DENTINAL

HYPERSENSITIVITY
 Contents
• Introduction
• Definitions
• History
• Etiology
• Mechanism of dentin sensitivity
• Theories
• Clinical considerations
• Methods of measuring hypersensitivity
• Management of hypersensitivity
• Summary & conclusion
Introduction
 Definitions

Dentin hypersensitivity can be described as an adverse reaction or

pain in one or more teeth resulting from either a thermal
mechanism, or chemical stimulus – Clark 1985

It is one of the most painful, ubiquitous and least satisfactory

treated chronic problems of teeth – Doran Zinner 1977

Hypersensitive dentin is an uncommonly sensitive or painful

response of exposed dentin to an irritation –Grossman 1935
 Definitions

Dentinal hypersensitivity is described clinically as an exaggerated

response to non noxious stimuli.
It is characterized by pain of short duration arising from exposed
dentin in response to stimuli, typically thermal, evaporative, tactile,
osmotic and chemical and which cannot be ascribed to any other
dental defect or pathology
 History

Tooth canals in dentin

• Leeuwenhoek, 1678

Dentinal pain caused by movement of fluid in dentinal tubules

• JD White,1855
Dental canaliculi are devoid of nervous substances,but at inner border
of dentine around odontoblast there is an “abundant network of finest
nerve fibers”
• Alfred Gysi,1900
 History

Described hypersensitivities in dentin as uncommon sensitivity or

painful response of the exposed dentin to an irritation
• Louis I Grossman,1935

Pain was not continous but was felt only as long as the irritant was
present
• MC Ghee,1936

Advocated sodium fluoride as a desensitizing agent

• Lukomsky 1941
 History

Hydrodynamic theory of dentinal pain

• Bransstrom,1962

Summarised different aprroaches to treat hypersensitivity

• Kleinberg,1986
 Incidence

• Incidence: 15% (4% to

57%)
• Age range: 15 – 70+ years
• Peak incidence: 20 – 40
years
• Gender: Female > Males
 Intraoral distribution
• Canines and
Teeth affected premolars
• Incisors and
molars

• Buccal cervical
area
Site of • Gingival
predilection recession
• Thinnest enamel
Canine

Canine Premolar
•Left sided tooth
Side affected sensitivity> right
sided tooth In: Pashley DH, Tay FR, Haywood VB, et al. Dentin
sensitivity Hypersensitivity: Consensus-Based Recommendations
for the Diagnosis and Management of Dentin
Hypersensitivity.
 Frequency of Dentate Adults who
Responded Positively to Having or Ever Having
In a multi-national survey Sensitive Teeth
conducted with 11,000 adults
in 2002, 48% of participants
said at some point they had
consulted a dentist due to
sensitive teeth.

11
• Association of noncarious cervical lesions (NCCL) and abfraction
with DH/RDS: the prevalence of NCCL may range from 5% to 85%
(Aw et al)
Reduced DH in old

Reparative processes

Secondary dentin formation

Decrease permeability

Reduced hydraulic conductance

 Mechanism of dentin sensitivity
Enamel

Dental Pulp
Oral Anatomy: Dentin

Dental Tissues

Cementum
 Mechanism of dentin sensitivity

• Presence of tubules renders

dentin permeable to fluid
Dentin
movement
Pulp
• Number of tubules per unit
area varies
• Dentinal tubules are
conical

Tubule

Fluid Nerve Fibers

Odontoblast
Cell
 Mechanism of dentin sensitivity

Superior cervical
Trigeminal nerve ganglion(sympathetic branch)

Pulpal nerve

Myelinated Non myelinated

Aδ (99%) Aβ(1%) C Sympathetic

1 to 6µm 6 to 12µm 0.4 to1.2µm fibers

Fast pain Slow pain

 Mechanism of dentin sensitivity
• A-delta and C-fibers -sub odontoblastic plexus-nerve fibers extend to
the odontoblastic layer, Predentin, denti-free nerve endings

A fibers C fibers
Brief, sharp,
Dull poorly
well localized
localized
pain

Dentinal
Pulpal pain
hypersensitivity

• The sensitivity of nerve units depends upon the condition of dentin

surface
Theories of dentinal hypersensitivity

Direct neural
stimulation

Odontoblastic Hydrodynamic Modulation

transducer
theory theory
mechanism

Gate-control
theory and
vibration
 Direct Neural Stimulation
Neural Theory Theory

An applied stimulus can directly influence the

nerve terminals within the dentinal tubules
through direct communication with nerve fibers
from the dental pulp

Nerve endings Parent primary

Stimuli within dentinal afferent nerve Brain
tubule fibers
 Drawbacks of Direct neural stimulation theory
• Anderson’s explanation

Histological studies failed to identify such pathways

Brances of pulpal nerves did not extend more than 100 µm

into peripheral dentin.

No nerve elements-pain evoked due to stimulation by non

neural means
 Modulation theory
Injury of
Irritating stimulus Dentin
odontoblasts

Increasing Neurotransmitters
Nerve fibres
neuronal cAMP and vasoactive
action potential
levels amines.

Pain
 Odontoblastic Transduction theory
Rapp et al 1960’s Odontoblasts-
receptor cells

Stimulation of odontoblast
processes in peripheral dentin

Changes in membrane potential of

odontoblasts

Via synaptic junctions with nerves

Pain
 Drawbacks of Odontoblastic
Transduction theory
Odontoblast Electron microscopy
processes may not failed to
extend peripherally demonstrate any
beyond one third to synaptic complexes
one half of the between pulpal
length of dentinal nerves and
tubules odontoblasts.

Fails to explain why

dentin continues to No evidence of a
be sensitive, despite neurotransmitter
destruction of like acetylcholine
odontoblast layer
 Gate control theory and vibration

• According to this, on application of a stimulus, all the nerves

in pulp become activated.

Larger myelinated fibres

Smaller C fibres
• Get accomodated
•Remain open
•‘ Pain gates’ - closed
•Become enhanced

• opened by anxiety
Pain gates • closed by distracting
stimuli like audio analgesia
 Drawbacks

The theory does not explain perception and transmission of the

responses by the free nerve endings

Pain responses from the dentin are transmitted and perceived by

the nerve endings of the pulp-only, how they may be centrally
interpreted.
 Hydrodynamic theory

•Actual
Fluid movement
within the dentinal
hydrodynamic
•Fish
tubules-1927
theory isput
the basis
forth by
•Dentinal fluid as
for the transmission
Brannstrom &
the “dental lymph”
of sensations
Astrom
accordingin to1960s
the
hydrodynamic theory.
 Hydrodynamic Theory
Physiology
Enamel

Two processes required:

• dentin must be exposed
• dentin tubules must be open
to:
Tubules
– dentin surface
– patent to the pulp

Exposed
Dentin

Receding
Gingiva

Odontoblast
Trigger stimuli include:
• Thermal
– Hot
– Cold
• Tactile
• Evaporative
• Osmotic
 The true physiologic Odontoblast
stimulus is the inward or Cell

outward fluid shifts, not the

actual trigger.

Fluid-filled Dentin Nerve

Tubules Fibers
 Variables affecting hypersensitivity :
For hypersensitivity to occur, permeation of substances into the
dentin is essential.
2 mechanisms –
Diffusion Convection
. High hydrostatic pressure

Low hydrostatic pressure

This fluid movement can be measured by measuring the hydraulic
conductance of dentin.
( given by Poiseuille Hagen Equation )
 Poiseuille Hagen Equation

ᴫPr4 N
Q=
8ηL

Q Flow rate
P Pressure
( hydrostatic or osmotic )
r Radius of tubule
( ± smear layer )
η Viscosity of fluid
( temperature dependant )
L Remaining dentin thickness
N Tubule density ( depth dependant)
Sensitive teeth Non-sensitive
Tubules are greater in number
(eight times) Fewer in number

Larger in diameter (two times) Smaller in diameter

Open Blocked

Rate of fluid flow α (radius of tubule)4

 Hyperosmotic
Dehydration Heat Cold solutions

Sensory nerves
 PREDISPOSING FACTORS AND
ETIOLOGY
• For dentin hypersensitivity to occur, dentin must become exposed
( “lesion localization”)

and

dentin tubules must be opened and patent to the pulp )

(“lesion initiation”)

• These two processes are multi-factorial

 Lesion localization

• Lesion localization occurs by exposure of dentin, either by loss

of enamel or by gingival recession.

• Gingival recession is the more important of these two factors

 Exposed dentin
The result of gingival
recession
(exposure of root surfaces)
Tooth
The result of loss of enamel Wear
from tooth wear or trauma

Loss of cementum

Removal or absence of a
smear layer
Receding
Gingiva
 Gingival Recession is caused by:

• Physiologic factors
• Chronic trauma
– Oral hygiene (toothbrushing) – Hormonal fluctuations
– Habits (tobacco smoking & – Poor nutrition
chewing) – Aging

• Predisposing anatomic factors • Periodontal diseases

– Thin gingiva – Gingivitis
– Prominent roots – Periodontitis
– Dehiscences
– Fenestrations • Periodontal therapy
– Frenum pulls – Scaling and root planning
– Surgery
– Roots moved outside alveolar
housing by orthodontics
• Restoration margins
Tooth Wear can occur as a result of:

• Physical Loss
– Abrasion—mechanical
– Attrition—tooth/tooth
– Abfraction—lesions

• Chemical dissolution
– Erosion
-Extrinsic acids
-Intrinsic acids

• Multifactorial etiology
– Erosion, abrasion, attrition, abfraction
 Lesion initiation

• Not all exposed dentin is Dentin

sensitive

Characteristics of Sensitive
Dentin:

• Open/patent tubules
• Greater number of
tubules
• Tubules larger in
diameter Tooth
• Absence of smear layer Wear

• Tubules open from

tooth wear Receding
Gingiva
• Erosion—acts alone, or in
combination with abrasion to
cause enamel loss

• Extrinsic/intrinsic acids cause

surface softening of enamel
which takes hours to re-harden
and results in greater
susceptibility to physical insult

3. Strassler HE, Drisko CL, Alexander DC.

 Clinical Manifestations

•Chronic condition
•Usually more with to
sensitive acute
coldepisodes of
than warm
exacerbation ( stimulus )
•Patient tends to avoid the stimulus
•Sharp pain of short duration.
•No tenderness on percussion
•Lasts as long as the stimulus is present.
•Radiographically, no periapical changes seen
•Characterised by good localisation
 Occurrence of pain:
• Cold beverages

• Eating cold food

• Breathing cold air

• Toothbrushing

• Improper dental floss use

• Eating sour/acid food

• Eating sweet/sugary liquids

and foods

• Bleaching/whitening procedures
Management of dentinal
hypersensitivity
 Management begins with patient education and
modification of risk factors

Differential diagnosis

Exclude or treat other causes

of dentin pain

Identify etiological factors

Prevent, remove or modify

etiological factors

Management/treatment
Dentin Hypersensitivity is a diagnosis of exclusion

Complete History Clinical Examination Radiographic

• Sign and symptoms • Visual assessment examination
• Intensity • Physical assessment • Rule out
• Frequency and – Dental explorer periapical lesions
duration (probe): tactile
• Dietary changes stimulus
• Other related events • Periodontal probe
– Depth of periodontal
pocket
• Percussion testing
• Response to cold air
 Needs to rule out:

Differential Diagnosis
• Cracked tooth syndrome
• Fractured restoration
• Chipped teeth
• Dental caries
• Periodontal disease
• Post-restorative sensitivity
• Marginal leakage
• Pulpitis
• Palatogingival groove
• Bleaching sensitivity
Methods of measuring dental hypersensitivity

• No ideal method.
– Tactile sensitivity method
– Thermal Sensitivity
– Electrical Sensitivity
– Osmotic Sensitivity
– Chemical Sensitivity
 Methods of measuring dental
hypersensitivity
• Subject Assessment
1. Verbal rating scale

0 • No discomfort

1 • Mild discomfort

• Marked discomfort
2
• Marked discomfort that
3 lasted for more than 10
seconds.
Visual analogue scale
3. McGill pain questionnaire
 Application of stimuli
• Whatever methods are used they should be

•Quantifiable
• reproducible
• Elicit dental pain
• Not pulpal pain
• Order of application of stimulus is important
• Least disturbing stimulus -first
• Most disturbing stimulus - last
 Mechanical or tactile stimuli

• Pass a sharp dental explorer- grade the response …..scale 0 –

3
– Collins used a no 23 explorer
– Simple yet effective
– 5 – 10 gm of force-Tip of the explorer -500/nm2-
compression and deformation of dentin
Smith and ash device
Yeaple probe
Scratchometer-Dr Kleinberg
Tine of #23 dental explorer

Arm

Modified strain-gauge

Instrument needle

Indicator needle
 Drawbacks of tactile method

• Testing and measuring tactile sensitivity levels depends

on the patience and expertise of the investigator.

• The force should be applied gradually .

• Only specific spots in a given cervical exposed dentine area

will be tactily sensitive
 Thermal stimuli
can be checked using either cold or warm stimuli.

These act as stimuli due to the differences in thermal conductivity and

co efficient of expansion of dentinal fluid and the tubule.

mismatch of volumetric changes

negative intrapulpal and intradental pressures

displacement of mechanoreceptors pain

 Thermal Sensitivity

• Directing a burst of warm temperature air from a dental syringe

onto the test tooth

• One second blast from the air syringe - temperature is b/n 650 and
700F and at a pressure of 60 psi

0 - No discomfort
1 - Mild discomfort, but no severe pain
2 - Severe pain when stimulus is applied
3 - Severe pain occurs and persists even after removal of
stimulus
 Measurement

a) Application of cold air blast from dental syringe for 1 sec

( 70 0 F ).The air is directed at right angles to surface specially near
CEJ

b) Temperature controlled stream of air used . Initial temperature of

1000F used which is reduced till pain felt or to 700F

c) Cold water testing – after isolating the tooth with a rubber dam,
the tooth is subjected to water of temperatures 20, 10 and 00C for
3 sec.
 Cold

Hot
 Thermal Sensitivity

• An air thermal device - dr. K.C. Yeh-yeh DEVICE

• Temperature controlled stream of air as the stimulus.
• Air was heated to 1000F close to temperature of the mouth.
• Temp reduced until the subject felt pain or discomfort.
• Disposible plastic tip
• Air emitted at 10 psi -1000 and 700F within about 2 minutes.
 Thermoelectric device
• Devices…. Electrical cooling or heating of direct contact metal probes.
 Electrical stimuli
Non physiologic way of stimulus
It directly stimulates the pulpal nerves
Thus of little value to evaluate dentin sensitivity

However, theoretically thought that electrical stimuli can induce

hydrodynamic fluid movements by a phenomenon called electro
osmosis.

It is a process of bulk movement of an electrolyte solution

through a porous substance when an electrical potential is applied.
•It is measured by application of electric current via pulp testers.

•It has been observed that, in case of hypersensitivity, these show a

lower threshold for both pre pain and pain sensation.
 Advantages of using electrical stimuli

1. The patients sensation of warmth or tingling is taken as

threshold, which is described as prepain or non pain sensation
2. It can be precisely defined by electronic method.
Stark Instrument for electrical
stimulation
 Osmotic sensitivity
• Popularised by Anderson
• Based on process of osmosis
i.e. if the dentinal tubules are surrounded by a hypertonic solution,
the fluid within the tubules tend to move outwards - thus
affecting the mechanoreceptors
 Measurement

a) Mc Fall & Hamrick used this method to measure response to

sweet stimulus.

• After isolation of teeth with cotton, saturated sucrose

solution -applied onto the sensitive area for about 10 sec.

• The subject then rated into 0 or 1 based on absence or presence

of pain.
 b) Saturated solution of CaCl2

•Used for checking integrity of margins of crown or

restorations.

•Solution applied on suspected margin for 5 – 30 sec.

•Lack of pain -margins are tight.

 Chemical sensitivity

• Used in clinical hypersensitivity studies

• Stimulus is not conducive to threshold measurement because

repeated applications of the chemical stimulus reduce the

sensitivity of the exposed dentin.

 Chemical sensitivity

Drawbacks

1. Inconvenience

2. Difficulty in administering and controlling the

stimulus

3. Injury to the adjacent soft tissue.

Classification of desensitizing agents

Mode of
administration

At home
In-office
desensitizing
treatment
agents
 On the basis of mechanism of action

Nerve desensitization Plugging dentinal

Potassium nitrate tubules
Burnishing of dentin
Calcium hydroxide
fluoride
Iontophoresis
Protein precipitation Strontium chloride
Gluteraldehyde Potassium oxalate
Silver nitrate Bioactive glasses
Zinc chloride
Strontium chloride
hexahydrate
 a
Dentine adhesive sealers Lasers
•Fluoride varnishes Nd-YAG laser
•Oxalic acid and resin
GaAlAs laser
•Glass ionomer cements
•Composites Erbium-YAG laser
•Dentin bonding agents

Homeopathic
medication
Propolis
 Selecting desensitizing procedures
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
Mechanisms of actions of
desensitizing agents

Blocking fluid movement by

occluding dentinal tubules.

Coagulating or precipitating
tubular fluids

Stimulating secondary
dentin formation

Blocking pulpal nerve

 Methods of tubule occlusion

1. Formation of calcium over sensitive tubules

2. Formation of intra tubular crystals from salivary
mineral
3. Formation of intra tubular crystals from dentinal
fluid.
4. Progressive formation of peritubular dentin
5. Invasion of tubules by bacteria
6. Formation of intratubular collagen plugs
 Methods of tubule occlusion

7. Formation of irritation dentin

8. Leakage of large plasma proteins into tubules.
9. Formation of smear layer by brushing, use of tooth picks
etc
10. Resin impregnation or covering
11. Topical application of calcium hydroxide, sodium fluoride
and oxalate
12. Restorations
 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

 Burnishing of dentin :

Done with a
formation of smear partially occludes
toothpick or
layer dentinal tubules
orangewood stick

Dry orangewood

Combination with
glycerin and Na F

•Found to reduce fluid movement by 50 – 80 %

 Cavity varnishes
• Brannstorm suggested the application of cavity lining and
varnishes under restorations so that the smear layer plugging
open tubules is retained

• Wycoff suggested the use of a copal varnish

• 2 % NaF varnish can be applied for more sustained relief-3
months

• Reduction in dentin permeability by 20-50 %

• 5 % NaF varnish forms a protective layer of calcium fluoride
that inhibits fluid flow in dentinal tubules

• Corona et al found no statistically significant difference

between fluoride varnish and gallium-aluminium-arsenide
laser
 Vanish XT

• Vanish XT, 3M ESPE)

• An extended-contact varnish

• Photocured fluoride varnish

• Forms an immediate layer of

protection to relieve dentin
hypersensitivity.
• Resin-modified glass ionomer
that contains glycerophosphate
for calcium and phosphate release
in addition to fluoride.

• The formation of resin tags

provides an immediate and
extended period of occlusion of
the dentinal tubules.
 Silver nitrate
Introduced in 1920s.

Mechanism of action- precipitates proteins within tubule with

formalin or eugenol, precipitated silver chloride which reduces
dentinal fluid flow.

Disadvantage
Pulpal inflammation in shallow
cavities

Staining of gingiva
 Corticosteroids

Anti inflammatory agents

•Induce mineralisation of the peritubular dentin

•Glucocorticoids( prednisalone) to cavity preparations and

expose dentin -by way of their effect on pain mediators - reduce
DH
 Corticosteroids
• paramethasone -significant desensitizing
Lawson Mjor action

Mjor and Furseth •complete obliteration of tubules

• liner -1% prednisolone +25%

parachlorophenol, 25% m-cresyl

Mosteller acetate +50% gum camphor

• ophthalmic solution -sensitive root -
relief
 Calcium hydroxide :
Produces immediate effect which is short lived

Mechanism of action

Occludes
Increases
tubules by
Physical peritubular Decreases
binding of
protection of dentin permeability
ca ions to
dentin mineralisatio
protein
n
radicals
 Method of use
After 5 min,
paste
Mixed with Applied onto
Removed,tooth
sterile water dried area
rinsed

Burnishing of the paste advised by -Hiatt & Johansen

•Short acting
•Multiple
applications
•Irritation to
Disadvantages gingiva
 Dibasic calcium phosphate
• Hott and Johansen studied the effectiveness of burnishing
CaHPO4

• Significant relief of discomfort

Formaldehyde (1.2 – 1.4 %)

1950s, 40 % formalin applied topically

Precipitates salivary proteins in dentinal tubules

Grossman- desensitising agent of choice as no

staining

Very strong tissue fixatives

Need utmost caution not to come in contact

with gingiva
• An aqueous solution of glutaraldehyde and HEMA, such as
Gluma Desensitizer (Heraeus Kulzer Inc.) or Calm-It (Dentsply
Caulk), has been used as a desensitizing agent, with
glutaraldehyde serving as the mechanism for tubule occlusion.
 Sodium citrate and Pluronic acid

Mechanism of action -Polyglycol has ability to precipitate

salivary & dentinal proteins

•Dibasic sodium citrate in pluronic acid F-124 ( Protect ) - most

safe and effective as given by ADA.

•Shown to reduce dentinal fluid flow by 19%.

 Casein phosphopeptides

• A relatively new product

• Thought to reduce sensitivity by
plugging of the dentinal tubules.
 Fluorides :

Mechanism of action

Peritubular Reduce diameter of

Flouride ions
precipitation tubules

Resistant to
replace ca in
Flouride ions Flourapatite acids
hydroxyapatite
insoluble

Synthesis of
Flouride ions Iontophoresis secondary
dentin
 Stannous flouride
used either in an aqueous solution OR in glycerin gelled with
carboxymethylcellulose

Acts by
occlusion of
dentinal tubules

gets precipitated
forms a calcific
on surface of
barrier
tubules
 Studies on Stannous fluoride
• Blank and Charbeneau -burnishing a 10% solution of stannous
fluoride

• Ellingsen and Rolla

 examined SnF2 treated dentin surface using S.E.M.
 observed a dense layer of tin and fluoride containing globular
particles blocking the dentinal tubules.

• Blank and associates-0.4% SnF2 gel effective

Topical application of 0.717% aqueous SnF2 provided

immediate relief from sensitivity
 Sodium flouride

2 % NaF can be used with iontophoresis or as topical agent.

2 % NaF used following pretreatment with 10 % strontium

chloride increase the efficacy.
 Sodium silico fluoride

• Bhatia- saturated solution of sodium silico fluoride for 5min

was much potent than 2% solution of NaF in desensitizing
painful cervical areas of teeth.

• Everett et al- silicic acid forms a gel with the calcium of the
tooth, thus producing an insulating barrier
 Silver Diamine Fluoride

• SDF is another emerging fluoride agent.

• Desensitizes dentin
• Arrests caries progression
• Saforide (toyo seiyaku kasei co., Ltd.) Contains 38% SDF, or
approximately 44,800 ppm of fluoride ion.
• Colorless solution
• Australia, china, and japan
• Transient mucosal irritation
 Flouride iontophoresis

• Introduced by Hiatt and Johansen in 1972

A process of facilitating the transfer of ions by means of an

electrical potential into soft or hard tissues of the body for
therapeutic purpose

• Used with sodium flouride, causes immediate relief .

• But, the symptoms gradually recur in about 6 months.

 Mechanism of action
Exactly not known.

1. Murphy et al - desensitisation due to formation of secondary

dentin by electric current

2. Gangarosa & Park- iontophoresis caused parasthesia by

reversibly altering sensory mechanism of pain conduction

3. Iontophoresis thought to increase conc and depth of penetration of

flouride ions into tubules
 Procedure
Isolation with Negative Positive to
cotton rolls & electrode attached patient’s face or
plastic strips to dentin arm

Application of
Current passed fluoride with
brush
 Strontium chloride hexahydrate ( 10 % )
•Dentifrice containing 10% strontium chloride hexahydrate as the
desensitizing agent

•Sensodyne tooth paste was formulated with strontium chloride

hexahydrate in 1961

•Kun- topical application of concentrated strontium chloride

solution

•penetrated the dentin to a depth of about 20 microns

 •Strontium ions are
exchanged with ca of
•Protein precipitant
dentin
•Adsorbed onto dentin
•Recrystallisation in
form of strontium
• Blocks outer organic
apatite complex
matrix of root surface.
•Promote calcification
blockage of tubules
• Dentrifices containing 10 % strontium chloride showed
complete relief of DH in a 2- month period (Cohen )

• Uchida et al found that 10 % strontium chloride dentrifice was

more effective in treating DH following periodontal surgery
than placebo groups
 Oxalates
Potassium oxalate and ferric oxalate solutions used popularly as
desensitizing agent

Mode of action

Ca ions Insoluble
Potassium
(dentinal calcium
oxalates
fluid) oxalate
 1. Ferric oxalate 6 %

2. Dipotassium oxalate
Commonly used oxalates - 30%

3. Monohydrogen
monopotassium oxalate 3 %

Advantages - •Inexpensive
• Easy to use
•Well tolerated by patients
Super Seal (Phoenix Dental)
is a potassium oxalate-based,
acid-resistant desensitizer that
can be applied with a cotton
pellet for root sensitivity after
periodontal treatment.
 Potassium nitrate

Introduced by Hodosh in 1974.

Highly effective home therapy.

Potassium salts block neural transmission at the pulp &

depolarize the nerve around the odontoblast

Incorporated into both toothpastes & mouthrinses

Mechanism of action of Potassium Nitrate
Through K ions
Potassium
dentinal To the nerve depolarise
nitrate
tubules the nerve

Prevent transmission
of the pain signals to Prevent it’s
brain. repolarisation
 Oxidising effect

K+ ions

Blocking of tubules
by crystallisation
 5 % potassium nitrate
• an excellent desensitizing agent

• reduces DH effectively at 1 week & up to 4 weeks

 Studies on Potassium Nitrate

Potassium nitrate ineffective in Decreasing any dentinal fluid flow

• Greenhill and Pashley

Compared potassium nitrate to calcium hydroxide in the desensitization from

mechanical, hot and cold stimuli

• Green et al

Called potassium nitrate a superior desensitizer and found it to be highly

effective at concentrations of 1 to 15 %
Sensitization
• Hodash (1974)
Studies on Potassium Nitrate…..

Found 5 % potassium nitrate able to desensitize the

dentin effectively at 1 week and 4 weeks compared to
control
• Tarbet et al

Potassium nitrate bioadhesive gels.. 5 % & 10%.

• Frecoso S et al 2002
• Combination of 5% potassium nitrate & 0.243% NaF in
dentifrice is significantly more effective than 10% strontium
chloride containing dentifrice.

• Chesters et al found that potassium citrate, sodium mono

fluoro phosphate was significantly more effective in reducing
dh compared to potassium nitrate.
 Lasers
The first laser used : Nd : YAG laser by Matsumito in 1985.

He – Ne laser
Low output
lasers –
Ga Al A lasers
Lasers
Nd : YAG
laser
Middle output
lasers –
CO2 laser
 Low Output Lasers

He-Ne laser

First used for treatment of DH reported by Senda et.al in

1985,then consecutively by others.

Senda et.al initially used an output power of 6mW.

Irradiation modes were two types-

Pulsed (5Hz only ) Continuous wave

mode
Treatment effectiveness ranged from 5.2 to 100 %.

Mech of action : affects electrical activity ( action potential )

which in a healthy nerve increased by 33 % following a single
irradiation.

– A long lasting effect inducing an increase in the size of the

nerve’s action potential for more than eight months after
cessation of irradiation.
 GaAlAs laser
• Introduced for treatment of hypersensitivity by Matsumito in
1985
• At 900nm, treatment effectiveness ranged from 73.3 to 100%.

• Mechanism of action :--This type of low output laser mediates

an analgesic effect related to depressed nerve transmission.

• At 830nm, this effect mediated by blocking the

depolarisation of the C- fiber afferents.
 Middle Output Lasers
Nd:YAG laser

• First use reported by Matsumoto et al 1985

• Output varied , ranged from 0.3 to 10mW but 1 or 2w was the

most common.

• Treatment effects ranged from 5.2 to 100%

• Mechanism of action - Laser induced occlusion or narrowing

of dentinal tubules as well as direct nerve analgesia
 CO2 laser
▪ First use reported by Moritz et al in 1996
▪ Treatment effectiveness ranged from 59.8 to 100%.

Mechanism of action:-

• Due to occlusion or narrowing of dentinal tubules- reduction

in the permeability of the dentinal tubules at moderate
densities.

• Cause dentinal dessication causing temporary relief

 Combination of laser treatment with
flourides

• The combined use of GaAlAs laser at 830nm with fluoridation

enhances treatment effectiveness by more than 20%over that
of laser treatment only.

• CO2 laser + DP-Bioglass paste (Lee et al): CO2 laser melts the
paste and creates about 10 microns of sealing depth
 Resins & adhesives :
Dayton, Brannstrom & Nordenval –

•Immediate and long lasting blockage upto one year

•Acts by physical protection of the dentin.

Dentin Glass
bonding Varnish ionomer
agents cements

Composites

Useful in cases of specific and localised hypersensitivity.

 In –office products
• Treatment agents that do not polymerize
A. Varnishes/precipitants
• Brannstorm suggested the application of cavity lining and
varnishes under restorations so that the smear layer plugging
open tubules is retained

• Wycoff suggested the use of a copal varnish

• 2 % NaF varnish can be applied for more sustained relief-3

months
• Reduction in dentin permeability by 20-50 %

• 5 % NaF varnish forms a protective layer of calcium fluoride

that inhibits fluid flow in dentinal tubules

• Corona et al found no statistically significant difference

between fluoride varnish and gallium-aluminium-arsenide
laser

• 1 % NaF, 0.4 % SnF, 0.14 % HF solutions, 6 % acidic ferric

oxalate, 3 % monopotassium mono hydrogen oxalate, CaPO4,
CaOH preparations
 In –office products
Primers containing HEMA

• Primer containing 5 % glutaraldehyde and 35 % HEMA

(Gluma Desensitizer) in water reduces DH in presence as well
as absence of smear layer

• Effective upto 9 months

 Treatment agents that undergo setting or
polymerization reactions

A. Conventional glass ionomer cements

- Low (1981) reported the use of GICs in treating cervical
abrasion lesions

b. Resin reinforced glass ionomers

- Hansen (1992) reported a 1 year success rate of 79 % to treat
DH
C. Adhesive resin primers
- Reduce dentin permeability as they have very thin residual
film thickness ( Simpson et al 1993)

- Problem associated: atmospheric oxygen may diffuse into the

thin films and interfere with free radical polymerization
reactions

- After light curing, unprotected resin films < 20µm thick may
remain unpolymerized and would be quickly lost
- An alternate resin desensitizer had been introduced: primers A
and B are mixed and gently rubbed on the hypersensitive
dentin for 30 s followed by air drying

- It contains oxalic acid and an emulsion of PMMA

copolymerized with p-styrenesulphonic acid

- The treated surface becomes covered with a layer of polymer

5-10 µm thick and some primitive resin tags are formed within
open tubules
- The long term effectiveness of this resin product may be
limited by the inability of the resin tags to bond to the walls of
the peritubular dentin matrix lining most dentinal tubules

- Only if the peritubular dentin is removed by acid etching to

expose collagen fibrils of the surrounding intertubular dentin
matrix, can liquid resin infiltrate into the demineralized dentin
and hybridize with it

- But acid etching may open up previously insensitive tubules,

making the treatment more difficult
• Adhesive resin bonding systems
- Yoshiyama et al(1993) reported that resin desensitization is
due to presence of resin tags in dentinal tubules

- Dayton et al (1974) evaluated the use of first generation dentin

adhesives

- All adhesives reduced sensitivity to tactile and osmotic stimuli

• Some dentin bonding agents, such as Clearfil New Bond
(Kuraray Dental) and Xeno III (Dentsply International), have
demonstrated success in sealing dentinal tubules to treat and
prevent sensitivity without an etching agent.

• A dentin bonding agent that requires an acidic agent opens the

pathway for the diffusion of monomers into the collagen
network, but it also facilitates the outward seepage of tubular
fluid from the pulp to the dentin surface.
• This process deteriorates bonding for some of the current
adhesives.
- Javed et al (1987) found that a single application of
cyanoacrylate to hypersensitive root surfaces cause an
immediate reduction in sensitivity to air blasts that returned
to pretreatment levels in 6 weeks

- Self etching bonding systems are also effective in treating DH;

Reevaluation of resin covered surface should be done with air
or cold water as the use of explorer may tear the resin and
reexpose the tubules

-
 Restorative materials

The use of restorative materials is generally an invasive

solution to the problem of hypersensitivity.

• Commonly used materials include composite resins and glass

ionomer restorations.

• Generally this approach is reserved for 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.
 Periodontal surgery
Soft tissue grafting procedures

•Lateral sliding grafts

•Free gingival grafts
•Connective tissue grafts
•Coronally repositioned flaps

• While these procedures may cover exposed dentinal tubules,

some are not very predictable in terms of their efficacy in root
surface coverage.
 Recent developments
• A dentifrice-containing potassium nitrate, in combination
with fluoride, a copolymer, and anti-calculus [tartar]
ingredients, has been formulated to reduce DH/RDS

• A dual-tube technology to deliver the active ingredients that

may interact if placed in the same tube onto the tooth surface

e.g Colgate Sensitive (Colgate–Palmolive Company,

Piscataway, NJ, USA) that incorporates potassium nitrate and
stannous ions
• Improvements in the abrasive (e.g. artificial silica) with low
Radioactive Dentin Abrasivity (RDA) values and detergent
systems

• It is possible that some of the anionic detergents systems

such as sodium lauryl sulfate may affect the attachment of
artificial silica to dentine possibly by ionic competition;

• An alternative nondetergent system such as tego betaine may

be used to prevent this interaction with the artificial silica
• Intra-oral fluoride releasing devices , bioadhesive potassium
nitrate 5/10% gels , and application of 3% potassium oxalate
or 6% ferric oxalate

• The combination of casein phosphopeptides (CPP) and

amorphous calcium phosphate (ACP) Recaldent[CPP–ACP] (GC
America Inc., Alsip IL, USA.) reduces DH

• ACP has also been used in bleaching trays to reduce DH

during the bleaching process and RDS
 Proargin technology
• Development of a new “saliva-based composition” for
treating dentin hypersensitivity.

• The essential components –are

• arginine, an amino acid
• calcium carbonate, which is a source of calcium.
• This desensitizing prophylaxis paste is effective in providing
instant sensitivity relief when burnished onto sensitive teeth
following scaling and root planing procedures

• Sensitivity relief lasts for at least 28 days following a single

treatment.

• The Colgate-Palmolive Company has further developed this

innovative technology by combining the key components,
arginine and calcium carbonate, with fluoride
• Bioactive and biocompatible glasses induce osteogenesis in
physiological systems and occlude tubules e.g NovaMin
(calcium sodium phosphosilicate) , Nucare Prophy Paste and
Oralief Therapy for Sensitive teeth
• Chewing gums containing potassium chloride
and mouthrinses containing potassium citrate
and potassium nitrate solutions (3%) or gels
(10%) in a mouthguard
 Fluorinex

• Fluoritray

• contains an anode and cathode is filled with the Fluoride.

• In the Fluorinex method, positive and negative electrodes are

within the gel when energized, and are a part of the tray itself.

• There is no passage of the current through the patient’s body

• Potassium nitrate has been used in bleaching trays to reduce
DH/RDS during and following the bleaching process

• The advancement in periodontal grafting procedures such as

bio-absorbable membranes to treat localized gingival
recession with DH/RDS may also enable the skilled
practitioner to treat DH/RDS successfully
 Summary

• Dentin hypersensitivity is 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
disease.”

• Prevalence of DH to be 4–69%

• Females > males

• End of the third decade and the beginning of the fourth

• Prevalence or incidence of RDS or RS following periodontal
therapy 60–98%

• Tooth type: canines and first premolars; incisors an second

premolars; molars (Graff and Galasse 1977)

• The buccal cervical area is the site of predilection

• THEORIES OF SENSITIVITY MECHANISM
• Odontoblast transducer theory: (Rapp et al 1960’s)
• Neural theory
• Hydrodynamic theory( Gysi 1900, Brannstorm 1963)

Two processes involved in DH:

• “lesion localization”
• “lesion initiation”
 Prevention of dentin hypersensitivity

• Suggestions for patients

- Avoid gingival recession due to poor plaque by practicing
good oral hygiene techniques
- Avoid using large amounts of dentifrice
- Avoid hard bristled toothbrushes
- Avoid brushing teeth immediately following ingestion of
acidic food or beverages
- Avoid overbrushing with excessive pressure for prolonged
periods of time
- Avoid using toothpicks
• Suggestions for professionals
• Avoid overinstrumenting the root surfaces during calculus
removal and scaling and root planing procedures

• Avoid overpolishing the exposed roots during stain removal

• Avoid violating the biologic width when placing crown

margins

• Avoid burning the gingival tissue during bleaching procedures

Management strategies
 Home use products
• Strontium salts
• Potassium salts
• Dibasic sodium citrate
• Flouride based interventions

 In-office products
 Treatment agents that do not polymerize
A. Varnishes/precipitants
B. Primers containing hema
 Treatment agents that undergo setting or polymerization
reactions
A. Conventional glass ionomer cements
B. Resin reinforced GICs
C. Adhesive resin primers
D. Adhesive resin bonding systems
• Iontophoresis
• Lasers
• Low out put Laser ( low power laser )
– He – Ne laser
– Ga Al As laser ( diode laser )
• Middle output Laser
– Nd : YAG laser
– CO2 laser

• Bioactive glass
• “saliva-based composition : ProArgin

• CPP-ACP containing formulations

 Conclusion

• Although dentin hypersensitivity is a common oral

health problem for many adult population groups, high-
quality scientific studies on the epidemiology, biologic
mechanism, and treatment of this condition are lacking.

• Many treatment methods have been proposed, yet no

universally accepted or highly reliable desensitizing
agent or treatment has been identified.
• When a patient has symptoms that can be attributed to dentin
hypersensitivity, the dentist should perform a thorough clinical
examination to rule out the other likely causes prior to
diagnosis and treatment.

• Depending on the identified cause, a combination of

individualized instructions on proper oral health behaviors, use
of at-home products, and professional treatment may be
required to manage the problem.
 References

• DCNA on Tooth hypersensitivity 1990, 34:3

• Text book of clinical periodontology – Newman Carranza
• Clincal periodontology & oral implantology – Jan Lindhe
• Text book of conservative dentistry – Sturdevent
• Dentinal sensation & hypersensitivity – A review of
mechanisms & treatment alternatives – JP 1984
• Role of dentin bonding agent in reducing cervical dentin
hypersensitivity – JCP 1998
 References
• Endodontic topics 2006, 13, 13–33
• The journal of clinical dentistry (ISSN 0895-8831)
• Walters PA. Dentinal hypersensitivity: A review. J contemp
dent pract 2005 may;(6)2:107-117
• Treatment of dentinal hypersensitivity by lasers j clin
periodontol 2000, 27; 715-721
• DCNA 2009 (53)