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 :

Tooth / dentin hypersensitivity is one of the oldest recorded

complaints of discomfort to people.

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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.

Leeuwenhock, shortly, after his invention of microscope described

“tooth canals in dentin”. In 1678, he reported “It is asserted that the tooth is

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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.

1st edition of a textbook of dental pathology and therapeutics

including pharmacology by Henry H. Burchard in 1898 provides a

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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

from the pulp and provides the necessary calcium phosphorus and carbonate

to carry on mineralization process.

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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 100C or above 400C 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.

4. It should be rapid in its action

5. It should be permanently effective

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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

hypersensitivity, based on this report sensodyne toothpaste was developed

with strontium chloride hexohydrate.

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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)

Berman proposed the term “dentinalgia” to differentiate sensitivity

from “Pulpalgia”. The “gate control therapy” and the hydrodynamic theory

were proposed as most probable mechanisms.

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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.

10) Dentrifices may provide one of the active ingredients above or

function by occluding tubular orifices.

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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

sense but can involve potential tissue damage with constant erosion of the

enamel or cementum along with the concomitant Pulpal response.

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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.

From this plexus, nerve fibers extend to the odontoblastic layer, predentin,

and dentin and terminate as free nerve endings. The sensory receptors

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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 m 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

classical signs of acute inflammation including heat, redness, and swelling

to some extent, but not pain and loss of function (sensitivity to chewing,

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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

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

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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.

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

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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 :

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 m of dentin is innervated, odontoblasts would act as receptor cells

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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 m, 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

outer part of the dentinal tubules does not contain any cellular elements but

is only filled with dentinal fluid.

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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 A 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

A-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 A-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 A-fibers. There is little evidence that stimuli other

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

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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

600C. 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 3.40C. 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.

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

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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

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

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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 m 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

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

19

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-, , or -

fibers, depending upon their axon diameter and their conduction velocity.

Most of the myelinated nerve fibers in teeth are A- 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- nerve activity. The

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

20

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- 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

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

21

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- 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- 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,

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.

22

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)

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

23

Q =IIPr4N

8nL

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

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 m2 (Pashley,

unpublished observation). If 5 gm of force is applied over 500 m2, 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

24

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

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

25

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

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.

26

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, 300C) 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

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- 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

27

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 250C air directed at a 320C 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

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

28

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

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

29

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

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.

30

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

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

31

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

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,

32

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

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.

33

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

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

34

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

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.

35

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

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

36

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 () is a factor that reports the relative ability of

a solute and a solvent to diffuse through a membrane. By definition,

= 1 when the membrane is impermeable to the solute but

completely permeable to the solvent, and when = 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

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.

37

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

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.

38

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.

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

39

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

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

40

(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.

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,

41

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

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.

42

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

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.

43

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 :

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

44

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

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

45

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

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.

46

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

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

47

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

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,

48

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

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,

49

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 :

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

50

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

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

51

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

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 200C and when gently blown

over a hypersensitive site at about 320C, 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.

52

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 120C; current flow in the other direction

heated the tip to 820C. 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

37.50C. For cold stimulation, the temperature was reduced in decrements of

approximately 10C. 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 37.50C in increments of 10C 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

and then applied to the root surface of the tooth and allowed to remain in

place for 10 seconds or until discomfort was perceived. The subject rated

the sensation as no pain or pain, which was recorded as 0 or 1, respectively.

The osmotic challenge was stopped by rinsing with warm water.

Electrical :

Electrical measurements differ from the others in that a pain response

can be obtained from non-sensitive as well as from sensitive teeth and with

either an enamel-covered crown or a cementum-covered root site of

stimulation. Until recently, instruments for applying electrical stimuli of

53

increasing intensity, generally referred to as pulp testers, were used mainly

to determine whether a pulp is vital or not. The answer determined the

treatment that would be carried out. Instrument improvement led to better

quantification of the electrical stimulus and discovery that a condition of

“pre-pain” consisting of a tingling or warm sensation is observed before real

pain and discomfort are felt by the subject as the magnitude of a stimulus is

increased. The pre-pain sensation has been attributed to the larger, more

rapidly conducting, nerve fibers located at or in the pulp reacting sooner,

than the smaller diameter nerve fibers that are also present.

The presence of a pre-pain zone of stimulation makes it possible to

obtain threshold stimulation levels without hurting the patient. This results

in less or no apprehension; such apprehension can have an adverse effect on

readings.

Instruments for stimulating a tooth electrically have as their basic

constituents an electrode or probe to apply the electrical stimulus to the test

tooth, a power source, a means of varying the electrical stimulus so that its

magnitude can be progressively increased, an a means of completing the

electrical circuit. Because of the high resistivity of teeth, toothpaste or a

similar material with high electrical conductivity is necessary to facilitate

transmission of the electrical stimulus to the tooth. In some cases, the

operator serves as a means of completing the circuit, with the finger of one

hand in contract with the patient’s mouth and the other hand in contract with

the casing of the probe. With the present need of the operator to wear

protective gloves, this method is not satisfactory. Also, alternate pathways

of current flow are more likely to occur if the operator is part of the

electrical circuit. Elimination of the operator from the circuit was

accomplished by Stark, who used as a reference electrode a saliva ejector

connecting the patient to a pulp-stimulating instrument that he called the

pulp stethoscope. As an alternative, the reference electrode can be applied to

54

the skin as in ECG measurements. The electrical resistance of the skin can

vary from 1000 ohms for damp skin to 1 million ohms for dry skin. By

using a conducting gel, this difference largely disappears. This method is

better than the saliva ejector method of Stark because there is less likelihood

of interruption of the electrical circuit during a measurement.

Alternate pathways of current flow that are of some concern are those

that can occur via the gingival adjacent to the site of electrode placement on

the tooth, via other oral; soft tissues such as the cheek or tongue, or via

saliva. All of these can be eliminated by carefully isolating and thoroughly

drying the tooth being tested and by having the insulation of the stimulating

probe extend right up to its tip. Fortunately, the sensation felt by a patient

when the gingival, tongue, or cheek is inadvertently touched with the probe

tip is very different and easy to distinguish from the sensation felt when

only the tooth is controlled and the pulp is stimulated.

By trial and error, an electrical stimulus consisting of a direct current

pulsed voltage between 0 and 150 (Digilog Pulp Tester) or between 0 and

300 volts (Analytic Technology Pulp Tester; Redmond, WA) has been

found suitable for eliciting a pulp response. If an alternating current supply

is used to power the unit generating the electrical stimulus, then for safety

reasons, it must provide for patient isolation. Although alternating current-

powered units are bulkier and less portable than direct current-powered

instruments, they do allow for easier addition of printers and other recording

devices, which are extremely useful for recording such information as the

tooth stimulated and the magnitude of the electrical stimulus that elicited a

pulpal response.

For safety reasons, any electrical current that is applied should be

limited to less than 1 milliampere, preferably 0.5 milliampere or less, which

is in the approximate range of the human body’s threshold of current

perception for 1 second hand-to-hand contact. The voltage of an electrical

55

stimulus should be in the from of pulses to avoid summation and a chance

of reaching voltage levels that might result in pain rather than pre-pain.

Pulses with a width of 0.05 to 0.20 millisecond each and spaced at 5 to 10

millisecond intervals will provide a stimulus of pre-pain instead of pain.

With a commercial digital pulp tester that contains this feature of

automatic ramping (Analytical Technology Pulp Tester), an indicator light

comes on when the probe tip contacting the surface of a tooth encounters a

circuit resistance below 5 million ohms.

Method use in studies :

It seems from the numerous studies that have been carried out on

tooth hypersensitivity that different types of teeth in the human dentition

and teeth of different ages and history will vary considerably in their

response to pain-producing stimuli so that testing of homologous pairs of

teeth would be prudent. To assess effects of an agent on dentinal sensitivity,

there need to be relatively large numbers of subjects with sensitive and non-

sensitive teeth in a cell. In general, we have found this number to be a

minimum of 25 but preferably 35.

Conclusion :

Hypersensitivity apparently affects one in seven dental patients. It is a

problem that should not be ignored because many of such teeth may become

non-vital with time. Now that such measurements are becoming possible,

practitioners should be able to monitor teeth that are sensitive to determine

whether they are getting better or worse following treatment. A chronically

sensitive tooth should be a warning sign that a pulp is under continual

trauma. With the aging of the population, greater retention of teeth, and

greater root surface exposure because of gingival recession and periodontal

surgery, one can expect the number of sensitive teeth to rise.

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DESIGNING HYPERSENSITIVITY CLINICAL STUDIES :

57

A clinical dentinal tooth hypersensitivity study is first and foremost a

clinical pain study. Critical design factors include proper selection of

investigator, subjects, hypersensitivity test measurement devices, agents to

be tested, and statistical analysis.

Investigator :

The central aspect of hypersensitivity studies is the investigator. The

investigator must know and understand the neurophysiologic explanations

for cause and effect of dentinal hypersensitivity.

The design and implementation of a research protocol require

comprehension of the proposed mechanism.

The investigator should be capable of designing a thorough and

efficient hypersensitivity study protocol. Sufficient time must be allocated

to manage every aspect of a hypersensitivity study. The test site must be

adequately staffed with trained auxiliary personnel. The best plans have

little chance to translate into a well executed study when crammed into a

busy schedule.

The investigator must understand that the sensitive region of the tooth

can be very specific. Not every exposed cervical dentin area not all points

within a known sensitive area will be hypersensitive.

The investigator must be thoroughly trained and experienced in the

use of the test devices. In becoming proficient, the investigator will develop

an intuitive feel for the sensitivity of the measuring device and when it is

being correctly applied to suspected sensitive areas.

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The investigator should be adept in evaluating prospective study

subjects fro their genuine interest in participating in the study. He or she

should be able to determine that each subject is properly relating when

sensitivity is first perceived, or when a subject is just giving answers to get

through the study for one reason or another. Most importantly, the

investigator must be capable of developing rapport with subjects so they

will be able to relax during hypersensitivity test examinations. A relaxed,

professional atmosphere will give subjects a chance to provide accurate and

reliable responses during the hypersensitivity testing procedures.

Overall design :

Principles of good clinical design must be followed in order to attain

reliable conclusions. When performing a dentinal hypersensitivity study this

usually means double-blind, parallel, randomized or stratified, and

comparative study designs.

In a double-blind study, neither the investigator (including research

personnel) nor the subject knows the identity of the test product assigned to

the subject.

In a parallel study, all test materials/products should be assigned to

separate subject groups/ cells and used by the respective subject cells. Thus,

each subject group tests only one product. In a cross-over design, each

subject uses one of the study products for a specified use-time. At the end of

the product use-time, the subjects use no study product for a brief period to

“wash out” the effect of the first study product. This wash-out period is then

followed by use of a second study product by each subject. The product-use

and wash-out period sequence is followed by the subjects until they have

used all study products. Cross-over designs are contraindicated because the

wash-out period is not usually known for most desensitizing agents.

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A comparative study compares one product to another. The simplest

study design tests an active product to a placebo control. More complicated

studies might compare two or more active products with each other and with

the placebo. Subject recruitment, experimental design and statistical

analysis become more difficult as the number of cells is increased.

Test materials :

The dentifrice with the active agent (active dentifrice) should be

compared with the same dentifrice without the active agent (placebo or

negative control). It must be emphasized that the placebo dentifrice should

possess the same color, taste, consistency and ingredients as the active

dentifrice except for the active agent.

The clinical dentinal hypersensitivity literature is replete with reports

demonstrating efficacy for the placebo dentifrice. This is common referred

to as the “placebo effect”. The use of a placebo control dentifrice will not

only enable demonstration of desensitizing efficacy by the active agent

alone; it will also rule out an additional potential placebo effect within the

active product itself.

Comparison of two or more desensitizing dentifrices is a frequent

objective of clinical hypersensitivity studies. One of the dentifrices might be

a well known and documented desensitizing product. This dentifrice could

be referred to as a “positive” control and lead the investigator to rationalize

that negative or placebo control is not necessary. A placebo control

(negative) should be included in studies comparing two active products to

verify that the design and conditions of the study will allow active agents to

overcome a placebo effect and demonstrate their potential efficacy.

Subject selection :

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Subject selection is the most demanding part of a clinical

hypersensitivity study. Specific subject selection criteria should be written

into the protocol and strictly adhered to.

The study should be designed to answer a question with regard to an

identified population. The study subjects should be a representative sample

of that population. Usually, the study subject population represents the

general population of those bothered with dentinal hypersensitivity.

Occasionally, the primary objective of the study is subset of the population,

such as post-periodontal surgery patients.

People troubled by hypersensitivity were found to range from 15 to

69 years of age. The greatest concentration were in their 20s and 30s.

sensitivity has also been reported to be evenly distributed in males and

females.

Ideal subjects should be :

1. Cooperative and relatively relaxed in the dental chair

2. Experienced in interacting with dentists as dental patients

3. Reliable in their responses to test measurements, use of assigned

product, and attendance at appointed examinations.

Prospective subjects should not be troubled with active periodontal

disease in the areas of their hypersensitivity teeth. Prospective subjects

should not have undergone periodontal surgery within 6 months prior to the

initiation of the study. Dental hypersensitivity is a particular problem in the

post-periodontal surgery patient. A study designed specifically to investigate

hypersensitivity in post-periodontal surgery patients would be appropriate.

Teeth with cracked tooth structure, large carious lesions, or restorations

should not be acceptable study teeth.

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Prospective subjects should be in good general health. They should

not be suffering from a chronic debilitating disease or a chronic disease that

is associated with daily episodes of pain, such as arthritis. Such conditions

would most probably interfere with obtaining representative hypersensitivity

pain data.

An important final consideration for subject selection would be the

level of hypersensitivity appropriate for inclusion in the study. For example,

the tactile sensitivity of a prospective study tooth should not be too close to

the tactile sensitivity of a prospective study tooth should not be too close to

the “low end” of tactile sensitivity, which precludes the opportunity to

demonstrate potential improvement, that is, non-responsive. On the other

end of the sensitivity range, it might not be appropriate to include a tooth

that is on the “high end” of tactile sensitivity. It might be difficult to

distinguish between pulpal and dentinal pain for those subjects. It is also

infinitely more difficult to reliably measure hypersensitivity pain at this end

of the range of pain.

Hypersensitivity measurement :

Whatever stimulus is used, the stimulus should be quantifiable and

reproducible. The stimulus should also elicit dentinal pain and not pulpal

pain. Dentinal pain is usually rapid in onset, sharp in nature, and of short

duration. Dentinal pain is produced by stimuli such as tactile, cold, heat, and

osmotic, which are applied to exposed dentin.

A general principle for all studies, clinical or laboratory, is to use

accepted methods. Unfortunately, acceptable devices/techniques have not

yet been established for measuring hypersensitivity. Thus, a large share of

the undertaking of a clinical hypersensitivity study is transformed from a

science to an art.

Tactile sensitivity :

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A dental explorer is passed over exposed dentin on the labial cervical

areas of suspected sensitive teeth. Subjects will then report their sensitivity

or lack of sensitivity to the examiner. Once sensitive teeth have been

designated and subjects enrolled in a clinical study, the dental explorer is

frequently used to measure tactile sensitivity levels throughout the study.

Subjects will then evaluate their level of tactile sensitivity to the explorer

using a verbal rating scale (VRS). A typical VRS might appear like this to

the subject:

0 = No discomfort, but aware of stimulus

1 = Mild discomfort

2 = Marked discomfort

3 = Marked discomfort that lasted more than 10 seconds

Measurement of tactile sensitivity by this method has two limitations.

First, the investigator should test all sensitive areas on all teeth of all

subjects during all examinations with the same tactile pressure. This would

be an almost impossible task. Second, the VRS offers a restrictive choice of

words that may not represent pain experience with sufficient precision for

all subjects.

An electronic pressure-sensitive probe (Yeaple probe) has been used

to measure levels of tactile sensitivity. The primary advantage of the probe

is that tactile sensitivity can be reported in terms of a quantified

reproducible grams force. The probe tip (dental explorer) can also reach all

tooth surfaces in all areas of the mouth.

Care must be exercised that the force is applied gradually so that the

applied force will not go beyond the point at which the subject actually

perceives sensitivity.

The investigator may “sweep” a suspected sensitive area with a tactile

probe several times before finding just one spot within the area that elicits

sensitivity by the subject. Patience is a virtue in these situations.

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Thermal sensitivity :

The cold stimulus appears to be the strongest and causes the greatest

problems to those troubled by dentinal hypersensitivity.

A method often reported in the literature for measurement of cold

sensitivity is the 1-second air blast at about 700F from a dental unit air

syringe. There are several problems associated with this apparently simple

quantifiable technique that render it difficult to reproduce accurately. First,

there always exists the problems of proper control f the temperature of the

air emanating from the syringe. The usual practice is to report a temperature

range of 680 to 730 F. such a relatively wide range has the danger of crossing

back and forth over the threshold temperature of cold air sensitivity for each

subject. The intensity of the stimulus could also vary in accordance with

variances in pressure (usually reported at 60 psi), the distance of the syringe

tip from the tooth being tested, and the actual duration of the 1-second air

blast. The latter of these two intensity factors are investigator controlled and

could easily vary from one test to another. The question of an “air drying”

effect on the exposed dentin area from the air blast has not been resolved.

Immediately after the cold air blast, the subject usually reports the

level of sensitivity via a VRS as discussed for tactile sensitivity.

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The pain threshold approach has also been used test sensitivity to

cool/cold air. A temperature-controlled stream of air was directed to the

exposed dentin of a sensitive tooth via a disposable plastic tip. The initial air

temperature of 1000F was reduced until the subject first experienced

sensitivity or until a lower limit of 700F was reached. The air stream was

generated by a compressor at 10 psi. the air temperature was controlled by

an intricate device and was monitored at all times by a temperature probe

just prior to the existing of the air through the tip. This technique would

appear to be quantifiable and reproducible, but it may have the advantage of

drying and sensitizing a test tooth as the investigator proceeds down through

a temperature range.

The thermocouple device used to test thermal sensitive provides a

continuous application of heat or cold via a probe tip to a point on the tooth.

The device has the advantage of precise control of temperature, but it suffers

from a lag between probe and tooth surface temperature. changes in

temperature must be made slowly so that a temperature threshold of

sensitivity is not bypassed. In addition, sensitivity measurement by this

device may not be representative of real world thermal sensitivity

experienced by subjects. Subjects usually complain of cold air or cold

liquids and not cold objects. Cold air or cold liquids produce sudden

changes in dentin temperature and thereby, sudden shifts in dentinal fluid in

the tubules result in hypersensitivity pain as described by the hydrodynamic

theory. The thermocouple would most likely produce more gradual changes

in dentinal temperature and dentinal tubule fluid movement.

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A cold water testing technique was developed and later modified to

include the use of different temperatures of water placed directly on the

exposed dentin. Plastic impression syringes were filled with water from

thermal insulated containers with temperatures equilibrated to 200, 100 and

00C. the investigators used the syringes to flow water over the exposed root

surface fro 3 seconds or until a positive response was noted by the subject.

Testing began with water at 200C and proceeded to 100 and 00 or until a

positive response was obtained. The intensity of pain perceived by the

subject at the temperature that first produced a positive response was not

evaluated. This method is, in effect, a threshold technique and should

include several more temperatures of water between 200 and 00C. to add

more temperatures would require more thermal insulated water containers.

The requirement of numerous water baths would make the technique

considerably more equipment intensive. Another concern about this

technique would be controlling the amount of water flowed over the

exposed dentin during each challenge.

Chemical sensitivity :

Chemical stimuli have been used in clinical hypersensitivity studies.

The stimulus is not conductive to threshold measurement because repeated

applications of the chemical stimulus reduce the sensitivity of the exposed

dentin. Problems such as inconvenience, difficulty in administering and

controlling the stimulus, and possible injury to the adjacent soft tissue de-

emphasize the chemical stimulus as a practical measurement of

hypersensitivity in clinical studies.

Electrical sensitivity :

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Application of electrical stimuli to either enamel or exposed dentin

has not been shown to result in any noticeable effect on tubule fluid

movements. The electrical stimulus would appear to be more appropriate for

measuring pulp vitality than dentinal sensitivity.

Subject assessment :

Word descriptors that patients use to describe their hypersensitivity

pain have not been documented. Clinical hypersensitivity studies should

provide an opportunity to indicate the key words that best describe

hypersensitivity pain throughout the use of an assigned product.

The subjects quantitative assessment of their own overall perception

of hypersensitivity pain has been used in clinical studies. When this method

of evaluating the level of hypersensitivity is used, subjects are asked to rate

the severity of sensitivity that they have been experiencing during their

everyday routine. They are to include stimuli from cold air, hot/cold foods

or drink, sweet and sour food, toothbrushing and so on in their overall

sensitivity evaluation. When provided a suitable method for evaluation of

perceived sensitivity, subject assessment of hypersensitivity during a

clinical study provides meaningful information. The visual analogue scale is

an acceptable method for providing this assessment.

Visual analogue scale :

A visual analogue scale (VAS) is a line, usually 10 cm in length. The

extremes of the line represent the limits of pain a subject might experience

during a dentinal hypersensitivity episode. One end could be labeled “no

discomfort” or “no pain”, whereas the other end could be labeled “severe

discomfort” or “severe pain”. Subjects are asked to place a “mark” on the

10cm line at a location between the no pain and sever pain ends that best

indicates their current level of hypersensitivity. When the VAS is properly

explained to subjects, they can easily understand its use and successfully use

it to indicate their level of pain response to a hypersensitive stimuli. The

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Vas offers a continuum between what the subjects would perceive as the

extremes of pain (none to severe). The VAS also offers a greater capacity to

change in response to a hypersensitive stimulus. On the other hand, the

verbal rating scale (VRS) is restrictive in that it does not offer enough

descriptions that can be placed in a continuous and ascending (or

descending) order of severity of pain. Use of the VAS has been found to be

reproducible because a very high correlation between successive

measurements of pain severity has been noted.

Application of stimuli :

When more than one stimulus is used, the application order of the

stimulus is very important. Care should be taken to insure, as much as

possible, that each stimulus does not interfere with other stimuli used in the

measuring procedure. The least disturbing stimulus should be used first,

with the most disturbing stimulus used last. Depending on which stimuli are

used, testing should begin with subject assessment and then followed by

tactile, heart and cold stimuli.

Control of extraneous factors that could potentially influence subject

response is important. Standardized instructions and stimulus demonstration

should be given. The examination room should be free of distractions

caused by noise, music, lights, temperature and so on. Avoid fear-generating

procedures. The subject should be allowed to adjust to the examination

room environment.

Test product assignment :

Subject assignment :

The first consideration in subject assignment should be the

establishment of two subject groups (cells) with equivalent level of dentinal

hypersensitivity. Treatment of equivalent levels of hypersensitivity is very

important for a meaningful comparison of the active dentifrice with the

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control dentifrice and the establishment of a desensitizing efficacy by the

active dentifrice.

Random assignment of subjects to treatment groups is the simplest

scheme to implement. By this method, however, an investigator is always at

risk of ending up with groups of different levels of hypersensitivity by this

method. The risk becomes greater as the group size is decreased, whereas

the risk is lessened as the group size is increased.

One easy method of stratification involves maintaining a cumulative

sum of the cold sensitivity measurements from the baseline examination of

subjects. Subjects are assigned to the two groups with the guideline of

maintaining equivalent sums of cold sensitivity data between the two

groups. The stratification process can be made more intricate by also

maintaining equivalent tactile sensitivity sums between the two groups in

addition to maintaining equivalent cold sensitivity sums.

The second consideration is subject group assignment based on “real

world” population variables. Generally, the subjects within each group

should be in the age range of 20 to 50. This age range should also be equally

represented between the two groups. Whenever possible, males and females

should be equally represented in each group.

Achieving the ideal representation of these population variables is

often very difficult because of the usual limited availability of

hypersensitivity subjects.

Product assignment :

The active and control dentifrices should be assigned to the subjects

so that the investigator, subject, and any other office staff do not know

which product each subject is using (double blind).

The active and control dentifrices should be packaged in plain

dentifrice tubes and properly coded for identity. A third person who has no

investigator or subject contact should be the only one who knows the code.

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Study length/examination periods :

The length of time subjects brush with their assigned dentifrice can be

a critical factor of dentinal hypersensitivity studies. Subjects should use

their assigned dentifrice over a sufficient time period to :

1. Demonstrate clinical efficacy on the part of the active desensitizing

dentifrice as compared to the control or placebo dentifrice.

2. Rule out a “placebo effect” on efficiency as compared with the active

dentifrice.

It has been the experience of the authors that a placebo effect by the

control dentifrice usually runs its course in about 6 weeks of treatment. In

order to confirm the course of the placebo effect, hypersensitivity

measurement should be obtained after 8 and 12 weeks of use of the study

dentifrices. Thus, a suggested examination/length of study format would be

two baseline hypersensitivity examinations 1 week apart, begin use of study

dentifrice immediately upon completion of the second baseline examination,

and hypersensitivity examinations obtained upon completion of 2, 4, 8 and

12 weeks of dentifrice use.

Statistical analysis :

Sound statistical principles of study design and analysis must be

considered at the outset of the trial, not at the conclusion. Failure to do so

could weaken the scientific validity of the study and lead to inaccurate

conclusions. Important factors to consider include representativeness of the

subject sample, number of subjects needed, treatment group allocation

methods, and selection of appropriate analytic methods.

The clinical investigator should not turn to the statistician after a

study has, been completed without prior consultation and expect the

statistician to derive statistical meaning from the data.

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Designing hypersensitivity study is in effect a clinical experiment of

testing the null hypothesis that the “active” desensitizing dentifrice is no

different than the control dentifrice in reducing hypersensitivity.

The ability to separate treatments in a statistical analysis is partly a

function of the statistical tests used. A desirable statistical test has a small

probability of rejecting the null hypothesis when it is true and a large

probability or rejecting it when it is false. Parametric tests usually have

higher probabilities of rejecting the null hypothesis when it is false than

non-parametric tests. When appropriately used, both parametric and non-

parametric tests have low probabilities of rejecting the null hypothesis when

it is true. The choice of which of these two statistical techniques and which

specific tests should be used depends on several factors and assumptions.

A good study should include enough subjects to have adequate

power. That is , the study should be able to identify, with high confidence,

when there is a meaningful difference between the treatment groups. This is

especially important when interpreting studies that show no statistically

significant difference between the treatment groups. For studies with an

adequate number of subjects, this result can be interpreted to mean that the

treatments are unlikely to differ by a meaningful amount. In studies with too

few subjects, the failure to differentiate treatments may simply be due to

insufficient power.

OVER-THE COUNTER DENTIFRICES IN THE TREATMENT OF

TOOTH HYPERSENSITIVITY :

Traditionally, a dentifrice has been defined as a substance used with a

toothbrush to aid in cleaning the accessible surfaces of the teeth. Pader has

expanded this definition to recognize the pharmacologic role of anticaries

therapeutic dentifrices by defining a dentifrice that falls into this category as

an abrasive-containing dosage from for delivering anticaries agents to the

teeth. A dentifrice formulated to alleviate or treat the symptoms of tooth

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hypersensitivity can be defined as an abrasive-containing dosage form for

delivering desensitizing agents to the affected teeth. It is important to note

that in the United Stages and many other countries, dentifrices that claim to

treat the symptoms of tooth hypersensitivity are regulated as drugs and thus

must meet strict standards of safety and effectiveness.

Dentifrice as a delivery vehicle :

Toothpaste, by far the commonest form of dentifrice, is apparently a

simple product but is actually quite complex in formulation terms. On the

one hand, consumers expect a toothpaste to extrude from its container

easily, spread onto and stick to the toothbrush, but then break apart and

foam almost instantly when brushing starts. Users also expect a pleasant and

refreshing flavor, a certain level of foam, and a lack of stringiness and

grittiness. Conversely, manufacturers must provide a product that is stable

and retains its rheologic characteristics for 2 or ideally 3 years and more

important, retains effective drug availability and delivery potential for this

length of time, often under less than ideal storage conditions.

Dentifrice components include abrasive, surfactant (foamer),

humectant, thickener, flavor, sweetener, coloring, and water. Therapeutic

dentifrices contain drug agents in addition to the other items. Desensitizing

dentrifices are, for the most part, standard in formulation except that a

concern for abrasivity exists because the condition is associated with

exposed cementum or dentin, structures that are much softer than enamel.

Abrasives are solid particles that clean or polish the tooth surface.

compounds used for this purpose include various insoluble calcium salts

(e.g., phosphate, pyrophosphate, and carbonate), sodium metaphosphate,

and alumina. In recent years, a shift toward silicas has occurred because of

their compatibility with fluoride, and their utility in formulating clear or

opacified gel dentifrices. In the United States the abrasiveness (abrasivity)

of a dentifrice is commonly determined by an in vitro procedure in which

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radioactive dentin is mechanically brushed with a standardized slurry of

dentifrice under a standard protocol developed by the American Dental

Association (ADA). The amount of radioactive material removed is

compared with that removed by a standard abrasive, which is given a value

of 100; hence, this scale is commonly referred to as the RDA100 (radioactive

dentin abrasivity) scale. Most toothpastes that are available today, including

desensitizing pastes, have RDA values from about 50 to 150. this is well

within the estimate of a safe and effective level of abrasiveness, 50 to 200

RDA, provided by Pader after extensive review. Dentifrice abrasives are

essential to prevent tooth staining. Because clinical studies have shown that

the degree of stain formation is inversely proportional to the abrasivity

level, a certain degree of abrasiveness in a dentifrice is cosmetically

essential. Clinicians, however, have sometimes noted wedge-shaped lesions

or defects at the cementoenamel junction, and the question has arisen as to

the role of dentifrice abrasives in the etiology of this condition. The results

of a clinical study designed to answer this question showed that the action of

brushing contributed substantially to the amount of dentin removed,

whereas the contribution of dentifrice abrasivity was not a major factor in

the progression of cervical lesions.

A second cosmetic attribute of dentifrices that is essential to

successful treatment of tooth hypersensitivity is flavor. In fact, the taste of a

dentifrice is one of the most important factors related to the continuous use

of a particular dentifrice, and, perhaps somewhat surprisingly, market

research has shown that most consumers will not continue to use a particular

dentifrice solely for its therapeutic benefit. Most desensitizing toothpastes

have a taste that is different from that of conventional toothpastes because

they incorporate therapeutic agents. When recommending or prescribing a

product, clinicians should explain this to the patient. The fact that a taste is

different does not mean that it is unacceptable. The pleasantness of a taste is

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a cultural, subjective, and personal phenomenon, and adaptation can rapidly

occur. If a patient reports that the flavor of a particular brand is

unacceptable for continued use, then the dentist should recommend another

brand that incorporates a different active system.

Using an in vitro dentin disc system, Pashley and co-workers found

that dentifrice components could occlude tubules, and that products differed

in their ability to produce this effect. Clinically, Addy and Co-workers

related decreased tooth sensitivity to an in vitro observation that the fine

silica abrasive particles in some toothpastes readily occluded open dentinal

tubules. Interactions among several potential dentifrice components affect

their uptake by dentin, and these interactions may have advantageous or

negative consequences for treatment.

RATIONALE FOR OTC TREATMENT OF TOOTH

HYPERSENSITIVITY

Up to one in seven adults screened in an office practice in

Switzerland had tooth hypersensitivity. In view of this incidence, home-use

OTC-desensitizing products appear to be the most realistic and practical

means of treating most patients with tooth hypersensitivity and should be

the first step in routine management. This presupposes that the diagnosis of

hypersensitivity has been made and the patient educated as to the proper

preventive measures to adopt.

First, they are readily and widely available, especially in pharmacies.

Second, the products are cost-effective. Repeated dental office visits for

desensitization treatments are costly in terms of time and money. Third, the

OTC products are simple to use and noninvasive. Fourth, the habit of tooth

brushing is almost universal in economically developed societies, the patient

is not required to do anything he or she would not normally do, thus easing

problems with regimen compliance. In 1981, the Council on Dental

Therapeutics of the American Dental Association established a category for

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acceptance of desensitizings agents. Products that meet the association’s

criteria for safety and effectiveness are allowed to display the ADA “seal of

acceptance” on the product and packaging, provided the manufacturer also

agrees to adhere to the association’s standards in promotion and advertising.

Currently, the council has accepted formulations containing three active

ingredients for OTC dentifrice use : potassium nitrate, strontium chloride

hexahydrate, and dibasic sodium citrate in a pluronic gel.

Clinical methods of efficacy assessment :

It is important to note that the ultimate criterion of success for a

hypersensitivity treatment is, in fact, the subjective opinion of the clinician

and patient : the former will not use a procedure or recommend a treatment

that is perceived to be ineffective, whereas the latter will not allow a

treatment regimen that does not alleviate the pain encountered in everyday

situations. Nevertheless, the unreliability of subjective opinions alone

necessitates that well-designed, double-blind, controlled clinical trials be

conducted to establish scientifically the effectiveness of hypersensitivity

treatment procedures before dissemination to the dental profession and the

public at large.

Pain perception, however, depends on several variables including

among other factors the significance of the pain, individual personality,

psychological factors, cultural attitudes, anticipation of pain, and the degree

of apprehension. That fact, along with other negative study design factors

including lack of stimulus standardization among investigators, led to

inconclusive or contradictory results in many studies in which the intensity

of pain perceived was the primary measurement criterion.

An ad hoc advisory committee on dentinal hypersensitivity appointed

by the ADA recommended the following study design features ; 1) the test

data should be quantifiable and reproducible ; 2) the threshold of response

should be established, preferably quantified, and correlated to a clinically

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definable intensity ; 3) the relationship between the experimental stimulus

and the defined area of hypersensitivity must be established by controlled

clinical research ; 4) if more than one stimulus is used, then these stimuli

should be reproducible, and interference between them must be minimized ;

and 5) appropriate statistics should be used, and these should be justified

according to the experimental design. The committee recommended, in

addition to sound clinical and statistical design, the use of variable stimulus

level-fixed threshold response as opposed to the earlier method of fixed

stimulus level-variable response for the evaluation of tooth hypersensitivity.

In evaluating the results of clinical desensitization studies, the

clinician should carefully determine how close the methodology used is in

conformance with the preceding guidelines and give greater credence to

results obtained with newer methods. Note that the terms “old methods” and

“new methods” are used for convenience; many studies conducted decades

ago essentially confirm to the guideline, whereas some studies conducted

recently do not.

CLINICAL RESULTS

Strontium chloride Dentifrices

Dentifrices containing 10% strontium chloride hexahydrate as the

desensitizing agent have been widely available for three decades. Sensodyne

tooth paste for Sensitive Teeth was the product tested; at least one other

brand (Thermodent Sensitive Teeth Toothpaste, Mentholatum Company,

Buffalo, New York) incorporating strontium chloride hexahydrate is

available commercially.

Ross in 1961 reported the results of a monadic study conducted

among 78 office patients who were instructed to use this dentifrice at home.

Subjectively, 73% of the subjects reported complete relief of the condition,

and this was confirmed by the clinician who observed the subjects’

involuntary response to artificially induced tactile and thermal stimuli.

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Alleviation of symptoms usually occurred within 1 month of use. Similar

results were reported in other monadic studies by Cohen, Skurnik, Meffert

and Hoskins, Zelman.

Although these early monadic studies showed that the use of a

strontium chloride dentifrice had a potential benefit, they did not establish

the efficacy of the drug agent itself because a placebo control was not used.

Subsequently, as clinical methodology evolved, several double-blind,

placebo-controlled clinical studies, were conducted two double-blind,

placebo-controlled clinical studies were conducted two double-blind studies

comparing the effectiveness of a strontium chloride dentifrice against that of

a placebo control, or placebo and monofluorophosphate-containing controls.

In the study against placebo, after 4 weeks of use, 68% of the sensitive teeth

in 38 subjects had improved in the active group as compared with 53% in

the 38 subjects using the placebo. This difference was significant at the 95%

confidence level. After 8 weeks of use, however, although the percentage of

improved teeth in both the active and placebo groups continued to increase

(76 vs. 71% respectively) the differences were no longer significant.

Subjects using the monofluorophosphate dentifrice experienced the same

degree of benefit in comparison with the placebo as did subjects using the

strontium chloride product.

Blitzer conducted a double-blind 1-month study in which the patients

subjectively rated their response to either an active (20 subjects) or placebo

(17 subjects) dentifrice into the categories of complete disappearance of

hypersensitivity, partial relief, or no improvement. In the active group, 75%

of the subjects rated their improvement as complete in comparison with

24% in the placebo group. The intergroup difference was significant at the

99% confidence level.

Smith and Ash conducted a double-blind, placebo-controlled study

over 60 days in 20 subjects using qualitatively applied thermal and

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mechanical stimuli to elicit a response. Subjects also self-rated their

hypersensitivity condition. The results showed that no improvement

occurred in either group regarding any of the parameters tested. Johnson and

co-workers found that after 12 weeks of unsupervised twice daily use, 28

subjects using the strontium chloride dentifrice demonstrated an increase in

the ability to tolerate a cold water stimulus of 5.330C, whereas an identical

number of subjects using a conventional stannous fluoride dentifrice showed

a smaller increase of 3.040C. The intergroup difference was significant at

the 99% confidence level.

Addy and coworkers found that a strontium chloride dentifrice was

significantly superior to a placebo dentifrice when measured by the graded

responses using the classical cold air method, but was inferior to the placebo

in terms of the number of sensitive teeth responding to a thermoelectric

probe set at 00C and 50C.

Minkoff and Axelrod :

Uchida and co-workers studied the effectiveness of a strontium

chloride dentifrice in treating hypersensitivity following periodontal

surgery. In the active group, the pain score (a summary of pain responses to

mechanical, cold water, and cold air stimuli) increased from 1.2 to 2.6, 1

week postoperatively, and then decreased to 0.6 (76%), 8 weeks

postoperatively or 7 weeks after the start of treatment. In the placebo group,

the pain score also increased from 1.0 to 2.2, 1 week postoperatively, but at

the end of treatment the value was still 1.4, a 34% reduction. The

significance of the Uchida study lies in the fact that the results quantitatively

confirmed the clinical impression that periodontal procedures often induce

tooth hypersensitivity, and, additionally, that a strontium chloride dentifirce

is effective in relieving the condition.

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Potassium Nitrate Dentifrices :

In 1974, a potassium nitrate-containing dentifirce was reported as

providing effective desensitization for 35 dental office patients who

experienced slight to severe tooth hypersensitivity. The positive results for

the agent provided by this type of quantifiable stimulation in double-blind

controlled studies led to the acceptance by the ADA of several commercial

products, Denquel Sensitive Teeth Toothpaste (Richardson-Vicks, Wilton,

Connecticut), Sensodyne-F, and promise with Fluoride.

Tarbet and co-workers compared the relative abilities of four active

ingredients present in OTC dentifrices to desensitize hypersensitive teeth.

They reported that 5% potassium nitrate was the most effective agent tested

and rank ordered the relative effectiveness of the other agents tested as

follows: strontium chloride, dibasic sodium citrate, formaldehyde.

On an overall basis, the clinical evidence supports the efficacy of a

5% potassium nitrate dentifrice for the alleviation of the pain of tooth

hypersensitivity.

Dibasic Sodium Citrate Dentifrices

Dibasic sodium citrate, formulated into a pluronic F-124 containing

dentifrice (Protect) is the final ingredient currently recorgnized by the ADA

as being safe and effective for the treatment of dentinal hypersensitivity.

Formaldehyde Dentifrices :

No longer sold in the united States, One brand, Emoform is available

in the United Kingdom. Actually, dentifrices that contain 1.2 to 1.4%

formaldehyde were the first widely available, commercially successful

desensitizing dentifrices. Clinically, however, the results have been

decidedly mixed. In early monadically designed studies, some investigators

reported a favorable effect. The results for formaldehyde dentifrice have

been generally negative. McFall and Morgan confirmed the negative tactile

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finding but also found a significantly increased ability to tolerate a

quantifiable cold stimulus. The ADA has not evaluated this agent to date.

Fluoride and other dentifrices :

One of the more popular early in-office treatments for treatment of

hypersensitivity was burnishing the affected sites with fluoride-containing

medicaments. The results of several studies, especially, those conducted

with sodium monofluorophosphate in comparison with nonfluoride control,

indicate a certain degree of effectivness. Kanouse and Ash found that after 3

months of use, subjects using the monofluorophosphate dentifrice had an

increased tolerance to cold and hot of 1.70C and 1.30C, respectively,

whereas subjects using a placebo showed increases of 0.50C for both

stimuli. The intergroup differences were significant at the 95% confidence

level.

RECOMMENDATIONS FOR FUTURE STUDY DESIGN

After reviewing the clinical desensitization literature of the last 30

years, one can conclude that a major obstacle impeding the development of

more efficacious products to treat tooth hypersensitivity is the lack of

standardization in study design. Clinical studies have been of varying

duration, from 4 to 12 weeks; numbers of subjects per experimental cell

vary widely; and the unit of data analysis has been the hypersensitive

surface, hypersensitive tooth, and the individual. Fleiss and Kingman state

that it is a mistake to employ statistical procedures that take individual sites

as the units of analysis; the patient must be the unit of analysis.

Although intrastudy comparisons are possible, and overall

assessments of drug efficacy are possible on the basis of the number of

studies and their overall quality, interstudy comparisons cannot be made.

Hence, questions such as the relative effectiveness of agents or the

comparative times required to observe an effect cannot be answered reliably

on the basis of published data.

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Contrast this situation with that in anticaries clinical research. In this

area, the units of measurements are well defined: decayed-missing-filled

teeth or surfaces. Measurements are usually made at yearly intervals. Even

the usual test population, school children, is well-defined because this age

group is both prone to the disease and is readily accessible to clinical

investigators. In earlier studies, the active products were compared with true

placebos; currently, new products are compared with clinically verified

positive controls. The net result of this has been the establishment of a large

data base suitable for interstudy comparisons, which will allow for future

advances in this area.

Choice of stimulus will remain a difficult issue because different

investigators have different opinions on this instrumentation. Nevertheless,

some have adopted tactile stimulation because at least one instrument is

widely available (Yeaple Probe, Vine Valley Research, Middlesex, NY).

A review of Current Approaches to In-Office management of tooth

Hypersensitivity :

CLINICAL CHARACTERISTICS OF DENTAL

HYPERSENSITIVITY

The terms dentin sensitivity and dentin hypersensitivity are often used

interchangeably, although the prefix hyper-denotes excessive sensitivity.

Whereas dentin sensitivity is a normal response to stimulation of freshly

exposed dentin, hypersensitivity may have a more pathologic basis.

In virtually all cases of hypersensitivity, it is the vestibular surfaces of

the teeth that are sensitive. Orchardson and Collins found that in different

tooth types the relative frequency of hypersensitivity was: premolars, 38

percent; incisors, 26 per cent; canines, 24 per cent; and molars, 12 per cent.

Dentinal hypersensitivity is subjective evidence that dentin has lost its

investiture of cementum. However, about 10 per cent of teeth have no

cementum covering the cervical portion of the root, and in these teeth

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gingival recession alone may lead to hypersensitivity. Most hypersensitive

teeth have associated gingival recession in excess of 1mm, and about 30

percent have cervical lesions. Gingival recession can be caused by

periodontal disease, periodontal therapy (including oral prophylaxis), and

improper tooth-brushing habits.

Typically, the chief symptom of dentinal hypersensitivity is a sharp,

sudden pain of short duration, although some patients complain of a dull,

lingering sensitiveness. The most frequent complaint is sensitivity to cold,

but pain may also be elicited by the use of a toothpick and /or brushing. In

some cases, hot liquids and sweet or sour foods may evoke a response.

Although most teeth are sensitive to more than one stimulus, not all

hypersensitive teeth respond to the same stimulus.

DIFFERENTIAL DIAGNOSIS :

In attempting to determine the cause of discomfort, teeth should be

examined for the presence of carious lesions, restorations, fractures,

discoloration, periodontal disease, occlusal trauma, and exposed dentin that

might be sensitive. Once the diagnosis of hypersensitivity has been

established, it may be advisable to obtain a written dietary history in order

to gather information regarding the possible etiologic role of acidic foods.

Incomplete tooth fracture can be associated with a number of

symptoms ranging from mild discomfort to severe pain. The most common

complaint is pain to pressure. Tapping the teeth or having the patient bite

down on an orangewood stick almost invariably evokes a sharp pain in the

affected tooth. Application of a dye such as methylene blue to suspected

tooth may aid in the diagnosis by disclosing the line of fracture.

Exposure of dentin due to chipped enamel is usually obvious.

Fractured restorations may be more difficult to visualize. Nevertheless,

careful examination of the restoration will usually reveal the fracture.

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Differentiating dentinal hypersensitivity from caries is realatively

easy, particularly in the case of a deep carious lesion. However, it must be

recognized that caries and dentinal hypersensitivity can coexist in the same

tooth.

Tooth sensitivity following a restorative procedure may resemble

hypersensitivity in that the tooth is particularly sensitive to heat and cold

and the evoked pain is generally of short duration and moderate intensity.

Acute hyperfunction. A common example is the new amalgam or

crown that has been placed without proper adjustment of the occlusion.

Although the recent operative procedure may be partially at fault,

hyperfunction alone can produce symptoms of pulpitis, Occlusal

equilibration has been reported as a treatment modality for hypersensitive

roots that did not successfully respond to accepted desensitizing methods.

Teeth in acute hyperfunction are typically responsive to temperature

changes and may mimic hypersensitive dentin, even though the investiture

of these teeth ay be intact.

Application of a saturated solution of CaCl2 (8.8m) on a cotton pellet

may be useful in identifying areas of hypersensitive dentin (Dr. David

Pashley, personal communication). Saturated CaCl2, a highly soluble salt, is

capable of evoking a sharp sensation by creating a strong osmotic pressure

across dentin, thus producing fluid movement in the tubules.

Diagnosis of pulpitis must be based on subjective and objective

findings. Diagnostic aids include history of pain, percussion and palpation

tests, inspection of the teeth and surrounding tissues, thermal and electric

pulp tests, and radiographic examination. The dental history should cover

the chronology, nature, location, radiation, and aggravating and alleviating

factors that influence the pain.

Dentinal hypersensitivity resembles reversible pulpitis in that pain is

generally mild to moderate and fairly well localized to the tooth in question.

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SPONTANEOUS REMISSION OF HYPERSENSITIVITY

It is well known that hypersensitivity often abates without treatment.

This is probably related to the fact that dentin permeability can decrease

spontaneously. Natural processes contributing to desensitization include the

formation of reparative dentin by the pulp, obturation of tubules by the

formation of mineral deposits (dentinal sclerosis), and calculus formation on

the surface of the dentin.

It has been estimated that approximately 20 to 45 per cent of patients

who receive no treatment or sham treatment experience relief.

PLACEBO EFFECT

A major factor in the establishment of a placebo response is the

doctor-patient relationship. Individuals afflicted with real or imagined

illness must have complete confidence in their doctor because patient

expectations are critical for the induction of the placebo response. Illness

and discomfort are perceived by the patient as threatening, and it is assumed

that practitioners are able to decrease the peril. A positive doctor-patient

relationship can motivate a patient to obtain relief. Furthermore, positive

emotional and motivational behavioral responses can activate the body’s

central pain-inhibiting system. this system modulates painful stimuli from

the periphery through the release of endorphins centrally.

PATIENT MANAGEMET

Informing a patient in advance regarding the possibility of a

potentially painful event can greatly strengthen the doctor-patient

relationship, alleviate anxiety, reduce unnecessary emergency calls, lower

the risk of litigation, and enhance the placebo effect. Proper patient

management relies heavily on good communication skills. Every patient

must be informed of the potential treatment risks, and post-treatment

dentinal hypersensitivity is no exception.

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IN-OFFICE TREATMETN PROCEDURES : RATIONALE OF

THERAPY

Treatment of hypersensitive teeth should be directed toward reducing

the functional diameter of the tubules so as to limit fluid movement. In order

to accomplish this objective there are several possible approaches :

1. Formation of a smear layer by brushing the exposed root surface.

2. Topical application of agents that form insoluble precipitates within

the tubules.

3. Impregnation of tubules with plastic resins.

4. Application of dental bonding agents to seal off the tubules.

Although most agents that are effective in reducing dentinal

hypersensitivity are also effective in partially occluding the dentinal tubules,

potassium nitrate (KNO3) is an exception.

SPECIFIC TREATMENT MODALITIES :

Prior to treating sensitive root surfaces, hard or soft deposits should

be removed from the teeth. Root planning with curettes or otherwise

manipulating sensitive dentin may cause considerable discomfort, in which

case teeth should be anesthetized prior to treatment. The teeth should be

isolated and dried with warm air. When using desensitizing agents that have

a caustic effect on sot tissue, care must be exercised to prevent them from

contacting the alveolar mucosa.

Cavity Varnishes :

Dentin often becomes insensitive when open tubules are covered with

a thin film of varnish. This may be an effective means of providing

temporary relief. Wycoff advocates the use of a cavity varnish such as

Copalite. For more sustained relief, a fluoride-containing varnish, Duraflor.

Can be applied

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Corticosteroids :

Mosteller reported that when a liner consisting of 1 per cent

prednisolone in combination with 25 per cent para-chlorophenol, 25 per cent

m-cresyl acetate, and 50 per cent gum camphor was applied to the walls of

cavities, it was completely effective in preventing postoperative thermal

sensitivity.

It has also been reported that burnishing an ophthalmic

corticosteroids solution into sensitive root areas achieved some success.

Studies involving the use of corticosteroids have provided little

evidence that desensitization was due to the hormone, particularly when it

was claimed that sensitivity was promptly relieved. Corticosteroids are not

fast-acting drugs.

Effects of Burnishing Dentin :

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Burnishing of dentin with a toothpick or orangewood stick results in

the formation of a smear layer that partially occludes the dentinal tubules.

Pashley and coworkers employed an in vitro method to study the effects of

burnishing NaF, kaolin, and glycerin, alone or in various combinations, on

dentin permeability. They observed that burnishing created a partial smear

layer that reduce fluid movement across dentin by 50 to 80 per cent.

Burnishing dentin with a dray orangewood stick was more effective in

reducing dentin permeability than burnishing with glycerin alone.

Formation of insoluble precipitants to block tubules :Certain soluble salts react with ions in tooth structure to form crystals

on the surface of the dentin. In order to be effective, crystallization should

occur within 1 to 2 minutes, and the crystals should be small enough to enter

the tubules. The crystals must also be large enough to partially obturate the

tubules. Although relatively large crystals such as calcium oxalate dihydrate

(which form when potassium oxalate is applied to dentin) are very effective

in reducing permeability smaller crystals such as CaF2 are les apt to be

effective.

Although it is used infrequently today, AgNO3 is time-honored

desensitizing agent. Numerous authors have attributed the effectiveness of

AgNO3 to its ability to precipitate protein constituents of odontoblast

processes (Tomes’ fibers), thereby partially blocking the tubules. However,

there are reasons to doubt this explanation.

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Gottlieb developed the zinc chloride – potassium ferrocyanide

impregnation method for desensitizing root surfaces and cavities. In this

procedure a 40 per cent solution of aqueous zinc chloride was rubbed into

the surface per cent aqueous solution of potassium ferrocyanide was

vigorously rubbed onto the dentin surface until an orange, curdy precipitate

formed. Scanning electron micrographs of this precipitate have revealed a

highly crystalline deposit covering the dentin surface. As most of the

crystals were too large to enter the tubules, it is doubtful whether this

method would provide a more efficient means of desensitizing dentin than

burnishing alone.

Grossman proposed formalin as the desensitizing agent of choice in

treating anterior teeth because, unlike AgNO3, it does not produce an

unsightly stain. Formalin has been used in the dental office in a

concentration of 40 per cent (full strength) for topical application by means

of cotton pellets or orangewood sticks.

CALCIUM COMPOUNDS :

Calcium hydroxide :

Calcium hydroxide (Ca(OH2) has been a popular agent for the

treatment of dentin hypersensitivity for many years, particularly after root

planning. The exact mechanism of action is unknown, but evidence suggests

that it may block dentinal tubules or promote peritubular dentin formation.

Using SEM, Brannstrom observed a variable constriction of the dentinal

tubules in the majority of teeth treated with Ca(OH)2, but only to a depth of

0.1 mm Mjor employed microradiograph to compare Ca(OH)2 – covered

dentin with normal dentin and demonstrated increased radiodensity in the

Ca(OH)2-covered dentin.

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Because increasing the concentration of calcium ions around nerve

fibers can results in decreased nerve excitability Ca(OH)2 might be capable

of suppressing nerve activity. However, Trowbridge and coworkers found

that application of Ca(OH)2 to the walls of deep cavities in cat canine teeth

had no effect on the excitability of nerve fibers in the underlying pulp.

Levin and associates applied Ca(OH)2 paste to the necks of 118 teeth

in 50 patients and found it to be immediately effective in reducing

sensitivity in 98 per cent of the teeth. First, sensitive teeth were isolated and

dried with cotton rolls. Next, a paste of Ca(OH)2 and sterile distilled water

was applied to the exposed root surfaces with a sable brush. The paste was

allowed to remain on the tooth for 3 to 5 minutes. After removal of the

paste, the tooth was tested sensitivity. If the dentin was still sensitive, the

paste was re-applied.

Pashely and coworkers found that Ca(OH)2 was effective in reducing

the permeability of acid-etched dentin as well as smear layers. However,

when 6 per cent citric acid was applied to the Ca(OH)2-treated smear layer,

dentin permeability returned to the initial acid-etched value. This would

suggest that ingestion of acidic foods and beverages might result in removal

of Ca(OH)2 from the dentin.

Dibasic Calcium Phosphate :

Hiatt and Johansen studied the effectiveness of burnishing CaHPO4

into sensitive areas of roots with a round toothpick and found that 93 per

cent to patient reported significant relief of discomfort, as compared with 25

per cent of the control group, which received burnishing only.

FLUORIDE COMPOUNDS :

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Lukomsky was the first to propose sodium for fluoride (NaF) as a

desensitizing agent. Later, Hoyt and Bibby developed a paste consisting of

equal parts of NaF, kaolin, and glycerin. The paste was burnished into the

exposed root surfaces with a porte polisher, an orangewood stick or a rubber

cup for 1 to 5 minutes. Although this procedure was considered to be a

success in decreasing sensitivity, at least part of the effect can be attributed

to burnishing. More recently, fluoride gels have been developed for in-

office treatment of hypersensitivity.

Because dentinal fluid is saturated with respect to calcium and

phosphate ions, application of NaF to dentin leads to precipitation of CaF2

crystals, thus reducing the functional radius of the dentinal tubules. The

crystal size of CaF2 is very small (approximately 0.5 m), and therefore as

single application of NaF has less effect on dentin permeability than agents

such as potassium oxalate that give rise to larger crystals. Furthermore, it

has been shown that fluoride is lost fairly rapidly following application of

NaF to dentin. This may explain why topical application of fluoride

solutions is of limited effectiveness in reducing sensitivity on a long-term

basis.

Evidence suggests that a small fraction of the fluoride initially applied

to dentin is retained in the insoluble apatitic form, thus making the lattice

more stable and less soluble in acid. This could protect the dentin from

dietary acids, which tend to open the tubules.

Acidulated Sodium Fluoride :

Laufer and colleagues observed that the concentration of fluoride in

dentin treated with acidulated NaF was significantly higher than dentin

treated with NaF. However, there was no difference after samples were

washed with synthetic saliva.

Sodium silicofluoride:

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Bhatia claimed that application of saturated solution (0.6 per cent) of

sodium silicofluoride for 5 minutes was much more potent than a 2 per cent

solution of NaF in desensitizing painful cervical areas of teeth. Everett and

associates postulated that silicic acid forms a gel with the calcium of the

tooth, thus producing an insulating barrier.

Stannous Fluoride :

Blank and Charbeneau advocate burnishing a 10 per cent solution of

stannous fluoride (SnF2) into sensitive root areas. Ellingsen and Rlla. This

observed a dense layer of tin- and fluoride-containing globular particles

blocking the dentinal tubules. The dentinal tubules were totally covered

even after treatment with relatively low concentrations of SnF2.

Blong and associates found that a 0.4 per cent SnF2 gel was an

effective agent in the control of pain associated with hypersensitive dentin.

However, prolonged use of the gel (up to 4 weeks) was necessary to achieve

satisfactory results.

Fluoride – Inotophorises :

Iontophresis is a term applied to the use of an electrical to transfer

ions into the body for therapeutic pusposes. The object of fluoride

iontophoresis is to drive fluoride ions more deeply of fluoride alone.

In a histologic study, leflkowitz observed secondary (reparative)

dentin in the pulps of teeth extracted soon after iontophoresis and concluded

that iontophoresis stimulates dentin formation. This inference is highly

suspect, as it takes several weeks for reparative dentin to form in human

teeth.

Iontophoresis is not a simple procedure. It involves the placement of a

negative electrode to dentin and a positive electrode to the patient’s face or

arm. If the negative electrode makes contact with salvia, gingival tissue or a

metallic restoration, the flow of current will follow the path of least

resistance and stream around the dentin rather than through. It for this,

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reason, Gangarosa recommended that teeth be isolated with plastic strips

and cotton rolls rather, than a rubber dam. He cautions that moisture can

accumulate between the tooth and the rubber dam, thus providing a low

resistance pathway for the current.

Although a number of authors have reported a significant reduction in

sensitivity with the use of iontophresis with 2 per cent NaF, Greenhill and

Pashely- found that the use of AgNO3 or potassium oxalate produced

significantly grater reductions in hydraulic conductance than fluoride

iontophoresis.

Although iontophoresis has gained some popularity, its effectiveness

needs to be demonstrated in well-controlled clinical studies. Iontophoresis

devices are expensive, somewhat difficult to use, and generally less cost-

effective than other treatment procedures.

Strontium chloride :

Kun found that (topical application of concentrated strontium chloride

(SrCl2) on an abraded dentin surface produced a deposit of strontium that

penetrated dentin to a depth of approximately 20 and extended into the

dentinal tubules.

It has been suggested that strontium deposits are produced by an

exchange with calcium in the dentin resulting in recrystallization in the form

of a strontium apatite complex. Gedalia and associates reported that topical

application of 10 per cent SrCl2 prior to application of 2 pre cent NaF was

more effective in decreasing sensitivity than NaF alone, as assessed 3

months following treatment.

Oxalates :

Since their initial development as a desensitizing agent, the oxalates

have gained great popularity, particularly among periodontitis. They are

relatively inexpensive, easy to apply, and well tolerated by patients.

92

Potassium oxalate and forric oxalate solutions make available oxalate

ions that can react with calcium ions in the dentinal fluid to form insoluble

calcium oxalate crystals that are deposited in the apertures of the dentinal

tubules. SEM revealed a high degree of tubule occlusion by crystals that

almost completely covered the orifices of the tubules. Subsequent

application of 6 per cent citric acid to the oxalate-treated dentin did not

increase dentin permeability, indicating that calcium oxalate should be

resistant to dietary acids.

In the development of an effective desensitizing system, there oxalate

compounds have been developed, 6 per cent ferric oxalate, 30 per cent

dipotassium oxalate, and 3 per cent monohydrogen-monopatssium oxalate.

Pashley and Galloway found that when reacting with ionized calcium, 30

per cent dipotassium oxalate produced fewer but significantly layer calcium

oxalate crystals than those produced by 3 per cent monohydrogen-

monopotasium oxalate. These investigators suggested that the larger crystals

are only effective in obturating wide open tubules, whereas the smaller

crystals are capable of obturating open as well as partially close tubules.

Application of KHOx to the etched dentin reduced sensory nerve

excitability to the level of unetched dentin.

KHOx is commercially available under the name of Protect. It comes

in a convenient unit-dose applicator tubules with a cotton tip that delivers

KHOx to the dentin surface. Ferric oxalate is currently marketed under the

Sensdodyne Sealant name. It is available as a professional desensitizing

treatment for unit-dose application with a disposable contra-angled

instrument.

DENTAL RESINS AND ADHESIVES :

The objective in employing resins and adhesives is to seal the

dentinal tubules to prevent pain-producing stimuli form reaching the pulp.

Several investigators have demonstrated immediate and enduring relief of

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pain for periods of up to 18 months following treatment. although not

intended for treatment of generalized areas of root sensitivity, this can be an

effective method of treatment when other forms of therapy have failed.

Brnnstrm and colleagues achieved excellent results by impregnating

the dentinal tubules with a restorative resin material. in this procedure, the

area of sensitive dentin was cleansed and etched with an acid conditioner for

5 seconds. The dentin was them dehydrated with a continuous blast of air

for a at least 15 to 20 seconds in order to dry the outer part of the dentinal

tubules. A drop of a Concise Enamelbond was then applied to the dentin.

Before the resin on the surface hardened into a thin film it carefully

removed to allow resin tags to occlude the outer part of the tubules without

covering the dentin between the tubules with resin.

The use of NTC-GMA and PMDM following ferric oxalate treatment

of the dentin smear layer led to a sustained decrease in dentin permeability.

This system spears to hold promise as a future treatment for dentinal

hypersensitivity.

Pashley and associates have shown that contamination of dentin with

blood or salvia lowers the bond strength of composite resin. However, they

found that contaminated surface could be removed with a high-speed bur.

During a 6-weeks study, Javid and coworkers compared the effects of

a single application of isobutyl cyanoacrylate with weekly applications of a

33 per cent NaF paste. The material is gradually lost, so that repeated

cyanoacrylate applications may be necessary.

Wycoff advocates the use of adhesives for severe cases of

hypersensitivity that do not respond to other therapy. He prefers a glass-

ionomer cement because it is hydrophilic acid conditioning is not required,

the material adheres well, and it is esthetically pleasing.

Copeland found that application of Scotchbond produced immediate

and lasting relief from hypersensitivity. Clinically superior results were

94

obtained by covering the resin with a drop of dilute restorative material.

Eighteen months following treatment, 89 per cent of 368 hypersensitive

teeth remained free of pain.

GLUMA- includes a 5 per cent gluteraldehyde primer and 35 per cent

HEMA. It provides an attachment to dentin that is immediate and strong.

GLUMA has been found to be highly effective when other methods of

treatment failed to provide relief.

It has been reported that the sequential use of GLUU<A followed by

Scotchbond produced impressive bond strength. Because. GLU<A has

excellent wetting characteristics, it should enhance bond strength of a resin

when the dentin has been contaminated with blood or saliva.

Recently Felton and coworkers have reported that GLUMA seems to

prevent bacterial growth in tooth/restoration interfaces. This could have a

beneficial effect in inhibiting plaque accumulation on sensitive root

surfaces.

PATIENT EDUCATION :

Dietary counseling :

Dietary counseling should focus on the quantity and frequency of acid

intake and intake occurring in relation to tooth brushing. Any treatment may

fail if these factors are not controlled. A written diet history should be

obtained on patients with dentinal hypersensitivity in order to advise them

concerning eating habits.

Addy and associates found that red and white wine, citrus fruit juices,

apple juice, and yogurt were capable of dissolving the smear layer in vitro.

They also found that formic and tannic acids, low-pH carbonated drink,

Coca-Cola and black currant cordial had no effect on smear layers.

Tooth brushing in combination with decalcification of superficial

dentin is capable of accelerating the loss of tooth structure. because loss of

dentin is greatly increased when brushing is performed immediately after

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exposure of the tooth surface to dietary acids, patients should be cautioned

against brushing their teeth soon after ingestion of citrus foods.

Tooth Brushing Techniques :

Because incorrect tooth brushing appears to be an etiologic factor in dentin

hypersensitivity, instruction in proper brushing techniques can prevent

further loss of dentin and the resulting hypersensitivity.

PLAQUE CONTROL :

Saliva contains calcium and phosphate ions and is therefore able to

contribute to the formation of mineral deposits within exposed dentinal

tubules. The presence of plaque may interfere with this process, as plaque

bacteria, by producing acid, are capable of dissolving any mineral

precipitates that form, thus opening tubules.

Periodontitis generally feel that patient who maintain effective plaque

control complain less about hypersensitivity. Recurrent of root sensitivity

has been noted in specific areas that were missed in home care.

It is difficult for patients of undertake desensitizing procedures such

as plaque control if the procedures cause pain. The goal of treatment is to

reduce sensitivity so that the patient is able to burnish sensitive dentin

surfaces with a toothpick, Stim-U-Dent, or abrasive-containing dentifrice.

This keeps the dentin surfaces clean and at the same time forms a smear

layer.

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