Hypersensitivity implies that the dentin of the tooth involved
is exposed. The prevalence of dentin sensitivity ranged
from 8 to 30%. The prevalence increase with age, peaking
at 25 to 30 years of age, then declining due to formatio
of sclerosis dentin and/or reparative dentin. Dentin sensitivity
can wax and wane over time in the same individual. Patient
diet and personal habit may play a major role. Acidic food
may attribute to the occurence of dentinal hypersensitivity.
Most importantly, the presence of plaque may exacerbate
the problem due to high amount of bacteria and bacterial
product, coupled with acid production and further causing
irritation. Dentin sensitivity usually observed on the buccal
cervical areas of canines and premolars, commonly occured
after oral prophylaxis or root planing due to exposed dentinal
tubules. Finally, dentinal hypersensitivity may occur due
to systemic problem such as in patient with bulimic problem
or stomach regurgitation, which in turn lead to loss of
enamel and expose coronal dentin. Exposed coronal dentin
is much more difficult to treat than cervical dentin because
of its higher permeability and innervation density.
To fully understand all the mechanism behind dentinal hypersensitivity,
we must understand the dentin formation and its structure.
Dentin is composed of inorganic and organic parts. Inorganic
compounds composed mainly of hydroxyappatite, whereas the
organic counterpart are mainly collagen. Dentinal tubule
is formed as the odontoblast layed down the predentin, the
odontoblast recede and leave behind the odontoblastic process
trapped within the tubule. The diameter of dentinal tubules
after demineralization and /or air drying has been quantified
using light microscopy and scanning electron microscopy
by J. Arens et al. in 1995. The tubule diameter was measured
in wet state, after 10 min and 12 hour air drying as well
as after critical point drying (CO2) by SEM. The results
show that the drying effects on tubule diameter are small
in sound tissue, but are sizeable in demineralized dentine.
Comparing the light microscopic and SEM observations show
that the difference in tubule diameter are small for sound
but substantial for demineralied dentine. The dentine tubules
in wet states are 2.5 micron, decrease in diameter as we
increase demineralization by drying. The decrease tubule
diameter with increasing demineralization occured may be
important for permeability and transport phenomena in dentine
caries and presumably hypersensitivity. As caries attack
the tooth, the acid produced by dnetal plaque demineralized
the mineralized tissue. The mineral crystallites in and
on collagenous structure prevent collagen expansion. If
the mineral is gradually removed by the acid system, the
collagenous structure expand. J. Aren showed in his investigation
that demineralization increase tubule size initially, but
increasing mineral losses decrease the tubule size, and
water loss caused by drying, increase tubule size in demineralized
dentine, and finally the tubule diameter in sound dentine
is not strongly influenced by air drying.
It has been demonstrated that the intradental A type (A
beta and A delta) nerve fibers are responsible for the sensitivity
of dentin and that the endings of the responding fibers
are located in the pulp-dentine area of the tooth. The nerve
fiber entering the teeth have been identified histologically
as myelineated A fibers and unmyelinated C-fibers. These
fibers are grouped in bundles, enter through the apical
foramina of the teeth, passing through the radicular to
coronal pulp where they fan out and diverge into smaller
bundle. The A fiber within small bundles lose there myelin
sheath and divide repeatedly before finally ramifying into
a plexus of single axon known as the subodontoblastic plexus
or plexus of Raschkow. From this plexus, nerve fibers are
distributed toward the pulp dentin border with terminals
showing a characteristic bead like structure. The fibers
are grouped into four types: the marginal fiber which extend
from suboddontoblastic nerve plexus to the odontoblast layer
but do not reach predentin, the simple predentinal fiber
which extend to the odontoblast/predentin border or enter
the predentin, the complex predentinal fibers which reach
predentin and undergo terminal ramification with multiple
branches and multiple ending like enlargement on each branch,
and the dentinal fibers which pass through the predentin
and enter the dentin throught he dentinal tubule (its penetration
is limited to approximately 100 microns). Ten Cate and coworker
reported that odontoblast cell process extended only to
the amelodentinal junction. Avery and Llja demonstrated
approximately 25-27% of dentinal tubules has associated
nerve fiber. More recently, sensory nerve fibers were identified
in dentinal tubules by autoradiography technique. The A
delta fibers are most responsible for the sensitivity of
dentin. The A beta fiber respond to the non painful sensation
induced by the low intensity electrical stimulation of human
teeth. The exact mode of transmission of stimuli (thermal,
chemical, mechanical) is investigated by D.G. Gilam in 1995.
Three hypothesis suggested the mechanism of dentinal sensitivity
transmission: a)nerve ending or nociceptor that respond
directly when the dentin is stimulated, located throughout
the dentin, b) the odontoblast, being chemically or electrically
related to the nerves, function when depolarized as receptors
generating nerve impulses; and c) stimuli applied to dentin
producing a displacement of dentinal tubule contents which
could excite mechanosensitive nerve endings near the pulpal
end of the tubules (hydrodynamic mechanism). The mode of
transmission to be explained here are direct nerve stimulation,
dentinal receptor (transducer/modulation), hydrodynamic,
and direct ionic diffusion hypothesis. Firstly, dentinal
sensitivity may be caused by direct stimulation of nerve
fibers. This theory was disproved in explanation of dentin
hypersensitivity since algogenic (pain inducing) substance
applied to the exposed dentin did not elicit a response.
Similarly, topical anaesthetic solution when applied to
the exposed sensitive dentin did not decrease sensitivity.
Possible explanation for these phenomena included there
is no nerve element in dentin or there are receptor mechanism
in dentin that could be stimulated indirectly, but cannot
be reached by direct stimulation from chemical agents becauses
of some barrier to diffusion in the tubules. Secondly, the
proponent of dentinal receptor mechanism hypothesis have
suggested that the odontoblast has a special sensory function
and that a functional complex with the terminal sensory
nerve endings in close proximity to the odontoblast layer
acts as an excitatory synapse. Several investigation however
have failed to establish the presence of any synaptic junction
or special form of connection between odontoblast process
and nerve endings. It was unlikely that the odontoblast
could perform the function of a special sensory receptor
cell, which at the same time functioning as the specialized
formation cell of dentin. Thirdly, the hydrodynamic theory
is suggest to explain the dentinal hypersensitivity phenomena.
The tubule contains fluid and the displacement of tubule
contents, if rapid enough, could deform nerve fibers in
pulp or predentin, or damage odontoblast cells; both effects
capable of producing pain. Minute fluid shifts, either dentinal
fluid or tubule contents, across dentin in either direction,
in response to tactile, thermal, osmotic (chemical) stimuli,
can stimulate mechanoreceptors in or near the pulp, which
in turn, excite sensory nerves (A beta and A delta classes)
to cause pain. According to Pashley, the hydrodynamic theory
of dentin sensitivity as proposed by Brannstrom is based
on the premise that sensitive dentin is permeable throughout
the length of the tubule. Brannstrom and other investigator
demonstrated in a series of experiment that fluid shifts
occurred through the dentinal tubules when pressure and
dehydration, as well as thermal stimuli, were applied to
dentin. Following a decrease in pressure, there appeared
an intense evaporation from the dentinal surface, producing
a rapid fluid shifts which activate nerves located at some
distance form the tubules corresponding to the exposed dentin.
Dehydration (may occur due to hypertonic solution such as
sugar and calcium chloride) causes the removal of dentinal
fluid from the exposed dentin surface and by capillary action
elicit an outward flow of tubule contents form the pulp,
stimulating the odontoblast structure and causing pain.
When cold or thermal change applied to the dentin, it was
observed to cause a contraction of tubule contents, which
in turn resulted in a rapid outward movement of fluid away
from the pulp. Heat usually produced a dull response and
took longer to develop, in contrast to the immediate sharp
pain elicited from the cold stimulus. This delay in response
may occurred due to a specific threshold of pulp temperature
must be reached before pain can be experienced. Finally,
several investigators suggested that application of various
chemical solution to dentin resulted in raising the intratubular
K+ content which in turn rendered the intradental nerves
less excitable to further stimuli by depolarizing the nerve
fibers membrane. Kim and Markowiz proposed the alternative
mechanism (modified hydrodynamic theory), namely desensitization
of dentin by blocking nerve activity.
Currently, the most accepted mechanism of intradental nerve
activation associated with dentin sensitivity appears to
be hydrodynamic in nature, although alternative mechanism
of transmission cannot be ruled out. Recent investigation
in the animal study (cat) has provided evidence substantiating
the hydrodynamic hypothesis.
Rimondini and Carrassi in 1994 determined the relationship
between the dentine ultrastructure and the clinical symptoms
in patients with cervical dentine exposures. Total of 28
teeth with cervical noncariouus lesions and dentine exposures
were obtained before and after acid etching. 120 areas were
randomly selected from the 28 dentine surfaces were analyzed.
The presence and morphology of smear layers and the density
and diameter of dentine tubules were recorded. In the unetched
specimens, the nonsensitive dentin surface were frequently
coated by the amorphous smear layer (88%) and occasionally
by a crystalline smear layer (2.7%). Only a few and narrow
tubules were observed on the nonsensitive dentine (9.3%).
On the other hand, the unetched hypersensitive specimen
exhibited less frequently (33.3%) an amorphous smear layer,
many and wider patent tubules, and grooves between tubules
due to loss of intertubular dentine. In hypersensitive dentine,
acid etching always removed the smear layer whereas removal
in nonsensitive dentine was partial or absence. The hypersensitiv
dentine smear layer was different in structure and undercalcified.
These findings are supportive of the theory of increased
hydrodynamic permeability of hypersensitive dentine.
During periodontal therapy, scaling and root planing removed
the outer layer of hypermineralized dentine and thus leaved
the surface expose to the effect of hydrodynamic phenomena.
Surgical periodontal treatment, similarly, usually involved
complete debridement of root surface. Post operative recession
of soft tissue further exposed the dentinal tubules. Patient
inability to maintain plaque control in the healing phase
further complicated the problem, as plaque and acid production
due to plaque accumulation could act as a noxious stimuli
and cause dehydration and lead to fluid movement across
the dentinal tubule. Instrumentation of the root creates
an outer contiguous smear layer covering the instrumented
surface as well as pushing debris into the dentin tubules
for several micrometer. The smear layer thus is a natural
iatrogenic yet transient treatment to dentin hypersensitivity.
Removal of the outer smear layer and smear plugs with acids
permits an increased in outward fluid flow and thus increase
the patient postoperative dentine hypersensitivity.
Grossman in 1931 suggested that the ideal desensitizer should
be: not unduly irritating to the pulp, painless when applied,
easy to apply, consistently effective, permanently effective,
quick acting, and not causing tooth discoloration. Another
quality that we might add is that the ideal densensitizer
should not interfere with the subsequent regenerative outcome,
if such procedures are deemed necessary at the future time.
We can break down the methods of desensitizing dentine into
topical methods, iontophoresis, use of restorative material,
electrosurgery, lasers, and guided tissue regeneration to
cover gingival recession.
Firstly, the topical methods included the topical applications
of caustics obtundants, fluorides, varnishes, oxalates,
and potassium nitrates. The caustics chemical are usualyy
silver nitrate, zinc chloride, phenol, formaldehyde, concentrated
alcohol, strong acid and alkalis. They are used in attempt
to precippitate proteins; however, they are harmful to the
pulp and should be avoided. Fluorides, on the other hand,
have been proven to be effective for several days to several
weeks (Hoyt and Bibby, 1943) when applied topically to the
area of dentinal exposure. Its mechanism of action involved
a formation of barrier by precippitating the CaF2 at the
tooth interface. However, this precipitate is slowly soluble
in saliva and thus the effect is temporary and needed to
be reapplied. The common commercial preparation of fluoride
is .4% stannous fluoride in glycerine vehicle; however,
the glycerine vehicle can activate the hydrodynamic mechanism
and cause pain upon application. Neutral sodium fluoride
should be used when patient had esthetic porcelain restoration
or implant in their mouth, since the acidity of stannous
fluoride may etch the restoration. Another topical method
is the copal varnish but its action only last several hours
and thus is used as the vehicle for fluoride. Oxalates consisting
of 3% KH2PO4 followed by 30% K2HPO4. Commercial product
including potassium oxalate and ferric oxalate are effective
in bloking the tubules. However, they have the same draw
back as in the case of topical fluoride: eventually the
saliva dissolves the surface precipitate that forms the
barrier. Finally, 5-30% potassium nitrate, as proposed by
Markowitz and Kim, can act directly on pulp nerves. However,
it would have to be applied frequently and reach a sufficient
concentration at the site of neural transduction.
Iontophoresis is the process of introducing ionic drugs
into the body surfaces for therapeutic purpose. Iontophoresis
requires that a charged drug (fluoride usually) be delivered
at the electrode of the same polarity, the condition or
disease under treatment be at or near surface, and a modern
sophisticated source of direct current, with appropriate
means of application be used. Murthy et al. in 1973 reported
the effectiveness of fluoride iontophoresis. They concluded
that the desensitization occurred immediately after iontophoresis
in most patients, whereas the placebo was ineffective. The
1% fluoride iontophoresis provided a statistically more
effective treatment than placebo or topical applications.
Also the burnishing of 33% topical fluoride paste was only
modestly effective. Gangarosa recommend that fluoride iontophoresis
is permanent in its effect when the dentist applies it correctly
to exposed dentine; however, highly sensitive teeth require
two or rarely three treatments about 1 week apart before
the effect can be considered permanent (lasting over 1 year).
The mechanism of action of iontophoresis have been proposed
as: a) rapid formation (7-28 days) of reparative dentine
following application of current, b) the alteration of the
sensory nerve condution by the electrical currents, and
c)fluoride ion, when introduced into dentinal tubule via
iontophoresis, can reduce dentine permeability. The third
mechanism has been supported the most by literatures. Iontophoretic
fluoride desensitization occurred by two mechanism: the
intratubular microprecipitation of CaF2 affecting dentine
permeability and an effect of fluoride on the neural transduction
The use of restorative material also have been proposed
to treat dentine hypersensitivity. Treating hypersensitivity
with resins was pioneered by Brannstrom and his colleagues.
Second generation composite (Scotch bond) can be laid down
successfully over lesions treated with fluoride iontophoresis.
Application of cyanoacrylate has been done with good desensitizing
effect. However, the complication of the first and second
generation composites was that the incidence of sensitivity
actually increased during use for aesthetic restoration.
The third and fourth generation bonding agents such as Gluma,
Scotchbond II, All Bond, and C&B metabond allow better
bonding to dentine, require less bulk for strength, penetrate
the tubules better. The use of restorative material to treat
dentine sensitivity is technique sensitive and expensive
but offer the hope of longer lasting and more predictable
results than topical agents. The choice of technique between
iontophoresis and restorative material may depend on availability
of the materials and the office personnel involved. Hygienist
can perform iontophoresis, whereas dentist must perform
all restorative technique.
Treatment of hypersensitivity by electrosurgery has been
advocated by Oringer in 1975. However, the postoperative
complications included irritation and pain due to pulpal
injury by excessive heat generation are the major draw back.
The Nd: YAG laser have been investigated in its use as
an ideal desensitizing agent, except for the long term effects,
which were not measured. The pulpal effect of laser requires
more investigation prior to its acceptance to be used with
the hard tissue. Currently, hard tissue application using
laser has not been approved.
Finally, the use of gingival graft on recession defect
has been documented successfully. Regenerative procedures
using resorbable membrane, free gingival graft for root
coverage, connective tissue graft have provided successful
result in terms of both functional and esthetics. The major
draw back is the selection criterias for each procedures,
the technique sensitive, and the cost of treatment. Nevertheless,
when can be done, periodontal plastic surgery is the best
and ideal treatment in providing a long lasting result and
The clinical goal to treat hypersensitive dentin is to provide
a permanent seal of dentin tubules. The seal can be established
by any of the above methods and if done correctly, will
provide the therapeutic effects. Patient must recognized
in some situation the condition may recur and require several
application or retreatment. His or her oral hygiene must
be emphasized to reduce the plaque accumulation in the area.
The dentist also required to evaluate his or her systemic
condition, nutritional diet, and be able to communicate
with the patient on issues regarding his or her periodontal
health and its correlation to the dentinal hypersensitivity.
1. Kleinberg, Kaufman, Wolff, M. Measurement of tooth hypersensitivity
and oral factors involved in its development. Archs oral
Biol., 39: 63S, 1994.
2. R. Orchardson and Peacock, J. Factors affecting the nerve
excitability and conduction as a basis for desensitizing
dentine. Archs oral Biol., 39: 81S, 1994.
3. Gangarosa, L. Current strategies for dentist applied
treatment in the management of hypersensitivity dentine.
Archs oral Biol., 39: 101S, 1994.
4. Jerome, C. Acute care for unusual cases of dentinal hypersensitivity.
Quintessence International, 26:715, 1995.
5. Touyz, L. The acidity and buffering capacity of canadian
fruit juice and dental implications. Journal of Canadian
Dentistry, 60: 454, 1994.
6. Cox, C. Etiology and treatment of root hypersensitivity.
American Journal of Dentistry, 7:266, 1994.
7. Griffith, H., Morgan, G., Williams, K., Addy, M. Dentine
hypersensitivity: the measurement in vitro of streaming
potentials with fluid flow across dentine and hydroxyapatite.
Journal of Periodontal Research, 28: 60, 1993.
8. Ramachandran Nair, P. Neural elements in dental pulp
and dentin. Oral surgery, oral medicine, oral pathology,
80: 710, 1995.
9. Rimondini, L., Baroni, C., Carrassi, A. Ultrastructure
of hypersensitive and non-sensitive dentine. A study on
replica models. Journal of Clinical Periodontology, 22:
10. Arends, J., Stokroos, I., Jongebloed, W.G., Ruben, J.
The diameter of dentinal tubules in human coronal dentine
after demineralization and air drying. A combined light
microscopy and SEM study. Caries research, 29: 118, 1995.
11. Gillam, D.G. Mechanisms of stimulus transmission across
dentin-A review. Periodontal Abstracts, 43: 53, 1995.
12. Pashley, D. Theory of dentin sensitivity. Journal of
Clinical dentistry, 5: 65, 1995.