DENTINAL HYPERSENSITIVITY

GUIDED BY:
DR.P.KARUNAKAR
DR.UMRANA FAIZUDDIN PRESENTED BY:
DR.ASHISH JAIN DR.M.RASAGNA
PG 2ND YEAR
CONTENTS
• Introduction
• Definitions
• History
• Etiology & predisposing factors 
• Mechanism of dentin sensitivity
• Theories
• Clinical considerations
• Methods of measuring hypersensitivity
• Management of hypersensitivity
• Summary & conclusion
INTRODUCTION
INTRODUCTION
• In 1982,Johnson and co-workers  stated that ''dentinal
hypersensitivity is an engima, being frequently encountered,yet ill
understood''.
• ''Common cold of dentistry ''. 
• ''Tooth brush disease''.
DEFINITIONS
DEFINITION
• Dentinal hypersensitivity is characterised by short sharp pain arising
from exposed dentine in response to stimuli typically thermal,
evaporative ,tactile, osmotic or chemical and which cannot be
ascribed to any other form of defect or disease.
                                                                                 (Holland Et al 1997)

• In 2003,Canadian Advisory  hypersensitivity recommend the use of

term disease instead of term pathology which will be accurate and
correct.
EXAMPLES OF CLINICAL CONDITIONS THAT NEED TO
BE EXCLUDED PRIOR TO A DEFINITIVE DIAGNOSIS OF
DH 
• Dental caries
• Cracked tooth
• Fractured restoration
• Post-restorative sensitivity
• Medication sensitivity
• Post –non surgical/post surgical periodontal sensitivity
• Palatogingival groove
• Non-odontogenic origin
• The terms dentinal,dentin, or tooth sensitivity frequently have been
used.
• The condition has also been referred to as cervical dentin
hypersensitivity and as cervical tooth sensitivity, adding a location
based descriptor to differentiate it from other types of tooth pain.
HISTORY
• Chinese-2000 years or more by the application of 'Xiao-shi' believed
to be niter or potassium nitrate ,in about third century B.C.

• The egyptian Medical Papyrus recommended a mixture of red and

yellow Vitriol and alum for ''teeth that suffer''.

• Leeuwenhoek (1678)-''tooth canals in dentin''.

• J.D.White(1855)- dentinal pain  was caused by the movement of fluid

in dentinal tubules.
• Cartwright in 1857- dentine sensitivity was observed when the
affected tooth was  struck and some areas of the tooth were
''exquisitely sensitive'' and a source of great discomfort.

• Chemical caustics could be used to desensitize dentin.

• In 1866,Francis presented ''sensitive dentine'' its cause and

treatment  with cavity liners.
• In 1898, Henry H.Buchard provided a categorization of the three
pharmacologic approaches for controlling the pain of dentin hypersensitivity.

The administration of agents to lower the pain perceptive centers of the

brain.

Use of agents to destroy or coagulate the dentinal protoplasm.

Use of local analgesic agents on the dentin.

• Herman prinz (1913)noted that aresnic was no longer used for
reducing sensitivity-damages or destroys the pulp.

• Suggested the application of local anesthetics directly to the exposed

dentin in prepared cavities.

• Louis J.Grossman described hypersensitiveness in dentin.

• King's speciality  Co. In Fort Wayne,Indiana,in 1932, produced

''sensitex'',commercial desensitizing solution,sold to dentists.
• Lukomsky(1941)-sodium fluoride
• Hoytt and Bibby (1943)-sodium fluoride,white clay and glycerin.
• Pawlowska(1956)- strontium chloride combined with bi-colloids of
teeth –favorable  effect on hypersensitivity.
• In 1962 Brannstorm-Hydrodynamic theory.
• In 1974 Hodosh-superior desensitizer-potassium nitrate.
• Summarized approaches to treat hypersensitivity-kleinberg (1986).
PREVALENCE 

• General population-15-18%
• Periodontal patients-60-98%
• Common occurrence- 20-50 years of age.
• Peak incidience –end of the third decade.
• In general, slightly higher incidence in females than males.
INTRAORAL DISTRIBUTION

Canines>first
premolars>incisors>
Teeth affected second
premolars>molars

Site of Buccal cervical area

predilection Gingival recession
Thinnest enamel
 Left sided tooth
Side affected sensitivity>right sided
tooth sensitivity
• Association of noncarious cervical lesions(NCCL) and abfraction with
DH/RDS:the prevalance of NCCLmay range from 5% to 85% (AW et al).
ETIOLOGY & PREDISPOSING FACTORS
• Two processes need to occur  to arise dentin hypersensitivity
Lesion localization
Lesion intitiation

• Lesion localization:
• Dentin has become exposed

Gingival
Enamel loss
recession
LOSS OF ENAMEL 
GINGIVAL RECESSION
• Pre-disposing factors
Alveolar bone
Tooth anatomy &position
Oral hygiene
Gingival diseases
Trauma
Other factors
ANATOMY OF ALVEOLAR BONE
• Most frequently cited predisposing factor.
• Thin, Fenestrated or even absent  labial alveolar bone may
cause gingival recession (Aldritt 1968,Bernimoulin J. , Curilovie Z.
1977, Lost 1984).
TOOTH ANATOMY &POSITION
• Tooth anatomy (Olsson and lindhe 1991) & tooth position (Gorman
1967,Modheer and Odenrick 1990) can influence  alveolar bone
thickness.
• Orthodontic tooth movement.
ORAL HYGIENE
• HIGH STANDARDS OF ORAL HYGIENE:
Overzealous tooth brushing cause gingival recession.
• POOR ORAL HYGIENE:
Leads to gingivitis(Loe et al 1995) and recession in chronically
inflammed tissue.
GINGIVAL DISEASES
• ANUP
• ANUG
• Chronic periodontitis with associated bone loss can cause gingival
recession although the Buccal area does not appear to be a site of
predilection for periodontal lesions.
TRAUMA
• Periodontal treatment(surgical or non-surgical)
• Impaction of foreign objects in the gingiva(Jenkins and Allen 1984)
• Factitious injury (Glenwright and Stranhan 1994)
OTHER FACTORS
• Frenal pull results in the tissues moving towards the CEJ may result in
recession.
• Occlusal trauma appears to be a risk factor for attchment loss in
individuals with active periodontal disease.
IATROGENIC FACTORS
• RESTORATIVE SENSITIVITY
• Restoration with composite material in which acid-etching step
performed beyond the CEJ margin.
•  sensitivity can also occur if the dentin tubule that is newly cut during
cavity preparation is left exposed during the restorative procedure.
• Bleaching sensitivity commonly associated with carbamide peroxide,
which breaks down into H2O2 and urea and bleach the tooth.
• This causes dehydration within the the tooth and symptoms of DH.
 LESION INITIATION
• Not all exposed dentin is sensitive.
• Characteristics of sensitive dentin:
MECHANISM OF DENTIN HYPERSENSITIVITY
• Presence of tubules renders dentin permeable to fluid movement.
• The dental pulp is richly innervated by
Myelinated-A fibers
B fibers-preganglionic autonomic function
C-fibers – Non-myelinated
A-alpha fibers- proprioception
A-beta fibers- touch&pressure
A-y fibers- motor function
A-delta-  pain,temp&touch
•  A-delta and C-fibers - subodontoblastic plexus, nerve fibers extend to the
odontoblastic layer, predentin and dentin free endings.
                

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

dentin surface.
DENTINAL SENSATION:MECHANISMS
• When dentin is exposed to thermal,osmotic or electrical stimuli,or
when air blasts or various drugs are applied to its surface,the host
feels pain which may be termed a ''dentinalgia'' .

• Although histochemical,autoradiographic and electron microscopic

studies have vividly described the relationship between the
odontoblast and the neural fibres of th pulp.

• the exact mechanism of  transmission of the pain response from the

dentin to the terminal nerve endings is only hypothesized.
THEORIES
• Direct Neural stimulation theory
• Odontoblastic transducer mechanism
• Modulation theory
• Gate control theory and vibration
• Hydrodynamic theory
Direct neural stimulation theory
• This theory states that Dentin hypersensitivity occurs due to direct
stimulation of nerve fibers present in the dentin.
 Drawbacks​:

• Nerves are present only in the predentine & inner dentinal zones but do

not extend upto the DEJ which is the most sensitive part of dentine.​
• Newly erupted tooth doesn't possess nerve  endings even though it
is sensitive.
Modulation theory

Irritating Injury of
stimulus Dentin odontoblasts

Nerve fibers Increasing Neurotransmitters

action neuronal and vasoactive
potential cAMP Levels amines

Pain
Odontoblastic Transduction Theory 
• Proposed by Rapp et al
• Synaptic like relation between the terminal sensory nerve endings
and odontoblastic processes.
Direct stimulation
of odontoblastic
Mechanical, chemical
processes in
or osmotic stimulus
dentinal tubules

Hypersensitivity Painful
response
 Drawbacks
• Failure to establish synaptic relation between the odontoblasts and
the pulpal nerves.
• Fails to explain why dentin continues to be sensitive,despite
destruction of odontoblast layer.
• Also does not explain why protein precipitation does decrease
sensitivity of dentin to osmotic stimuli.
Gate control theory and vibration
•  When the dentin is irritated, all of the pulpal nerves become
activated from the vibrations.

Larger myelinated
fibers Smaller C fibers
Get accomodated Remain open
''pain gates''-closed Become enhanced
Drawbacks
• Little to explain how pain responses from dentin transmitted and
perceived by the  nerve endings of the pulp-only how they may be
centrally interpreted.
Hydrodynamic theory
• Fish in 1927 observed the interstitial fluid of the dentin and pulp-
dental pulp.
• Flow of this fluid is in both outward or inward direction.
• Fluid movement within the dentinal tubules is the basis for the
transmission of sensations according to  the hydrodynamic theory.
• Brannstrom and Astrom, proposed that  dentinalgia results from a
stimulus Causing minute changes in the fluid movement within the
dentinal tubules –deform the odontoblasts or its process-pain.
Variables affecting hypersensitivity
• For hypersensitivity to occur,permeation of substances into the
dentin is essential.
• 2 mechanisms
• The fluid movement can be measured by the hydraulic condutance of
dentin (given by Poiseuille Hagen Equation).
Rate of fluid flow α (radius of tubule)4
• The presence of tube like structures in hypersensitive dentin is important in
maintaining the patency of dentinal tubules.

• These contain sulphur rich, non collagenous acidic phosphoproteins .

• These phosphoproteins cause stabilization of tube-like lamina limitans and

may prevent the mineralization of hypersensitive dentin.

• Yoshiyama et al found that 75.8 % of of dentinal tubules in hypersenstive

dentin contain hollow tube like structures while in non-sensitive areas, tube
like structures were present in 20.4 % of dentinal tubules.
• Mechanism creating hypersensitive dentin:
Increase in hydraulic conductance of dentin.
Decrease in A-delta nerve threshold.
ALTERNATIVE MECHANISM (MODIFIED
HYDRODYNAMIC THEORY)
• Narhi in 1982, Kim in 1986 and berman in 1984 and other investigators…

• Application of various chemical solutions (in particular potassium

containing compounds) to dentin resulted in raising the intratubular
potassium content, which in turn rendered the interdental nerves les
excitable to further stimuli by depolarizing the nerve fiber membrane.
Clinical Manifestations
• Usually more sensitive to cold than hot.
• Patient tends to avoid stimuli.
• No tenderness on percusion.
• Radiographically,no periapical changes seen.
DIAGNOSIS 
• Following are the important points that have to be evaluated during
the diagnosis of dentine hypersensitivity
History and nature of the pain
Number and location of sensitive teeth.
Area of origin of sensitivity from tooth.
Intensity of pain,frequency and duration of each episode.
Triggering factor or stimulus for dentinal hypersensitivity.
DIFFERENTIAL DIAGNOSIS
CLINICAL ASSESSMENT OF DENTINAL
HYPERSENSITIVITY
• Traditionally, dentinal hypersensitivity mainly evaluated on the
individual patient's response to the stimulus.

• According to the recent reccomendations by Holland et

al (1997),dentin hypersensitivity may be evaluated either in terms of
the stimulus intensity to evoke pain or response based methods.

• Stimulus based methods usually involve the measurement of a pain

threshold;response based methods involve the estimation of pain
severity.
SUBJECTIVE EVALUATION
Verbal rating scales
• Described by Keele(1948)
• Has a 4-point scale grading pain as slight,moderate,severe,agonizing.
• Recently modified in the form of mathematical interpretation of scoring
system i.e. scores an often arbitrarily assigned numerical values.
Drawbacks
• Assigned scores were analyzed as if these numbers reflected true
quantiative differences in pain rather simple qualitiative differences.
• These scales are restrictive because they may not offer enough
descriptions that can be placed in a continuous and ascending or
descending order of  severity of pain.
VISUAL ANALOG SCALE(VAS)
• It is a line 10cm in length.
• The extremes of the line representing the limits of pain a pt might
experience from an external stimulus.
• NO pain at one end.
• Other end-most severe pain.
• Pt are asked to place a mark on the 10cm line which indicates
intensity of their current level of intensity/discomfort.
  VERBRAL DESCRIPTOR CHECKLISTS

• Allows quantitative assessment of both the sensory and affective

dimensions of pain using a continuum across different pain conditions
instead of words intended to distinguish conditions.
 MCGILL  WORD  DESCRIPTORS(MPQ)
• It is used to determine the nature of the discomfort & to monitor
response to treatment.
• The patient is shown 20 sets of words and asked to select a word from
each set which best describes the present pain experience.

• Advantages
• Provides additional data  as  both the quantitative and qualitative
ascepts of pain.
Disadvantage
• Relies on the subject's vocabulary and consquently subject who do
not understand certain words  in a subgroup will ignore the group or
choose a word which they understand.
HOSPITAL ANXIETY AND DEPRESSION SCALE
• Zigmond and Snaith in 1983.

• It is one –way of determining whether well-being has an impact on the

efficacy of dentrifice during study.

• As of today, only few  published studies on   dentine hypersensitivity   have

looked at the influence of well-being(mood) on dentrifice efficacy(Gilliam et
al 1994,1995).

• It is evident from these studies that this scale is not sensitive enough to
detect changes from low grade levels of pain.
OBJECTIVE EVALUATION

• The presenting stimuli can be grouped into five categories:

Mechanical/Tactile.
Chemical/Osmotic.
Electrical.
Evaporative.
Thermal.
APPLICATION OF STIMULI
STIMULI TO ASSESS DENTINAL HYPERSENSITIVITY
(GILLAM ET AL)
Mechanical/tactile method
Pass the sharp dental explorer-grade the response using a scale (0-3).
• 0-no pain felt.
• 1-slight pain or discomfort.
• 2- severe pain.
• 3-severe pain that lasts.
Mechanical pressure stimulators
• Smith &Ash(1964).
YEAPLES PROBE(1980)
• An electronic pressure –sensitive probe presented by Polson et al.
SCRATCHOMETER
• Hand-held scratch device developed by kleinberg(1990) consists of
• Torsion gauge
• Sharp explorer like probe
• A tooth that fails to respond  to a force of 80 centi-newtons is classified as
non-sensitive tooth.
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 and only specific spots in a
cervical exposed dentine area will be tactily sensitive.
Thermal stimuli
THERMAL
• Directing a burst of air at room temperature from a dental syringe on
to the test tooth.
• One second blast from the air syringe -temperature is b/n 65 and 70
degree F and at a pressure of 60 psi.
• Application of cold air blast from dental syringe for 1 sec ( 70 degree F).The air
is directed at right angles to surface specially near CEJ.

• Temperature controlled stream of air used . Initial temperature of 100 degree F

used which is reduced till pain felt or to 70 degree F.

• Cold water testing – after isolating the tooth with a rubber dam,  the tooth is
subjected to water of temperatures 20, 10 and 0 degre C for 3 sec.
 Electronic thereshold measurement device​
•Appartus consists of a miniature thermistor connected to a
medical multichannel recorder with a handheld event recorder.​

 Thermoelectric device(Bio-mat thermal probe)​

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.
 Electric pulp tester
• They were used to quantify pain;however they are not useful in quantifying
dentinal hypersensitivity.
• Since increase in one unit on pulp tester did not produce a linear increase in
voltage.

q Dental pulp stethoscope

• Devloped by stark et al (1977).
• Consists of a digital read out sensitive voltameter connected to a digital
printer teeth activated by push button control.
• The stimulus intensity was measured in volts.
• The pulp  test  lip is placed on the gingival 1/3rd of enamel and tooth
stimulated.
• Electrolytic gel with ph of 5.4-5.6 is used.
• When patient  feels tingling  warm sensation, it is switched off
and voltage is read in digital read out.15 volts and above range of
non-sensitivity.
Advantages of electrical stimuli
• The patients sensation of warmth or tingling is taken as a threshold,
Which is described as prepain or non-pain sensation.
• It can be precisely defined by electronic method.
CHEMICAL/OSMOTIC STIMULI
• Popularized by Anderson.
• Based on the 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.
• 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.
Saturated solution of CaCl2
Drawbacks

• Inconvenience
• Difficulty  in administering and  controlling the  stimulus
• Injury  to  the  adjacent  soft  tissue.
EVAPORATIVE(DEHYDRATING) STIMULI
Cold air blast from a dental air syringe
• Directing a burst of air at room temperature from a dental syringe
onto the test tooth.
• Also  an air current from the dental chair can be applied for one second
at a pressure of 45 psi ,at a distance of 1cm to the sensitive tooth.
• This procedure is generally used to screen the patients.

Yeh air thermal system

• An air thermal device devised by Dr.K.C.Yeh used a temperature
controlled stream of air as the stimulus.
• Air was heated to 100 farenheit close to the temperature of the mouth.
• Its temperature was then  reduced until the subject felt pain or
discomfort.
• Drawbacks​
•Moisture content.
​
 Temptronic device​
•It is a microprocessor temperature controlled air delivery systems.​
•Air temp varied in the range of -5 to +85 degrees.​
•Air flow is regulated at a constant rate of 60psi.​
 Air jet stimulator
• Developed by Orchardson and collius (1987).
• Consists of a controlled jet of air (20+/-1 degree) from compressed air
supply .
• Flow of air is regulated by flowmeter.
• Activated by footswitch, which diverts airflow to the tooth and
started a three-decade digital clock.
• Pt feels discomfort switch off which automatically stops the clock.
MANAGEMENT OF DENTINALHYPERSENSITIVITY
• The pt is monitored and reviewed in a management strategy based on recognised
treatment paradigms.
Step wise approach to treating dentin hypersensitivity
Classification of desensitizing agents
BASED ON MECHANISM OF ACTION
Selecting desensitizing procedures
• Criteria ….. Grossman(1935).
Mechanism of actions of desensitizing agents
Methods of tubule occlusion
• Formation of calcium over sensitive tubules.
• Formation of intra tubular crystals from salivary mineral.
• Formation of intra tubular crystals from dentinal fluid.
• Progressive formation of peritubular dentin.
• Invasion of tubules by bacteria.
• Formation of intratubular collagen plugs.
• Formation of irritation dentin.
• Lekage of large plasma proteins into tubules.
• Formation of smear layer by brushing,use of tooth picks etc.
• Resin impregnation or covering.
• Topical application of calcium hydroxide,sodium fluoride and oxalate.
• Restorations.

  INSTRUCTIONS TO THE PATIENT

• Occurs as a result of exposure of dentin

• Disappers over a few weeks
• Plaque control is important
• Desensitizing agents do not produce immediate relief
IN OFFICE TREATMENT MODALITIES
• Office treatment for dentinal hypersensitivity as given by
Trowbridge(1990)
• 1.cavity varnishes
• 2.anti-inflammatory agents.
• 3.treatments that partially obturate dentinal tubules
Burnishing of dentine
Silver nitrate
Zinc chloride
Potassium ferrocyanide
formalin
Calcium compounds
Dibasic calcium phosphate
Dibasic calcium phosphate
Fluoride compounds
Sodium silicofluoride
Sodium fluoride
Stannous fluoride
Restorative resins
Dentine bonding agents
• Pashley in 1986 placed the in-office treatment for hypersensitive dentine as
follows:
Treatment agents that do not polymerize are
• Varnishes/precipitants
Shellac
5% sodium fluoride varnish
1% sodium fluoride,HF solution
6% acidic ferric oxalate
Calcium phosphate preparation
Calcium hydroxide
• Primers containing HEMA
5% glutaraldehyde,35% HEMA in water
35% HEMA in water
Treatment agents that undergo setting or polymerization reactions
• Conventional glass ionomer cements
• Resin reinforced glass-ionomers/compomers
• Adhesive resin primers
• Adhesive resin bonding systems
Mouth guards
Iontophoresis
Lasers
Varnishes
• Wycott advocated the use of a cavity varnish such as copalite.
• Dentin becomes insensitive.
• Topical application of fluoride varnishes was thought to create a
barrier by ppt of  CaF2 on to exposed dentine surface.
• The use of 5% sodium fluoride(NAF) in a thich varnish as dentine
desensitizer has been reported by Clark et al. (1985).
• Corona et al. found no statistically significant difference between
fluoride varnish and gallium-aluminium-arsenide  laser.
Oxalates
• Potassium oxalate and ferric oxalate solutions used primarily as
desensitizing agent.
• Mode of action:
 Advantages

Superseal(phoenix Dental) is a potassium oxalate- based,acid resistant

desensitizer that can be applied with a cotton pellet for root sensitivity after
periodontal treatment.
 Calcium hydroxide
• Produces immediate effect which is short lived.
• Mechanism of action
• Method of use :

Dibasic calcium phosphate

• Hott and johansen studied the effectiveness of burnishing CaHPO4.
• Significant relief of discomfort.
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
• Conventional glass ionomer cements
• Low(1981) reported the use of GICs in teating cervical abrasion
lesions.
• Resin reinforced glass ionomers
• Hansen (1992) reported a 1 yr success rate of 79% to treat DH.
• Adhesive resin primers
• Reduce dentin permeability as they  have  very thin residual film
thickness.
• Problems associated :atmospheric oxygen may diffuse into thin films
and interfere with free radical polymerization reactions.
• After light curing,unprotected resin films <20um thick  may remain
unpolymerized and would be quickly lost.
• Adhesive resin bonding systems
• Examples: Fluoride-containing adhesive resin
                   Dentin bonding agents
                    Self etching /self priming bonding system

• All bonding agents 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.
• 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.

• Mouth guards
• The use of mouth guards type appliance  used to deliver  desensitizing agents are
5% potassium nitrite/silica/sodium fluoride mouth rinse,10% potassium nitrite.
• Reinhart  et al (1990) first used mouth guard type appliance to deliver potassium
nitrite(10%) for  5 min.They had only partial success rate. In that they obtained a
significant  reduction only after 2 weeks of treatment.
Fluoride iontophoresis
• Introduced by Hiatt and Johansen in 1972

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
Murphy et al   -   desensitisation due to formation of secondary
dentin by electric current
• Gangarosa & Park-   iontophoresis caused parasthesia by reversibly
altering sensory mechanism of pain conduction
Iontophoresis thought to increase conc and depth of penetration of
flouride ions into tubules
Lasers
•     The first laser used : Nd : YAG laser by Matsumito in 1985.
• Mechanism of action:
• Coagulation and precipitation of plasma  proteins in dentinal
fluid(Goodies et al 1994)
• The thermal energy liberated alters the inter-dental activity(orcharelous
et 1998).
• Low-output lasers
• First used for  treatment of  DH reported by Senda et.al in 1985,then
consecutively by others.
• Irradiation modes were two types-  
• 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.
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%.
• 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
• Corticosteroids

    
Burnishing of dentine
• Tooth pick or ''orange wood stick'' …..creates a  partial smear layer on
dentin surface.
• Reduced fluid movement by 50% to 80%.
• More effective in reducing dentin permeability that burnishing
with glycerin alone or glycerin in combination with sodium fluoride.
• Silver nitrate
Disadvantage:
• Pulpal inflammation in shallow cavities.
• Staining of gingiva.
• Formaldehyde(1.2-1.4%)
 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.
• Casein phosphopeptides  
• A relatively new product
• Thought to reduce sensitivity by plugging of the dentinal tubules.
 Fluorides
• Sodium fluoride
• 2 % NaF can be used with iontophoresis or as topical agent.
• 2 % NaF used  following  pretreatment with 10 % strontium chloride
increase the efficacy.
• Stannous flouride
• used either in an aqueous solution OR  in glycerin gelled with
carboxymethylcellulose
• Acidulated sodium fluoride
• The conc of F in dentin treated with acidulated NaF was significantly higher
than dentine treated with NaF.
• Sodium silicofluoride
• Application of staturated solution of sodium silicofluoride for 5 minutes
was much more potent than a 2% solution of  NaF in desensitizing painful
cervical areas of teeth.
• Periodontal surgery
• A tissue grafting procedure can be used to cover the sensitive surface and
protect the dentinal tubules from the oral environment.
• The outcomes of this procedure to relieve sensitivity is unpredictable.
Home –desensitizing agents
• 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
• Penerated  the dentin to a depth of 20 microns
• 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
 Potassium nitrite
• Introduced by Hodosh in 1974
• Highly effective home therapy
• Potassium salts block neural transmission at the pulp& depolarize the
nerve around the odontoblast
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
• 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.
• 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
• 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
• 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.

• 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

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
• 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)
• Taha, S., & Clarkson, B. H. (Eds.). (2014). Clinician’s Guide to the
Diagnosis and Management of Tooth Sensitivity.