Dentinal hypersensitivity /certified fixed orthodontic courses by Indian dental academy

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com


CONTENTS
Introduction
Definition
Anatomy & histology of dentine
Mechanism of stimulus transmission
Clinical features
Prevelance
Distribution
Etiology
Methods of measurement
Management protocols

INTRODUCTION
One of most important and main objective of dentist has been the
control or elimination of pain. Painful symptoms arising from
exposed dentine are a common finding in Adult population &
have been reported to effect as many as 1 in 7 of patients
attending the dental operatory. (Graf & Galasse, 1977)

Although many individuals seem to have exposed dentine but not
all experience symptoms. There is no clear cut explanation for this
but certain factors may be implicated age, rate of exposure of

•Definition:
Dentinal hypersensitivity may be defined as short sharp pain
arising from exposed dentin, typically in response to stimuli-
typically thermal, chemical, tactile or osmotic that cannot be
ascribed to any other dental defect or pathology (disease).
[Canadian Advisory Board on Dentinal Hypersensitivity; 2003]

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. www.indiandentalacademy.com

Anatomy and histology of dentin:
Dentine is the hard tissue portion of the pulp dentin complex and
forms the bulk on the tooth.

ENAMEL
GINGIVA
DENTINE

PULP
CEMENTUM

PERIODONTAL
ALVEOLAR BONE LIGAMENT/ PDL


material mainly of
hydroxyapatite,
20% organic material - type I
collagen with glycoproteins,
proteoglycans,
phosphoproteins and plasma
MATRIX of type – I collagen fibrils
proteins and 10% water.
glycoproteins, proteoglycans
It is Characterized by closely
packed dentinal tubules that Mineral crystals - Hydroxyapatite

surround its entire thickness
and contain the cytoplasmic
extensions of odontoblasts,
cells that once formed the
dentin and now maintain it.
The cell bodies of
odontoblasts are aligned along
ODONTOBLASTS & their processes
the aspect of the dentine,
where they also form the

Contents of tubule:
Odontoblast and its process, nerves are also found in some tubules.
Fluid that is assumed to be present which might be equivalent to serum.
It is thought that apart from collagen and nerve fibrils, the fluid might
contain proteoglycans, tenascin, the serum protein albumin, transferrin
and type V collagen.


DENTINE: Composition

MATRIX subdivided into

Peritubular dentine

Inter-tubular dentine

TUBULES 1-3 µm wide


Types:
Predentin:
It's a layer of variable thickness 10 - 47 mm that lines the inner most
portion of the dentin. It is unmineralized and consists principally of
collagen, glycoproteins and proteoglycans.
Primary dentin:
Most of the tooth is formed by primary dentin, which outlines the pulp
chamber. The outer layer of primary dentin is called mantle dentin.
This is the l st layer formed by newly differentiated odontoblasts. The organic
matrix lacks phosphate and loosely packed coarse collagen fibrils.
Secondary dentin:
It develops after root formation. It was thought that secondary dentin is
formed only in response to stimuli but it has been found in unerupted teeth
as well.
Thus secondary dentin represents the continuing but much slower

Enamel
PREDENTINE

DENTINE

Odontoblasts

Direction of growth -
pulpward from DEJ


MATURE DENTINE: Varieties
MANTLE DENTINE just below
DEJ coarser fibrils

PRIMARY (CIRCUMPULPAL)
DENTINE - main mass of dentine
{
P
U TERTIARY DENTINE - slow
L increment to pulpal surface
P
REPARATIVE DENTINE -
response to caries/erosion


Dentine permeability:
It is constant interchange of fluid between dentine & pulp. It differs from one person to
another and from one area to other.

FACTORS GOVERNING DENTINAL PERMEABILITY:

•Types of dentine
•Type & nature of diffusants
•Degree of mineralization
•Dentine exposed during g tooth preparation
•Effective depth
•Induced stresses
•Hydraulic pressure
•Deficient resistance and retention form
•Micro leakage
•Cracks & micro cracks in dentine & enamel
•Types of intermediary base or restorative material

NEUROANATOMY OF PULP AND DENTINE:
Nerve fibers entering the teeth have been identified histologically as
myelinated A - fibers and unmyelinated C-fibers. Both A and C and provide
both fast and slow conduction.
They are grouped in bundles and enter through the apical foramina of the
teeth and pass through the radicular to the coronal pulp where they fan out
and diverge into smaller bundles.
Nerve divergence continues, individual A-fibers within small bundles lose
their myelin sheath and divide repeatedly before finally ramifying into a
plexus of single axons known as the subodontoblastic plexus or plexus of
Rashkow.
From this plexus, nerve fibers are distributed toward the pulp dentin border

Trow bridge summarized 4 types of nerve endings where they terminated

1. Marginal fibers: simple pulp fibers extending from sub odontoblastic
nerve layer; don’t reach predentine.

2. Simple predentinal fibers: extend upto odontoblast predentine border or
enter predentine.

3. Complex predentinal fibers: reach predentine; undergo terminal
ramification with multiple branching and multiple ending like branching
on each branch

4. Dentinal fibers: these pass through predentine with branching and enter
dentin through dentinal tubule

By tooth eruption, both myelinated and unmyelinated nerves
reach the odontogenic regions and lie close to the odontoblast.
According to Narhi and co-workers, it would appear that A-
fibers account for the sensitivity of dentin (dentinal pain).
Most are Aδ fibers, where as C fibers respond when external
irritants (i.e. chemical agents) reach the pulp (pulpitis).


MECHANISM OF STIMULUS TRANSMISSION ACROSS
DENTIN
Pashley & Parson suggested mechanism of dentinal
hypersensitivity to be classified according to three hypothesis:
1. nerve endings/ nociceptors respond directly when dentine is
stimulated(threoughout the dentin)
2. odontoblasts being chemically or electrically related to nerves
3. stimuli applied to dentine- produce displacement of dentinal
tubule content- excite mechanosensitive nerve endings near
pulpal end of tubules [hydrodynamic mechanism]

Theory ]:
This theory of dentinal sensation takes into consideration the "synaptic-
like" relationship between the terminal, sensory nerve endings and the
odontoblastic processes. If a true synapse were present between these two
elements to facilitate the transmission of dentinal sensations, then a neural
transmitting substance such as acetylcholine would be expected in this area
of the odontoblastic process and the predentin. There is no direct evidence
for the presence of acetylcholine activity in the neural transmission in the
pulp.

Modulation Theory:
Upon an irritating stimulus to the dentin, the odontoblasts may become
injured and subsequently release a variety of neurotransmitting agents as
well as vasoactive and pain producing amines and proteins. These
substances may modulate associated nerve fiber action potentials by

Gate Control Theory:
When the dentin is irritated, for example, by cavity preparation, all of the
pulpal nerves become activated from the vibrations.
The larger myelinated fibers may accommodate to the sensations. The smaller
C-fibers may tend to be maintained and not adjust to the stimulus.
Thus, as the low-intensity "pain gates" from the larger fibers are closed, the
high-intensity "pain gates" from the smaller fibers are enhanced.
However, the gate theory does little to explain how pain responses from the
dentin are transmitted and perceived by the nerve endings of the pulp and
how they may be centrally interpreted.

Hydrodynamic Theory:
Fish in 1927 observed the interstitial fluid of the dentin and
pulp, referring to it as the "dental lymph."
He postulated that the flow of this fluid could take place in
either an outward or inward direction depending on the pressure
variations in the surrounding tissue.
This idea of fluid movement within the dentinal tubules is the
basis for the transmission of sensations according to the
hydrodynamic theory.

According to the hydrodynamic theory, as put forth by Brannstrom and
Astrom, a dentinalgia results from a stimulus causing minute changes in the
fluid movement within the dentinal tubules.
This may subsequently deform the odontoblast or its process and hence cause
an elicitation of pain via the intimately associated "mechano-receptor-like"
nerve endings.
i.e this increased flow, in turn, causes a pressure change across the dentine,
which activates A- delta intradental nerves at the pulp-dentine border or
within the dentinal tubules.

It is also a common clinical finding that pain is produced when
sugar or salted solutions are placed in contact with exposed
dentin.
When the irritant is rinsed or brushed away, the discomfort
subsides.
This again can be explained by dentin tubule fluid movements.
Fluids of a relatively low osmolarity (i.e., dentinal tubule fluid)
will have a tendency to flow towards solutions of higher
osmolarity (i.e., salt or sugar solutions).
When isoosmotic solutions are applied, no stimulus is felt.

Cold

Hot


Clinical features:

•It’s a symptom complex rather than true disease
•The teeth diagonosed as exhibiting dentine sensitivity when extracted and
studied under by SEM, exhibited in excess of seven times the mean surfaces
tubule count at buccal cervical dentinal sitescompared with teeth classified
as non sensitive
•Tubules at hypersensitive sites had a mean diameter twice that at a non
sensitive sites.
•Dentinal hypersensitivity is uisually dioagonosed after other possible
conditions havbe been eliminated like chipped or fractured teeth, fracturted
restorations, caries etc.

Prevelance:

The prevelance of DH varies from 45-57%. Cause for variation is attributed
to differences in the population studied and methods of investigation 9for
eg questionaires & clinical examinations
Prevelance of DH is between 60-98% in patients with periodontitis.
[Chabanski MB et al . Prevelance of cervical dentine sensitivity in a
population of patients reffered to a specialist periodontology department:
JCP 1996; 23: 982-92]

Schuurs & colleagues reported that dentists believe DH represents a severe
problem for only 1% of their diagnosed patients.

Distribution

•It mostly occurs in patients who are between 30 & 40 yrs old, it may
effect patients of any age
•It affects women more often than men though sex difference rarely is
statically significant
•The condition may effect any tooth but it most often affects canines &
premolars; buccal cervical zones of permanent teeth.
•In right handed patients, dentinal hypersensitivity is obseved on left side
of mouth of patients.

ETIOLOGY :
Essentially exposure of the dentin may result from one of the
processes:
either removal of the enamel covering the crown or
denudation of the root surface by loss of cementum and
overlying periodontal
tissues.
Removal of the enamel may result from :
attrition
occlusal abnormalities
tooth brush abrasion
dietary erosion
habit/ parafunction

Denudation of the root surface is multifactorial with
acute & chronic periodontal disease
following non-surgical periodontal therapy
incorrect tooth brushing
chronic trauma from habits
gingival recession increasing with advancing age
Factors such as method and frequency of brushing, the brush
type, the dentifrice used all relate to the effects produced on soft
and hard tissues.
Erosive agents primarily acids, environmental, dietary or
endogenous are known to cause the damage.
Occupational:Workers exposed to fumes of HC1, sulfuric, nitric,

METHODS USED TO MEASURE /TEST HYPERSENSITIVITY :
Tactile
Thermal
Osmotic
Electrical
Tactile method :
A.The simplest tactile method used to test for hypersensitivity is
to lightly pass a sharp explorer over the sensitive area of tooth
(usually along the CEJ).
Patient response is graded on a scale.
0 - No pain felt
1 - Slight pain or discomfort
2 - Severe pain

A device with a 15 mm (0.26 gauge) stainless steel wire with a tip ground to
a fine point & movable across the highest arc curve of facial surface of the
sensitive tooth under test.
Pressur in wire is increased with adjustment screw incrementally in ¼ or
1/3 of mm until subject is able to feel a pain sensation. At that point , the
scratching force expressed in mm is taken as threshold value. If no pain is
felt tooth is considered as Non sensitive.

C. force sensitive electronic probe by Yeaple
used for measurement of periodontal pocket at fixed pressure. In dentinal
hypersensitivity test, probe force can be increased in steps of 5 gms until
the subject experience discomfort, that point is taken as pain threshold.

Hand held scratch device by Kleinberg:
Another tactile method is a hand held scratch device developed by
Kleinberg (1990) which consists of torsion gauge and a sharp
explorer like probe that can be passed easily across a sensitive
tooth.
It has an indicator that is displaced by the arm of the explorer
that records the force of displacement in centi-newtons .
A tooth that fails to respond to a force of 80 centi-newtons is
classified as non sensitive.

Thermal:
A simple thermal method for testing is directing a burst of air at
room temperature from a dental syringe on to the test tooth.
Room air is cooler than teeth and cooling by this means is easily
detected as pain if tooth is sensitive.
Air stimulation has been standardized in number of studies as a
one second blast from the air syringe of a dental unit, where its
temperature is set generally between 65° and 70° F and a
pressure 60 psi. (the air is directed at right angles to test surface
with adjacent teeth usually isolated by operators fingers).
0 - No discomfort
1 - Discomfort but no severe pain
2 - Severe pain-during application

contact metal probes have been used in a number of
Hypersensitivity studies.
The tip diameter of these probes is usually small enough to permit
placement in the cervical area of a tooth.
One such device developed by Smith and Ash, the temperature of
the probe tip was measured with a thermistor embedded in the
tip.
A flow of current in one direction was used to cool the probe tip
from room temperature to 12°C, current flow in the other
direction heated the tip to 82°C.
Intensity of the current to the probe from a power supply
controlled the temperature. The initial temperature (standard)
37.5°C
For cold stimulation 1°C is reduced and the tip is placed in
contact with tooth, for heat stimulation it is increased in 1°C
increments and placed in contact with tooth. Temperature at

Osmotic :
This method is based on the principle of osmosis i.e. movement of
fluid from higher concentration to lower concentration.
An osmotic method consisting of the subjective pain response to a
sweet stimulus was used by Mcfall and Hamrick in 1987 to
measure the effect of several test dentifrices on dentinal
sensitivity.
This was done by preparing fresh saturated solution of sucrose
allowing it to reach room temperature.
After isolation of the test tooth with cotton rolls, a cotton
applicator was saturated with sucrose solution and then applied
to the root surface of the tooth and allowed to remain in place for

Electrical :

Electrical measurements differ from the others as in this a pain response
can be obtained from non-sensitive as well as from sensitive teeth.
Instruments for application of electrical stimulus of increasing intensity,
e.g: pulp testers, were used mainly to determine the vitality.
Instrument improvements led to better quantification of the electrical
stimulus and discovery, that a condition of "pre-pain" consisting of a
tingling or warm sensation is observed before real pain and discomfort are
felt by the patient as the magnitude of stimulus is increased.
For stimulating a tooth electrically, the basic constituents are an
electrode or probe to apply the electrical stimulus so that its magnitude
can be progressively increased and a means of completing the electrical
circuit, electrolyte (eg. tooth paste) required.

MANAGEMENT OF DENTINAL HYPERSENSITIYITY:

History :
Opium therapy, the earliest recorded treatment method, dates to
400 BC and was still advocated as late as 1000 AD.
A wide variety of treatments such as henbane plant and crushed
beetles were recommended until the late 1800s.
Cocaine was introduced in 1859 and other medicaments such as
creosate and tannic acid and arsenic were used at the turn of the
century.
In the 1920s, aqueous solutions of iodine with silver iodide were
reported to be effective for relieving dentinal sensitivity and did
not blacken the tooth surface as did silver nitrate.

In 1935, Grossman suggested the criteria for the ideal
desensitizing agent.
Desensitizing agents should be
nonirritating to the pulp,
relatively pain less on application,
easily applied,
rapid in action
permanently effective,
consistently effective and
cause no staining.
Hot olive oil, formaldehyde, silver nitrate, zinc chloride, sodium
carbonate, and sodium fluoride were used in the 1950s, many of
these materials are used to stimulate the formation of secondary
dentin, and some are adhesive and used for covering the sensitive
areas.

Dental conditions with symptoms similar to dentine hypersensitivity :
Cracked tooth syndrome
Fractured restorations
Chipped teeth
Dental caries
Post-restorative sensitivity
Teeth in acute hyperfunction


Office treatments for dentinal hypersensitivity :
Cavity varnishes Stannous fluoride
Anti-inflammatory agents
Ionotophoresis
Burnishing of dentin
Strontium chloride
Silver nitrate
Potassium oxalate
Zinc chloride - potassium ferrocyanide
Formalin Restorative resins
Calcium compounds Dentin bonding agents
Calcium hydroxide
Diabasic calcium phosphate
Fluoride compounds
Sodium fluorides

Desensitizing agents:
Pattisson and Pattison listed the following possible mechanism of action for
desensitizing agents.
Precipitating or denaturing organic material at the exposed end of the
(odontoblastic process) tubule.
Depositing an inorganic salt at the supposed end of the dentinal tubules
Stimulating secondary dentin formation with in the pulp.
Suppressing pulpal inflammation
Myjor suggests that the treatment should be aimed towards a reduction in
the permeability of the dentin rather than towards an attempt to stimulate
secondary dentin .
Treatment through tubules occlusion:
Several therapeutic approaches to tubule occlusion have been developed with
promise as dentin desensitizing agents.

There are variety of physiochemical mechanisms that can lead to such
reduction in permeability and sensitivity of dentin.

Formation of calculus over sensitive tubules.
Formation of intra tubular crystals from salivary mineral
Intratubular crystals from dentinal fluid
Progressive formation of peritubular dentin
Invasion of tubules by bacteria
Formation of caries crystals
Formation of intratubular collagen plugs
Leakage of plasma proteins up into tubules
Formation of smear layer by brushing, tooth pick etc.
Formation of irritation dentin
Resin impregnation or covering
Topical application of calcium hydroxide, sodium fluoride .

The concept of tubule occlusion as a method of dentin
desensitization is logical extension of Hydrodynamic theory.
But not all agents that decrease dentin sensitivity do so by
occluding dentinal tubules.
This is because there are 2 mechanisms of action of desensitizing
agents.
One involves blocking fluid movements by occluding dental
tubules.
The other involves blocking pulpal nerve activity by altering the
excitability of sensory nerves.

Fluorides:
Sodium fluoride:
Clinical investigations have shown fluoride tooth paste and
concentration of fluoride solutions are highly efficient
especially with iontophoric technique.
Fluoride was first proposed as a desensitizing agent by
Lukomsky in 1941.
The use 2% sodium fluoride following pretreatment with, 10%
strontium chloride was observed to have an additive effect in
reducing sensitivity ( Gedalia et al 1978) although sodium
fluoride alone was still significantly effective.

It has been demonstrated that aqueous solutions of stannous
fluoride in low concentration will effectively control Dentin
hypersensitivity (Miller et al 1949).
Two concepts have been put forward for the mechanism of action
of stannous fluoride.
That it acts as an enzyme to inactivate the odonotoblastic
process. (Kutsches 1967).
That it induces high mineral content which creates a calcific
barrier on the dentin surface ( Furseth 1970).
In view of the questionable importance of the odontoblast process
in pain transmission the former suggested mode of action appears
unlikely.
As with sodium fluoride the formation of a calcific barrier

Strontium :
A possible explanation for the mechanism of action of strontium ion in
suppressing Dentin Hypersensitivity had been advanced by Gutentag.
He proposed that because calcium has been shown to establish excitable
neural membranes by modifying their permeability to Na + and K + the effect
was more pronounced and long lasting with strontium.
As a result effects in Dentin Hypersensitivity were attributed to a blockage
of the organic matrix of the tooth ( Powlowska 1956) .


Calcium hydroxide :
Calcium hydroxide has been a popular agent for the treatment of dentin
hypersensitivity for many years particularly after root planing.
The exact mechanism of action is unknown, but evidence suggests that it
may block dentinal tubules or promote peritubular dentin formation.
Increasing the concentration of calcium ions around nerve fibers can result
in decreased nerve excitability and thus suppresses nerve activity.
Potassium nitrate :
The desensitizing effectiveness of potassium nitrate used in professional
hands has been reported by Hodosh in 1974 and Green et al 1977.
Tarbet et al (1980) demonstrated for the first time that the daily use of 5%
potassium nitrate delivered in low abrasive toothpaste constituted a highly
effective home therapy regime for patients with Dentin hypersensitivity.
Penetration of K + ions into pulp, there by sensory nerves are prevented to
repolarise after depolarization.

The use of a dentifrice containing formalin was reported by Fitzgerald
(1956) who noted excellent results in most of patients seeking relief from
cervical hypersensitivity.
However, Smith and Ash 1964 using as more objective method of evaluating
responses to thermal and mechanical stimuli, found no significant alteration
of Hypersensitivity after use of dentifrices containing formalin.

Resin and adhesives :
The rationale for the use being the possibility of sealing dentinal tubules.
Results of studies were promising and have demonstrated an immediate and
long lasting blockage of sensitivity on most surfaces for between 1 month
and 1 year.
Doereig and Jensen (1985) have used light cure dentin bonding agents out of
12 participants withwww.indiandentalacademy.com
hypersensitivity, 74% reported no pain three months

Oxalates :
Oxalates have been used popularly as desensitizing agent, they are
relatively inexpensive, easy to apply and well tolerated by the patients.
6% Ferric oxalate 30% potassium oxalate and 3% Monohydrogen
monopotassium oxalate solutions are used as desensitizing agents.
The oxalate ions react with calcium ions in the dentinal fluid to form
insoluble calcium oxalate crystals that are deposited within the tubules.

Corticosteroids :
Myjor and Ferseth have reported that application of corticosteroids
preparation to dentin caused complete obliteration of tubules thus
decreasing dentin permeability.
Bowers and Elliot concluded that 1.2% solution containing 25% by weight
the parachlorophenol, 25% metacrystal acetate, 49% gumcomphor, 1%
prednisolone was effective in treatment of sensitivity due to incisal or
occlusal fracture, periodontal surgery, occlusal adjustment and post

Iontophoresis is a method of facilitating the transfer of ions by means of an
electrical potential into soft or hard tissues of the body for therapeutic
purposes.
The object of fluoride Iontophoresis is to drive fluoride ions more deeply
into the tubules than can not achieved with topical application of fluoride
alone.
It is hypothesized that fluoride Iontophoresis may increase the
concentration and depths of penetration of calcium fluoride there by
occluding the tubules and reducing the conduction of hydrodynamically
mediated stimuli.
Iontophoresis is not a simple procedure it involves the placement of a
negative electrode to dentin and a positive electrode to the patients face or
forearm. Although iontophoresis has gained some popularity, its

Lasers :
Types used : Argon, Co2, Ho:YAG, Nd:YAG, erbium YAG etc. These systems
have become available which are tailored specifically for dental surgery
using fibre optic delivery to a hand piece, smaller than a conventional
rotary dental instrument.
The availability of laser would potentially satisfy all the requirements of a
desnsitizing agent .
However question whether laser may be thermally damaging to vital tooth
structure has been raised by some investigators.
Action :
Blocks the tubules probably by fusion of crystals (Hydroxyapatite), as low
intensity defocused beam is used.
Side effects :

Burnishing of dentin :
Burnishing of dentin with tooth pick or orange wood stick will
create a partial smear layer on dentin surface, there by occluding
the orifices of dentinal tubules.


SUMMARY AND CONCLUSION
Dentin hypersensitivity is a problem that plagues many patients.
The initial or continued clinical cause, in the majority of situations, is
gingival recession.
The first step should be to identify and eliminate the cause.
Patients should be informed of all the possible steps that may be necessary
to eliminate their hypersensitivity.
The next is to rectify the recession or seal the exposed dentinal tubules
from the oral environment.
If the patient is thoroughly informed of all the possible steps then they
become a partner in the treatment process, identifying for the dentist when
they want to proceed to the next step.
This minimizes frustration on the patient's part and facilitates the process
by which the dentist solves the problem.

REFERENCES


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