GOOD MORNING

DENTIN
HYPERSENSITIVITY

TABLE OF CONTENTS

Introduction
Definition
History
Prevalence and distribution
Etiology - Enamel loss
Cementum loss
Role of saliva in dentin hypersensitivity
Pulp-dentin complex
Pulp innervation

Theories of dentin hypersensitivity

Direct innervation theory
Odontoblast deformation theory
Hydrodynamic theory
Clinical features
Diagnosis
Case history
Clinical features
Methods of evaluating pain associated
with dentin hypersensitivity
Subjective evaluation
Objective evaluation

Differential diagnosis
Prevention
Management of dentin hypersensitivity
Home use products
In office products
Conclusion

INTRODUCTION

Term dentin hypersensitivity has been

used for many decades to describe a
common painful condition of the tooth.
These patients complain of sharp pain in
response to various stimuli like
heat,cold,chemicals etc.
Alternative terms such as cervical
dentinal sensitivity has been suggested
[Chabanski & Gilan 1997] ,but not
generally accepted.

Careful clinical examination may reveal no

obvious pathology.
Though many theories have been proposed
and several treatment options suggested ,
dentin hypersensitivity is still a vexing
clinical problem to diagnose and manage.

DEFINITION

Hypersensitive dentin is an uncommonly

sensitive or painful response of exposed
dentin to an irritation Grossman 1935.

It is one of the most painful, ubiquitous

and least satisfactory treated chronic
problems of teeth Doran Zinner 1977.

Dentin hypersensitivity is characterized

by short, sharp pain raising 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.
Dowell, 1985
Orchardson and Collins, 1987

This definition provides a clinical

description of the condition and identifies
hypersensitivity as a distinct clinical
entity.

History

Chinese 2000 years or more by the

application of xiao-Shi believed to be
niter or potassium nitrate.
The Egyptian Medical Papyrus
recommended a mixture of red and
yellow vitriol and alum for "teeth that
suffer"
In 1855 J.D.White .dentinal pain was
caused by movement of fluid in dentinal
tubules

Chemical caustics (Copper sulphate;

Mercury bichloride, silver nitrate, Zinc
chloride, antimony chloride, arsenous
acid) could be used to desensitize dentin.
Alfred Gysi in 1900 stated unequivocally
that dental canaliculi are devoid of
nervous substances .. the first to
suggest relieving hypersensitivity by
coagulating its protein content.

In the First half of the twentieth century

Herman Prinz 1913 noted that arsenic
was no longer used for reducing
hypersensitivity since it invariably
severely damages or destroys the dental
pulp. Best results are obtained by the
application of local anesthetics directly to
the exposed dentin in prepared cavities.

Louis J. Grossman in 1935 described

hypersensitiveness in dentin
In 1941. Lukomsky . Sodium fluoride
1956Pawlowska . strontium chloride
combined with the bi-colloids of teeth ...
favourable effect on hypersensitivity..
sensodyne tooth paste was formulated
with strontium chloride hexahydrate.

In 1962 Brannstrom . Hydrodynamic

theory

In 1966.. Therapies
deposit

an insoluble substance on the

ends of the fibers or nerves to act as a

barrier
To

stimulate secondary dentin

formation.

In 1974 Hodoshsuperior

Prevalence

The age range early teenage to 70

years
Peak incidence 3rd and 4th decades of
life
Gender differences females more than
males

DISTRIBUTION

Dentin hypersensitivity can occur

anywhere in the oral cavity and effect any
tooth,

Areas of higher predilection are:

Buccal cervical area of teeth is the site of

predilection for dentin hypersensitivity

Other areas of predilection include areas of gingival

recession and where enamel is thin.

Most commonly effected are the canines

and 1st premolars, then incisors and 2nd
premolars and least often molars.

Tooth sensitivity is more common on the

ETIOLOGY

Dentin hypersensitivity can occur by

dentin exposure which can be by 2
methods
Loss

of enamel due to tooth wear.

Conditions

leading to recession of
gingiva and subsequent loss of
cementum.

One of the iatrogenic cause of tooth

sensitivity is vital tooth bleaching.

Not all exposed dentin is sensitive. It

occurs only when dentin is exposed and
dentinal tubules are patent from the
surface till the pulp.

Enamel loss
Occlusal wear
Tooth brush abrasion
Dietary erosion
Abfraction
Para functional habits
Cemental loss
Gingival recession
Periodontal disease
Root planing
Periodontal surgery

Predisposing factors for

gingival recession

Aging is a physiologic etiologic agent

Anatomy of the alveolar bone

Tooth anatomy and tooth position

Excessive tooth brushing to maintain good

oral hygiene

Non surgical and surgical periodontal

procedures

Acute gingival infections and periodontal

diseases.

Role of saliva in dentin

hypersensitivity

It has multiple functions in preventing

demineralization and even promoting
remineralisation
Protein rich biofilm layer or salivary pellicle has
more protective effect on enamel than dentin.
Ability of bio film to neutralize acid attack ,as we
as to initiate and support the remineralisation of
the dentin surface, appears to be critical step in
determining whether a tubule remains patent
even in the face of dentin tissue loss.

It is the patency of tubules that helps

predicting whether the dentin will be
hypersensitive to external stimuli.

DEVELOPMENT

Lesion localization- requires exposure of

dentin

Lesion initiation- requires removal of the

cementum or smear layer.

PULP DENTIN COMPLEX

Dentin is formed by cells called odontoblasts.

Odontoblasts are part of both dentin and pulp
tissue ,because their cell bodies are in pulp
but their long, slender cytoplasmic processes
extend well into tubules.
Unmineralized zone of dentin is called
predentin is always on the pulpal surface and
next to the cell bodies of odontoblasts.
Dentin formation begins at areas subadjacent
to the cusp tip or incisal ridge and gradually
spreads to the apex of root.

Dentinal tubules are small canals that

extend across the entire width of dentin,
from the DEJ to the pulp .
Each tubule contains cell process of an
odontoblast.

Pulp innervation

Dental pulp is richly innervated

Myelinated A delta fibres -20%
Non-myelinated C fibres -80%
B fibres Preganglionic autonomic function
A delta and C fibres subodontoblastic
plexus
A delta fibres are distributed in the
odontoblastic and subodontoblastic zones
and are associated with dentinal pain
Excitation of C fibres associated with pulp
tissue injury.

THEORIES

Direct innervation theory

Odontoblast deformation theory
Hydrodynamic theory

Direct innervation theory

This was one of first theory put forth to

explain hypersensitivity
According to this theory,nerve fibres present
with in dentinal tubules initiate impulses
when they are injured and this causes
hypersensitivity.
However ,histologic studies have shown that
nerve fibres are present only in the
predentin and inner dentinal zone but dont
extend all the way upto the DEJ which is
most sensitive area of the dentin.

Another drawback when pain inducing

substances like potassium chloride,
acetylcholine and histamine are applied
to exposed dentin, they fail to elicit a
painful response.

ODONTOBLAST DEFORMATION
THEORY

This theory suggested the odontoblasts

or their processes are damaged when
external stimuli are applied to exposed
dentin.
As a result of this study conduct impulses
to the nerves in the predentin and
underlying pulp from where they proceed
to the central nervous system.

Drawbacks
Research has shown that the odontoblast
processes extend only partly through the
dentin and not up to the DEJ.
Also invitro studies have shown that
odontoblast membrane potential is too
low to permit transduction.

HYDRODYNAMIC THEORY

Given by Brannstorm in 1964

Most accepted mechanism to explain
dentinal hypersensitivity.
Structurally dentin has over 300,000
dentinal tubules /mm ,these are filled
with dentinal fluid.
In a vital tooth, there is a constant ,slow
outward movement of this fluid through
the dentinal tubules.

The hydrodynamic theory states that

whenever exposed dentin is stimulated
by tactile,chemical,thermal or osmotic
stimuli, there is rapid movement of
dentinal tubule either towards the pulp or
outward.
This can cause direct stimulation of low
threshold A delta nerve fibres in the pulp.

This rapid displacement of dentinal fluid

in thousands of dentinal tubules at the
same time produces a cumulative layer
and this hypersensitivity.
Studies have shown that stimuli like
cold,sweets,airblasts etc can cause a
rapid outflow of dentinal fluid causing
pain.

DENTIN CONSIDERATIONS

There are two mechanisms responsible

for the permeation of substances across
dentin:

diffusion and
convection

Diffusion is the process by which

substances are transported from an area
of high concentration to an area of low
concentration.
there is no bulk fluid movement but
only molecular translocation.
driving force is a concentration gradient
or chemical potential energy

Convective transport or filtration - bulk

fluid movement occurs from an area of
high hydrostatic pressure to an area of
low hydrostatic pressure

According to the hydrodynamic theory of

dentin sensitivity, it is fluid movement that is
responsible for transducing a variety of
physical stimuli into electrical nerve activity.

This type of fluid movement can be

quantitated by measuring the hydraulic
conductance of dentin which is the reciprocal
of resistance.

Dentin with a high conductance has a low

resistance .

For hydrodynamic theory to be accepted

as valid, teeth presenting with
hypersensitivity must have dentinal
tubules which are open at the dentin
surface and patent till the pulp.

CLINICAL FEATURES

Patient usually experiences a short,sharp

pain in response to heat, cold, tactile
stimuli.
Its considered to be exaggerated
response of normal dentin complex and is
felt only on application of external
stimuli.
There is no lingering discomfort once the
stimulus is removed.

Diagnosis

This requires a careful history and clinical

examination
CASE HISTORY :
History or nature of pain.
No. and location of sensitive teeth
Intensity of the pain
The stimuli which initiates the sensitivity.
Frequency and duration of sensitivity
History of recent restorative or periodontal
treatment.

Clinical examination
Includes the following tests and
observations
Evidence of dentin exposure
Sensitivity or pain on tactile examination
Percussion sensitivity
Pain lingering after the stimulus is
removed.
Vitality tests to rule out pulpal
involvement
Signs of fractured or poor restorative

METHODS OF EVALUATING PAIN

Subjective evaluation
Verbal

rating scales

Visual

analogue scales

Verbal

descriptor checklists

McGill

word descriptors

Objective assessment
Mechanical

stimuli

Chemical

(Osmotic) stimulation

Electrical

stimulation

Dehydrating
Thermal

(evaporative) stimuli

stimulation

Hydrostatic

pressure

Subject Assessment
1.

Verbal rating scale is a simple descriptive

pain scale which includes the following
(Gillam and

Newman 1993)

0 No discomfort

1 Mild discomfort

2 Marked discomfort

3 Marked discomfort that lasted for

more than 10 seconds.

2 Visual analogue scale is a line 10 cm in length,

the extremes of the line representing the limits
of pain, a patient might experience from an
external stimulus.
3. McGill pain questionnaire the patient is
shown 20 sets of words and asked to select a
word from each set which best describes the
present pain experience.

Stimuli used to access dentin

hypersensitivity

Mechanical {tactile} stimuli

Explorer probe
Constant pressure probe (Yeaple)
Mechanical pressure stimulators
Chemical {osmotic} stimuli
Hypertonic solutions, e.g. sodium
chloride, glucose, sucrose and calcium
chloride

Evaporative stimuli
Cold air blast
Yeh air thermal system
Air jet stimulator

Thermal stimuli
Electronic threshold measurement device
Cold water testing
Heat
Thermo-electric devices (e.g. Biomat
Thermal Probe)
Ethyl chloride
Ice-stick

Electrical stimulation
Electrical pulp testers
Dental pulp stethoscope

Application of stimuli

Whatever methods are used they should

be quantifiable and reproducible.

Should be designed to elicit dental pain in

preference to pulpal pain.

When more than one stimulus is used

the order of application of the stimulus is
important.

The least disturbing stimulus should be

used first, with the most disturbing

Testing should begin with subject

assessment and then followed by tactile,
heat and cold stimuli.
Control of extraneous factors that
could potentially influence subject
response is important.
Standardized instructions and stimulus
demonstration should be given.

DIFFERENTIAL DIAGNOSIS

Its difficult when there are other conditions

causing reversible pulpitis present in
combination with exposed dentin.It has to
be differentiated from :
Fractured restoration
Fractured enamel exposing dentin
Dental caries
Post restoration sensitivity
Cracked tooth syndrome
Bleaching sensitivity

PREVENTION

Tooth brushing with an abrasive

toothpaste can abrade the dentin surface
and may open up dentinal tubules
.Patient should avoid brushing for at least
2 to 3 hrs after consuming food of drinks.
Patient may be asked to maintain diary of
their food and drink consumption.

For patients who are suffering from

dentinal hypersensitivity,dentist can
provide valuable device to prevent or
reduce the clinical symptoms this
includes :
Diet counselling
Correction of brushing techniques
Care during operative procedures and
while restoring teeth to avoid iatrogenic
damage
Care during periodontal procedures.

MANAGEMENT

Two basic mechanisms by which dentin

hypersensitivity can be managed :
Desensitization by occluding the dentinal
tubules
Desensitization by blocking the pulpal
sensory nerves.

Selection of desensitizing agents

Criteria . Grossman (1935)

Provide immediate relief of pain

Easy to apply

Well tolerated by patients

Not injurious to the pulp

Will not discolor the tooth

Relatively inexpensive.

Instructions to the
patients

Occurs as a result of exposure of dentin

Disappears over a few weeks

Plaque control is important

Desensitizing agents do not produce

immediate relief

Pain ladder showing increasing

pain and complexity of treatment

Potential treatment modalities

Home use products

In office products

Homeuse products

The products include agents such as potassium

salts, strontium salts and fluoride salts in
toothpaste, mouthwash and gel formulations.

These reduce the symptoms by

Occluding dentine tubules and/or
Intercepting the neural response by chemical
intervention

Advantages
Readily and widely available
Cost effective
Simple to use
Non invasive

Potassium nitrate

Potassium ions from potassium nitrate

tooth paste can easily pass through the
dentin into the pulp .Here they depolarize
the sensory nerve endings present closed
to the odontoblasts thus preventing the
impulses to the brain.
It requires two application a day for a
minimum of two weeks.

Recently novel method of applying

potassium nitrate has been suggested to
reduce hypersensitivity.
This consists of using the potassium
nitrate paste in a mouth guard type soft
tray.

Mouthwashes and chewing

gums

Studies have found that mouthwashes

containing potassium nitrate and sodium
fluoride,potassium citrate or sodium
fluoride or mixture of fluoride can reduce
sensitivity.
Another study by Krahwinkel 2001
,concluded that chewing gum containing
potassium chloride significantly reduce
sensitivity.

INOFFICE DESENSITIZING
AGENTS

In-office treatment of dentine hypersensitivity should

be performed in all cases of severe hypersensitivity

The treatment options are often dictated by the

clinical condition.

All in-office treatments are designed to decrease the

hydraulic conductance of dentin by partial or
complete tubule occlusion

The most difficult sites to treat are those where there

is no loss of tooth structure

It is crucial that the exact region of

hypersensitivity be identified.

Air blasts are useful as a screening tool, they

cannot identify the exact site

Surfaces should be gently evaluated with a

dental explorer

All treatments should be done on

unanesthetized patients

The clinical use of these agents will

depend on
the

degree of sensitivity,

the

number of teeth involved,

the

amount of tooth structure lost and

the

amount of treatment time that

would be required

RECOMMENDED TREAMENT
APPROACHES

Isolated cases/ few teeth are affected :

Try application of varnishes,dentin
adhesives
Generalized hypersensitivity Prescribe
desensitizing toothpastes and
mouthwashes.
Severe hypersensitivity consider
endodontic therapy

INOFFICE TREAMENTS

Cavity varnishes
Anti-inflammatory agents
Treatments that partially obturate dentinal
tubules

Burnishing of dentin
Silver nitrate
Zinc chloride-potassium
ferrocyanide
Calcium compounds
Calcium hydroxide
Dibasic calcium phosphate
Fluoride compounds
Sodium fluoride
Sodium silicofluoride
Stannous fluoride

Primers containing HEMA

5% glutaraldehyde, 35% HEMA in water
35% HEMA in water

Strontium chloride
Potassium oxalate
Iontophoresis
Lasers

Restorative methods
Conventional glass ionomer cements
Resin-reinforced glass ionomers / compomers
Adhesive resin bonding systems

CAVITY VARNISHES

Act by forming a barrier over the exposed

dentin.
Cavity varnishes containing copal rosin
etc provide only a temporary relief as
they can readily dissolve in the oral
environment.
Fluoride varnishes like duraphat provide a
more sustained relief.

Corticosteroids

Use of corticosteroids is based on the

assumption that hypersensitivity is linked
to pulpal inflammation
Corticosteroids caused complete
obliteration of tubules, thus decreasing
dentin permeability.
Mosteller (1962) used liner consisting of
1 % prednisolone in combination with
25 % para-chlorophenol,
25 % M-cresyl acetate,
50 % gum camphor.

BURNISHING OF DENTIN

Its achieved by isolating the affected

tooth and burnishing the dentin dry for
few minutes with an orangewood stick.
Results in the formation of a smear layer
that partially occludes the dentinal
tubules
Burnishing created a partial smear layer
that reduced fluid movement across
dentin by 50 to 80 per cent .

Formation of insoluble
precipitants to block tubules

Certain soluble salts react with ions in

tooth structure to form crystals on the
surface of the dentin.
AgN03 is a time honored desensitizing
agent.
It has ability to precipitate protein
constituents of odontoblast processes
thereby partially blocking the tubules.

Other protein precipitants such as zinc chloride

and phenol can also be used

Zinc chloride-potassium ferrocyanide

impregnation method
40

% solution of aqueous zinc chloride for 1

minute, followed by a 20 % aqueous solution of

potassium ferrocyanide rubbed on dentin surface.
Scanning

electron micrographs of this precipitate

have revealed a highly crystalline deposit

covering the dentin surface.

CALCIUM COMPOUNDS

It can be mixed with water to form a thick

paste .
This is then applied on the exposed
dentin for few minutes.
It increases the remineralization of the
exposed dentin thus reducing dentin
permeability.

Calcium phosphate pastes

Paste of amorphous calcium phosphate is

applied over exposed dentin.
This method reduces hypersensitivity by
blocking the tubules and that dentin
permeability is by 85%.
Commercially available product
introduced are GC tooth mousse
containing ACT and CPP is recommended
for dentin hypersensitivity.

FLUORIDE COMPOUNDS

Agents such as sodium fluoride, stannous

fluoride or acidulated phosphate fluoride
used for few minutes as mouthrinses
,toothpaste or as topical application over
exposed dentin.
They act by forming fluorapatite within
tubules

STRONTIUM CHLORIDE

Its incorporated in desensitizing

toothpastes
Strontium strongly binds to calcified
tissues.
Strontium deposits are produced by an
exchange with calcium in dentin resulting
in recrystallization in form of strontium
apatite complex.
Topical application of 10% strontium
chloride prior to application of 2% NaF
was more effective in decreasing

OXALATES

Application of potassium oxalate solution

over exposed dentin also reduces dentin
hypersensitivity.
Oxalate ions react with calcium ions in
the dentinal fluid to form insoluble
calcium oxalate crystals.
They are relatively inexpensive, easy to
apply, and well tolerated by patients.

IONTOPHORESIS

Term applied to the use of an electrical

potential to transfer ions into the body for
therapeutic purpose.
Objective is to drive the topically applied
therapeutic agents more deeply into the
dentinal tubules.
Fluoride iontophoresis transfer fluoride
ions into the dentin.

Ionotophoresis unit consists of an adapted

plastic tip placed around the tooth.
This serves as a negative electrode while
the positive electrode is placed on the
patients face.
2% solution of sodium fluoride is applied
on the exposed dentin and this transferred
deep into dentin on activation of unit.
It provides a long term relief from
hypersensitive dentin.
This method is expensive as it needs
special equipment and often requires
more than one application.

LASERS

Laser like CO2 lasers,Nd: YAG lasers ,Er:YAG

lasers have been employed to treat
hypersensitive dentin.
Mechanism of action is by :
Coagulation and precipitation of plasma
proteins in dentinal fluid.
The thermal energy can alter intradental
nerve activity.

RESTORATIVE MATERIALS

Glass ionomer and composite

restorations may be placed to replace the
lost tooth structure.
Adhesive resin primers use of adhesive
primers to occlude the open tubules is
popular.

ADHESIVE RESIN BONDING

AGENTS

Resin desensitization is due to the

formation of resin tags in the tubules
These materials are somewhat technique
sensitive and should be used carefully
The latest generation of adhesive
bonding systems are hydrophilic and
provide better bonds in wet environments
The disadvantage of the adhesive
systems is that their polymerization is
inhibited by atmospheric oxygen to a
depth of 10-15m

A single application of cyanoacrylate to

hypersensitive root surfaces, and found a
significant immediate reduction in
sensitivity

Recent progress

New proposal presented by Gandolfi et al

in 2008
Application of calcium silicate paste
derived from portland cement ,shown to
be effective in tubular occlusion and
reduction of dentin permeability.
Indicated for treatment of dentin
hypersensitivity.
(J Of Oral Science ,Vol 51 ,Issue 3, 2009)

CONCLUSION

BIBLIOGRAPHY

DCNA ,tooth hypersensitivity in the spectrum of

pain ,Vol 34.No 3 ,July 1990, 429-436,448-469
Tooth wear and sensitivity clinical advances in
restorative dentistry,1st edition ,Martin
dunitz,2000 ,239-244
Clinical operative dentistry -Ramya raghu and
Raghu Srinivasan
Sturdevant art and science of operative
dentistry ,4th edition ,2002
Clinical periodontolology and implant dentistry
,5th edition, Jan Lindhe

JADA, 2006,Vol 137,990-998 : managing

dentin hypersensitivity
J Of Oral Science ,Vol 51,Issue 3, 2009