Dentine hypersensitivity

ETIOLOGY AND CLINICAL IMPLICATION OF DENTINE
HYPERSENSITIVITY
Introduction :
• Relatively common cause of pain associated with teeth.
• “An enigma”, frequently encountered but ill understood :
•
• Suitability of term questionable. In most cases pain is initiated and
persists only during the application of a suitable stimulus to the
exposed dentin surface, associated with many conditions including
dental caries.
• There is no evidence to indicate that “Hypersensitive” dentin differs
in anyway from normal dentin or that specific pulpal changes occur.
Term “Dentine sensitivity” may be more appropriate.
Definition : Dentin hypersensitivity may be defined as pain arising from
exposed dentine, typically in response to chemical, thermal, tactile or
osmotic stimuli that cannot be explained as arising from any other form of
dental defect or pathology.
It is perhaps a symptom complex rather than a true disease and results
from stimulus transmission across exposed dentine.
Other conditions which may produce some symptoms include:
• Chipped teeth
• Fractured restorations
• Restorative treatments
• Dental caries
• Undisplaced cracked cusps.
• Palatogingival grooves / other enamel invaginations.
History :
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Tooth / dentin hypersensitivity is one of the oldest recorded
complaints of discomfort to people.
Inspite of a considerable amount of research over the last 50 years
clinical management of dentin hypersensitivity still remains largely
empirical because the physiologic mechanism remains ill defined and to
some extent poorly understood.
Mid 19th
Century :
Dr. John Neill of Philadelphia, postulated that “Dentin consists of
hallow tubules filled with a fluid secreted by the pulp, and pressure applied
without, by compressing the enamel and fluid of the tubules, affects the
nervous pulp within, by subjecting the letter to a species of hydrostatic
pressure, the amount of which can be measured. Whatever reduces the
thickness of the enamel or uncovers any portion of the dentin, increases the
painful impression caused by external pressure”.
100 years later Kramer proposed the “Hydrodynamic theory” as “The
dentinal tubules contain fluid or semifluid materials and their walls are
relatively rigid. Peripheral stimuli are transmitted to the pulp surface by
movements of this column of semifluid material within the tubules.
Work by Braunstrom resulted in widespread and current acceptance
of the hydrodynamic theory.
The early years from BC to 20th
century :
Pain in the teeth “Ya-Tong” treated by Chinese some 2000 years ago
by application of “Xiao –Shi” believed to be Niter or potassium nitrate.
Egyptian papyous Ebers, (3700 BC to 1550 BC), described gingivitis,
the pain associated with tooth erosion and tooth ache. Rhages an Arabian
physician 875 AD, first recognized the pain associated with gum recession,
which occurred mostly in older people, and observed that it may be a
difficult ailment in some and simple in others. Suggested treatment with
astringent salts.
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Leeuwenhock, shortly, after his invention of microscope described
“tooth canals in dentin”. In 1678, he reported “It is asserted that the tooth is
formed from very narrow, transparent tubes six or seven hundred of these
pipes put together exceed not the thickness of one hair of a man’s beard”.
Mid 1860’s Francis presented view of fluid movement impinging on
pulpal nerves and causing pain and supported the practice of using cavity
liners to promote the development of secondary dentin for “Better self
protection”.
For serious sensitivity problems, he recommended a paste of arsenous
acid, tannin and creosote.
Late 1880’s use of carbolized potash (Robinson’s Remedy)
(trituation of equal proportion of carbolic acid and potassium hydroxide)
came into widespread use for treating sensitivity of dentin. (No one had yet
ascribed the effect to potassium ions until quite recently i.e.
In 1900 issue of British Journal of Dental Sciences, a published report
appeared by Alfred Gysi, stated that “dental conaliculi are devoid of
nervous substances”, but that at inner boundary of dentine around the
odontoblasts there is an “abundant network of finest nerve fibers. He
proposed that movement of fluid in dental canuliculi in either direction
results in a sensation of pain in the nerves interwoven with the odontoblasts.
“Drawing” or movement of fluid away from pulp can be induced by “salt,
sugar, alcohol etc.” He also stated that “when however the externalportion
of the contents of the tubuli is caused to coagulate albumen, such as by
carbolic acid or formed of sublimate and thereby loses its mobility, then
also the great sensibility disappears”.
Although Gysi was not the first to describe fluid movement in
dentinal tubules, he was among the first to suggest relieving dentin
sensitivity by coagulating its protein content.
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1st
edition of a textbook of dental pathology and therapeutics
including pharmacology by Henry H. Burchard in 1898 provides a
categorization of 3 approaches for controlling pain of hypersensitivity of
dentin.
1. Administration of agents to lower the pain perceptive centers of the
brain (anesthetic and analgesic agents)
2. Use of agents to destroy or coagulate the dentinal protoplasm (zinc
chloride, silver nitrate, carbolic acid, mineral acids, concentrated
alkalies and others).
3. Use of local anesthetic agents on the dentin (essential oils, sedative
alkaloids, morphine, atrophine, cocaine etc.)
Suggestion was made for the use of an electric current to deliver
medicaments more effectively.
First half of twentieth century :
Textbook dental pathology and therapeutics, Henry Burchard states
“The exposure of dentine to external agencies is so commonly followed by
an increase in sensitivity that the condition requires description in itself. It is
a general condition attendant upon abrasion, erosion and caries, and has a
therapeutics of its own”.
The nitrate of silver powerfully coagulates fibrillar protoplasm,
forming albuminate of silver, which turns black upon exposure to light.
Subsequent use of sodium chloride reduces staining.
“Potassium carbonate in glycerin may be given to the patient for self
treatment at home”.
Mid 1930’s, 2 important publications appeared that include Charles F
Bodecker and Edward Applebaum’s and second by Louis I. Grossman.
First was regarding active metabolism in the dentin. Their
conclusions were that there is an active exchange between the fluids of the
dental pulp and the structure of the teeth. In young teeth, fluid flows readily
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from the pulp and provides the necessary calcium phosphorus and carbonate
to carry on mineralization process.
The odontoblasts that line the pulp chamber and pulp canal are
probably secretory cells. Residual fluid, depleted of salts, passes back
through Neumann’s sheath into the circumtubular space. When caries
threatens the tooth structure, a defensive mechanism occurs to put down a
layer of secondary dentin to help protect the pulp.
In young teeth, this process is not yet well developed, and the carious
process proceeds rapidly to involve the pulp.
2nd
publication by Louis I. Grossman 1935 gave a comprehensive
summary of causes of hypersensitive dentin and the methods used to treat it.
According to him, hypersensitiveness in dentin describes an
uncommonly sensitive or painful response of the exposed dentin to an
irritation. This includes dentin exposed by caries, attrition, abrasion or
erosion, by failure of the enamel to meet the cementum and by marked
atrophy of the alveolar process, exposing both dentin and cementum.
Chemical stimuli that affect hypersensitive dentine include citrus fruits,
berries, acid food stuffs such as tomatoes or rhubarb, vinegar, candy, sugar,
salt and other condiments and many raw and cooked foods.
Physical stimuli include temperature below 100
C or above 400
C or
tactile pressure.
He pointed to Gysi’s explanation that because fluid in tubules is
incompressible, a stimulus induces a wave like motion transmitted to the
pulp.
Grossman listed the requirements for an ideal therapy :
1. It should not usually irritate or in any way endanger the integrity of
the pulp.
2. It should be relatively painless on application or shortly afterward.
3. It should be easily applied.
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4. It should be rapid in its action
5. It should be permanently effective
6. It should not discolor tooth structure.
1936, Dr. Hartmann proposed application of a balanced micture of ether
chloroform and thymol based on the theory that lipoids present in dentin
play an important role in transmission of sensation.
“Semitex” a commercial densitizing agent in solution form was a
chloride of metals : sodium, magnesium, zinc, potassium, aluminium,
calcium, aluminium oxide, and triple distilled water.
In 1941, Lukomsky advocated sodium fluoride as a desensitizing
obtundent.
Hoyt & Bobby (1943) reported an effectiveness of a paste made of
equal parts of sodium fluoride, white clay and glycerin. Since this report, it
has probably been the most extensively used dental office therapy to treat
hypersensitivity.
2nd
half of 20th
century :
Emoform toothpaste was introduced in Switzerland by Dr. Wild in
late 1940’s. It contained :
- Formaldehyde 1.4%]
- Calcium carbonate 14%
- Magnesium carbonate 15%
- “Mineralizing salt” mixture of Sodium bicarbonate 3.4%
Sodium chloride 1.45%
Potassium sulfate 0.0075%
Sodium sulfate 0.0075%
Introduced in U.S. as Thermodent.
Pawlowska 1956 published a report stating that strontium chloride
“combined with biocolloids of teeth” exerted a favourable effect on
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hypersensitivity, based on this report sensodyne toothpaste was developed
with strontium chloride hexohydrate.
A possible explanation for mechanism of strontium ion was advanced
by Gutentag. He proposed that since calcium has been shown to stabilize
excitable neural membranes by modifying their permeability to sodium and
potassium, the effect is more pronounced and longer lasting with strontium.
In 1962, Bromstrom summarized the “Hydrodynamic theory of
dentinal pain excitation.
Everett and colleagues summarized in 1966 therapies popular for
treatment.
1. A paste containing 2% formaldehyde in a vehicle of calcium
carbonate, magnesium carbonate, sodium bicarbonate and soap
powder.
2. A formaldehyde containing mouthwash.
3. Fluorides in various forms and their vehicles, applied either alone or
by a sequential treatment with calcium hydroxide.
4. Strontium chloride
5. 28% Ammoniacal silver nitrate.
6. Zinc chloride – potassium ferrocyanide impregnation (Gottlieb’s
solution) in which the active ingredients are applied sequentially.
7. Corticosteroids
8. Sontophoresis with fluoride
In 1974, Hodosh proposed a “superior” densensities, potassium nitrate.
Presumably, the mechanism depends on the ability of K+
to permeate
through the dental tubules to nerve endings at the dentin-pulpal junction and
there to modify the usual exchange of sodium and potassium in nerves (Na+
K+
Pump)
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Berman proposed the term “dentinalgia” to differentiate sensitivity
from “Pulpalgia”. The “gate control therapy” and the hydrodynamic theory
were proposed as most probable mechanisms.
Orchardson and coworker published reports on some characteristics
of tooth hypersensitivity. In one report, 109 patients in Scotland were
examined for hypersensitive dentin 80% were sensitive to cold alone or to
cold and some other stimuli.
Lower 1st
molars and upper canines were most frequently affected,
and 68% of hypersensitive teeth had significant recession but only 25
percent had evidence of abrasion, attrition or erosion.
Use of iontophoresis with sodium fluoride has been reevaluated in
recent years. Carla Ciancio and Seyrek reported that over 90% of patients
thus treated had a significant reduction in sensitivity.
Kleinberg (1986) summarized the different approaches that have been
used to treat hypersensitive dentin.
1) Remineralization by saliva deposits of calcium phosphate complex
within dentinal tubules.
2) Formation of secondary dentin, which may occur naturally or can be
stimulated by daily burnishing.
3) Calcium hydroxide facilitates calcium phosphate deposition from
dentinal fluid and saliva.
4) Potassium oxalate forms calcium oxalate within dentinal tubules.
5) Sodium fluoride promotes the deposition of less soluble fluoropatite
6) Sliver nitrate precipitates proteins within dentinal tubules
7) Strontium chloride forms strontium hydroxyapatite and strontium
phosphate within dentinal tubules.
8) Resins seal the outer ends of dentinal tubules.
9) Potassium nitrate appears to be effective.
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10) Dentrifices may provide one of the active ingredients above or
function by occluding tubular orifices.
Krawer pointed out that severe cases of sensitivity can be so
problematic as to cause an emotional change among sufferers that can alter
lifestyle.
SUMMARY :
For well over a century, there has been cognizance that sensitivity is a
serious problem, that is arises when the dentin and cementum are exposed,
that fluid movement within the dentinal tubules acts as a provocative
stimulus, that tubules can be sealed off (apparently in most instances)
without damage to the tooth or the dental pulp, and that the problem can
also be at least partially resolved by suppressing nerve firing within the
pulp.
Sealing off the dentinal tubules or dampening neural impulses,
although admittedly none meet all of the hypothetic requirements proposed
by Grossman over 50 years ago. Fluorides, strontium chloride, potassium
nitrate, potassium oxalate, sodium citrate, surface sealing agents (varnishes,
resins, cyanoacrylate), calcium hydroxide, and others.
Tooth hypersensitivity in the spectrum of pain :
As an exaggerated response to a non-noxious sensory stimulus. The
sensory stimuli usually considered are thermal by the application of a burst
of air to the tooth and tactile by running a metal instrument across the
hypersensitive region of the tooth. Tooth hypersensitivity is viewed as
originating from the underlying exposed dentin. Merskey for the
international association for the study of pain (IASP). Pain is described as
an unpleasant sensory and emotional experience associated with actual or
potential tissue damage or described in terms of such damage. Tooth
hypersensitivity is not associated with actual tissue damage in the acute
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sense but can involve potential tissue damage with constant erosion of the
enamel or cementum along with the concomitant Pulpal response.
Allodynia pain resulting from a non- noxious stimulus to normal skin.
“Allodontia” to describe appropriately tooth hypersensitivity is a chronic
condition with acute exacerbations. Chronicity ends when the enamel or
cementum defect is restored; however, differs from dentinal and Pulpal pain
in that the patient’s ability to locate the source of pain is very good. Aside
from that characteristic Tooth hypersensitivity is similar in its description to
dentinal pain – i.e., in terms of its differential diagnosis. The character of the
pain does not outlast the stimulus, the pain in intensified by thermal change,
and sweet and sour. Pain intensity is usually mild to moderate; both can be
associated with caries, defective restorations, and exposed dentin. The pain
can be duplicated by hot or cold application or by scratching the dentin, and
both tooth hypersensitivity and dentinal pain usually show a normal
radiographic architecture of the peripheral region.
Dentinal hypersensitivity is a response from a non-noxious stimulus
and a chronic condition with acute episodes; whereas dentinal pain is a
response from a noxious stimulus and usually an acute condition. A clear
understanding of tooth sensory conduction still needs further elucidation to
aid the clinical investigator in choosing the most appropriate clinical model.
The fact that local anesthetics applied topically to dentin are not affective
and that one can still elicit a pain response from a root-canaled tooth (from
exteroceptors from the periodontal ligament) present challenging in vitro
and in vivo hurdles to overcome in the future by dental scientists in
deciphering the mechanism of action.
DENTAL HYPERSENSITIVITY :
Pulpal considerations :
The tooth pulp and dentin are now known to be innervated by A-delta
and C-fibers that form an interlacing network, the subodontoblastic plexus.
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From this plexus, nerve fibers extend to the odontoblastic layer, predentin,
and dentin and terminate as free nerve endings. The sensory receptors
respond to chemical, thermal and mechanical stimuli and are thus termed
polymodal. It has been proposed that A-delta fibers are responsible for
dentinal pain, and C-fiber nociceptors (receptors preferentially sensitive to a
noxious or potentially noxious stimulus account for the pain from external
irritants that reach the pulp. Morphologically, nerve fibers may penetrate
into the dentin as far as 150 to 200 µm only. Except possibly for serotonin,
many vasoactive substances implicated in pain (such as substance P,
bradykinin, and histamine) appear to have no direct effect on A-delta Pulpal
afferent but may activate C-fiber Pulpal afferents. Sympathetic nerve
simulation and changes in blood flow can alter Pulpal afferent activity, and
it now seems likely that these substances may have indirect effects by
altering blood flow.
The neural theory attributes activation to an initial excitation of those
nerves ending within the dentinal tubules. These nerve signals are then
conducted along the parent primary afferent nerve fibers in the pulp into the
dental nerve branches and then into the brain. The hydrodynamic theory
proposes that the stimuli cause a displacement of the fluid that exists within
the dentinal tubules. This mechanical disturbance activates the nerve
endings in the dentin or pulp. The odontoblastic transduction theory
proposes that the stimuli initially excite the process or body of the
odontoblast, the membrane of which may come into close apposition with
that of nerve endings in the pulp or in the dentinal tubule, and that the
odontoblast transmits the excitation to these associated nerve endings.
Technically, enamel and cementum erosion of a tooth would satisfy
the definition of inflammation (i.e., a localized protective response elicited
by injury or destruction of tissue), which serves to destroy, dilute, or wall
off both the injurious agent and the injured tissue. The tooth can mask the
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classical signs of acute inflammation including heat, redness, and swelling
to some extent, but not pain and loss of function (sensitivity to chewing,
percussion and air). It is interesting to speculate the role, if nay that the
process of inflammation plays in the chronic conditions of dentinal
hypersensitivity. The biochemical cascade involved would allow a wide
range of clinical and Pharmacologic approaches for its treatment.
Currently the treatment of choice for the chronic management of
dentinal hypersensitivity. The active agent that has the widest data base of
in vivo as well as in vitro studies is strontium. 1) cariostatic effects,
especially in the pre-eruptive phase of tooth formation, 2) strontium can be
taken up at extra-vascular site and the retention is by surface adsorption; 3)
strontium can be sued to differentiate two different forms of acetylcholine
(ACh) secretion and is effective in supporting asynchronous, neurally
evoked ACh release asynchronous ACh secretion is the delayed, residual
increase in miniature end-plate potential frequency evoked by repetitive
nerve impulses that can be analogous to dentinal hypersensitivity; 4) in
many secretory processes, strontium can substitute for calcium in activating
the secretory mechanism, and can possibly affect or modulate the Pulpal
cholinergic and adrenergic mechanisms involved in dentinal
hypersensitivity; and 5) strontium can increase the time of the rat trial-flick
response suggesting analgesia and may possess central analgesic potency
similar to narcotic drugs by possibly altering the calcium disposition
including binding or transport. Strontium chloride dentifrices have been
suggested to work by occluding dentinal tubules by binding to the tubules
matrix and / or stimulating reparative dentin formation.
The simplest conclusion to be drawn is that in vitro models do not
provide a good model to extrapolate data to explain human dentinal
sensitivity. In humans stimuli are applied to outer dentin, whereas in animal
models the stimuli are applied to deep cavities, where the length and width
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of the tubules would facilitate a direct action on nerves in the inner dentin or
pulp. Additionally, dentin electrodes can record from only a limited sample
of the total intradentinal nerve population, not taking into account neural
convergence or summation. More than twenty peptides have been identified
in the nervous system; some (such as bradykinin, serotonin, and substance
P) have been identified or associated with sensitization of the tooth.
Sensitization of tooth neciceptors after repeated exposure to noxious stimuli
can lower the nociceptor threshold, allowing for increased sensitivity to
what was normal and is now a suprathreshold stimuli (hypersensitivity) and
if persistent to spontaneous activity (odontalagia).
Subjective considerations :
To evaluate the subjective responses of pain, many pain-word
questionnaires, visual analog scales, and lists of worlds are currently
available and have been used to assess various pain syndromes with
controversy as to which are the most appropriate. To assess a patient
completely an evaluation of the physical determinants of pain should be
supplemented by an assessment of at least two other components – one
observable, the other more subjective.
Gracely has listed five properties for an ideal pain measure to both
optimize the information gained on the subjective component, and to relate
the clinical and experimental assessment of pain. They are 1) sensitive
measurement free of biases inherent in different assessment methods; 2)
provision of immediate information about the accuracy and reliability of the
subject’s performance in the task; 3) separation of the sensory –
discriminative aspects of the pain experience from its hedonic qualities; 4)
usefulness for clinical as well a experimental pain measurement, allowing
reliable comparisons between these fundamentally different types of pain; 5)
absolute measures that increase the validity of pain comparisons between
and the within groups over time.
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Chronic pain is a learned behavior, and the chronic pain patient is a
person who acts like a chronic pain patient. It is immaterial whether the pain
is somatogenic, neurogenic, or psychogenic (or for that matter, whether
there “really” is any subjectively experienced pain). Chronic dentinal
hypersensitivity patients acquire learned behavior characteristics such as
avoiding cold drinks and certain foods, not opening their mouths, on cold
days, and avoiding tooth brushing in sensitive areas – possibly making them
susceptible to gingival and periodontal problems.
Recently, Woolf described a distinction that should be made between
two forms of organic pain: physiologic and pathologic. The distinction
between the two depends on the premise that physiologic pain is a “normal”
sensation, whereas pathologic pain is the consequence of an “abnormal”
state. Dynamic sensations perceived as a result of stimuli “of sufficient
intensity to threaten to damage tissue or produced small localized areas of
injury, but which neither provoke an extensive inflammatory response nor
damage the nervous system” as physiologic pain. It can be manifested in
response to mechanical, thermal, or chemical stimulation. It is characterized
by quantifiable stimulus-response relationships, yet it is particularly
susceptible to interference from psychologic factors. This definition aptly
describes dentinal hypersensitivity, takes into account the polymodal nature
of the nerve fibers, and considers the psychological component.
SUMMARY :
It is estimated that the frequency of dentinal hypersensitivity affects
one of six people, and one or more teeth can be affected. The incidence of
dentinal hypersensitivity appears to peak around the third decade of life and
may appear as root sensitivity in the fifth decade of life as root sensitivity
particularly in patients undergoing periodontal surgery.
The neurophysiology of the teeth :
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It is well known that even the most peripheral part of dentin can be
sensitive. Recent neuroanatomic studies have shown that only the inner 100
to 200 µm of dentin is innervated, odontoblasts would act as receptor cells
and mediate the effects of external stimuli to the nerve ending located in the
pulp – dentin border. However, there are few experimental data supporting
this theory. Moreover, combined electrophysiolgic and histologic studies
have shown that dentin can be sensitive despite irritation – induced
odontoblasts aspiration and other tissue injury in the pulp-dentin border
area. Also, the nerve endings in dentin were found to be injured in these
studies. Human dentin can be sensitive despite considerable tissue trauma in
the pulp-dentin border.
INNERVATION OF THE PULP AND DENTIN :
As already mentioned, the dental pulp is enormously richly
innervated. The mean number of axons entering one human premolar tooth
is 926. a great majority of the axons are unmyleinated. To Byers, one axon
may innervate more than a hundred dentinal tubules. The density of the
innervation in the pulp-dentin border is enormous.
However, most of the recent studies indicate that only the inner 100
to 200 µm, of dentin is innervated. This has been confirmed with electron
microscopic techniques as well as with light microscopic studies employing
autordiographic and immunohistochemical nerve labeling methods. The
density of the innervated tubules is highest in the area of pulp horns.
Although close contacts have been shown to exist between the nerve
fibers and the odontoblasts synapses or other junctions that would allow
nerve impulse transduction between the cells do not seem to exist.
Although the results of many histologic studies are conflicting, the
most recent results indicate that the odontoblast process is restricted to the
inner third of the dentinal tubule. Accordingly, it seems probable that the
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outer part of the dentinal tubules does not contain any cellular elements but
is only filled with dentinal fluid.
THE FUNCTION OF INTRADENTAL NERVES :
Much of the information concerning the function of intradental
nerves, especially that of C-fibers, originates from single unit recordings
performed on experimental animals.
The recent electrophysiologic recordings indicate that intradental
nerves in cats, dogs, and monkeys function in the same way as those in
human teeth. Also the structure of intradental innervation is similar in all
these species.
As already mentioned, the dental pulp is innervated by both
myelinated and unmyelinated axons. Correspondingly, according to
conduction velocities (c.v.), the nerve units can be classified into A- (c.v >2
m/s) and C-groups (c.v. ≤2 m/s). Most of the A-fibers have their conduction
velocities – velocities within the Aδ range (<30 m/s). This functional
organization of intradental innervation is significant because in other parts
of the body the first, sharp, better localized pain is mediated by Aδ-fibers,
whereas C-fiber activation seems to be connected with the second, dull,
radiation pain sensations.
Some intradental nerve axons have conduction velocities higher than
30 m pre second and thus they can be classified as Aβ-fibers. They have bee
suggested to mediate non-painful sensations induced by low-intensity
electrical stimulation of human teeth. However, their responses to other
stimuli applied to the tooth indicate that they belong to the same functional
group as the intradental Aδ-fibers. There is little evidence that stimuli other
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than electrical can induce non-painful sensation when applied to human
teeth.
Intradental A-fibers respond to drilling of dentin. They also respond
to probing and air drying of dentin and hyperosomotic solutions applied to
the exposed dentin surface as well as to direct mechanical irritations of the
pulp. The C-fibers of the pulp do not respond to the same type of dentinal
stimulation. A fibers also respond to rapid heating of the tooth. The nerve
firing starts within a few seconds few the beginning of stimulation. In this
stage, no considerable change in the temperature of the pulp-dentin border
has occurred. Accordingly, the nerve responses cannot be due to a direct
effect of heat on nerve terminals. If heating of the tooth crown is slow, A-
fibers do not respond, even if the pulp temperature is elevated up to 50 to
600
C. Temperature changes are able to induced fluid flow in dentinal
tubules. With intense heating, the fluid flow is strong enough to induce
activation of intradental A-fibers (see Pashley’s article, Mechanisms of
Dentin Sensitivity).
A common effect of the stimuli activating A-fibers is that they can
induce fluid flow in dentinal tubules, as studied in vitro.
The C-fibers of the pulp are polymodal and respond to several
different stimuli when they reach the pulp proper. In heat stimulation their
mean threshold temperature is 43.8 ± 3.40
C. Considering the function of
both intradental nerve fiber groups, rapid heating induces A-fiber activation
within a few seconds followed by a delayed C-fibers firing. Sharp pain is
induced within a few seconds, and if stimulation is continued, a dull, aching,
and radiating pain sensation is evoked.
Intradental C-fibers also respond to direct mechanical irritation of the
pulp tissue and to such chemicals as bradykinin and histamine. A-fibers are
not activated by these chemicals. From this point to view, it is interesting
that bradykinin applied on the exposed human pulp induces dull pain.
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In general, unmyelinated axons are more resistant to the effects of
pressure and hypoxia than myelinated fibers. Both pressure elevation and
hypoxia may occur in the pulp during inflammation. Accordingly, the
function of intradental A-fibers may be locked. On the other hand, such
inflammatory mediators as histamine and bradykinin are released and are
able to activate intradental C-fibers. Explain why the pain connected with
advanced pulpitis is dull, aching, and poorly localized.
THE MECHANISMS OF DENTIN SENSITIVITY :
Myelinated A-fibers seem to be responsible for dentin sensitivity. The
sensitivity of the nerve units is very dependent on the condition of the
dentin surface, with either open or blocked dentinal tubules. Acid etching of
the drilled dentin surface removes the smear layer and pen the dentinal
tubules, and the sensitivity of the nerve fibers to dentinal stimulation is
increased to a great extent. Blocking of the tubules with resin impregnation
or potassium oxalate treatment prevents the nerve activation.
Because pain in general is evoked by intense stimuli that induce
tissue damage (noxious stimuli), a clinically relevant problem is whether
stimulation of dentin, for example with air blasts, is noxious to the pulp. On
the other hand, if tissue damage is induced in connection with dentinal
stimulation and pulp nerve activation, it would be important to know how
the nerve function might be affected by the injury.
Air drying of human dentin induces odontoblast aspiration into
dentinal tubules. Moreover, chronic dentin exposure may result in
considerable tissue damage and inflammation in the pulp-dentin border area.
It seems that thee morphologic change do not affect dentin sensitivity that
much. In dog teeth, dentinal stimulation causes tissue damage in the pulp
dentin border area, and the dentinal innervation is injured. The
responsiveness of the units seems to be more dependent on the openness of
the dentinal tubules than the tissue injury in the pulp – dentin border. These
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results from human and animal experiments support the view that the
activation of intradental nerves by dentinal stimulation must be induced by
an indirect effect. These result also indicate that sensitive dentin does not
necessarily mean that the dental pulp is healthy. Neither does insensitive
dentin mean that the pulp is dead. Sometimes patients may have wide areas
exposed dentin without feeling any discomfort or pain. In these the dentinal
tubules may be blocked by dentinal sclerosis or irritation dentin formation
in the pulp –dentin border area.
Certain inflammatory mediators, such as prostaglandins, histamine,
serotonin (5-HT), and neuropeptides, such of the nerve endings.
Accordingly, their thresholds to external irritation may change. For
example, after local application of serotonin on dentin close to the pulp, the
responses, of the intradental nerve fibers to dentinal stimulation are much
enhanced.
MECHANISMS OF DENTIN SENSITIVITY :
HISTORIC CONSIDERATIONS :
Clinician knew that freshly exposed dentin was extremely sensitive
and concluded (erroneously) that nerve fibers in teeth must extend to the
DEJ to be responsible for such pain. When histologists began looking for
nerve fibers in peripheral dentin using light microscopy and special heavy-
metal stains, they found that branches of Pulpal nerves did not extend more
than 100 µm into peripheral dentin.
Rapp and his colleagues, proposed that odontoblasts could serve as
receptors. Stimulation of odontoblast processes in peripheral dentin was
proposed to cause change in the membrane potential of odontoblasts via
synaptic junctions with nerves, thereby causing pain. However, careful
electron microscopy failed to demonstrate any synaptic complexes between
Pulpal nerves and odontoblasts. Perhaps the most damaging blow to that
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hypothesis was the observation that odontoblast processes may not extend
peripherally beyond one third to one half of the length of dentinal tubules.
Anderson and colleagues and Brannstrom, working independently,
found that peripheral dentin, although very sensitive to a variety of physical
stimuli (tactile, thermal, evaporative) was uncreative to KCI and local
anesthetics, which normally modified nerve activity. Brannstrom
reintroduced Gysi’s concept that sensitivity may be due to the movement of
tubule contents, the so called hydrodynamtic theory of sensitivity. Unlike
Gysi, Brannstrom accumulated a great deal of laboratory and clinical
evidence to support the concept that, although the peripheral one half of
dentin is devoid of nerve or odontoblastic processes, movement of fluid
within dentin transduces surface stimuli by deformation of Pulpal
mechanoreceptors, which in turn, cause pain. This hypothesis, which is
currently the most popular theory.
PULPAL INNERVATION :
Nerve type :
The dental pulp is richly innervated with a variety of nerve fibers.
Only a few of the 1000 to 2000 nerves found in each tooth reach the dentin.
Of these nerves, approximately 75 per cent are nonmyelinated and 25 per
cent are myelnated. The myelinated nerves are classified as A-α, β, or -δ
fibers, depending upon their axon diameter and their conduction velocity.
Most of the myelinated nerve fibers in teeth are A-δ nerves, which are
thought to be responsible for the brief, sharp, well-localized pain associated
with dentin sensitivity. These fibers have a relatively low stimulation
threshold. As they are relatively large, their depolarization causes much
more current flow than smaller nerves, and their activity can be recorded
extracellular from cavities cut into dentin. When investigators measure
intradental nerve activity, the implication is that it is A-δ nerve activity. The
20

unmyelinated nerve of the pulp are composed of small c-fibers and
sympathetic nerves. The c-fibers contain peptides that may contribute to
both pain sensation and local inflammation. The poorly localized, dull,
burning ache of Pulpal pain is thought to be due to c-fiber. They are too
their fibers from the mandibular nerve as “single units,” which are then
placed on recording electrodes. The stimulation threshold of c-fibers is
relatively high. The proportion of sympathetic nerves in the total number of
unmyelinated nerves has been reported to vary from 10 pre cent to a
majority of the fibers.
Normal electric pulp testing stimulates the lowest threshold nerves
first which are A-δ fibers. Higher currents are required to activate c-fibers.
Few electric pulp testers used in clinical practice can stimulate c-fibers,
although the development of such devices may be useful in future clinical
research.
Nerve Reactions :
Vasoactive peptides such as substance P, calcitonin gene – related
peptide (CGRP), and neurokinins A and B (NKA, NKB) are found in c-
fibers often in close association with blood vessels. They can be released by
tissue destruction (pulp exposure, elevated cutting temperature, antigen-
antibody reactions, complement activation) or by antidromic stimulation of
the inferior alveolar nerve.
These peptides all promote vasodilation and plasma extravasation.
These agents contribute to the phenomenon called “neurogenic
inflammation and they have been demonstrated in the dental pulp. The
utility of neurogenic inflammation was developed in Lewis’s nocifensor
system, which consisted of a peripheral neurogenic defense mechanism by
which exogenous or endogenous toxic material was removed by local
increases in tissue blood flow, interstitial fluid production, and lymph
drainage. The dental pulp contains for more unmyelinted than myelinated
21

neurons. These nerves proliferated in response to bacterial challenge. In the
low-compliance environment of the pulp, neurogenic inflammation may,
under some conditions, promote and sustain dentin sensitivity rather than
leading to its resolution. The wave of depolarization traveling along the
nerve which depolarize back toward the periphery. Recent modifications to
the original concept suggest that the nerve can act as both receptors and
effectors. In this way, painful impulses may perpetuate Pulpal inflammation
and perhaps aggravate it. Nerves that contain these neurogenic peptides are
capsaicin-sensitive. The most interesting effect of capsaicin is its ability to
desensitize tissues to the effects of SP, CGRP, and NKA. Capsaicin itself
can cause pain when applied to dentin, presumably by causing the release of
substance P.
A-δ fibers can be stimulated repeatedly for hours with no apparent
change in their sensitivity. They are polymodal (sensitive to changes in
temperature, osmotic pressure, or tactile stimuli) fibers that are not sensitive
to bradykinin or histamine. They mediate the sharp, transient pain that is
typical of dentinal sensitivity. In contrast, c-fibers are activated by chemical
mediators of inflammation. They produce a dull, aching pain when
bradykinin or histamine is placed in deep cavities cut into human teeth. A
brief application of hot gutta-percha on crown enamel can produce a
transient burst of A-δ nerve active. If a tooth is heated continuously but very
slowly, no nerve activity is produced until tissue damage results, causing c-
fibers to fire.
Based on indirect evidence, Kim has suggested that vasodilating
agents may actually decrease Pulpal blood flow following a transient
increase in blood flow. As the pulp is a low-compliance environment, any
increase in its volume, whether due to dilation of vessels or filtration of
fluid across capillaries following dilation, would increase tissue pressure,
22

which would compress local venules, thereby increasing postcapillary
resistance and decreasing blood flow.
DENTIN CONSIDERATIONS :
When the Pulpal terminations of the tubules are sealed by reparative
dentin, the dentin is generally insensitive for two reasons. First, reparative
dentin generally has fewer tubules than primary dentin. Second, reparative
dentin generally has few nerves innervating the dentin.
There are two mechanisms responsible for the permeation of
substances across dentin: diffusion and convection. Diffusion is the process
by which substances are transported from an area of high concentration to
an area of low concentration. In pure diffusion, there is no bulk fluid
movement but only molecular translocation. In convective transport or
filtration, bulk fluid movement occurs from an areas of high hydrostatic
pressure to an area of low hydrostatic pressure. This type of fluid movement
can be quantitated by measuring the hydraulic conductance of dentin.
Hydraulic conductance is the reciprocal of resistance. That, is dentin with a
high conductance has a low resistance. The important variables regulating
hydraulic conductance of dentin are the length of the tubules (that is, dentin
thickness), the number of tubules per unit surface area, the applied pressure,
the viscosity of the fluid, and the radius of the tubules raised to the fourth
power. These are expressed in the Poiseuille-Hagen equation.
Where:
Q = Fluid flow
∆P = applied pressure (hydrostatic or osmotic)
r4
= radius of tubules (that is, ± smear layer)
N = tubules density (depth – dependent)
n = viscosity of fluid (temperature –dependent)
23
Q =
II∆Pr4
N
8nL

L = length of tubule (remaining dentin thickness)
The amount of fluid that can shift across a full preparation is much
larger than the amount that can shift across a buccal pit preparation. The
most important variable is the radius of the tubule because it is raised to the
fourth power. The creation or dissolution of smear layers and smear plugs
from dentinal tubules can have a profound influence on the hydraulic
conductance of that dentin and hence its sensitivity. However, the hydraulic
conductance of dentin is not uniform but is highest over pulp horns, high on
axial walls, and relatively low on root surfaces. This is due in part to
regional differences in tubules density and diameter and in part or regional
differences in the amount of intratubular material. The surface resistance of
dentin is variable owing to the presence or absence of the smear layer or the
growth calculus or other surface deposits. Patients with sensitive dentin
generally lack smear layers and have open tubules orifices. Several therapies
bases on tubule occlusion have been proposed that were designed to
decrease fluid flow by decreasing the hydraulic conductance of dentin.
Exposed dentin free of a smear layer should have a high hydraulic
conductance. If these tubules are open all the way to the pulp, Pulpal fluid
should slowly filter down its hydrostatic pressure gradient to the surface.
This has actually been demonstrated by Linden and Brannstrom and by
Pashely and associates in vivo. Apparently, the spontaneous rate of fluid
filtration across open, sensitive dentin is too slow to activate the
mechanoreceptors. When an additional stimulus is superimposed on it,
however, then the receptors are activated. Steadily applied pressures do not
cause as much pain as when the pressure is suddenly applied or released.
MECHANISTIC EVALUATION OF ADEQUATE STIMULI :
Tactile :
All clinicians use a dental explorer to identify regions of sensitive
dentin. It is simple yet effective. Although the use of a gently force of 5 to
24

10 mg on the explorer (measured by performing such maneuvers on an
analytical balance) seems as though it would be a trivial stimulus, that force
is localized on the tip of the explorer, which is only about 500 µm2
(Pashley,
unpublished observation). If 5 gm of force is applied over 500 µm2
, the
resulting pressure is gm/5 X 10-6
cm2
= 1000 kg/ cm2
= 102 Mpa. This is
sufficient to overcome the elastic limit of dentin, leading not only to
compression of dentin and smear layer creation under the explorer tip but
also to permanent (yet incroscopic) deformation of dentin, (scratch
development). This compression of dentin can presumably cause
displacement of fluid inwardly at a rapid rate, which activates
mechanoreceptors. Tactile stimuli can be made quantitative by incorporating
a calibrated strain gauge in the explorer or by using a Yeaple probe. A
Yeaple probe is a compact handpiece that contains an explorer tine in an
adjustable electromagnetic fluid. The probe is calibrated such that one can
apply forces sequentially to sensitive dentin in a graded manner. The force
should be applied to the same area at 900
to the surface in a static inwardly
directly manner. The patient is asked to respond whether there is either pain
or no pain at each test. The instrument is adjusted in 5 to 10-gm increments
from 10 to 70 gm. Each increasing force compresses more and more dentin.
This is a variable stimulus / constant response type of test. If different
laboratories wish to compare testing data, they should all use the same type
of explorer tine (that, is identical surface area, sharpness and so on).
Osmotic stimuli :
The use of osmotic stimuli for evaluation of dentin sensitivity was
popularized by Anderson and his colleagues. At the time they developed
this methodology, the smear layer had not yet been discovered and the
hydraulic conductance of the dentin that they studied was probably very
low. This required them to use very large osmotic stimuli (very concentrated
25

solutions of various solutes) in order to induced enough fluid movement to
cause, pain. The same concentrations of different solutes amounts of fluid
movement. This was due to differences in the reflection coefficients of these
solutes for dentin. Reflection coefficients are values that correct the
theoretical osmotic pressure of a solution for the relative permeabilities of
the solute versus the solvent.
Anderson’s group found that repeated applications of the same
hypertonic solutions to cavity preparations in the teeth of unanesthetized
subjects evoked fewer and fewer reports of pain. They also demonstrated
that repeated applications of these solutions induced successively smaller
amounts of fluid movement across dentin in vitro. This was due to the
diffusion of the solute into the dentinal fluid, which “loaded” them so that
subsequent applications of the solution produced smaller and smaller
osmotic gradients. Osmotic stimuli are effective because the chemical
activity of water in these solutions is les than that of the chemical activity of
water in dentinal fluid. Water flows from the area of higher activity to the
area of lower activity, which is, by definition, osmosis. Horiuchi and
Matthews reported that than were osmotic pressure. However, osmotic
stimulation continues to be a convenient, popular method of evoking pain in
neurophysiologic studies in cat teeth, where it is technically difficult to
produce hydrostatic stimulation. Calcium chloride, has multiple effects.
when applied to superficial dentin, it excites intradental nerve owing to
osmotic movement of fluid. In deep dentin, it may depress nerve activity
owing to the direct effect of calcium at stabilizing excitable membranes.
Solutions of sodium chloride tend to excite nerves owing to indirect osmotic
effects on superficial dentin and direct effects on intradental nerves in deep
dentin. Thus, for a variety of reasons, osmotic stimuli are not generally used
clinically to quantitate dentin sensitivity although some have tried. For a
review of this topic see pashely. Saturated solutions of calcium chloride
26

may be useful for exploring the integrity of margins of drowns or other
restorations. A cotton pellet saturated with the solution is place on a suspect
margin. There is usually a delay of 5 to 30 seconds as the osmotic stimulus
diffuses into any defects. The lack of a painful response in an
unanesthetized patient indicates either that the margin is tight or that the
dentin in insensitive. Margins should be tested individually to limit
identification to a specific leaky margin.
Thermal stimuli :
Thermal stimuli have been used ever since endodontists began using
hot gutta percha to elicit Pulpal nerve responses. Thermoelectric devices are
useful for delivering cold or warm stimuli in a controlled quantitative
manner. Because patients are generally more sensitive to cold than to hot
stimuli, the use of cold water (10,15,20,25, 300
C) as a simple, quantitative
stimulus is gaining in popularity. In using cold water, each tooth tested is
isolated with a rubber dam and water at a known temperature is slowly
flowed on the exposed dentin surface for a maximum of 3 seconds from a
disposable plastic syringe. The patient is forced to decide if that temperature
causes pain or not and then the next lower temperature is tried until the
patient responds unequivocally. Thermal stimuli are effective hydrodynamic
stimuli because of the differences in thermal conductivity and coefficients
of expansion or contraction of pula/dentinal fluids and their containers,
enamel and dentin. This is, application of cold causes a more rapid
volumetric contraction of dentinal fluid than occurs in dentin. This
mismatch of volumetric changes produces negative Intrapulpal (and
presumably intradental) pressures that displace mechanoreceptors and cause
pain. Because many thermal stimuli require that the tooth be touched with a
device, they are actually both tactile and thermal. Application of a water
stream is almost purely thermal, as there is no pressure application. The use
27

of a thermally – adjusted air stream provides a “no-touch” thermal
stimulation. Unfortunately, it provides both thermal and evaporative stimuli
simultaneously.
Thermal stimuli to vital dentin cause sharp, well-localized pain (that
is, activation of A-δ fibers) before there is a change in dentin temperature
near the pulp where the nerves are located. Many seconds later, the thermal
wave or pulse arrives at the pulp and may activate other nerves. however.
The thermal stimuli that the used in testing dentin sensitivity should be
regarded as hydrodynamic stimuli rather than thermal stimuli pr se. That is,
they induce fluid movement or pressure changes indirectly rather than
directly stimulating temperature –sensitive receptors. Thus, the term thermal
stimuli actually a misnomer. Prolonged application of hot or cold stimuli to
dentin eventually cause changes in the temperature of Pulpal nerves.
Although this is useful in endodontics it is not used in testing dentin
sensitivity. Clinically, cold stimuli are more useful than hot stimuli for
testing dentinal sensitivity. Patients tolerate cold stimuli better than hot
stimuli, and there is less danger of causing Pulpal damage.
Evaporative Stimuli :
The use of an air blast as a noxious stimulus in testing for dentin
sensitivity has been widely used since Brannstrom, Londen, and Astrom
first demonstrated that air blasts to cut dentin caused evaporative fluid
movement across dentin. There are two mechanisms operating to cause pain
under these conditions. The first is the evaporation of fluid from the dentin
by relatively dry 250
C air directed at a 320
C toot. This occurs very quickly
(within 1 second). If longer blasts of air are used, one begins to cool the
tooth, and the stimulus becomes complex owing to the addition of a thermal
stimulus with an evaporative stimulus. A thermal testing device has been
developed that blows air of progressively lower temperature on sensitive
28

teeth. Although it is regarded as primarily a thermal stimulus, it includes an
evaporative component.
Air blasts are useful stimuli during patient screening. They quickly
identify individual sensitive teeth but they are not useful at identifying
sensitive tooth surfaces. That is, an air syringe does not identify exactly
where, on a tooth, the sensitive dentin is located. The exact location of
dentin sensitivity often dictates the type of therapy that might be employed.
Whenever permeable dentin is exposed to an environment in which
the relative humidity is less than 100 percent, water in dentinal fluid will
change from the liquid state to the gaseous state, which, by definition, is
evaporation. The important variables in evaporation are the tooth or dentin
temperature, the ambient relative humidity, and the presence or absence of
convective air movement.
Spontaneous evaporation of water from exposed dentin is the same
regardless of the presence or absence of a smear layer. However, the
accelerated evaporative water loss seen during an air blast is much higher in
the absence of a smear layer (Goodis, Tao, Pashley). The direction of the air
blast should be 900
to the dentin surface to obtain maximal rates of water
evaporation.
There is no standard air blast, although perhaps there should be
clinicians direct air at teeth at varying distances for varying periods of time.
It would be desirable to standardize to a 1-second air blast, 1 cm from the
tooth, directed at 900
using room temperature air.
Orchardson and Collins - an air syringe that uses a prolonged air
blast. The patient holds a cut-off switch that they activate when pain is
perceived. A timer begins when the clinician activates the air syringe. The
time in milliseconds between the onset of the stimulus and the patients
cancellation of the stimulus was found to be proportional to dentin
sensitivity. One criticism of the use of prolonged evaporative stimuli is that
29

sufficient water can evaporate from the dentin to cause partial tubule
occlusion by the salts and proteins left behind. Prolonged air blasts also tend
to decrease dentin sensitivity until the dentin becomes rehydrated. Finally
prolonged air blasts cause temperature changes on and in the dentin that can
be avoided by using 1-second air blasts.
If prolonged air blasts are directed at exposed dentin, the rate of
evaporative water loss may occur faster than dentinal fluid can flow into the
dentin, causing negative intradental pressures. This may be responsible for
the displacement of nerves and odontoblasts nuclei from the cell body into
the cytoplasmic processes inside dentinal tubules. Although this
phenomenon has been called ‘aspiration’ of odontoblasts, the preferred term
is ‘displacement’. These cells die and are generally replaced by underlying
mesenchymal cells.
Filtration of fluid :
The most physiologic stimulus for evoking dentin sensitivity should
be the graded, quantitative movement fluid across dentin. Ahlquist and
colleagues, by preparing circular cavities on the facial surface of incisors
and cementing conical plastic chambers into the preparation with
cyanoacrylate. The chamber was connected to a fluid reservoir with
polyethylene tubing. Uanesthetized subjects reported the quality and
magnitude of their sensation of pain by means of an intermodal matching
technique, finger-span potentiometer, and verbal descriptors. In the presence
of the smear layer, no pain could be evoked. After using 0.5M EDTA (pH
7.4) for 2 minutes, fluid flow in either direction elicited sensations of sharp
pain. Rapid changes evoked higher pain intensities than slow changes in
flow. When the dentin was treated topicaly with 3 percent oxalic acid (2
minutes) to occlude the tubules with calcium oxalate crystals, the same
stimuli were prevented from producing sufficient fluid flow to evoke pain.
This effect could be reversed by EDTA treatment, which restored both
30

dentin permeability and its sensitivity. These results tend to support the
hydrodynamic theory of dentin sensitivity.
There is a linear relationship between applied pressure and the flow
of fluid through dentinal tubules. The hydraulic conductance of dentin is the
slope of the linear relationship between fluid flow and the applied
hydrostatic pressure gradient. The presence or absence of smear layers has a
profound influence on the magnitude of the hydraulic conductance, which
also varies inversely with dentin thickness.
The histologic appearance of the odontoblast process in dentinal
tubules would suggest that it should have an enormous effect on the
hydraulic conductance of dentin. However, if one removes the smear layer
of dog dentin in vivo and measures the hydraulic conductance of the dentin
before and after filtration of water (which should osmotically swell
odontoblast processes in tubules) across dentin, there are no statistically
significant changes. Similarly hypertonic (3M) NaCl across dentin (which
should osmotically shrink the odontoblast process), one sees no change. A
prolonged (10 minute) air blast to dentin to cause displacement of
odontoblast nuclei up into the tubules, there is not change in Lp even though
subsequent histologic examination revealed that more than 50 percent of the
tubules contained displaced nuclei.
Presence of irregularities in the walls of the tubules, the presence of
organic partitions, mineralized and unmineralized collagen fibers, and so on.
Their summed effects are apparently much more important in modifying
fluid movement across dentin than is the presence of the odontoblast
process.
Electrical stimuli :
Criticized on several grounds as being nonphysiologic, rather than
testing the pulpodentin complex via hydrodynamic stimuli, it has been
argued that electrical stimulation of teeth directly stimulates pulpal nerves
31

and hence is of little value in evaluation of dentin sensitivity. That is, it only
evaluates the presence or absence of nerve vitality rather than the degree of
sensitivity. Further, most clinical devices that are used to test pulp vitality
pass different currents through teeth because of the different resistances
offered by varying enamel and dentin thicknesses. Constant-current
stimulators are used in neurophysiology to deliver an exact current flow
regardless of the resistance of the tooth. Because current flow is the critical
variable in stimulating nerves, constant current stimulators, as they are
called, are absolutely necessary in studies of nerve thresholds and
sensitivity.
There are regional differences in nerve distribution within teeth. One
might expect to obtain differences in nerve responses if the electrode was
placed on the incisal versus the middle third of coronal enamel. Bender and
associates demonstrated that the incisal third of the crown was more
sensitive to electric pulp testers than the cervical third.
Karlsson and Penney study, the root surfaces became more sensitive
after periodontal treatment, whereas coronal sensitivity remained
unchanged.
It is theoretically possible for electrical stimuli to induce
hydrodynamic fluid movements through open dentinal tubules via a
phenomenon called electro-osmosis. Electro-osmosis is the bulk movement
of an electrolyte solution through a porous substance in response to the
impression of an electrical potential.
Until we know much more about electro-osmosis in dentin, we cannot
dismiss electrical stimulation of teeth as being unphysiologic.
Bacterial contributions to dentin sensitivity :
Periodontists have long thought that patients who keep their root
surfaces free of plaque will exhibit less dentin sensitivity. Overzealous tooth
brushing by some patient may abrade radicular dentin and remove surface
32

salivary mineral deposits, thereby creating dentin sensitivity rather than
preventing it. Indeed, Addy and colleagues reported a higher amount of
gingival recession and dentin sensitivity on the left side of right-handed
individuals than on the teeth on the right side of their mouth. They found an
inverse correlation between plaque scores and dentin sensitivity. That is,
low plaque scores were associated with high levels of sensitivity.
Adrians and coworkers found far more microorganisms in the dentin
adjacent to periodontal pockets than in normal radicular dentin. Further,
more bacteria were found in superficial root dentin than in middle dentin.
However, they found a significant number of bacteria in the pulps of
periodontally involved teeth even though these teeth were asymptomatic. A
relatively common histologic observation of bacterial penetration into
dentin is that it is extremely localized. A few tubules may be filled with
bacteria while most of the adjacent tubules remain bacteria free.
Bergenholtz clearly demonstrated that bacterial products placed on
dentin can induce pulpal inflammation. Some bacterial substances can
activate complement, whereas others are strongly chemotactic for PMNs.
Still others may activate macrophages to release tumor necrosis factor.
bacterial products may have direct vasoactive properties on pulpal vascular
smooth muscle. Alternatively, they may have indirect effects on the
vasculature through their direct effects on the release of neuropeptides from
pulpal nerves.
Bacterial products may have cytotoxic effects on pulpal fibroblasts
that may modify areas of the pulp during inflammation. They may damage
or kill the odontoblast and their mesenchymal stem cells. If there had been
multiple episodes of acute pulpal inflammation immediately beneath open
sensitive entinaltubules followed by healing, one result might be a local
accumulation of fibrous tissue (that is, scarring) and a reduction in capillary
density. Such relatively avascular regions would not clear bacterial products
33

diffusing into the pulp from open tubules, thereby permitting their local
concentrations to rise to levels that were cytotoxic. The relative lack of
capillaries would tend to interfere with or retard the transport of fibrinogen
and globulins that might reduce the rate of entry of bacterial products
through dentin to the pulp.
Dentin hypersensitivity :
Some authors use the term hypersensitivity dentin or dentin
hypersensitivity, whereas others simply refer to it as dentin sensitivity. Can
dentin become hypersensitivity and if so, how ?
The hydrodynamic theory of dentin sensitivity implicates both dentin
and nerves as important elements. it follows, then, that one could have
“dentin hypersensitivity” or nerve hypersensitivity or both. As dentin
becomes thinner (from multiple root planings or tooth abrasion), its
hydraulic conductance increases. The most important variable is the
condition of the tubule apertures. Tubule orifices plugged with smear plugs
have a much lower hydraulic conductance than those same tubules devoid of
smear plugs and smear layers. As dentin loses its smear layer, it becomes
hyperconductive and hence “hypersensitivity” relative to what it was when
it was covered with a smear layer, especially from the patient’s perspective.
Alternatively, changes may occur in nerve sensitivity. The ionic
concentration of sodium and potassium of predentin fluid, in nonexposed
dentin determined by micropuncture technique, has been reported to be 48.0
and 9.0 mEq per L, respectively. The concentrations of the same ions in
exposed dentin have been reported to be 150 and 3 mEq per L, respectively.
Because resting membrane potentials of nerves are more sensitivity to
changes in extracellular potassium than sodium, one would expect the
34

membrane potential of intradental nerves to be more negative (and less
excitable) in open, exposed dentinal tubules (owing to the lower, more
plasma like potassium concentration) than the same nerves in nonexposed
dentin.
Hypersensitive states may also develop during inflammation via
several mechanisms. The small unmyelinated c-fibers that are normally
thought of as nociceptors may release small but important quantities of
neuropeptides without firing. They increase local blood flow and increase
capillary permeability. Extravasation of plasma tends to cause local
elevations in pulpal tissue pressure that may lower the excitatory threshold
of mechanoreceptor nerves, thereby contributing to a true hypersensitivity
of that dentin.
The supporting of nerves may increase the innervation density of
dentin or the subodontoblastic regions, further increasing dentin sensitivity.
Clinical considerations :
Generally, patients who have had extensive root planning will have
lost all of the cementum on the cervical third of the root as well as variable
amounts of root dentin. These patients seldom complain of dentin sensitivity
until their periodontal packs are removed. Although the subsequent events
vary considerably among individuals, many patients complain of increases
in dentin sensitivity of the planed teeth over the next 7to 10 days. This is
generally followed by a gradual decline in sensitivity over the following 7 to
10 days.
As saliva is saturated in calcium and phosphate with respect to most
forms of insoluble calcium phosphate at normal salivary flow rates and pH,
there are numerous physiochemical mechanisms tending to occlude dentinal
tubules with a wide variety of crystal types. This may lower the hydraulic
conductance of the exposed dentin below levels that permit activation of
mechanoreceptors hydrodynamically. The transudation of plasma and the
35

macromolecules that it contains may tend to fill tissue spaces and perhaps
even the pulpal ends of the tubules with fibrin, thereby decreasing the size
of diffusion channels, decreasing dentin permeability. The pulp may then
have an opportunity to heal and the thresholds and distribution of sensory
fibers should return to normal leaving the patient relatively comfortable.
DENTINAL PERMEABILITY IN ASSESSING THERAPEUTIC
AGENTS
Isotonic potassium chloride does not elicit pain when applied to
dentin but does when in direct contact with the pulp ; and acetic acid buffer
(pH 5.7), reported to induce pain in subcutaneous injections, had no effect
on the dentin or the pulp.
Brannstrom observed that dentin exposed by drilling was less
sensitive than dentin exposed by fracture, which he attributed to the
blockage of tubule openings caused by the debris produced during drillings.
These observations together with the observations that pain could be
produced from air blasts, application of sugar solution, and dry absorbent
paper led to the conclusion that a central vital part of the tooth pulp acts as a
mechanoreceptor, and any stimulating agent causing mechanical disruption
or movement of fluid flow through the tubules is a potential cause of pain.
Furthermore, Brannstrom reasoned that the geometry, that is, the conical
shape, of the dentinal tubules combined with capillary action could make
instaneous minute amounts of fluid flow possible, and could explain the
acute pain reported in the clinical operatory.
Citing three natural defense mechanisms for reducing dentin
permeability as formation of irregular atubular dentin at the pulpal wall,
obturation of dentinal tubules by sclerosis, and mineralization of a
36

superficial layer of pellicle or plaque, Brannstrom proposed a clinical
technique for sealing dentin using a resin material.
Brannstrom later suggested the application of cavity lining and
varnishes under restorations, the retention of smear plugs in restorative
procedures, and use of calcium hydroxide and non-abrasive fluoride gels for
treatment of exposed sensitive dentin.
Following Brannstrom, the greatest protagonist of the hydrodynamic
theory and the role of dentin permeability has been D.H. Pashley who has
presented numerous reports in the field of evaluating agents for the
treatment of hypersensitivity.
1) Hydraulic conductance (Lp) measures the ease with which fluid
movement occurs across a membrane in a hydraulic gradient.
2) Permeability coefficients (P) are a property of solutes for a particular
membrane. In the absence of bulk fluid movement, P is a measure of
the ability of solute to diffuse across a membrane because of a
concentration gradient. In an analysis of factors influencing P,
molecular size, configuration, polarity, Van der Waals forces,
London forces, and interaction potentials need be considered.
3) Reflection coefficient (σ) is a factor that reports the relative ability of
a solute and a solvent to diffuse through a membrane. By definition,
σ = 1 when the membrane is impermeable to the solute but
completely permeable to the solvent, and when σ = 0 the membrane
cannot distinguish between the solvent and solute.
In 1974, Pashley published the first experimental work utilizing a
laboratory method to measure dentin permeability by hydraulic
conductance. In this work, a split chamber device was described wherein
thin slices (0.99mm) of coronal dentin from extracted human third molars
were placed between fixed surface area plexiglass reservoirs, one end of
37

which could be connected to a source of hydrostatic pressure or treatment
solution and the other end to a means of measuring flow rate or to collect
diffused fluid. Movement through a micropipette was found to be an
accurate flow meter.
Fluid movement through dentin was nil with no hydrostatic pressure,
flow was a linear function of hydrostatic pressure, acid-etched discs had
flow rates nearly 32 times greater than unetched discs, permeability was
inversely proportional to dentin thickness, and permeability was directly
proportional to surface area.
86 percent of the resistance to dentinal fluid flow was due to the
surface characteristics of dentin, strongly suggesting that the alteration of
permeability by surface agents could be a useful clinical treatment modality.
Flow was greater in the direction from the enamel to the pulp.
In 1983, Pashley measured the effect of temperature on the flow rate
of saline solutions, through etched and unetched dentin. Generally,
permeability increased with temperature, however, the increases were
greater with etched dentin.
In 1982, Pashley measured the influence of saliva, bacterial
suspensions, and plasma proteins on fluid movement across dentin. Pashley
speculated that after injury, a natural defense mechanism originating from
the pulp could be the formation or release of plasma proteins, leaked into
the dentinal fluid in an attempt to occlude tubular passageways and reduce
hydrodynamic transmission to the mechanoreceptors in the pulp.
Using a modification of the split chamber deice wherein the enamel
side was acid etched and then brushed with slurries of a series of dentifrices,
Pashley determined fluid flow through dentin in the direction pulp to
enamel, and interpreted the reduction in flow as a measure of the dentifrices
ability to occlude dentin. In the series of products tested, no significant
differences were reported among Sensodyne, Crest, Denquel, Promise, and
38

Thermodent, but an experimental oxalate dentifrice developed by Pashley
was significantly more able to reduce hydraulic conductance (Lp).
Pashley also applied iontophoretic currents in the range 0 to 1.0 mA
to dentin discs in a further modification of the split chamber device. Using
Na I and C lidocaine as test materials, iontophoresis was reported to
significantly increase the permeability of dentin, and it was concluded that
iontophoresis may be useful for enhancing dentin permeability to deliver
therapeutic agents to the pulp.
Pashely and colleagues in 1985 evaluated a series of commercial
cavity varnishes and bases for their ability to reduce dentin permeability.
The split chamber device was employed in two ways. 1) to measure
permeability by a radiotracer applied to the top reservoir of a split chamber
device, collecting the perfusion in the bottom portion with a fraction
collector and 2) to measure hydraulic conductance by fluid filtration through
dentin as driven by 30 cm of hydrostatic pressure. the products tested were
Copalite, Tubulitec, Dropsin, Universal Cavity Varnish, Durelon, Dycal,
ZnPO4 cement, and ZnO/ eugenol cement. All cavity varnishes decreased
dentin permeability by 20 to 50 percent. In the filtration method, only
Tubulitec produced a statistical reduction in Lp. Furthermore, the effect of
varnishes was found proportional to their solid content, but cavity bases and
liners produced larger reductions in dentin permeability.
Burnishing dentin with orangewood and a paste composed of sodium
fluoride, kaolin and glycerin. Act of burnishing with orangewood alone was
the most effective part of the therapy, reducing permeability by 80 percent.
NaF had no appreciable positive contribution, and kaolin and glycerin
slightly diminished the reduction in flow rates. Oxalic acid reduced flow by
95 percent.
39

Smear layers produced by burnishing were found to be more resistant
to acid than those produced by a bur. Burnishing may force more debris
deeper into the tubule openings than bur cutting could.
Multistep dentin bonding procedure containing ferric oxalate, NTG-
GMA (N-tolyl glycine-glycidlymethacrylate), and PMDM (pyromellitic
dianhydride + 2-hydroxyehtylmethacrylate) developed by Bowen and
associates.
Ferric oxalate – reducing dentin permeability by 65 percent. Ferric
oxalate at pH 0.9 may dissolve the smear layer and then re-precipitate as
calcium oxalate and ferric phosphate salts, occluding the patent and exposed
tubules.
Takahashi - the lactate, tartarate, citrate, maleate, and chlorides of Al,
Zn, Ca, Sn and Mg were evaluated, with Saforide (diamine silver fluoride),
silver nitrate, calcium hydroxide, Hyperband Kimura (paraformaldehyde),
and Gottlieb’s recipe (zinc chloride and potassium ferrocyanate solutions)
serving as positive controls. 2.18 percent aluminum lactate (pH 17) emerged
as the agent of choice for further clinical investigation.
Addy and his coworkers - the sensitive teeth were found to have an
average number of 59.9 open tubules per unit area versus 7.47 for the
nonsensitive examples. The average tubule diameter was estimated as 0.83
microns for the sensitive teeth and 0.43 microns for the non-sensitive
exposed dentin areas.
Addy and associates also reported the effects of acids and acidic
dietary substances on root-planed and bur-cut dentin. Using SEM, the
authors observed that the strong mineral acids such as nitric, sulfuric, citric
and lactic removed the smear layer, as did red wines, citrus fruit juices,
apple juice and yogurt.
Finally, the recent work by Absi and colleagues, which involved the
development of a replica technique to study sensitive and non-sensitive
40

cervical dentin, is a rather novel approach. Silicone impressions were taken
of extracted human teeth that had been root planed to expose dentin and
then acid etched to expose dentinal tubules. These replica SEMs were
compared with SEMs of the original dentin surfaces. Excellent correlation
between the original and replica SEMs in terms of tubule cunts was reported
as well as excellent resolution of surface details such as tubule diameters as
low as 1 micron, illustrating patent tubules.
Kim used a refined electrophysiologic method on the vital teeth of
cats, dogs, and humans to measure baseline pulpal sensory nerve activity
(SNA) or electric potential and the effects of therapeutic agents on their
activity.
Kim reported for the first time that potassium ion is the active portion
of potassium nitrate and any other potassium compound. When potassium
ions reached the pulpal sensory nerve, after passage through dentinal tubules
in Kim’s deep-cut cavities, the external part of the nerve membranes
became regions of greatly increased potassium concentration. This localized
increase in potassium caused rapid firing of the sensory nerve that ceased
quickly because the extracellular potassium ions subsequently inhibited
hyperpolarization of the pulpal sensory nerve, that is, they raised the nerve
action potential and produced a desensitizing effect.
HYPERSENSITIVE TEETH :
Experimental studies of dentinal desensitizing agents :
Not all teeth with exposed dentine are sensitive. Teeth with
toothbrush or other forms of abrasion and erosion may have extensive loss
of tooth structure without sensitivity.
1) The dentinal smear layer consists of small amorphous particles of
dentin, minerals, and organic matrix, which cover the cut surface of
dentine, obstructing the orifices of the tubules.
41

2) Salivary proteins adhere to the outer dentine surface and, in addition,
plasma proteins can adhere to the inner dentine surface, blocking the
tubules.
3) Reparative dentine forms in response to chronic irritation. This type
of dentine is less permeable than primary dentine and serves to
insulate the pulp from irritating stimuli.
Anatomic study of pulpal nerves shows that in the coronal area of the tooth
there is extensive peripheral branching of axons and many axons entering
the dentine. This is in sharp contrast to the cervical and radicular areas,
where most of the axons are found in central bundles and very little
branching occurs.
How then can the roots becomes so sensitive ? One possible
explanation is provided by Byers and coworkers. Following grinding of the
roots f rat molars they found sprouting of new axons branches in the area of
injury. Thus, the dentine in the area of injury may be more richly innervated
than intact sites.
1) It can reduce fluid flow through the dentine by clogging the tubules.
2) It can decrease the activity of the dentinal sensory nerves, preventing
the pain signal from being transmitted to the central nervous system.
Toothpastes containing SrCl2 and KNO3 have gained wide popularity.
Both agents have been hypothesized to cause blockage of dentinal tubules.
Historically, KNO3 was preceded by silver nitrate, and this substance was
reported to be effective but permeability stained teeth black and was never
popular in our cosmetically conscious society.
Method for measuring sensory nerve activity :
In order to study the effects of desensitizing agents, the multi-unit
intradental recording method developed by Scott and modified by others
was used. In the canine teeth of anesthetized cats and dogs, two dentinal
cavities were prepared, one deep cavity over the incisal pulp horn and a
42

second less deep cavity near the gingival margin. The incisal cavity an
active low impedance platinum or silver / silver chloride electrode was
placed. The incisal cavity was also used to apply various stimulating and
desensitizing solutions. The gingival cavity held a reference electrode and
was always filled with saline. The electrodes were connected to standard
pre-amplifier and recording equipment. Using this method, many intradental
nerve units can be recorded simultaneously.
In order to study the effect of desensitizing agents, some means of
stimulating neuronal firing had to be used.
First the excitatory solution 3M NaCl was applied to the cavity for 2
minutes. The nerve activity during this time constitutes the control sensory
nerve activity. Then, following a 2-minute saline rinse, the test desensitizing
agent was placed in the cavity for 2 minutes. Immediately following
removal of the test desensitizing agent, the 3M NaCl was reapplied.
KNO3, the active ingredient in Sensodyne F and Denquel,
significantly reduced the sensory nerve activity.
Strontium chloride, which is the active ingredients in Sensodyne
toothpaste, was shown to be effective only at the higher concentration.
1) The NO3
–
anion is not effective as a desensitizing agent.
2) K+
is an effective desensitizing agent regardless of the anion with
which it is combined.
3) Divalent cation solutions were effective in reducing sensory nerve
activity but less effective then K+
.
Both K+
and divalent cation solutions had a reversible effect, that is,
they did not appear to damage the dentinal sensory apparatus.
Mode of action of effective agents :
The extracellular potassium ion concentration is the principal
determinant of the nerve resting electrical potential. The normal resting
potential for nerve fibers is approximately – 90 mv measured from the
43

inside of the cell. When the concentration of K+
is increased above the
normal physiologic level the cell depolarizes, that is, the inside becomes
less negative. Once a certain critical (threshold) potential level is reached,
action potentials begin to occur. Owing to the properties of the membrane
gates that mediate the action potential, the burst of spikes in response to
increase K+
does not last long. After 15 to 20 seconds of prolonged
depolarization, the action potentials cease as a result of the closing of the
action potential membrane gates.
Divalent cations such as Ca++
, Mg++
, and Sr++
can act to stabilize the
nerve membrane by raising the membrane threshold without actually
changing the resting potential. Recent evidence also suggests that divalent
cations may block the membrane channel that mediates the action potential.
Patients who brush with KNO3
–
containing toothpastes do not
complain of pain when applying these agents. Also, in our experiments,
desensitization occurs immediately and is of short duration in contrast to the
clinical situation, in which all desensitizing agents require time and repeated
application of the agent of order to have maximal benefit.
Future directions :
Pain and inflammation are interconnected phenomena. The presence
of inflammation in hypersensitive teeth has yet to demonstration.
Inflammation is marked by an increase in blood flow.
The laser Dopper flowmeter – allows continuous monitoring of pulpal
blood flow. When the effect of agents that stimulate sensory nerve activity
such as hypertonic NaCl and KCl solutions are tested, these solutions cause
an increase in pulpal blood flow. When lidocaine is applied to block nerve
activity, the blood flow changes evoked by KCl are greatly attenuated.
ETIOLOGY AND CLINICAL IMPLICATIONS OF DENTINE
HYPERSENSITIVITY :
44

Dentine hypersensitivity may be defined as : pain arising from
exposed dentine, typeically in response to chemical. A number of other
dental conditions are associated with dentine exposure and therefore may
produce the same symptoms. Such conditions include chipped teeth,
fractured restorations, restorative treatments, dental caries, undisplaced
cracked cusps (the cracked tooth syndrome), and palato-gingival grooves or
other enamel invaginations. Thus, a careful history, together with a thorough
clinical and radiographic examination, is necessary before arriving at a
definitive diagnosis of dentine hypersensitivity. However, the problem may
be made difficult when two or more conditions co-exist.
There can be few other conditions or diseases in man besides dentine
hypersensitivity that are treated apparently successfully by so many
compounds. Some authors have commented that “because of their
subjective nature many of the earlier reports on desensitization have little
scientific basis and belong in the realms of testimonials.
The lesion :
Direct evidence has been gathered of tubule patency associated with
dentine hypersensitivity. Thus, teeth diagnosed as exhibiting dentine
hypersensitivity, when extracted and studied by scanning electron
microscopy, exhibited in excess of seven times the mean surface tubule
count at buccal cervical dentine sites compared with teeth classified as non-
sensitive.
Incidence and distribution :
Cross-sectional prevalence studies for dentine hypersensitivity have
been limited in number and there are no longitudinal incidence figures for
the condition. The available prevalence data vary considerably, and dentine
hypersensitivity has been stated to range from 8 to 30 per cent of adult
dentate populations. Most sufferers range in age from 20 to 40 years a peak
occurrence is found at the end of the third decade. The reduced incidence of
45

dentine hypersensitivity in older individuals despite increasing dentine
exposure with age, particularly through gingival recession, presumably
reflects age changes in dentine and the dental pulp. Sclerosis of dentine, the
laying down of secondary dentine, and fibrosis of the pulp would all
interfere with the hydrodynamic transmission of stimuli through exposed
dentine and the response of pulpal nerves.
A slightly higher incidence of dentine hypersensitivity is reported in
females than in males, however, the differences are not usually statistically
significant. Most surveys do not conform to standard epidemiologic
methods, and therefore a gender difference may or may not exist.
Dentine hypersensitivity is most commonly reported from the buccal
cervical zones of permanent teeth. Dentine exposure may occur occlusally
and at lingual cervical sites, but in many populations this is less frequently
found and sensitivity only rarely reported. Canines and premolars in either
jaw are the most frequently involved. Additionally, in a group of patients
characterized as moderate to severe sufferers, the dominant factor
influencing the distribution of recession and dentine hypersensitivity was
the side of the mouth.
Etiology and predisposing factors :
Dentine may become exposed by two processes either loss of enamel
or loss of covering periodontal structures, usually termed “gingival
recession”. Loss of enamel occurs by attrition associated with occlusal
function and may be exaggerated by habits or Parafunctional activity such
as bruxism; by abrasion from dietary components or habits such as
toothbrushing; or by erosion associated with environmental or dietary
components, particularly acids. Probably rarely, if ever, is enamel loss due
to a single agent. Exposure of root dentine by gingival recession similarly is
multifactorial, but acute and chronic periodontal diseases, toothbrushing, or
46

chronic trauma from other habits and some forms of periodontal surgery are
important causal factors.
Indirect and direct evidence indicates that for dentine to be sensitive,
not only must it be exposed to the oral environment but dentinal tubules
have to be patent at the surface. Clearly not all factors that expose dentine
necessarily open dentinal tubules. Indeed, most mechanical influences
applied to dentine, including abrasion and attrition, cause this plastic tissue
to flow, producing the so-called smear layer. This very thin layer thus will
cover the dentine surface and obturate the tubules.
The buccal cervical site predilection for dentine exposure and
sensitivity is consistent with toothbrushing practices, with lingual sites
receiving little attention during the brushing cycle of most individuals. The
particular involvement of canines and premolars is therefore not surprising,
because epidemiologic evidence and data from dentine hypersensitivity
sufferers indicate these are the most well cleaned teeth.
Interestingly, the finding that females are more commonly affected by
dentine hypersensitivity than males, if actually correct, would also relate in
part to oral hygiene practices. Females have increased grooming behavior
compared with males, and this is associated with better oral hygiene.
In vitro studies suggest that brushing with water will remove the
dentine smear layer to expose tubules only after protracted periods of
continuous brushing. Brushing with a toothpaste may produce occlusion of
tubules both by a smearing effect on the dentine and by the deposition of
toothpaste ingredients on the dentine and into the tubule orifices. Some
artificial silicas readily adhere to dentine, occlude open dentinal tubules, and
are resistant to removal by washing or dietary acids.
Workers exposed to fumes of hydrochloric, sulfuric, nitric, picric and
tartaric acids exhibit extensive tooth decalcification as do individuals with a
high dietary acid intake or suffering gastric regurgitation. Organic hydroxy
47

acids, in particular citric acid, appear more erosive than inorganic acids, and
clearly activity is not directly pH dependent. The rate of erosion is rapid,
and buffering by saliva is probably too slow to prevent the initial
decalcification. Loss of enamel or dentine due to toothbrushing is very
markedly increased with prior exposure to dietary acids.
The role of plaque as an etiologic factor in dentine hypersensitivity
would appear to be an area of controversy. Through, even over-enthusiastic,
toothbrushing has long been associated with gingival recession and
sensitivity, yet other authors have suggested that plaque causes dentine
hypersensitivity. Marginal leakage around restorations leading to bacterial
activity may be responsible for pulpal pathology and sensitivity beneath
restorations. The possible role of saliva and bacterial contamination of
exposed dentine in dentine hypersensitivity has been proposed but not
proved. Bacteria do penetrate into tubules of dentine left open to the oral
environment and therefore toxins may diffuse to the pulp. This diffusion
would have to occur over relatively large distances and against the outward
flow of dentinal fluid. Additionally, the concentration gradient would be just
as great if not greater in an outward direction. Plaque-induced dentine
sensitivity is considered in the differential diagnosis, in which the emphasis
of management would be quite different from that of dentine
hypersensitivity.
Clinical implications :
The possible consequence of dentine hypersensitivity could be
reduced oral hygiene. Thus, the scenario has been proposed of pain on
toothbrushing leading to a vicious circle of reduced plaque control, more
gingival disease, more recession, and more sensitivity.
The dental surgeon will have to choose the treatment to provide from
an extensive range of possibilities. Indeed, different treatments may be
chosen for different teeth in the same mouth. Whatever is decided, all
48

treatments are designed either to block the dentine sensitivity mechanisms
or to interrupt nerve transmission. These treatment modalities encompass
extremes, from the use of toothpaste and applications of restorative
materials to dentine, to endodontia or even exodontias. There is a need for
greater public awareness, through education, of the effects of exposure to
acids on the teeth, particularly dietary acids. Accepting the nutritional and
health value of many acidic foods and beverages, as with any item in the
diet, excessive quantities or frequency of intake rarely produce proportional
increase in benefits and may have deleterious effects on certain systems,
including the teeth. The need to determine etiologic factors in dentine
hypersensitivity is essential if management is to be successful, and this
should include the taking of a diet history or evaluating the less common
possibilities of exogenous erosive elements in an individual’s living or
occupational environment. In the light of the aggravating effect of
toothbrushing, advice on method and frequency would appear sensible.
Excessive force should be avoided, as should the use of very abrasive
toothpastes. Little benefit to periodontal health is obtained with frequencies
of toothbrushing in excess of twice a day. Indeed, advice to brush before
meals should be provided, and because there are clear benefits from such a
regimen derived not only from mechanical cleaning but also from the
properties of toothpaste, before-meal brushing should be the norm for all
individuals.
Summary :
Management requires the determination of etiologic factors and
predisposing influences, and where possible, their control or modification.
METHODS OF MEASURING TOOTH HYPERSENSITIVITY :
Electrical stimulation differs from the other stimuli in that the
stimulus is not transmitted by the movement of the dentinal fluid. Rather, it
is transmitted by the passage of electrical charge via the moisture associated
49

with the organic material in enamel, cementum, and dentine as well as that
in dentinal tubules, especially if they are open.
Factors affecting measurement of hypersensitivity :
Using a silicone rubber impression method to obtain replicas of root
dentine surfaces in vivo, Absi, Addy and Adams showed that non-sensitive
teeth have closed dentinal tubules, whereas tubules of sensitive teeth are
open. Because enamel is thicker than cementum, it generally provides
greater protection of the underlying coronal dentinal tubules except perhaps
near the cemento-enamel junction where the enamel is thin. Enamel,
because of its thickness, also provides greater electrical resistance. A greater
electrical stimulus is required to produce a sensation in molars because of
their thicker enamel coverings than in premolars and cuspids and in turn,
incisors.
Loss of the thin protective cementum easily occurs with use of a hard
toothbrush and/or an abrasive toothpaste, or by root scaling and planning
during oral hygiene and periodontal therapy.
Another factor that may affect hypersensitivity values is the state of
the pulp. Inflamed pulpal tissue could result in a reading of greater
sensitivity than normal, whereas necrotic pulp tissue generally results in
readings of lower sensitivity or non-sensitivity.
Still another factor is the fact that stimuli for some sensitivity
measurements persist. This means that more time is required for the tooth
and pulp tissues to return to baseline values before another or a repeat
stimulus can be applied.
A placebo effect occurs remarkably frequently in clinical studies on
tooth hypersensitivity. McFall and Hamrick and Addy and his coworkers
suggest that toothpaste components may also contribute to this frequently
observed placebo effect.
Methods used to measure tooth hypersensitivity :
50

Tactile :
The simplest tactile method used to test fro hypersensitivity is to
lightly pass a sharp dental explorer over the sensitive area of a tooth (usually
along the cemento-enamel junction) and to grade the response of the patient
on a severity scale, generally 0 to 3. a score of 0 is assigned if no pain is
felt, 1 if there is slight pain or discomfort, 2 if there is severe pain, and 3 if
there is severe pain that lasts.
Smith and Ash a device with a 15mm (0.26 gauge) stainless steel wire
with a tip ground to a fine point and moveable across the highest arc of
curvature of the facial surface of the sensitive tooth under test. The
scratching force could be increased with a small screw that moves the tip
closer to or away from the totoh surface. As the wire is passed across the
surface of the test tooth it bends, and the amount of bending of the wire and
therefore the force applied can be measured from a scale on the device. To
start the measurement, the screw for adjustment of the wire tip is set so that
the tip just barely touches the root surface being tested. Then the wire is
moved laterally in an arc across the area of sensitivity. This procedure is
repeated after the pressure is increased with the adjustment screw. This is
continued, usually in steps of 1/4 or 1/3 of a millimeter, until the subject is
able to feel a pain sensation. At that point, the scratching force, expressed in
millimeters, is taken as the threshold value.
To permit accurate repositioning for a subsequent re-examination, a
matrix of dental compound is fitted over the lingual and occlusal surfaces of
two or three teeth near the tooth being measured. While the compound
material is still soft, the frame of the device is impressed in the compound
material.
Another tactile device that has been used is the force-sensitive
electronic probe devised by Yeaple for measurement of the depth of
periodontal pockets at fixed pressures. Such a pressure sensitive probe has
51

been modified to accept the tine of a dental explorer tip. The operator can
vary the force applied to the tip of this device by regulating the amount of
current to an electromagnet controlling the tip position. The probing force is
set, and when reached, the probe tip is retracted by an electromagnet; a red
light on a control panel goes on, and the applied force is released. The
handle of the probe is about the size of a fountain pen and is connected by a
flexible electrical lead to the control panel.
The probe force is controlled within ± 1 gram. Calibration is carried
out by using a top loading balance to relate probe meter readings in
microamperes with probe force in grams. In a dentinal sensitivity test, the
probe force can be increased in steps of 5 grams until the subject
experiences discomfort. That point is taken as the pain threshold. If a
maximum force of 70 grams is reached with no discomfort, the tooth is
scored as non-sensitive. The probe emits a buzzing sound when a
predetermined pressure is applied.
Thermal :
A simple thermal method for testing for tooth sensitivity is directing a
burst of room temperature air from a dental syringe onto the test tooth.
Room air is cooler than the teeth, and cooling by this means can be easily
detected as pain if the teeth are sensitive. Blowing air on a tooth also
involves drying, which as pointed out above could also be stimulatory.
Air stimulation has been standardized in a number of studies as a 1-
second blast from the air syringe of a dental unit, where its temperature is
set generally between 650
and 700
F and at a pressure of 60 psi. usually, the
air is directed at right angles to the test surface near the cemento-enamel
junction and/or exposed root surface, with adjacent teeth usually isolated by
the operator’s fingers. Responses are assessed on a severity scale such as 0
where there is no discomfort, 1 if there is some discomfort but no severe
52

pain, 2 if severe pain is felt during application of the stimulus, and 3 if
severe pain occurs during and persists after stimulus application.
The temperature of room air is about 200
C and when gently blown
over a hypersensitive site at about 320
C, the temperature of the site
decreases. By using a miniature thermistor connected to a multi-channel
recorder, Thrash and associates found that the temperature could be easily
measured. Measurement of the drop in temperature is usually repeated three
times and the average taken. Tactile stimuli are applied before thermal
stimuli if the two are being used in the same subject.
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 120
C; current flow in the other direction
heated the tip to 820
C. the temperature was controlled by regulating the
intensity of the current to the probe from a power supply.
The initial temperature for thermal sensitivity testing was set at
37.50
C. For cold stimulation, the temperature was reduced in decrements of
approximately 10
C. at each lower decrement, the instrument was shut off
and the stimulator tip was then placed in contact with the root surface. The
subject raised his or her hand when pain was first detectable.
Testing with heat was carried out in exactly the same way except that
the temperature of the stimulating tip was increased from the initial
temperature of 37.50
C in increments of 10
C to the point at which pain could
be felt.
Osmotic :
The subjective pain response to a sweet stimulus was used by McFall
and Hamrick to measure the effect of several test dentifrices on dentinal
sensitivity. This was done by preparing fresh a saturated solution of sucrose
and allowing it to reach room temperature. After isolation of the test tooth
with cotton rolls, a cotton applicator was saturated with the sucrose solution
53

Dentine hypersensitivity

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