DENTIN

HYPERSENSITIVITY

CONTENTS

INTRODUCTION
CLINICAL FEATURES
PREVALENCE
THEORIES
ETIOLOGY
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
PREVENTION&TREATMENT
CONCLUSION

INTRODUCTION
Root hypersensitivity is a relatively
common problem in periodontal practice.
It may occur spontaneously when the root
becomes exposed as a result of gingival
recession or pocket formation/it may occur
after scaling &root planing&surgical
procedures

DEFINITION
Definition:
DENTINHYPERSENSITIVITY is characterized by short sharp
pain arising from exposed dentin in response to stimuli
typically thermal, evaporative, tactile, osmotic or chemicalthat
cannot be ascribed to any other dental defect or disease.1
(Addy

M. )

Dentine hypersensitivity is sensation felt when the

nerves inside the dentin are exposed to the
environment

 The sensation can range from irritation all the way

to intense, shooting pain.
This sensitivity can be caused by several factors,
including wear, decaying teeth or exposed tooth
roots.

Sensitive teeth

DENTINAL
TUBULES

Images of dentin surface(2000x)

Enamel loss exposing dentin

Gum loss exposing dentin

 It is manifested as pain induced by cold or hot

temperature by citrus fruits or sweets,or by contact
with a toothbrush or a dental instrument.
Root sensitivity occurs more frequently in the
cervical area of the root,where the cementum is
extremely thin
Scaling &root planing procedures remove this thin
cementum inducing the hypersensitivity

 Transmission of stimuli from the surface of the

dentin to the nerve endings located in the dental
pulp or in the pulpal region of the dentin could
result from the hydrodynamic mechanism or from
the odontoblastic process
An important factor for reducing or eliminating
hypersensitivity is adequate plaque control

 Dentine contains many thousands of microscopic tubular

structures that radiate outwards from the pulp

These dentinal tubules are typically 0.5-2 microns in

diameter.

Changes in the flow of the plasma-like biological fluid

present in the dentinal tubules can trigger
mechanoreceptors present on nerves located at the
pulpal aspect thereby eliciting a pain response.

 This hydrodynamic flow can be increased by cold,

air pressure, drying, sugar, sour (dehydrating
chemicals), or forces acting onto the tooth.
Hot or cold food or drinks, and physical pressure
are typical triggers in those individuals with teeth
sensitivity

CHARACTERISTIC OF DENTIN
HYPERSENSITIVITY
Clinical features.
DENTIN HYPERSENSITIVITY usually is diagnosed after other
possible conditions have been eliminated.

Alternative causes of pain include chipped or

fractured teeth, cracked cusps, carious lesions, leaky
restorations and palatogingival grooves.
The clinical features of DENTINHYPERSENSITIVITY
are well-documented.
PREVALENCE:The prevalence
ofDENTINHYPERSENSITIVITY varies from 4 to 57
percent.6

 These variations are likely due to differences in the

populations studied and the methods of investigation
(for example, questionnaires or clinical
examinations).
The prevalence of DH is between 60 and 98 percent
in patients with periodontitis.

 A majority of patients, however, do not seek

treatment to desensitize their teeth because they do
not perceive DH to be a severe oral health problem.
In response to questionnaires, dentists have reported
that DH affects between 10 and 25 percent of their
patients.
Schuurs and colleagues also reported that dentists
believe DH presents a severe problem for only 1
percent of their diagnosed patients

DISTRIBUTION

While DH mostly occurs in patients who are between

30 and 40 years old,it may affect patients of any age.
It affects women more often than men, though the
sex difference rarely is statistically significant.
The condition may affect any tooth, but it most often
affects canines and premolars.
The affected teeth tend to vary among studies and
populations, and different distribution patterns have
been described

ETIOLOGY
Mechanisms of sensitivity

Dentin is naturally sensitive owing to its close

structural and functional relationship with the dental
pulp.
This inherent sensitivity usually is not a problem
because other tissues cover the dentin.
Microscopic examination reveals that patent dentinal
tubules are more numerous and wider in
HYPERSENSITIVE DENTIN than in Non sensitive
dentin

 These observations are consistent with the

hypothesis that dentinal pain is mediated by a
hydrodynamic mechanism.
In the hydrodynamic sequence, a painprovoking stimulus applied to dentin
increases the flow of dentinal tubular fluid.
In turn, this mechanically activates the
nerves situated at the inner ends of the
tubules or in the outer layers of the pulp .

 Cooling, drying, evaporation and hypertonic

chemical stimuli that stimulate fluid to flow
away from the pulp more effectively activate
intradental nerves than do stimuli such as
heating or probing that cause fluid to flow
toward the pulp.
The observation that about 75 percent of
patients with DH complain of pain on
receiving cold stimuli supports this hypothesis

 During periodontal therapy, scaling and root planing

removed the outer layer of hyper mineralized dentine and
thus leaves the surface expose to the effect of
hydrodynamic phenomenon.
Surgical periodontal treatment, usually involves complete
debridement of root surface.
Post operative recession of soft tissue further exposes the
dentinal tubules.
Patient inability to maintain plaque control in the healing
phase further complicates the problem,

 ACID PRODUCTION DUE TO PLAQUE

ACCUMULATION could act as a noxious stimuli
and cause dehydration and leads to fluid
movement across the dentinal tubule.
Instrumentation of the root creates an outer
contiguous smear layer covering the instrumented
surface as well as pushing debris into the dentinal
tubules for several micrometer.
Thus The smear layer is a natural iatrogenic yet
transient treatment for dentin hypersensitivity.

 Another quality is that the ideal desensitizer should not interfere with
the subsequent regenerative outcome, if such procedures are deemed
necessary at the future time.
We can break down the methods of desensitizing dentine into
topical methods,
iontophoresis,
use of restorative material,
electrosurgery,
lasers, and
guided tissue regeneration to cover gingival recession.

THEORIES OF PAIN TRANSMISSION

THROUGH DENTIN

DIRECT NEURAL STIMULATION

The nerves in the dentinal tubules are not
commonly seen &even if they are present
they do not extend beyond the inner dentin.
Topical application of local anesthetics do
not abolish sensitivity.Hence this theory is
not accepted

FLUID/HYDRO DYNAMIC THEORY

Various stimuli as heat,cold,air blast
desiccation/mechanical/osmotic pressure affect
fluid movement in the dentinal tubules.
This fluid movement,either inward(due to cold
stimuli)/outward(due to drying of exposed
dentinal surface),stimulates the pain mechanism in
the tubules by mechanical disturbance of the
nerves closely associated with the odontoblast
&its process

 Thus these endings may act as

mechanoreceptors as they are affected by
mechanical displacement of the tubular
fluid

TRANSDUCTION THEORY
Odontoblast process is the primary structure
excited by the stimulus &that the impulse
transmitted to the nerve endings in the inner
dentin.
This is not a popular theory since there are
no neurotransmitter vesicles in the
odontoblast process to facilitate the synapse
Or synaptic specilization

HISTORY, EXAMINATION&
DIAGNOSIS

A diagnosis of DH should be determined only when

the practitioner has considered differential diagnoses
after conducting a methodical history and
examination of the patient.
The other causes of transient tooth pain must be
excluded for a diagnosis of DH to be made.
Quantifying the initial degree of sensitivity provides a
baseline from which to chart subsequent changes in
the condition

 Although dentin hypersensitivity is

a common clinical problem, there
is no standard method of
diagnosis, and confusion exists
about the most effective treatment

 The condition should be diagnosed only after

excluding other possible causes of pain.
Flowchart for the clinical management of
dentin hypersensitivity (DH). (Adapted with
permission of George Warman Publications
[UK] Ltd., from Addy and Urquhart.) Note 1.
Pain evoked by thermal, evaporative (jet of
air), probe, osmotic or chemical stimuli. Note
2.

DifferentialDiagnosis
Crackedtoothsyndrome.
Fracturedrestorations.
Chippedteeth.
Dentalcaries.
Post-restorativesensitivity.

Categorizing Dental Pain

Dental pain can be categorized using

different taxonomies.
It may arise from a problem in the tooth or
its supporting structures, or it may be due
to a problem elsewhere that is
misperceived by the patient as originating
there (e.g., referred pain).
Dental pain can also be classified by
etiology. All occurrences require dental
referral.

Pain Originating in the

Tooth or Periodontium
This type of pain can be due to trauma, a cracked
tooth, pulpitis, or a host of other causes.
Trauma: Dental pain may be caused by a
traumatic event, perhaps a recent fall, a blow to
the face from sports or fighting, or other facial or
dental trauma.
Trauma may have occurred some time ago, and
the patient may have endured longstanding pain.

Cracked Tooth Syndrome

The patient may have "cracked tooth syndrome"
from trauma, as well as from tooth grinding,
accidental insults (e.g., biting down on an
unpopped kernel of corn or a concealed olive pit),
or bad habits, such as compulsively chewing ice.
In all of these cases, a living tooth can suffer a
partial fracture that extends into the dental pulp
(connective tissue lying beneath enamel and
dentin in the central portion of the tooth housing
the nerve).

 This problem is more common in older patients,

whose water may not have been fluoridated when
they were young.
As a result, many have extensive dental
restorations (i.e., fillings).
As those restorations age, they are prone to
damage.
Patients with cracked tooth syndrome feel pain
when biting down to chew; the pain usually
remits when chewing ceases.
Thus, patients often stop chewing on the
troublesome side for a period of time.

Irreversible Pulpitis
Some tooth problems are too
extensive to repair.
Perhaps the tooth has developed a
large cavity in a previously unfilled
area or there is extensive erosion
beneath an older amalgam.

 If the cause is addressed properly, it

may cease.
If the patient is unable or unwilling to
see a dentist, the tooth may progress
to irreversible pulpitis.

 In these cases, if the damage reaches an

area proximal to the pulp, repair cannot be
done.
Advanced periodontal disease that leads
to bone loss may also be the cause.
The tooth affected with irreversible
pulpitis causes moderate to severe pain
and is also painful after cold, heat, or
other stimuli, but in this case, the pain
lasts for minutes to hours.
The pain can be severe and disrupt sleep.

 Investigators hypothesize that tiny air

bubbles trapped under a root filling or
adjacent to dentin expand or contract.
Patients experience a sensation of sharp
or squeezing tooth pain.
In the worst case, alveolar mucosa may
rupture.
If the patient describes a pressure-related
problem, treatment may be restoration of
damaged teeth.

REVERSIBLE PULPITIS
This term refers to inflammation of the dental
pulp that can be reversed with a professional
appointment.
Patients complain of discomfort lasting less than
five seconds when the tooth is contacted by cold,
an air blast, or ingestion of sweet foods.
The cause can be minor (e.g., dentinal
hypersensitivity, a new filling, recent dental
cleaning) or due to such problems as gingival
recession, caries, or a defective restoration.

 Nonsteroidal nonprescription
products can be recommended as an
emergency measure until patients
see the dentist.
However, ibuprofen or naproxen
does not affect the underlying
pathology and the problem will
continue to worsen until a
professional intervenes.

Referred dental pain

Dental pain may occur as a result of
extradental causes.
For instance, several types of headache
can cause pain in the teeth and jaw.
A cluster headache can result in
toothache.
Migraine and paroxysmal hemicrania can
produce pain in the maxillary molars.

 Barodontalgia: Barodontalgia is tooth pain

resulting from extremes of pressure.
Pilots in unpressurized cabins (e.g., highperformance aircraft) experience barodontalgia
from low pressures at about 3,000 feet, and scuba
divers experience the same problem at the
elevated atmospheric pressures encountered 10
meters below the surface and deeper.

 Hemicrania continua is a headache that can

produce toothache in the maxillary premolars.
In each case, the dentist may discover that the
pain does not originate in the teeth or
periodontium.
A physician may use diagnostic criteria to
identify the type of headache that caused the
tooth pain.
Jaw/tooth pain can be caused by trigeminal
neuralgia, characterized by pain on one side of
the head, in most cases the right side

 The pain occurs in the areas innervated

by the trigeminal nerve's mandibular
and/or maxillary branches.
Some patients insist that the pain started
without any provoking factor, while others
recall that it began after trivial stimulation
of the mucosa around the teeth, tongue, or
skin (e.g., chewing, yawning).
Attacks come in waves of electric-like
pain, lasting from a few seconds to
several minutes.

 Temporomandibular disorders, involving

the temporomandibular joints, chewing
structures, and other associated areas,
may produce dental pain.
Appropriate treatment for this condition
may encompass such interventions as
intraoral appliances, prescription drugs,
moist heat, ice, ethyl chloride spray,
exercise, physiotherapy, electrotherapy,
and iontophoresis.

Methods used to measure tooth

hypersensitivity
Tactile
The simplest tactile method used is to lightly pass a sharp dental
explorer over the sensitive area of the tooth (usually the cemento
enamel junction) and to grade the response of the patient on a severity
scale from 0 to 3.
If no pain is felt 0,
slight pain or discomfort 1,
severe pain 2,
severe pain that lasts 3
Other sophisticated tactile methods used were a device by Smith and
Ash, force sensitive electronic probe devised by Yeaple, pressure
probe device used by McFall and Hamrick and a hand held scratch
device.

YEAPLES PROBE

SCRATCHOMETER

 Electrical Electrical measurements differ from others in that a pain response can
be obtained from nonsensitive as well as from sensitive teeth and with
either an enamelcovered crown or a cementumcovered root site of
stimulation.
Improvements in pulp testers led to better quantification of the electric
stimulus and discovery that a condition of pre-pain consisting of a
tingling or warm sensation is observed before real pain and discomfort
are felt by the subject as the magnitude of a stimulus is increased.
A stark device and a commercial digital pulp tester have also been
tried.

 Osmotic
An osmotic method consisting of the
subjective pain response to a sweet stimulus
was used to measure the effect of several
test dentifrices on dentinal sensitivity.

 Thermal
A simple thermal method for testing for tooth sensitivity is directing a
burst of room temperature air from a dental syringe onto the test tooth.
Blowing air on a tooth involves drying and pain can be easily detected
by this method if the teeth are sensitive.
Air stimulation has been standardized as a one second blast from the
air syringe of a dental unit, where its temperature is set generally
between 65 70 degrees fahrenheit and at a pressure of 60 psi.
An air thermal device has been devised.
Instruments that involve electric cooling or heating of direct contact
metal probes have also been used in some studies.

DENTIN DISK MODEL

Small dentin disks prepared from extracted teeth can
be used to measure the permeability of dentin.
Permeability is derived from the hydraulic
conductance or ease of fluid flow through the dentin.
Some desensitizing agents such as oxalates reduce
dentin permeability, while others such as potassium
nitrate do not.

 Treated dentin disks can be examined using

a scanning electron microscope to visualize
surface deposits and tubule occlusion.
By incorporating the dentin disk specimens
in intraoral appliances, experiments can be
conducted in situ under natural conditions in
the mouth.
It is possible to replicate the outward flow of
dentinal fluid, which can oppose pulpward
diffusion of desensitizing agents.
.

 An in vitro study of hydraulic conductance in dentin

disks confirmed the findings of these clinical trials.
The product containing 5 percent potassium nitrate
and 0.454 percent stannous fluoride in a silica base,
which caused significantly greater reduction in DH,
also demonstrated the lowest hydraulic conductance
(permeability) and greatest inward potassium ion flux
in dentin disks.

RECORDING CONDUCTION IN
ISOLATED NERVE FIBERS
. This model identifies agents (e.g., potassium
salts) or procedures (e.g., use of lasers) that
may block nerve conduction.
Although these in vitro methods allow for
rapid screening of potential desensitizing
agents, they generally do not mimic natural
conditions or indicate how the agent will
behave when exposed to saliva and
masticatory forces.

CLINICAL TRIALS

The ultimate test of any treatment is how well it

works in the clinic.
A randomized, blinded and controlled trial is the gold
standard for determining efficacy.
In such a clinical trial, the product is compared with
the same formulation minus the active ingredient,
which can be called "minus active," "negative control"
or "placebo.
A product also can be tested "head-to-head" against
existing products to determine its effective
equivalency or superiority with its comparators

MANAGEMENT
Classifying treatments for DH can be
challenging because its modes of action often
are unknown.
It can be simpler to classify treatments
according to their mode of delivery.
Treatments can be self-administered by the
patient at home or be applied by a dental
professional in the dental office.

 At-home methods tend to be simple and

inexpensive and can treat simultaneously
generalized DH affecting many teeth.
In-office treatments are more complex and
generally target DH localized to one or a few
teeth.
These various treatment options can be
graded by their complexity

PREVENTION OF DENTIN
HYPERSENSITIVITY
Prevention of dentin hypersensitivity should include
identifying and eliminating predisposing etiologic
factors such as endogenous or exogenous acids and
toothbrush trauma.
The role erosive agents play in the development of
DH is well-established.
Exogenous dietary sources like fruits, fruit juices and
wine contain acids that can remove smear layers and
open dentinal tubules.

 Endogenous acids arising from gastric acid reflux or

regurgitation also can produce DH, which
characteristically affects palatal surfaces.
Toothbrushing with an abrasive toothpaste can
abrade the dentin surface and may open up dentinal
tubules if combined with erosive agents.
Patients should avoid toothbrushing for at least two to
three hours after consuming acidic foods or drinks to
reduce the deleterious co effects of acids and
abrasion.

 Most patients are unable to remember details of their food and

drink consumption.
They should be asked to keep a daily diet diary in which they
record their food and drink consumption over a period of
consecutive days spanning a week and weekend.
The diary may reveal changes in the patients diet that may
contribute to DH.
The diary also could present an opportunity for practitioners to
review their patients oral hygiene practices.

TREATMENT
A.
NERVE DESENSITIZATION

POTASSIUM NITRATE
B)ANTI INFLAMMATORY AGENT

CORTICO STEROIDS
C) COVER /PLUGGING DENTINAL TUBULES

I.
1.
a)
b)
c)
d)
e)
f)
g)
h)

PLUGGING/SCLEROSING DENTINAL TUBULES

IONS /SALTS
CALCIUM HYDROXIDE
FEROUS OXIDE
POTASSIUM OXALATE
SODIUM MONOFLUORO PHOSPHATE
SODIUM FLUORIDE
STANNOUS FLUORIDE
SODIUM FLUORIDE/STANNOUS FLUORIDE
COMBINATION
STRONTIUM CHLORIDE

2)PROTEIN PRECIPITANTS
a.
b.
c.
d.

FORMALDEHYDE
GLUTARALDEHYDE
SILVER NITRATE
IONOTOPHORESIS

II)DENTIN SCALERS
a)
b)
c)
d)
e)
f)

GLASS IONOMER CEMENT

COMPOSITES
RESINS
VARNISHES
SEALANTS
METHYL METHACRYLATE

III)PERIODONTAL SOFT TISSUE GRAFTING

IV)CROWN PLACEMENT/RESTORATIVE
MATERIAL
V)LASERS

NERVE DESENSITIZATION BY
DESENSITIZING AGENTS
Desensitizing agents do not produce immediate
relief &must be used for several days or even
weeks to produce results
Desensitizing agents can be applied by the patient
at home or by the dentist or hygienist in the dental
office
The most likely mechanism of action is the
reduction in the diameter of the dentinal tubules so
as to limit the displacement of fluid in them

Desensitizing toothpastes/dentifrices

Tooth-pastes are the most widely used dentifrices for

delivering over-the-counter desensitizing agents.
The first desensitizing toothpastes to appear on the
market claimed either to occlude dentinal tubules
(those that contained strontium salts and fluorides) or
destroy vital elements within the tubules (those that
contained formaldehyde).

 Now, most desensitizing toothpastes contain a

potassium salt such as potassium nitrate, potassium
chloride or potassium citrate,
Though one study reported that a remineralizing
toothpaste containing sodium fluoride and calcium
phosphates reduced DH.

Grossman in 1931 suggested that the ideal desensitizer

should be:
NOT UNDULY IRRITATING TO THE PULP
PAINLESS WHEN APPLIED
EASY TO APPLY
CONSISTENTLY EFFECTIVE
PERMANENTLY EFFECTIVE
QUICK ACTING
NOT CAUSING TOOTH DISCOLORATION

Potassium salts
Toothpastes containing potassium nitrate have been
used since 1980.
Since then, pastes containing potassium chloride or
potassium citrate have been made available.
Potassium ions are thought to diffuse along dentinal
tubules and decrease the excitability of intra dental
nerves by altering their membrane potential.
The efficacy of potassium nitrate to reduce DH,
however, is not supported strongly by the literature,
according to Poulsen and colleagues.

 Two studies support the desensitizing effectiveness

of pastes containing potassium citrate.
Many toothpastes contain other ingredients such as
fluorides (for example, sodium monofluorophosphate, sodium fluoride, stannous fluoride) and
antiplaque agents in conjunction with desensitizing
and abrasive agents.
Further studies are needed to determine that these
various ingredients do not interfere with each other.

Toothpaste application
Practitioners should educate patients on
how to use dentifrices and monitor their
toothbrushing techniques.
Dentifrices should be applied by
toothbrushing.

 There is no evidence to suggest that finger

application of the paste increases effectiveness.
Many patients habitually rinse their mouths with water
after toothbrushing.
Rinsing with water may cause the active agent to be
diluted and cleared from the mouth and, thus, reduce
the efficacy of the caries-reducing effect of fluoride
toothpastes.

Mouthwashes and chewing gums

Studies have found that mouthwashes containing
potassium nitrate and sodium fluoride, potassium
citrate or sodium fluori deor a mixture of fluorides can
reduce DH.
In only one of these studies, however, was the effect
of the active mouthwash significantly greater than that
of the control product.
Another study concluded that a chewing gum
containing potassium chloride significantly reduced
DH, but the study did not include a control group.

 DH severity should be reassessed two to four

weeks after commencement of treatment to
determine the effectiveness of the first level of
desensitizing treatment .
If at-home care fails to reduce DH compared
with baseline levels, the next level of
treatment, an in-office method should be
started.

 Desensitizing agents intended for athome use by patients generally are

simple to administer.
Dental professionals can deliver a wider
range of more complex and more potent
desensitizing treatment.

Sodium fluoride
Treatment of exposed root surfaces with fluoride
toothpaste and concentrated fluoride solutions has
been found to be very efficient in managing
dentinal hypersensitivity.
The improvement appears to be due to an increase
in the resistance of dentine to acid decalcification
as well as precipitated fluoride compounds
mechanically blocking exposed dentinal tubules or
fluoride within the tubules blocking transmission
of stimuli.

 As alternatives with more accessible cost and simpler

techniques of hypersensitivity treatment which aim at producing
an occlusive effect on the dentin tubules, blocking the
hydrodynamic flux,there are the application of fluoridated
varnish, restorative or adhesive systems, e.g
silver nitrate,
formalin,
zinc chloride,
calcium hydroxide,
strontiumchloride,
potassium oxalate (PEREIRA22, 1995),
propolis (MAHMOUD et al.17, 1999)
potassium nitrate (TOUYZ & STERN25, 1999).

POTASSIUM NITRATE
Potassium nitrate in bioadhesive gels at 5%
and 10% have been shown to be highly
effective in reducing hypersensitivity.
Potassium ions are the active component,
and potassium nitrate can reduce dentinal
sensory nerve activity due to the
depolarizing activity of the K+ ion.

STRONTIUM CHLORIDE
It has been effectively and widely used to
reduce hypersensitivity.
It has been suggested that strontium
deposits are produced by an exchange with
calcium in the dentin resulting in
recrystallisation in the form of a strontium
apatite complex.

Restorative resins&composite resins

The use of restorative material also have been
proposed to treat dentine hypersensitivity.
Treating hypersensitivity with resins was
pioneered by Brannstrom and his colleagues.
Second generation composite (Scotch bond) can
be laid down successfully over lesions treated with
fluoride iontophoresis.

 Application of cyanoacrylate has been done with good

desensitizing effect.
However, the complication of the first and second
generation composites was that the incidence of sensitivity
actually increased during use for aesthetic restoration.
The third and fourth generation bonding agents such as
Gluma, Scotchbond II, All Bond, and C&B metabond
allow better bonding to dentine, require less bulk for
strength, penetrate the tubules better.

 The use of materials like composite resins and

glass ionomer restorations can be used in
situations where there has been significant prior
loss of cervical tooth structure or as a last resort
for a tooth which does not respond to other less
invasive desensitizing protocols

 The use of restorative material to treat dentine

sensitivity is technique sensitive and expensive but
offer the hope of longer lasting and more
predictable results than topical agents.
The choice of technique between iontophoresis
and restorative material may depend on
availability of the materials and the office
personnel involved.

TOPICAL METHODS
Firstly, the topical methods included the topical
applications of caustics ,obtundants, fluorides,
varnishes, oxalates, and potassium nitrates.
The caustics chemical are silver nitrate, zinc
chloride, phenol, formaldehyde, concentrated
alcohol, strong acid and alkalis.
They are used in attempt to precipitate proteins;
however, they are harmful to the pulp and should
be avoided.

 Fluorides, on the other hand, have been proven to

be effective for several days to several weeks
(Hoyt and Bibby, 1943) when applied topically to
the area of dentinal exposure.
Its mechanism of action involved a formation of
barrier by precipitating the CaF2 at the tooth
interface.
However, this precipitate is slowly soluble in
saliva and thus the effect is temporary and needed
to be reapplied.

 The common commercial preparation of fluoride

is 4% stannous fluoride in glycerine vehicle;
however, the glycerine vehicle can activate the
hydrodynamic mechanism and cause pain upon
application.
Neutral sodium fluoride should be used when
patient had esthetic porcelain restoration or
implant in their mouth, since the acidity of
stannous fluoride may etch the restoration.

 Finally, 5-30% potassium nitrate, as

proposed by Markowitz and Kim, can act
directly on pulp nerves.
However, it would have to be applied
frequently and reach a sufficient
concentration at the site of neural
transduction

 Another topical method is the copal varnish but its action

only last several hours and thus is used as the vehicle for
fluoride.
Oxalates consisting of 3% KH2PO4 followed by 30%
K2HPO4.
Commercial product including potassium oxalate and
ferric oxalate are effective in bloking the tubules.
However, they have the same draw back as in the case of
topical fluoride: eventually the saliva dissolves the surface
precipitate that forms the barrier.

Sodium monofluorophosphate
Toothpastes containing this agent have been
shown to be effective in reducing hypersensitivity

Stannous fluoride
This agent either in aqueous solution or in glycerine has
been found effective.
The mode of action appears to be through the induction of
a high mineral content which creates a calcific barrier
blocking the tubular openings on the dentine surface.
Alternatively, it may precipitate on the dentine surface
leading to occlusion of the exposed dentinal tubules.

Oxalates
Since their initial development as a desensitizing
agent, the oxalates have gained rapid popularity.
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
apertures of the dentinal tubules.

Resins and adhesives

Sealing of dentinal tubules with resins and
adhesives have been advocated for managing this
condition with encouraging results however
problems arise when they break away resulting in
exposure of the tubules.
It is usually reserved for cases of specific and
localized areas of hypersensitivity rather than
generalized dentinal pain.

Combination agents
A combination of 5% potassium nitrate:fluoride
dentifrice has been found to be safe and effective
in providing patients relief from sensitivity and
protection against dental caries.

DENTAL IONTOPHORESIS is used most often in

conjunction with fluoride pastes or solutions and
reportedly reduces DH.
LASERS. The effectiveness of lasers for treating DH
varies from 5 to 100 percent, depending on the type
of laser and the treatment parameters.
Studies have reported that the neodymium:yttriumaluminum-garnet (YAG) laser, the erbium:YAG
laser and galium-aluminium-arsenide low level
laser all reduce DH.

Low level laser therapy for

dentin hypersensitivity
Dentine hypersensitivity is a disease that
affects both man and women, and it is an
overreaction for a stimulus that normally
would not cause pain in a healthy tooth.
The etiology is multifactorial, and the pain
appears specially when the cervical region
dentine is exposed to the oral environment.

 The laser therapy has been proposed

for the treatment of cervical
hypersensitivity because it is painless
for the patient.
The GaAlAs laser has been used for
the treatment of dentin hypersensitivity.

BIOSTIMULATION
It increases the production of mitochondrial
ATP, increasing the threshold of the free
nerve endings, providing an analgesic effect
due to the increase of b-endorphine in the
cephalorrhachidian liquid (BENEDICENT
1982).
The reduction of pain occurs because of the
inhibition of the cyclooxygenase enzyme,
which suspends the conversion of the
arachidonic acid into prostaglandin

 The laser also increases the formation of a

secondary dentin by the odontoblasts.
The GaAlAs laser is easy to apply and
presents good results as described in the
literature (MEZAWA et al. 1988; FURUOKA
et al., 1988, YAMAGUCHI et al.1990;
GROTH)

BDP 660 class IIIb Laser

MMOPTICS

 The laser therapy is a painless, safe, fast,

conservative treatment, and it is well
accepted by the patients (MARSLIO, 1999).\
However, the lasers,especially high-level
ones, are very expensive and the
professional has to be qualified to its use.
The low-level ones, on the other hand, are
more accessible to most professionals

Long-term studies are necessary to confirm the durability of the

therapeutic effect of the treatment with low-level lasers
compared to conventional forms of treatment, bearing in mind
that the search for the cause of the problem is extremely
important,
such as:

diet regularization

occlusal adjustment,

strength control and hygiene habits

 CO2 laser irradiation and stannous fluoride gel has

also been shown to be effective for inducing
tubule occlusion for upto 6 months after treatment.
The pulpal effect of laser requires more
investigation prior to its acceptance to be used
with the hard tissue.
Currently, hard tissue application using laser has
not been approved.

IONOTOPHORESIS
Iontophoresis is a technique using a small electric charge
to deliver a medicine or other chemical through the skin.
Basically an injection without the needle.
The technical description of this process is a non-invasive
method of propelling high concentrations of a charged
substance, normally medication or bioactive agents,
transdermally by repulsive electromotive force using a
small electrical charge applied to an iontophoretic chamber
containing a similarly charged active agent and its vehicle.

 To clarify, one or two chambers are filled with a

solution containing an active ingredient and its
solvent, termed the vehicle.
The positively charged chamber, termed the anode
will attract a negatively charged chemical, while
the negatively charged chamber, termed the
cathode, will attract a positively charged chemical
into the skin.

 Iontophoresis is well classified for use in

transdermal drug delivery. Unlike transdermal
patches, this method relies on active transportation
within an electric field.
In the presence of an electric field electro
migrationand electro osmosis are the dominant
forces in mass transport
These movements are measured in units of
chemical flux, commonly mol/cm2h

Fick's laws of diffusion

describe diffusion and can be used to solve for the diffusion

coefficient,
They were derived by Adolf Fickin the year 1855
Fick's first law relates the diffusive flux to the concentration field, by
postulating that the flux goes from regions of high concentration to
regions of low concentration, with a magnitude that is proportional
to the concentration gradient (spatial derivative). In one (spatial)
dimension,

 Fick's second law predicts how diffusion

causes the concentration field to change
with time

 Iontophoresis is the process of introducing ionic

drugs into the body surfaces for therapeutic
purpose.
Iontophoresis requires that a charged drug
(fluoride usually) be delivered at the electrode of
the opposite polarity, the condition or disease
under treatment be at or near surface, and a
modern sophisticated source of direct current, with
appropriate means of application be used

MECHANISM OF ACTION OF
IONOTOPHORESIS
The mechanism of action of iontophoresis have been
proposed as: a) rapid formation (7-28 days) of reparative
dentine following application of current,
b) the alteration of the sensory nerve condution by the
electrical currents, and c)fluoride ion, when introduced
into dentinal tubule via iontophoresis, can reduce dentine
permeability.
The third mechanism has been supported the most by
literatures. Iontophoretic fluoride desensitization occurred
by two mechanism: the intratubular microprecipitation of
CaF2 affecting dentine permeability and an effect of
fluoride on the neural transduction mechanism.

FLUORIDE IONOTOPHORESIS
Murthy et al. in 1973 reported the effectiveness of fluoride
iontophoresis.
They concluded that the desensitization occurred
immediately after iontophoresis in most patients, whereas
the placebo was ineffective.
The 1% fluoride iontophoresis provided a statistically more
effective treatment than placebo or topical applications.
Also the burnishing of 33% topical fluoride paste was only
modestly effective.

 Gangarosa recommended that fluoride

iontophoresis is permanent in its effect
when the dentist applies it correctly to
exposed dentine
however, highly sensitive teeth require two
or rarely three treatments about 1 week
apart before the effect can be considered
permanent .

 Iontophoretic fluoride desensitization occurred by

two mechanism:
the intratubular microprecipitation of CaF2
affecting dentine permeability
an effect of fluoride on the neural transduction
mechanism.

ELECTROSURGERY
Treatment of hypersensitivity by
electrosurgery has been advocated by
Oringer in 1975.
However, the postoperative complications
included irritation and pain due to pulpal
injury by excessive heat generation are the
major draw back.

REGENERATIVE PROCEDURES
Finally, the use of gingival graft on recession
defect has been documented successfully.
Regenerative procedures using resorbable
membrane, free gingival graft for root coverage,
connective tissue graft have provided successful
result in terms of both functional and esthetics.

 The major draw back is the selection criterias for each

procedures, the technique sensitive, and the cost of
treatment.
Nevertheless, when can be done, periodontal plastic
surgery is the best and ideal treatment in providing a long
lasting result and esthetically pleasing.
The clinical goal to treat hypersensitive dentin is to provide
a permanent seal of dentin tubules.
The seal can be established by any of the above methods
and if done correctly, will provide the therapeutic effects.

 Patient must recognized in some situation the

condition may recur and require several
application or re treatment.
Patient oral hygiene must be emphasized to reduce
the plaque accumulation in the area.
The dentist also required to evaluate Patient
systemic condition, nutritional diet, and be able to
communicate with the patient on issues regarding
his or her periodontal health and its correlation to
the dentinal hypersensitivity.

MISCELLANEOUS TREATMENTS
. A large number of reports support alternative approaches for
tooth desensitization.
Although these reports are not truly evidence-based, they may
apply to some clinical situations.
For example, periodontal surgery involving coronally positioned
flaps reportedly eliminates DH in extensively exposed root
dentin.
If the DH is associated with an ABFRACTION LESION,
OCCLUSAL ADJUSTMENT may be effective.

CONCLUSION
Professionals should appreciate the role
causative factors play in localizing and
initiating hypersensitive lesions.
It is important to identify these factors so that
prevention can be included in the treatment
plan.
Active management of DH usually will involve
a combination of at-home and in-office
therapies.

 Root dentin hypersensitivity frequently

develops as an uncomfortable& sometimes
difficult ailment to treat,subsequent to
scaling&root planing procedures in
periodontal therapy.(jan lindhe 4th edition)

REFERENCES
REFERENCES
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THANK
YOU

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