calcium hydroxide direct pulp
capping: an analysis of the clinical treatment outcome, J Endod 36:806, 2010
152

153. 153

154. • Other calcium silicate–based materials are gaining popularity as
pulp capping agents and appear to have properties and effects
similar to MTA.
• Biodentine deserves special reference because in addition to the
biocompatibility, it has physical properties that are similar to
dentin.
154

155. Tricalcium silicates as direct pulp capping
materials 155
BIODENTINE
composed of pure
tricalcium silicates
and calcium chloride
as a setting
accelerator
It is presented as
powder and liquid to
be prepared by mixing
both components with
an amalgamator
sets in 12min
Resin free

156. 156
THERACAL 43% Resins
presented as a ready-to-
use material in a syringe
sets by
photopolymerization (20
s per 1mm increment) in
a hydrophobic
environment

157. 157

158. • Investigating the effects of adding extracts of TheraCal® or
BiodentineTM demonstrated that pulp capping materials modulate
the inflammatory response. Inflammatory THP1 cells adhesion to
endothelial cells and their activation were reduced by
BiodentineTM and TheraCal® . However, their migration decreased
only with BiodentineTM
• Giraud T, Jeanneau C, Bergmann M, Laurent P, About I. Tricalcium silicate capping materials
modulate pulp healing and inflammatory activity in vitro. J Endod 2018,
158

159. • It appears clearly that the presence of resins in CSC pulp capping
materials such as TheraCal® shifts the balance towards
inflammation. Their incomplete photopolymerization leads to free
monomers release.
• When these monomers reach the underlying pulp, they exert their
toxicity as demonstrated by decreased cell viability, release of
pro-inflammatory cytokines and recruitment of inflammatory
cells. It can be assumed that this creates an inflammatory state
which compromises the regenerative process
159

160. • . In addition, the incomplete TheraCal® hydration due to the
presence of a high percentage of resin, leads to a reduced Calcium
ion release and the absence of Ca(OH)2, both of which are known
for their positive impact on the mineralization process (Fig. 7).
Thus, pulp capping with TheraCal® can be held responsible for a
disorganized pulp tissue without dentin bridge formation
160

161. 161

162. THE USE OF HEMOSTATIC AGENTS AND
DISINFECTANTS ON DIRECT PULP EXPOSURES
• Given the difficulty in creating a bacteria-free operating
environment during tooth preparation, the ideal hemostatic agent
also would have the ability to kill bacteria.
162

163. • One study compared the effects of two hemostatic/ disinfectant
agents on the healing of experimental pulp exposures created in
human third molar teeth and capped with calcium hydroxide.
• Pulp exposures were made in 45 maxillary wisdom teeth scheduled
for extraction for orthodontic reasons.
• Teeth were randomly assigned to receive hard-setting calcium
hydroxide pulp caps after a 30-second surface treatment with one
of three agents: 0.9% saline, 2% chlorhexidine, or 5.25% sodium
hypochlorite.
163

164. • Although the 7-day saline specimens showed slightly less
inflammatory response, there were no statistically significant
differences between the groups with respect to all dependent
measures over the course of the study.
• Complete healing was seen in 88% of all specimens at 90 days.
164

165. Response to impression material
• Impressions for inlay and crown – serious hazards to pulp
• Seltzer et al showed that-more pressure while taking impression-
pulpal trauma
• Negative pressure-removing an impression-odontoblastic
degeneration
165

166. PULPAL REACTIONS TO LASER PROCEDURES
• Laser use on hard tissue has been a popular area of research
because of the potential benefits of efficiency, reduced
sensitivity, disinfection, and precision.
• Several types of laser technologies are available that depend on
the wavelength, active medium, emission mode, delivery system,
power output, and duration of application
166

167. • The CO2 laser is historically the oldest type used on soft tissues .
• It has the longest wavelength (10,600 nm).
• It cannot be delivered in an optic fiber, thus it must be used in a hollow-
tube-like wave guide in continuous gated-pulse mode.
• This means that the operator does not feel a solid resistance when using
this laser
167

168. • Er:YAG, Nd:YAG or Ho:YAG lasers all have an active medium of a
solid crystal of yttrium-aluminum-garnet, which is impregnated in
erbium, neodymium, or holmium, respectively.
• Er:YAG has a wavelength of 2940 nm and is delivered using a solid
optic fiber. It has a high affinity for water and hydroxyapatite,
thus it can be used to remove caries and cut dentin with coolant.
It can also be used on soft tissue.
168

169. • Ho:YAG laser has a wavelength of 2120 nm and has high affinity to
water but not to tooth structure, thus it is used primarily for soft
tissue surgery.
• Nd:YAG laser is also delivered fiberoptically, has a wavelength of
1064 nm, and has been used extensively in dentistry because it
has a high affinity for water and pigmented tissues and offers good
hemostasis; thus is used extensively in surgery.
169

170. • there are some low-power output lasers such as HeNe (helium-
neon) (632 nm), and GaAlAs (gallium-aluminum-arsenide) (diode;
semiconductor) (720-904 nm) lasers, which have been used in
laser Doppler flowmetry and in treating dentin hypersensitivity
170

171. Lasers in the Prevention, Diagnosis, and
Treatment of Caries
• Laser irradiation of deep susceptible pits and fissures may reduce
the incidence of dental caries.
• Once caries develops, some lasers may be effective in removing
the carious lesion and sparing undemineralized dentin, because of
their differential absorption by water and hydroxyapatite.
Furthermore, if caries exposes the pulp in young teeth,
particularly those with immature apices, lasers may be able to
effectively excise coronal infected pulp in pulpotomy, because of
their hemostatic and antibacterial properties
171

172. • Laser fluorescence is used by the DIAGNOdent and DIAGNOdent
pen, which are laser devices that have been introduced for the
diagnosis of noncavitated caries.
• Laser ablation of superficial carious lesions may be more
conservative than bur preparation.
172

173. • Earlier studies showed reduced permeability of dentin in vitro
with a XeCl excimer laser (a laser with a relatively short
wavelength of 308 nm in the ultraviolet range).
• The apparent fusion of tubules in superficial layers of dentin was
shown to occur with CO2, Nd:YAG, and Er:YAG lasers in vitro.
• The pulpal responses to Nd:YAG and CO2 lasers were not
favorable. It was shown that Nd:YAG and to a lesser degree CO2
lasers may be associated with charring and significant
inflammation in the pulp compared with the Er:YAG laser.
173

174. • For pulpotomy procedures, such as in primary teeth, permanent
teeth with immature apices, or pulps that are exposed due to
fracture and treated promptly, the lasers, particularly
• CO2 lasers, may be useful in achieving precise surgical excision of
coronal pulp and immediate hemostasis.
• A controlled clinical study showed that CO2 laser pulpotomy was
comparable to traditional methods in experimental pulpotomies of
primary teeth scheduled for extraction for orthodontic reasons.
174

175. Lasers in the Treatment of Dentin
Hypersensitivity
• Earlier studies have shown effectiveness ranging from 5% to 100%
of low-output lasers on dentin hypersensitivity.
• a reduction of hypersensitivity in 73% of mild cases, 19% of
moderate cases, and 14% of severe cases after 4 months using a
GaAlAs laser
• Low-output lasers do not have any effects on the morphology of
enamel or dentin, but they are thought to cause a transient
reduction in action potential mediated by pulpal C-fibers, but not
Aδ-fibers, although this finding was not consistent
175

176. • Nd:YAG lasers have also been used in dentin hypersensitivity.
Because of the higher power output, these lasers cause superficial
occlusion of dentinal tubules of up to 4 µm, in addition to action
potential blockage within the pulp in vitro or in experimental
animals
176

177. Use of Lasers as a Protective Measure for
Dentin, Under Traditional Cavity Preparation
• One clinical study has proposed that if lasers are used to prepare
cavities or used on prepared dentin after traditional cavity
preparation with burs, this would protect the dentin, as its
permeability and bacterial content may decrease
177

178. • In this study, two patients were scheduled to have six teeth
extracted during orthodontic treatment.
• In the teeth that had laser irradiation (GaA1As laser, lambda =
660 nm, power of 30 mW and energy dose of 2 J/cm2 ) and were
examined with transmission electron microscopy (TEM)
• after 28 days, the odontoblastic process had increased contact
with the extracellular matrix, and the collagen fibrils appeared
more organized than those of the control group (traditional bur
preparation only). The study concluded that laser irradiation
accelerates the recovery of the dental tissues in the predentin
region
178

179. THERMAL EFFECTS OF LASER 179
Ansari MA, Erfanzadeh M, Mohajerani E. Mechanisms of Laser-Tissue Interaction: II. Tissue Thermal Properties. J Lasers
Med Sci 2013; 4(3):99-106

180. PULPAL REACTIONS TO VITAL BLEACHING
TECHNIQUES
• Vital bleaching techniques employ strong oxidizing agents, namely
10% carbamide peroxide and hydrogen peroxide, to bleach enamel
of teeth with vital pulp.
• There have been concerns about the potential for pulpal irritation
during these procedures because of the long duration that the
chemicals are in contact with the teeth, particularly if dentin with
open tubules or cracks is present
180

181. • Histologic or histochemical analysis of the pulp following
bleaching for up to 2 weeks showed minor inflammatory changes
in the pulp of the bleached teeth that were reversible.
• One clinical report documented that if 16% carbamide peroxide
was used, gingival irritation was evident; however, no changes in
pulp vitality or in symptoms were noted.
181

182. • Even in patients who develop symptoms postoperatively, these
tend to be reversible and could be prevented by treating the teeth
with fluorides and by correcting restorative deficiencies
preoperatively
• Clinical symptoms are likely to be due to increases in
neuropeptides, such as substance P, in the pulp.
182

183. • In one clinical study, premolars scheduled for orthodontic
extraction had 38% H2O2 bleaching gel with and without a halogen
light source applied. There were no histologic effects on the
dental pulp at 2 to 15 days after bleaching
Kina JF, Huck C, Riehl H, et al: Response of human pulps after professionally applied vital tooth
bleaching, Int Endod J 43:572, 2010.
183

184. • When the study was performed on incisors with the same
treatment for 45 minutes, areas of coagulation necrosis could be
seen in the pulp. Therefore, caution should be exercised when this
caustic agent is used for extended bleaching.
• Costa CA, Riehl H, Kina JF, et al: Human pulp responses to in-office tooth bleaching, Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 109:e59, 2010.
184

185. Conclusion
• Pulp is a unique tissue and is the formative organ of the tooth.
• The value of pulp as an intergral part of the tooth, both anatomic and functional
should be recoginised and every effort should be made to protect it.
• Diseases affecting the hard tissues of the tooth as well as most operative procedures are
traumatic to the pulp
• Though the pulp has remarkable recuperative powers all efforts must be made to minimise
insults to it
185

186. • Hence a gentle approach to cavity preparation and restoration should be
employed
• An accurate diagnosis and case selection plays a major role in the
predictable outcome of pulp protection procedures
186

187. REFERENCES
• Cohen’s pathways of dental pulp- 10th edition
• Ten Cate’s Oral Histology
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