3. INTRODUCTION
•Tooth hypersensitivity is one of the oldest recorded
complaints of discomfort to the patient. It is one of the
most common painful dental conditions.
•Dentin hypersensitivity is a common condition of
transient tooth pain caused by a variety of exogenous
stimuli.
• The exogenous stimuli include thermal (cold), tactile
(touch), or osmotic changes (sweets or drying the
surface).
3
4. •The response to a stimulus varies from person to
person due to differences in pain tolerance,
environmental factors, and emotional state.
•The primary underlying clinical cause for dentin
hypersensitivity is exposed dentinal tubules.
•The only hypersensitivity not associated with this
etiology is the transient spontaneously resolving
hypersensitivity associated with the dental
bleaching process.
4
5. DEFINITION
―Dentin Hypersensitivity is a condition characterized by
short , sharp pain arising from exposed dentin in response
to stimuli typically thermal , evaporative,tactile, osmotic
or chemical and which cannot be ascribed to any other
form of dental defect or pathology‖.
Holland et al 1997
5
6. Many other conditions exits where dentin is exposed and
sensitivity ,identical to that experience with DH occurs
• Chipped or fractured teeth
• Caries
• Marginal leakage of restorations
• Cracked cusps of teeth
• Palato-gingival groove.
6
7. PREVALENCE AND
DISTRIBUTION
Age
is broad , spanning from early teenage to more than 70
years. (Fischer et al 1992)
however peak incidence is between 20-40 years.
7
8. Numerical gender differences have been reported in
males and females.
Females tend to have more sensitivity than males. This
has been attributed to their practicing better oral hygiene.
Interestingly, the prevalence of cervical dentine
sensitivity, another term used to describe dentine
hypersensitivity, was found to be much higher in
periodontal patients, ranging between 72.5–98%.
8
9. Regarding the intra-oral distribution, dentine
hypersensitivity is most commonly reported from the
buccal cervical zones of permanent teeth.
Sites of predilection in descending order are canines and
first premolars, incisors and second premolars and molars
9
10. ETIOLOGICAL AND
PREDISPOSING FACTORS
There are potentially numerous and varied etiological and
predisposing factors to dentine hypersensitivity.
Certainly, no prime cause can be identified.
By definition, dentine hypersensitivity may arise as a
result of loss of enamel and or root surface denudation
due to gingival recession with exposure of underlying
dentine.
Enamel loss as a part of tooth wear may result from
attrition, abrasion,abfraction or erosion.
10
11. Attrition describes the wear of teeth due to direct contact
between teeth.
Attrition is associated with occlusal function and may be
exaggerated by habits or parafunctional activity
such as bruxism.
11
13. Abrasion describes the wear of teeth caused by objects
other than another tooth, examples include
toothbrush/toothpaste abrasion and the variety of facets
which can be caused by pipe smoking or other similar
habits.
Typical toothbrush abrasion lesions are side dependent,
for example being greater on the left-side in right-
handed people.
The buccal cervical area of the teeth are the sites of
predilection. Furthermore, canines and premolars are
most affected because of their position within the dental
arch where they receive the most attention during tooth
13
cleaning.
17. Erosion is defined as the loss of hard dental tissue, due to
chemical means which are non-bacterial.
Erosion may be by either extrinsic or intrinsic acids.
Extrinsic erosion can be subdivided into dietary and
environmental, while intrinsic erosion is the result of
exposure of teeth to gastric juice.
Dietary erosion may result from foods or drinks
containing acids such as citrus fruits, pickled food, fruit
juices, carbonated drinks, wines and ciders.
17
20. Abfraction
Abfraction or cervical stress lesions has been
hypothesized as an etiological factor in tooth wear.
The process is thought to involve eccentric occlusal
loading leading to cusp flexure.
This in turn leads to compressive and tensile stresses at
the cervical fulcrum area of the tooth with the resultant
weakening of the cervical tooth structure .
There is progressive disruption of the hydroxyapatite
crystals leading to dentin exposure.
20
23. Gingival recession
Gingival recession and subsequent root surface exposure
allow more rapid and extensive exposure of dentinal
tubules because the cementum layer overlying the root
surface is thin and easily removed.
Gingival recession, as with dentine hypersensitivity, has
been described as enigma, having what appears to be a
multifactorial etiology.
23
24. Tooth brushing has long been implicated in gingival
recession on buccal surfaces and is a frequent finding in
subjects with a high standard of oral hygiene,or with a
history of hard toothbrush use.
Gingival recession is frequently cited to result from
periodontal treatment particularly surgery as is dentine
hypersensitivity.
24
25. Common Reasons for Gingival Recession
1. Inadequate attached gingiva
2. Prominent roots
3. Toothbrush abrasion
4. Pocket reduction periodontal surgery
5. Oral habits resulting in gingival laceration, i.e.,
traumatic tooth picking eating hard foods
6. Excessive tooth cleaning
7. Excessive flossing
8. Gingival loss secondary to specific diseases, i.e., NUG,
periodontitis, herpetic gingivo stomatitis
9. Crown preparation
25
10.Ageing
27. Other related factors
• Diet sensitivity. Generally associated with a low pH
material, such as fresh tomatoes, orange juice, cola
drinks.
• Genetic sensitivity. Patients reporting history of
sensitive teeth. It is not known whether sensitivity
correlates to the 10 per cent of teeth that do not have
cementum covering all the dentine at the DEJ, or is a
factor of lower overall patient pain threshold values.
27
28. Restorative sensitivity Triggered following placement
of a restoration for several possible reasons:
• during setting; contamination of composites during
placement or improper etching of the tooth, which
results in micro-leakage
• incorrect preparation of glass ionomer or zinc
phosphate cements;
• general pulpal insult from cavity preparation
technique;
• thermal or occlusal causes; galvanic reaction to
dissimilar metals that creates a sudden shock or ‗tin
foil‘ taste in the mouth.
28
29. Medication sensitivity
• Due to medications that dry the mouth (e.g.
antihistamines, high blood pressure medication),
• thereby compromising the protective effects of saliva
and aggravating diet-related trauma or proliferating
plaque.
• Even a reduction in salivary flow due to aging or
medications can lower the pH of the saliva below the
level at which caries occurs (6.0–6.8 for Dentine
caries; < 5.5 for enamel caries) and increase erosive
lesions to exposed dentine.
29
30. Bleaching sensitivity
• Commonly associated with carbamide peroxide vital
tooth bleaching and thought to be due to the by-
products of 10 per cent carbamide peroxide (3 per cent
hydrogen peroxide and 7 per cent urea) readily passing
through the enamel and dentine into the pulp in a
matter of minutes.
• Sensitivity takes the form of a reversible pulpitis
caused from the dentine fluid flow and pulpal contact
of the material, which changes osmolarity, without
apparent harm to the pulp.
30
31. • Sensitivity is caused by all other forms of bleaching
(in-office, with or without light activation, and new,
over-the-counter) and depends on peroxide
concentration.
31
33. INNERVATION OF DENTIN
• Dentinal tubules contain numerous nerve endings in
the predentin and inner dentin no further than 100 to
150 micrometer from the pulp.
• Although most of the nerve bundles terminate in the
sub-odontoblastic plexus as free unmyelinated nerve
endings, a small number of axons pass between the
odontoblast cell bodies to enter the dentinal tubules in
close approximation to the odontoblast process.
33
35. • No organized junction or synaptic relationship has
been noted between axons and the odontoblast process.
Intra tubular nerves characteristically contain
neurofilaments, neurotubules, numerous mitochondria
and many small vesicular structures.
• Most of these small vesiculated endings are located in
tubules in the coronal zone, specifically in the pulp
horns. It is believed that most of these are terminal
processes of the myelinated nerve fibers of the dental
pulp.
35
36. The mechanism underlying dentin hypersensitivity have
been the subject of keen interest in recent years.
Converging evidence indicates that movement of fluid in
the dentinal tubules is the basic event in the arousal of
pain.
It now appears that pain producing stimuli such as heat,
cold, air blasts and probing with the tip of an explorer
have in common the ability to displace fluid in the
tubules.
36
37. The thermal diffusibility of dentin is relatively low, yet
the response of the tooth to thermal stimulation is rapid
often less than a second.
Evidence suggests that thermal stimulation of the tooth
results in a rapid movement of fluid in the dentinal
tubules that results in the deformation of the sensory
nerve terminals in the underlying pulps .
37
38. Heat would expand the fluid within the tubules,
causing it to flow towards the pulp whereas cold
would cause the fluid to contract producing an
outward flow.
Presumably the rapid movement of fluid across
the cell membrane of the sensory receptor activate
the receptor.
38
41. The dentinal tubule is a capillary tube having an
exceedingly small diameter.
Therefore the effects of capillarity are significant, as the
narrower the bore of a capillary tube, the greater the effect
of capillarity.
Thus if fluid is removed from the outer end of exposed
dentinal tubules by dehydrating the dentinal surface with
an air blast or absorbent paper, capillary force will
produce a rapid outward movement of fluid in the tubule.
41
43. According to Braunstrom desiccation of dentin can
theoretically cause dentinal fluid to flow outward at a rate
of 2 to 3 mm per second.
In addition to air blasts, dehydrating solutions
containing hyper osmotic concentrations and sucrose or
calcium chloride can produce pain if applied to exposed
dentin.
43
44. Investigators have shown that it is the A fibres
rather than the C fibres that are activated by stimuli such
as heat, cold and air blasts applied to exposed dentin.
However if heat is applied long enough to increase the
temperature of the pulp-dentin border by several degrees
Celsius the C-fibres may respond.
It seems that the A fibres are only activated by a very
rapid displacement of the tubular contents.
Slow heating of the tooth produced no response until the
temperature reached 43 C, at which time C fibres were
activated presumably because of heat-induced injury to
the pulp.
44
45. The most different phenomenon to explain is pain
associated with light probing of dentin.
Even light pressure of an explorer tip can produce strong
forces.
These forces mechanically compress the openings of the
tubules and cause sufficient displacement of fluid to excite
the sensory receptors in the indulging pulp.
45
47. Many theories explain dentinal hypersensitivity
Proposed theories are:
Direct neural theory
Odontoblasts receptor theory
Transducer theory
Gate control theory
Fluid or Hydrodynamic theory
47
48. 1)DIRECT NEURAL THEORY
The dentin contains nerve endings that respond when it is
stimulated.
The pulp is well innervated, especially below the
odontoblasts (the plexus of rack show)and that some
nerves penetrate a short distance in to some tubules.
Whether these intratubular nerves are involved in dentin
sensitivity is not known.
No evidence has been found for nerves in the outer
dentin, which is most sensitive .
48
49. 2)ODONTOBLAST RECEPTOR THEORY
This mechanism explains dentin sensitivity considers
the odontoblasts to be a receptor cell. This attractive
concept has been considered, abandoned and
reconsidered for many reasons.
It was once argued because the odontoblasts is of neural
crest origin it retains an ability to transducer and
propagate an impulse what was missing was the
demonstration of a synaptic relation between the
odontoblasts and the pulpal nerves.
49
50. 3)TRANSDUCER THEORY
This theory of dentinal sensation takes into consideration
the synaptic –like relationship between the terminal
,sensory nerve endings and odontoblastic process.
If a true synapse were present between these two
elements to facilitate the transmission of dentinal
sensations,then a neural transmitting substance such as
acetylcholine could be expected,but there no direct
evidence of its presence.
50
51. 4)GATE CONTROL THEORY AND
VIBRATION
When the dentin is irritated, for example, by cavity
preparation, all of the pulpal nerves become activated from
the vibrations.
The larger myelinated fibers may accommodate to the
sensations. The smaller C- fibers may tend to be
maintained and not adjust to the stimulus.
Thus, as the low-intensity pain gates from the larger fibers
are closed, the high-intensity "pain gates" from the smaller
fibers are enhanced. 51
52. "Pain gates" may be opened by some stimuli, such as
anxiety, and may be closed by distracting stimuli such as
"audio-analgesia" or gingival stimulation.
However, the gate theory does little to explain how pain
responses from the dentin are transmitted and perceived
by the nerve endings of the pulp-only how they may be
centrally interpreted.
52
53. 6.)FLUID OR HYDRODYNAMIC THEORY:
By Brannstrom
This mechanism proposed to explain dentin sensitivity
involves movement of fluid through the dentinal tubules.
This "hydrodynamic theory" which fits much of the
experimental and morphological data proposes that fluid
movement through the dentinal tubule distorts the local
pulpal environment and is sensed by the free nerve
endings in the plexus of Raschkow.
53
55. Thus, when dentin is first exposed, small blebs of fluid
can be seen on the cavity floor. When the cavity is dried
with the air or cotton wool, a greater loss of fluid is
induced, leading to more movement and a further painful
experience.
The increased sensitivity is at the dentino-enamel junction
is explained by profuse branching of tubules in this
region.
Interestingly stimuli, such as cold, which cause fluid flow
away from the pulp produce more rapid and greater pulp
nerve responses than those, such as heat, which cause an
55
inward flow.
56. This certainly would explain the rapid and severe response
to cold stimuli compared to the slow dull response to heat.
The hydro dynamic hypothesis explains why pain is
produced by thermal change, mechanical probing,
hypotonic solutions and dehydration.
56
58. The pain producing stimuli can be thermal, tactile,
osmotic, chemical or evaporative, but the cold stimulus
appears to be the strongest and causes the greatest problem
to those troubled by dentine hypersensitivity.
WHY ALL EXPOSED DENTINE IS NOT
SENSITIVE???
Evidence from a scanning electron microscopic
investigation of extracted teeth would suggest that there
are differences between ‗hypersensitive‘ and ‗non-
sensitive‘ dentine in that there are more and wider open
dentinal tubules in sensitive dentine.
58
59. Additionally, another scanning electron micro-scope
study, based on replica models of hypersensitive and non-
sensitive dentine, showed that, in hypersensitive dentine,
the smear layer was thinner, different in structure and
than in non sensitive dentine.
These findings appear consistent with the hydrodynamic
theory.
The greater number of open and wider tubules at the
dentine surface would enhance fluid permeability through
dentine and as such increase the possibility for stimulus
transmission and subsequent pain response.
59
62. CLINICAL FEATURES.
• Pain is only consistent symptom of dentin
hypersensitivity.
• However it is not known whether hypersensitive
teeth lie at one extreme of a normal distribution of
dentin sensitivity or they represent a separate
population of teeth that are abnormally sensitive.
• Not all areas of exposed dentin are sensitive and
hypersensitive surfaces can vary in their sensitivity
to different stimuli. 62
63. PRESENT AND FUTURE METHODS
FOR ASSESSMENT AND EVALUATION
OF PAIN ASSOCIATED WITH DENTIN
SENSITIVITY
63
64. Traditionally dentin hypersensitivity mainly evaluated on
the individual patients' response to the stimulus.
According to recent recommendations by Holland et al
(1997), dentin hypersensitivity may be evaluated either in
terms of the stimulus intensity to evoke pain or response
based methods.
Stimulus based methods usually involve the measurement
of a pain threshold; response based methods involve the
estimation of pain severity .
64
65. The presenting stimuli can be grouped into five
categories:
•mechanical
•chemical
•electrical
•evaporative
•thermal.
65
67. Electrical stimulation - electrical pulp testers
Evaporative stimuli - cold air blast, air thermal
system, air Jet stimulator,
Thermal stimuli - electronic threshold measurement
device, cold water testing, heat,
Ethyl chloride, ice stick, thermo-
electric Devices (e.g.: bio mat thermal
probe).
67
68. SUBJECTIVE EVALUATION:
VERBAL RATING SCALES:
Keele 1948 described four point scale grading pain as
slight, moderate, severe and agonizing.
Verbal rating scales (VRS) offer a choice of words that
may not represent pain experience with significant
precession for all patients.
68
69. SUBJECT EVALUATION TACTILE AND OR
THERMAL STIMULATION:
a) simple binary pain scale pain -before treatment pain/no
pain after treatment(Hansen 1992)
b)
0 - no discomfort .
1 - Mild discomfort .
2 - Marked discomfort
3 - Marked discomfort that lasted 10 sec. (Gilliam and
Newman1993)
69
70. VISUAL ANALOGUE SCALES:
A visual analogue scale (V AS) is a line 10 cm in length,
the extreme of the line representing the limits of pain a
patient might experience from external stimulus.
No pain at one end and most severe pain at the other end.
Patients are asked to place a mark on the 10 cm line
which indicates the intensity of their current level of
sensitivity or discomfort following application of stimuli.
V AS can give only a one -dimensional assessment of pain
and as such cannot distinguish between the sensory,
intensity and affective aspects of pain.
70
72. AIR INDEXING METHOD
An ―air indexing method‖ was developed in the late
1970‘s to detect and quantify CDH. (In 2000, an
introduction of the technique was published by
Coleman et al.)
The method was developed to diagnose CDH in a
manner that minimizes thermal or evaporative stimuli
to sensitive teeth.
72
73. A minor puff of air from a standard air/water syringe
was directed to the CEJ region at a 45-degree angle to
the long axis of a test tooth at a distance of
approximately one-half centimeter for a duration of one-
half to one second.
A ―threshold patient response‖ was recorded as none
(0), slight (1), moderate (2), or severe (3) for test
zones of teeth
An ―air index mapping‖ was obtained by patient
responses to the air stimulus beginning on the most
distal upper right tooth, going toward the upper left,
then mandibular left and so on for both buccal and
lingual CEJ regions .
73
75. When a patient presents with what appears to be
sensitive dentin, the initial diagnosis should eliminate
any possible reasons such as decay, cracked tooth, or
irreversible pulpitis that may mimic dentin
hypersensitivity.
The next appropriate step, once the problem has been
identified as dentin hypersensitivity, is to identify the
reason for the exposed dentinal tubules and to see if the
etiology process causing the hypersensitivity can be
eliminated.
75
76. The greatest clinical implication of dentine
hypersensitivity is how the condition may be prevented
either from occurring or recurring, and this can only be
debated by considering the probable etiologic factors.
Grossman has stated, ―The best treatment for
hypersensitivity lies in its prevention.‖.
76
78. Patient communication
Finally successful patient management relies heavily on
good communication skills which are of vital importance
in dentistry because it improves the quality and amount of
information obtained from the patient, increases the
likelihood of patient compliance, decreases the patient
anxiety and improves the probable outcome of treatment.
78
79. Clinical management:
Often dentin hypersensitivity abates without treatment.,
This is probably related to the fact that dentin
permeability can decrease spontaneously. This may
be probably due to the natural process contributing
by;
• formation of reparative dentin by pulp.
• obturation of the tubules by the formation of mineral
deposits (Dentinal sclerosis)
• Calculus formation on the surface of the dentin
79
80. There are essentially two basic approaches to the
treatment of dentin hypersensitivity
1) Direct inhibition of sensory nerve activity
2) Tubule occlusion
80
83. •Criteria for the selection of desensitizing procedures
•Provides immediate and lasting relief of pain
•Easy to apply
•It should be well tolerated by patients
•It should not be injurious to the pulp.
•It should not discolour the tooth.
•It should be relatively inexpensive.
83
84. Two types of procedure for
desensitization
I. IN OFFICE TREATMENT PROCEDURES:
Evidence indicates that areas of hypersensitive dentin
have significantly more open dentinal tubules
compared with non-sensitive dentin and that these
open tubules are patent throughout their length.
This enables fluid to move freely between the oral
environment and the pulp.
It has also been established that exposed but sensitive areas
of dentin have tubules that have become occluded.
A rapid movement of fluid in the tubules is capable of
activating intradental sensory nerves, therefore
treatment should be directed toward reducing the
functional diameter of the tubules to limit fluid
movement. 84
85. Specific treatment modalities
Some of the materials used for in-office treatment are
•cavity varnishes
•anti-inflammatory agents
•treatments that partially obturate dentinal tubules.
Burnishing of dentin
silver nitrates
zinc chloride-potassium Ferro cyanide
Formalin
85
87. –Strontium chloride
–potassium oxalates
Treatment agents that undergo setting or
polymerization reactions
•Glass ionomer cement
•Dentin bonding agents
•Restorative resins
and
Lasers
Prior to treating sensitive tooth surfaces, hard or soft
deposits should be removed from the teeth. The teeth
should be isolated and dried with warm air.
Most of the in-office treatment procedures are aimed at
obturating the tubules. 87
88. 1.)Cavity varnishes:
The varnish does temporarily occlude dentinal tubules but
the material is readily lost over time.
Dentin often becomes insensitive when open tubules are
covered with a thin film of varnish.
WyCoff advocated the use of cavity varnish such as
copalite.
For more sustained relief, a fluoride containing varnish,
Duraflor can be applied.
The use of 5% sodium fluoride (NaF) in a thick varnish
as a dentine desensitizer has been reported by Clark et al.
88
(1985).
89. Duraphat
5% sodium fluoride varnish
quick and easy application
natural resin base
pleasant taste
adheres to dry or moist teeth
sets in contact with saliva
ask patient not to brush or floss for 3-4 hours. Can
drink or eat a soft meal immediately.
calcium fluoride can persist for weeks or months on
the tooth surface .
89
90. 2.)Corticosteroids:
Mosteller reported that when a liner consisting of 1 %
prednisalone in combination with 25 para-chlorophenol
25% M-cresyl acetate and 50% gum camphor was
applied to the walls of cavities, it was completely
effective in preventing post-operative thermal
sensitivity.
Many studies have given reports of prompt relief from
hypersensitivity with similar preparations.
90
91. 3.)Treatments that partially
obturate dentinal tubules
Effects of burnishing dentin:
Burnishing of dentin with a tooth pick or orange wood
stick results in the formation of a smear layer that
partially occludes the dentinal tubules.
Pashley et al employed an in vitro method to study the
effects of burnishing NaF, Kaolin and Glycerin alone
or in various combinations on dentin permeability.
It was observed that burnishing created a partial
smear layer that reduced fluid movement across
91
dentin by 50-80%
92. Formation of insoluble precipitants to block
tubules
Certain soluble salts react with ions in tooth structures to
form crystals on the surface of the dentin.
In order to be effective, crystallization should occur
within 1 to 2 minutes and the crystals should be small
enough to enter the tubules.
The crystals must also be large enough to partially
obturate the tubules although relatively large crystals such
as calcium oxalate dihydrate are very effective in reducing
permeability.
Smaller crystals such as calcium fluoride are less apt to be
effective.
92
93. Silver nitrate
is a time honored desensitizing agent
The effectiveness of silver nitrate has been attributed to
its ability to precipitate protein constituents of
odontoblastic process, thereby partially blocking the
tubules.
Calcium hydroxide
For many years calcium hydroxide has been a popular
agent for the treatment of dentin hypersensitivity.
The exact mechanism of action is unknown. But
evidence suggests that it may block dentinal tubules or
promote peritubular dentin formation.
93
94. FLUORIDE COMPOUNDS
Lukoinsky was the first to propose sodium fluoride as a
desensitizng agent.
Because dentinal fluid is saturated with respect to
calcium and phosphate ions, application of Fluoride to
dentin leads to precipitation of CaF2 crystals, thus
reducing the functional radius of the dentinal tubules.
The crystal size of CaF2 is very small and therefore a
single application of Fluoride has less effect on dentin
permeability than agents such as potassium oxalates that
give rise to large crystals.
94
95. Acidulated sodium fluoride
The concentration of fluoride in dentin treated with
acidulated NaF was significantly higher than dentin
treated with NaF.
Sodium silicofluoride
Application of a saturated solution of sodium
silicofluoride for 5 minutes was much more potent than
a 2% solution of NaF in desensitizing painful cervical
areas of teeth
95
96. Stannous fluoride:
Blank and charbeneon advocate burnishing a 10%
solution of stannous fluoride into sensitive root areas.
It has also been reported that topical application of
0.717% aqueous SnF2 provided immediate relief from
sensitivity.
The ADA has recognized the desensitizing properties of
stannous fluoride gel by granting the ADA Seal of
Acceptance to a nonaqueous stannous fluoride gel
formulation (Gel-Kam) for the therapeutic prevention of
sensitivity and caries.
96
98. Fluoride iontophoresis :
Iontophoresis is a term applied to the use of an electrical
potential to transfer ions into the body for therapeutic
purposes.
The objective of fluoride ionotophoresis is to drive
fluoride ions more deeply into the dentinal tubules
than can be achieved with topical application of fluoride
alone.
Iontophoresis is not a simple procedure.
It involves the placement of a negative electrode to dentin
and a positive electrode to the patients face or arm.
98
99. If the negative electrode makes contact with saliva,
gingival tissue or a metallic restoration the flow of
current will follow the path of least resistance and
stream around the dentin rather than through it.
For this reason, it is recommended that teeth be isolated
with plastic strips and cotton rolls rather than a
rubber dam.
To use these battery-powered devices, the patient holds
the positive electrode in his hand and the dentist, using
the negative electrode, applies a 2% solution of
sodium fluoride to the sensitive areas of the teeth. 99
100. Although a number of authors have reported a
significant reduction in sensitivity with the use of
iontophoresis with 2% NaF others found no striking
difference between topical application of NaF with or
without iontophoresis.
The authors concluded that ―iontophoresis with 1%
sodium fluoride is the method of choice for the treatment
of hypersensitive dentin, as it meets all the requirements
of an ideal desensitizing agent except permanency of
effect, which requires further investigation‖ .
100
101. Iontophoretic application of fluoride by tray
techniques:
This new technique offers three improvements
1) A safer, more powerful voltage source providing upto
40 volts.
2) Insulation of gingival tissues and metal restorations.
3) A flexible electrode system adaptable to all areas of
the mouth.
101
102. OXALATES
These are relatively inexpensive, easy to apply and well
tolerated by patients.
Potassium oxalate and Ferric oxalate solutions make
available oxalate ions that can react with calcium ions in
the dentinal fluid to form insoluble calcium oxalate
crystals that are deposited in the aperture of the dentinal
tubules
BISBLOCK
Dentin Desensitizer, Oxalate
102
104. • Potassium oxalate
as a desensitizing agent was developed by Greenhill
and Pashley.
• It is sold commercially as PROTECT (John O.
Butler Co., Chicago, Ill.).
• Applying potassium oxalate to the dentin surface,
which, in turn, produces ―calcium oxalate crystals‖
of different particle sizes within the dentinal tubules,
is a means of obstructing the tubules apertures.
104
105. • ―Calcium oxalate is poorly soluble and is formed
when the potassium oxalate contacts the calcium ions
in the dentinal fluid.‖
• A single-dose applicator permits pinpoint delivery,
to the sensitive area, of monopotassium-
monohydrogen oxalate.
• Although the degree and duration of relief will vary
from patient to patient, the effectiveness of a single
application by the dentist can last up to 6 months.
• It has been found that application of potassium
oxalate to the etched dentin reduced sensory nerve
excitability to the level of unetched dentin.
105
106. 4.)Treatment agents that undergo setting or
polymerization reactions
A. Conventional glass Ionomer cements
• One of the first clinical evaluations of the use of glass
ionomers for the treatment of hypersensitive dentine in
cervical abrasion lesions was reported by Low (1981).
• The cervical lesions were etched with 50% citric acid
for 30- 45 s, then rinsed and dried prior to placement
of the glass ionomer cement.
• Although the method of evaluating sensitivity was not
described and no controls were used, the author
reported complete loss of hypersensitivity in 89.7% of
all patients. 106
107. B. Resins and Adhesives:
The objective in employing resins and adhesives is to seal
the dentinal tubules to prevent pain producing stimuli
from reaching the pulp.
107
108. Javid et al during a 6 week study compared the effects
of a single application of isobutyl cyanoacrylate with
weekly applications of 33% NaF paste.
The cyanoacrylate was applied to sensitive root
surfaces with a small cotton pellet and allowed to dry,
this procedure provided immediate desensitization and
proved to be significantly more effective than the NaF
treatments. However during a 6 week interval,
sensitivity slowly returned.
This suggests that the material is gradually lost, so
repeated application of cyanoacrylate becomes
108
necessary.
109. GLUMA
is a dentin bonding system includes a 5% gluteraldehyde
primer and 35% HEMA.
It provides an attachment to dentin that is strong and
immediate.
It has been reported that GLUMA seems to prevent
bacterial growth in tooth/restoration interfaces.
This could have a beneficial effect in inhibiting
plaque accumulation on sensitive root surfaces.
109
110. Indications :
–As a normal part of resin bonding with a Gluma 3-step.
–Under any indirect resin-bonded inlay, onlay, crown or
veneer.
–Under amalgam fillings.
–Under crowns cemented with zinc phosphate cements.
–In conjunction with other dentin bonding systems
which may not provide a desensitization effect.
110
111. • Pulpdent Dentin Desensitizer contains 5%
glutaraldehyde in water. It can be applied to all
dentin surfaces, including cavity, crown and inlay
preparations and cervical areas, as a desensitizing
agent.
111
112. • In summary, the effectiveness of Adhesive resins in
reducing dentine sensitivity has improved as bonding
techniques and formulations have improved
(Nakabayashi and Pashley, 1998).
• These materials are somewhat technique sensitive and
care must be taken to avoid creating a rough ledge of
resin in the gingival crevice
112
113. 5.)Lasers
The NdYAG Laser has been used experimentally in
dentistry since 1970's.
Recently systems have become available which are
tailored specifically for dental surgery using fiber optic
delivery to a hand pieces.
113
114. The tool was effective in reducing dentin
hypersensitivity to cold stimuli, although the
mechanism of laser action has yet to be confirmed, it
would appear that obturation of the dentinal tubules
may be the most logical hypothesis.
It has been found to produce quick response with few
side effects, it is also simple and fast to administer,
results are consistent, statistically significant and
reproducible, high success rate, the patient find the
treatment procedure less traumatic
114
115. The presumed mechanism of action is the
coagulation and precipitation of plasma proteins in
dentinal fluid.
It is also possible for the thermal energy to alter
intradental nerve activity.
Periodontal surgery—
A tissue grafting procedure can be used to cover the
sensitive surface and protect the dentinal tubules from
the oral environment.
The outcomes of this procedure to relieve sensitivity is
unpredictable.
115
116. II. Home and desensitizing agents :
During the years, a wide variety of professionally
applied and home care products have been
advocated for treatment of the hypersensitivity
condition.
Most of the dentifrices used as home remedies are in
dentifrice form.
Pashley et al found that dentifrice components could
occlude tubules and the products differed in their
ability to produce this effect.
116
117. Strontium chloride
Strontium chloride is contained in two toothpastes on
the market, Sensodyne and Thermadent .
Strontium combines ―with phosphate in the dentinal fluid
and exchanging for calcium in the hydroxyapatite of the
dentinal tubule walls may produce strontium phosphate
crystals and dentinal tubules closure.‖
Goodman believes that the strontium ion alters neural
transmission, which may account for the immediate
improvement in relieving sensitivity.
117
118. • Strontium may also stimulate the formation of
irritation dentin, and it has been reported ―as well to
bind to the matrix of the tubule, thus reducing its
radius.‖
• Kun found that topical application of concentrated
strontium chloride on an abraded dentin surface
produced a deposit of strontium that penetrated
dentin to a depth of approximately 20~ and extended
into the dentinal tubules
• Strontium deposits are produced by an exchange
with calcium in the dentin resulting in
recrystallisation in the form of a strontium apatite
complexes 118
119. It was found that the radiodensity of dentin samples
immersed in strontium chloride was significantly
increased as compared with control specimens
suggesting that strontium is incorporated into tooth
structure.
119
120. Potassium nitrate
as a desensitizing agent was developed by Hodash, who
reported the use of saturated solutions and pastes to be
used for home care that contain up to 5% potassium
nitrate.
These pastes are sold over the counter as Promise and
Sensodyne Fresh Mint and Denquel .
120
121. Goodman has shown some impressive clinical results
using dentifrices containing potassium nitrate.
He suggested that desensitization may occur either by the
oxidizing nature of potassium nitrate or by crystallization,
which blocks the tubules, or both.
Goodman also believes that the ―potassium ion
depolarizes the nerve fiber membrane…in which few or
no action potentials can be evoked.‖
121
124. Dibasic sodium citrate:
Another type of dentifrice for home therapy of
sensitivity was introduced by Jenner, Dnany and Tutz in
the year 1977 which was based on mixture of sodium
citrate and pluronic a surface active agents.
The citrate pluroxia dentifrice was some what more
effective than 10% strontium chloride and 0.4%
stannous fluoride in axhydrons glycerol.
The substance has been recognised by American
dentinal association as been safe and effective for
treatment
124
126. Future therapies for dentine hypersensitivity
Gene therapy in the future may include treatment of sensory
nerves to dental restorative procedures as well as surgical and
non surgical debridement that elicits its dentin
hypersensitivity.
One such method may include blocking the increased
production of nerve growth factor(NGF)by pulpal fibroblasts
near the lesion thought to contribute to tooth hypersensitivity
after restorative procedures.
126
128. • If, the patient has lost tooth structure at the cervical
area and presents with dentin sensitivity, the best
treatment is the use of restorative materials.
• Restorative treatment of cervical dentinal sensitivity
can be successfully accomplished using any currently
marketed third generation dentin bonding agent or
glass ionomer cement.
• The newer light cured glass ionomer cements are
easy to work with and have been used to successfully
treat dentin sensitivity.
128
129. • The use of restorative materials to treat dentin
sensitivity requires more time and is more expensive,
but it is also more long lasting and predictable.
• If patients have moderate to severe sensitivity in
multiple teeth with minimal loss of tooth structure,
clinicians should consider the use of topical agents
such as oxalates or fluorides.
• If one or two teeth remain sensitive after such
treatment, they can then be treated with restorative
resin materials.
129
131. • If the patient has previously bleached their teeth with
the night guard vital bleaching technique, then the
custom-fitted tray can be used as the carrier for the
anti sensitivity toothpaste.
• If the patient is not a candidate for bleaching but has
a history of chronic sensitivity, then non-scalloped,
no reservoir designed tray can be fabricated.
131
133. • Since tooth sensitivity during bleaching is common,
yet unpredictable, it must be addressed clinically
when it occurs.
• Often the sensitivity experienced is ‗mild‘ and
required no alteration in the treatment protocol.
• In cases where it cannot be ignored, the dentist may
have to instruct the patient to decrease the frequency
(typically, to every other day) and duration of
treatments.
• When this protocol fails, some practitioners advocate
the use of topical fluorides in conjunction with the
beaching treatments.
133
134. • Others recommend using desensitizing toothpaste for
2-3 weeks prior to initiating as well as during
bleaching.
• Persons experiencing nighttime sensitivity may switch
to daytime wear and reduce contact time of the
peroxide to 2-4 hours.
• In severe cases patients may have to stop bleaching
for a few weeks or even altogether.
• Use of calcium and fluoride added to bleaching agents
• eg.calcium peroxide.
134
135. CONCLUSION
Dentinal hypersensitivity is a problem that plagues
many dental patients. When a patient presents with
dentinal hypersensitivity symptoms, they should be
examined and informed of the multiple treatment
options that may be necessary to eliminate the problem.
•The patient should be responsible for the decision
making process since some of their daily habits may be
contributing to the problem and if not changed the
condition will persist.
135
136. •Up to 90% of patients suffering from Dentin
Hypersensitivity claim that in particular a cold stimulus
causes the painful condition, whereas a tactile stimulus
affects up to10 per cent of patients
136
