Dentin is a hard connective tissue characterized by dentinal tubules and is composed of approximately 75% inorganic material, primarily hydroxyapatite. Different types of dentin, including primary, secondary, and tertiary dentin, have distinct formation processes and properties that affect dental health, particularly in relation to dentin hypersensitivity. The management of dentin hypersensitivity, which involves sharp pain from exposed dentin, has gained attention in recent years, highlighting the need for clear definitions and treatment strategies.

1. INTRODUCTION TO DENTIN
Dentin is characterized by the presence of a multitude of closely packed
dentinal tubules that traverse its entire thickness and contain the cytoplasmic
extensions of the odontoblasts that once formed the dentin and now maintain it.
Dentin is a hard connective tissue.
It is yellowish in color.
Chemically composed by weight approximately,
75% INORGANIC
20% ORGANIC
05% WATER
Chemically composed by volume approximately,
45% INORGANIC
33% ORGANIC
22% WATER
Inorganic component consists mainly of hydroxyapatite.
Organic component consists mainly of type I collagen with fractional inclusions of
glucosaminoglycans, proteoglycans, phosphoproteins, glycoproteins and other
plasma proteins. Dentin has an elastic quality which provides flexibility to prevent
fracture of the overlying brittle enamel.
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2. PREDENTIN
Predentin is a newly formed umicrometerineralized matrix of dentin located
at the pulpal border of the dentin.
Predentin is evidence that dentin forms in 2 stages ie, first organic matrix is
deposited and second one inorganic mineral substance is Added.
Predentin is thickest where active dentinogenesis is occurring and its
presence is important in maintaining the integrity of dentin.
Absence of predentin appears to leave the mineralized dentin vulnerable to
resorption by odontoclasts.
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3. PRIMARY DENTIN
It is composed peripherally of a thin layer of MANTLE DENTIN. It is the
initial dentin formed. Its collagen fibers are larger i.e., 0.1 to 0.2 micrometer in
diameter in contrast to the remaining dentinal matrix which is 50 to 200micrometer
Mantle dentin is slightly less mineralized and has fewer defects than
circumpulpal dentin.
CIRCUMPULPAL DENTIN forms the remaining primary dentin or bulk
of the tooth. It represents all of the dentin formed before root completion. Its
collagen fibrils are smaller in diameter 0.05micrometer. and it constitutes most of
the dentin in both the crown and root.
Primary dentin is characterized by the continuity of tubules from the D.E.J
to the pulp and by incremental lines indicating a daily pattern of rhythmic
deposition of dentin of approximately 4micrometers per day.
SECONDARY DENTIN
It is formed internal to the primary dentin of the crown and root.
Develops after the crown has come into clinical function and the roots are
nearly completed.
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4. Deposited more slowly than the primary dentin and as result the
incremental lines are only about 1.0 to 1.5 micrometer per day in the manner the
pulp is not obliterated by an excessive rate of dentin formation.
Contain fewer tubules than primary dentin. There is usually a bend in the
tubules at the primary and secondary dentin interface. Tubules of primary and
secondary dentin are generally continuous.
Secondary dentin scleroses occur more readily than primary dentin. This
tends to reduce the overall permeability of the dentin, thereby protecting the pulp.
In molar teeth greater deposition of secondary dentin on the roof and floor
of the coronal pulp chamber occurs than on the lateral walls. This leads to
protection of the pulp horns as aging occurs. These changes in pulp space clinically
referred to as PULP RECESSION can be readily detected in rAdiographs and are
important in determining the form of cavity preparation in certain dental restorative
procedures.
TERTIARY DENTIN
Also referred to as REPARATIVE or REACTIVE dentin.
Dentin is deposited rapidly in which case the resulting dentin appears
IRREGULAR WITH SPARSE AND TWISTED TUBULES.
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5. It results from pulp stimulation and forms only at the site of odontoblastic
activation.
May be due to,
 Attrition
 Abrasion
 Caries
 Restorative Procedures
Dentin is deposited underlying only those stimulated areas.
No continuity with the primary and secondary dentin. This decreases dentin
permeability.
INTERGLOBULAR DENTIN
Mineralization of dentin begins in small globular areas but fails to coalesce
into a homogenous mass. This results in zones of hypomineralization between the
globules. These zones are known as "GLOBULAR DENTIN" or "INTER
GLOBULAR SPACES"
This dentin forms in the crowns of teeth in the circumpulpal dentin just
below the mantle dentin and follows the incremental pattern.
The dentinal tubules pass uninterruptedly through interglobular dentin.
Especially noticeable with,
1) Vitamin D deficiency
2) Exposure to high levels of fluoride at the time of dentin formation.
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6. TOMES GRANULAR LAYER
When ground sections of root dentin are viewed under transmitted light,
there is a granular zone underlying the cementum covering the root known as
"TOMES GRANULAR LAYER"
Increases in width from C.E.J to the apex of the tooth.
It is due to a coalescing and looping of the terminal portions of the dentinal
tubules.
These true spaces appear dark when viewed with transmittal light.
Peripheral to the granular layer of Tomes and separating it from the
cementum is a very thin hyaline layer.
HYALINE plays a functional role in "cementing" cementum to the dentin
and is a product of root sheath cells.
INCREMENTAL LINES
INCREMENTAL LINES OF VON EBNER :
Dentin is deposited incrementally which means that a certain amount of
matrix is deposited daily. This lack of formation results in these lines also known
as "IMBRICATION LINES."
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7. Incremental lines indicate a daily pattern of rhythmic deposition of dentin
of approximately 4 micrometer per day. They run at right angles to the dentin.
CONTOUR LINES OF OWEN:
Another type of incremental pattern found in dentin.
They are resulted due to,
1) Coincidence of the secondary curvatures between neighboring dentin
tubules.
2) Disturbances in the matrix.
3) Deficiencies in mineralization.
Microscopically seen at the junction of primary and the secondary dentin. It
is seen easily in longitudinal ground sections.
NEONATAL LINE
In the primary dentition and the first permanent molar teeth in which dentin
is formed partly before and partly after birth, the prenatal and post natal dentin are
separated by on accentuated Contour line known as "NEONATAL LINE".
It reflects the abrupt change in environment that occurs at birth.
These result due to,
1) Physiological trauma at birth.
2) Periods of illness.
3) InAdequate nutrition.
DENTINAL TUBULES
DENTINAL TUBULES are small, coral like spaces within the dentin filled
with tissue fluid and occupied by odontoblast processes.
They extend the entire thickness of dentin from the D.E.J to the pulp.
They follow 'S'- SHAPED path from the outer surface of the dentin to the
perimeter of the pulp.
This S- shaped curve is less pronounced in root dentin and is least
pronounced in the cervical third of the root and beneath incisal edges and cusps,
where they run an almost straight course.
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8. These curvatures called the "PRIMARY CURVATURES" which arise as a
result of the crowding of center of the pulp. "SECONDARY CURVATURES" are
smaller oscillations within the primary curvatures.
In coronal dentin approximately 20,000 tubules are present per square
micrometer near the enamel and 45,000 per square micrometer near the pulp. This
increase in number per unit volume is associated with a crowding of the
odontoblasts as the pulp space becomes smaller.
The terminal part of the tubules branches, resulting in an increased number
of tubules per unit length in mantle dentin. This terminal crowding is more in root
dentin.
DENTINAL TUBULE DIAMETER
8
900 micrometer near
the D.E.J
1.2 micrometer in the
middle
2.5 micrometer near
the pulp

9. Dentinal tubules are tapered in out line, measuring approximately 2.5
micrometer in diameter near the pulp, 1.2 micrometer in the mid portion of the
dentin and 900 micrometer near the D.E.J.
Tubules begin perpendicular to the Dentino-enamel junction and Dentino-
cemental junction to the pulp.
Few dentinal tubules extend through the D.E.J into the enamel for several
millimeters. These are termed "ENAMEL SPINDLES".
They have lateral extensions that branch from the main tubule at intervals
of 1 to 2 micrometer along its length and that may or may not house lateral
cytoplasmic extensions of the odontoblastic processes.
These lateral extensions are termed CANALICULII, SECONDARY or
MICROTUBULES. These are less than a micrometer in diameter and arise at right
angles to the tubules. Some canaliculii enter Adjacent main tubules and some
appear to terminate in the inter-tubular matrix.
The clinical significance is that dentinal tubules make the dentin permeable
providing a path way for the invasion of caries.
ODONTOBLASTIC PROCESS
The odontoblastic cell processes are the cytoplasmic extensions of the
odontoblast which exists in the peripheral pulp.
These processes extend through the entire thickness of dentin.
In some instances they also extend into the enamel for a short distance as
"ENAMEL SPINDLES".
The odontoblast cell bodies are approximately,
7micrometer → In diameter and
40 micrometer → In length
The odontoblastic processes are largest in diameter near the pulp 3 to 4
micrometer and taper to 1 micrometer near the D.E.J.
Lateral branches arise at near right angles to the main odontoblastic process
and extend into the inter-tubular dentin as into the Adjacent tubules.
Loss of the odontoblastic process usually results in the appearance of
"DEAD TRACTS" in dentin. In the dentin underlying an area of attrition or a
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10. carious lesion the odontoblast may die and disintegrate, producing a band of dead
tracts in the dentin. Then the tubules become filled with air. When ground section
is made it results in a black appearance of these tubules.
The odontoblastic process contains,
• Microtubules
• Small filaments
• Occasional Mitochondria
• Micro vesicles.
This is indicative of the PROTEIN-SECRETING nature of the
odontoblasts.
Nerve terminals can also be seen in the dentinal tubule in the region of
predentin.
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11. INTRATUBULAR DENTIN
The dentinal matrix that immediately surrounds the dentinal tubules is
termed "INTRATUBULAR" or "PERITUBULAR DENTIN"..
Since it is formed within and at the expense of the dentinal tubules INTRA
TUBULAR DENTIN is a more accurate term.
40% more highly calcified than the Adjacent intertubular dentin.
It is missing from the dentinal tubules in interglobular dentin, indicating
that this is a defect of mineralization.
Formation is a slow continuous process which can be accelerated by
external stimuli. By growth it constricts dentinal tubules to a diameter of
1micrometer near the D.E.J. In some areas the intratubular dentin completely
obliterates the tubules for example near the D.E.J overlying the pulp horns and
especially in the root. When the tubules are completely obliterated in an area of
dentin, this is called ''SCLEROTIC DENTIN'' OR TRANSPARENT DENTIN”.
The clinical significance is sclerotic dentin increases in amount with age
and is believed to be a protective mechanism of pulp, to decrease permeability in
area of overlying attrition, abrasion, fracture or caries on the tooth. SCLEROTIC
dentin is most frequently encountered in the apical third of the root and in the
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12. crown midway between the D.E.J. and the surface of the pulp. Helps to protect
pulp vitality.
In demineralized dentin there is loss of the peritubular dentin. This is
important clinically as etching of a cavity floor will open up the tubules.
Calcified tubule wall has an inner organic lining termed the ''LAMINA
LIMITANS''. This is described as a thin organic membrane high in
glucosaminoglycans and similar to the lining of lacunae in cartilage and bone.
INTERTUBULAR DENTIN
Main body of dentin, known as INTERTUBULAR DENTIN is located
between dentinal tubules. It is the primary secretory product of the odontoblasts
and consists of tightly interwoven network of TYPE I collagen fibrils measuring
50 to 200micrometer in diameter in which hydroxyapatite crystals are deposited.
Collagen fibrils are aligned roughly at right angles to the tubules and the
apatite crystals raging 100 micrometer in length and are generally oriented with
their long axis parallel to the collagen fibrils. The ground substance consists of
phosphoproteins, proteoglycans, glucosaminoglycans, glycoproteins and some
plasma proteins. Less highly mineralized and unlike intra tubular dentin changes
little throughout life. It is retained after calcification.
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13. DENTINO ENAMEL JUNCTION
The junction between the dentin and enamel is scalloped or has ridges. The
dentin supports enamel and the junction between two is "DENTINO ENAMEL
JUNCTION".
Convexities of the scallops are directed toward the dentin.
Scalloping has been reported greatest in the area of cusps where the
occlusal trauma is intense.
In ground section D.E.J. can be seen as a series of scallops with extensions
of odontoblast tubules occasionally crossing the junction and passing into the
enamel.
In demineralized section where the enamel has been removed, the scalloped
nature of the junction can be clearly seen.
In ground section a hypermineralized zone about 30micrometer thick can
sometime be demonstrated at the D.E.J.
Several features are noted in the area of D.E.J.
• Scalloping
• Appearance of spindles
• Branching of dentinal tubules
The clinical significance is during cavity preparation while the D.E.J is
reached; there is dentin sensitivity because of fluid movement that occurs at D.E.J
as well as near the pulp which is explained by hydrodynamic theory.
INNERVATION OF DENTIN
Dentinal tubules contain numerous nerve endings in the predentin and inner
dentin no further than 100 to 150 micrometer from the pulp. Although most of the
nerve bundles terminate in the sub-odontoblastic plexus as free unmyelinated nerve
endings, a small number of axons pass between the odontoblast cell bodies to enter
the dentinal tubules in close approximation to the odontoblast process.
No organized junction or synaptic relationship has been noted between
axons and the odontoblast process. Intra tubular nerves characteristically contain
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14. neurofilaments, neurotubules, numerous mitochondria and many small vesicular
structures.
Most of these small vesiculated endings are located in tubules in the
coronal zone, specifically in the pulp horns. It is believed that most of these are
terminal processes of the myelinated nerve fibers of the dental pulp.
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15. INTRODUCTION TO DENTINAL HYPERSENSITIVITY
The ever-changing profiles of human diseases in mankind’s history have
not left dentistry untouched. The improving oral health status of populations,
people keeping teeth for longer, for example, has brought impressive benefits, but
at the same time has created or raised awareness of other oral and dental health
problems. Following the decline of dental caries, the management of periodontal
diseases gained priority, and other, painful dental problems, such as dentin
hypersensitivity stepped forward.
Dentin hypersensitivity was discussed in the dental literature over 100
years ago when Gysi attempted to explain ‘the sensitiveness of dentin’ and
described fluid movement in the dentinal tubules.
In the past, little attention has been paid to scientific research and practical
management of this condition. The last twenty years have brought a change in the
attitudes of dental researchers and practitioners concerning dentin hypersensitivity.
DEFINITION & TERMINOLOGY
The term hypersensitive dentin is widely used but poorly defined. A
definition for dentine hypersensitivity was suggested in 1983 and, with minor
amendment was adopted in 1997 by an international workshop on the design and
conduct of clinical trials for treatments of the condition. The definition states:
“Dentine hypersensitivity is characterized by short, sharp pain arising from
exposed dentine in response to stimuli typically thermal, evaporative, tactile,
osmotic or chemical and which cannot be ascribed to any other form of dental
defect of pathology”. The Canadian Advisory Board on Dentine Hypersensitivity
in 2002 suggested that it would be more correct to substitute ‘disease’ for
‘pathology’. The definition provides a clinical descriptor of the condition and
identifies dentine hypersensitivity as a distinct clinical entity, thereby encouraging
the clinician to consider a differential diagnosis. Other causes of the typically
short, sharp, dentinal pain include caries, chipped teeth, fractured restorations,
marginal leakage around restorations, some restorative materials, cracked tooth
15

16. syndrome and palato-gingival grooves. Such conditions clearly require treatment
options that are usually quite different from those used for dentine hypersensitivity.
The terminology for this condition is extremely varied: in Addition to
‘hypersensitive dentine’ other names such as sensitive dentine, cervical dentinal
sensitivity, cemental hypersensitivity and root sensitivity have been applied. There
is a need for a uniform nomenclature and a precise definition of the condition, as
well as agreement about what should be included within its classification.
Actually exposed dentin is sensitive because it is innervated tissue.
Hypersensitivity implies that the dentin is more sensitive than normal. Normally,
dentin is sealed peripherally by enamel or cementum and hence is not very
sensitive. When it is suddenly exposed, as occurs in tooth fracture or periodontal
surgery, the patient becomes acutely aware that the dentin is sensitive, but regards
it as hypersensitive relative to their previous experience. Similarly, patients with
sensitive root surfaces can become more sensitive if those surfaces are acid-etched.
Scientists have suspected that bacterial products or endogenous mediators of
inflammation might lower the threshold of pulpal nerves, making the dentin truly
hypersensitive. There is little published evidence to support that idea as occurring
commonly in most cases of cervical dentin sensitivity. Cementum is not innervated
and hence can not be sensitive. Thus, the old term, ‘hypersensitive cementum’ is a
misnomer, which should be discarded. In fact, the presence of sensitive root
surfaces indicates that the cementum is not present and that the underlying dentin
has become exposed.
Appreciating the fact that the term, dentin hypersensitivity, may be
inaccurate and even inappropriate, alternative descriptors would be difficult to
introduce. The term has been commonly used and accepted for many decades to
describe a specific painful condition of teeth, which is distinct from other types of
dentinal pain having differing etiologies.
Dentin sensitivity is a sharp, transient, well-localized pain in response to
tactile, thermal, evaporative or osmotic stimuli. The pain does not occur
spontaneously and does not persist after removal of the stimulus. Generally, this
definition has been applied to exposed cervical dentin, but should include any
sensitive dentin. As some sensitive dentin is not exposed but beneath restorative
materials, biting force could be added as a stimulus as well.
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17. INCIDENCE AND PREDISPOSING FACTORS
Hypersensitive dentine affects between 10-20 % of the population. The
prevalence appears to be fairly similar in different parts of the world, although
there are some regional differences. The prevalence of dentin sensitivity ranges
from 8% to 30%. This wide range is due, in part, to widely different methods used
to diagnose the condition. Most clinicians use a 1- second air blast, while others
ask the patient to fill the mouth with ice-cold water. Hypersensitive dentine may
affect any tooth, but most studies agree that it is most common in canines and first
premolars, and is almost exclusively found on the vestibular surfaces.
Hypersensitive dentine may also be present on other surfaces, including cuspal and
incisal edges, and on lingual or palatal surfaces; in the latter case, it is usually
indicative of acid regurgitation. However, not all exposed dentinal surfaces are
sensitive, and not all regions of hypersensitive dentine are the same: they vary in
extent, and also in sensitivity to different stimuli. For example, it is often found
that hypersensitive teeth are sensitive to one form of stimulus e. g. cold, but not to
another, e. g. probing. The reasons for these differences require further
investigation.
Age seems to be a factor with most complaints of dentin sensitivity peaking
at 25-30 years of age (range 20-40). The incidence of exposed root surfaces rises
with age from 21% in 16 to 24 year -olds to 81% in 34 to 44 year- olds, and to
98% in 55 to 64 year -olds. The decline in the degree of sensitivity with age, even
in the face of increased gingival recession and root surface decay, may be due to
sclerosis of dentin and/or the formation of reparative dentin. Anecdotal reports of
frequent cervical dentin sensitivity in geriatric populations need to be confirmed in
scientifically designed epidemiologic studies. Most studies have been limited to
cervical root dentin. High incidence of dentin sensitivity would be reported if the
authors included restored teeth.
Another problem is that dentin sensitivity can wax and wane over time in
the same individual. For instance, patients may develop dentin sensitivity when
they begin a grapefruit diet regiment, which then disappears when they stop eating
acidic foods. Root sensitivity commonly occurs following oral prophylaxis or
root planing, but this slowly resolves over the next week or weeks, similarly, in
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18. restorative dentistry, dentin sensitivity often follows cavity or crown preparation
and insertion of restorative material, but disappears over time. Dentin sensitivity is
often observed on the buccal cervical areas of canines and premolars, especially on
the left side of right handed individuals. Most cervical dentin sensitivity is caused
by improper tooth brushing, and is seldom seen on the lingual surfaces of teeth,
except in bulimic patients. The sensitive teeth are often absolutely free of bacterial
plaque because they are brushed 3-4 times a day. Thus, the treatment of dentin
sensitivity requires careful questioning of the patient’s dietary history and oral
hygiene efforts. Clinicians should observe the patient’s brushing technique to offer
corrective suggestions, especially if they suspect obsessive or compulsive habits.
Excessive loss of tooth structure such as occurs in bulimic patients,
leaving smooth but sensitive dentin surfaces exposed, is another problem. As will
be discussed exposed coronal dentin is such more difficult to treat than cervical
dentin because of its higher permeability and innervation density. Females tend to
have more sensitivity than males. This has been attributed to their practicing better
oral hygiene
HYDRODYNAMIC THEORY OF DENTINAL PAIN
PERCEPTION
The pain sense in human teeth has some important differences from pain
perception in other organs such as the skin: It is considered to be the only sensation
which can be elicited by any stimulus applied to the teeth (excluding the
periodontal receptors). Thus, there is no sense of warmth or cold, but only pain if
the temperature exceeds certain limits - lower than 27o C or higher than 45°C
(Matthews, 1977). While some authors have regarded the teeth as pressure-
sensitive over a very high range of pressures, the most common sensation we
usually experience is pain, whether with exposed dentin from enamel attrition or
from pulpal inflammation acting directly on nerve endings.
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19. DISTRIBUTION OF PAIN SENSITIVITY IN TEETH
Most dental pain researchers agree on at least two things: (1) the enamel of the
teeth is completely insensitive, and (2) the dentin and pulp are sensitive to a variety
of stimuli, including mechanical, thermal and chemical. The insensitivity of the
enamel is not surprising, as that substance consists primarily of dry hydroxyapatite
crystals with no demonstrable innervation. The pulp and dentin, on the other hand,
are living structures which contain body fluids and identifiable nerve endings. One
seemingly paradoxical finding is the sensitivity of the dentin-enamel junction;
although no nerve endings can be seen in this region of the tooth, when the
junction is inadvertently touched by a dental drill, the pain reaction can be sudden
and severe.
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20. NERVE ENDINGS IN DENTIN
The sensory fibers in the pulp are branches of a plexus underlying the
odontoblastic layer, the Plexus of Raschkow. The pulp nerves approach the horns
of the pulp, then branch diffusely to form the plexus. Fibers arising from this
network occasionally appear to cross the odontoblastic layer into the dentin.
There has been some controversy over the years about whether or not
nerve endings are present in the dentinal tubules. From light microscopic
observations, R.W. Fearnhead (1963) stated that, "The question whether calcified
dentin is innervated I now regard as settled. It is no longer a controversial topic. In
suitable specimens nerve fibres can be demonstrated within the dentinal tubules".
This is shown in the next two figures.The histologist T. Arwill (1963), however,
claimed that the fibers were located in the intertubular ground substance, and not in
the tubules themselves.
With the Advent of auto radiographic studies, researchers were able to
study the distribution of trigeminal sensory branches. Byers and Dong (1983)
injected radioactive proline into the trigeminal ganglion and waited 20 hours until
the isotope had been carried to the teeth by axoplasmic transport in sensory fibers.
Their radiographs clearly showed label reaching as much as 120 micrometers into
the dentinal tubules, indicating the presence of sensory axons. Less than half the
tubules showed the presence of label, but this was "hard" evidence of sensory
endings in dentin.
RESPONSES OF DENTAL PAIN ENDINGS
D.S. Scott, in the 1960s, attempted to demonstrate the activity of nerves in the
dentin directly. Plastic tubes filled with conductive solutions were placed in freshly
prepared cavities in the dentin of a cat's canine tooth. Then heat was applied to the
opposite side of the tooth, and the electrical responses recorded between the two
electrodes.
When the temperature of the tooth was increased sufficiently, the frequency
of firing of nerve impulses increased. A small drop of acetylcholine applied to one
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21. of the cavities would produce a burst of impulses. And treatment of a cavity with
acetylsalicylate would block the response to heating. (This was considered one of
the early demonstrations of a peripheral analgesic action of aspirin.) Scott and
others interpreted these findings as demonstrating unequivocally the presence of
active nerve fibers in dentin.
At about the same time, a group in Sweden carried out a series of experiments
which they believed to prove the active pain endings in teeth were not in the
dentin, but in the pulp below the predentin layer (Brännström, 1963; Brännström
and Åström, 1964). Using a premolar tooth about to be extracted for orthodontic
reasons, they cut a groove around the cusp and broke it off, exposing fresh dentin.
One observation was that the intertubular substance was a fluid, which beaded up
on the dentin surface a few minutes after it was exposed.
This finding supports the theory that sensory endings are in the pulp: It is
assumed that stimuli to the dentin which cause pain do so by movement of the
tubular contents and the resulting displacement of nerve endings in the pulp. This
is known as the hydrodynamic theory of dentinal pain perception. Some of the
experiments which Brännström and co-workers did were:
(1) Stimulating with a puff of air applied to the freshly exposed dentin resulted in
a pain sensation.
(2) Drying the dentin for a few minutes with an air stream reduced the sensitivity
to air puffs.
(3) Application of dry filter paper to exposed dentin caused a pain sensation.
(4) Application of filter paper soaked in isotonic potassium chloride, which is a
potent nerve stimulator, did not cause pain.
These results were all interpreted to mean that no nerve fibers were present in
the dentin. The results of Scott were explained by assuming that the nerve impulses
he had recorded were electrically conducted from the pulp nerves to the electrodes
by the conductive fluid in the tubules. Thermal stimuli were thought to produce
movement of tubular contents because the coefficient of expansion of the fluid was
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22. much greater than that of the tubular walls. As a kind of confirming experiment,
Brännström (1963) applied suction to the exposed dentin and then extracted the
tooth soon after and made a histological preparation.
The tubular fluid was evidently so free to move that the negative pressure
had caused odontoblastic nuclei to be sucked up into the tubules. The obvious
conclusion was that with much less suction or positive pressure, the pulpal
elements near the odontoblasts could be moved around significantly, disturbing the
local nerve fibers.
The next piece in the puzzle came from Matthews (1970), who repeated
Scott's experiments and then pushed the recording electrodes further and further
into the dentin cavities. The result was that, the closer the electrodes were to the
pulp, the larger were the recorded action potentials in response to heating. This
indicated that the major source of nervous signals in the teeth was indeed in the
pulp. Confirming evidence of the hydrodynamic theory came from the work of Tal
and Oron: A scanning electromicroscopic picture of freshly cut dentin, as shown in
the next figure, reveals open dentinal tubules with Tomes' fibers protruding into
the open space.
Topical fluoride, which is used as a treatment for abrasion hyperalgesia,
resulted in the deposition of crystals within the dentinal tubules. It was assumed
that part of the reduction of pain with fluoride treatment was a result of this
occlusion of the dentinal tubules.
Summary of the innervation of the pulp and dentinal tubules. Fibers from
the plexus of Raschkow arise and innervate the spaces between odontoblasts, and
some fibers do reach into the tubules, but only for 100 micrometers or so. Stimuli
reaching the dentin may stimulate intratubular fibers, but also displace nerves in
the pulp through hydrodynamic movement of the tubular fluid.
Interestingly, the hydrodynamic theory is able to account convincingly for
the sensitivity of the dentin-enamel junction: If that junction is breached by a
dental bur or other injury, the tubular fluid will be exposed to the outside pressure
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23. and undergo a sudden movement, causing excitation of sensory endings far from
the enamel.
INNERVATION OF THE TEETH: PAIN SENSORY
PATHWAYS
From electronmicroscopic studies, it has been shown that pulp nerves in
both feline and human teeth contain Ad and C fibers (Beasley and Holland, 1978;
Byers, 1984; Reader and Foreman, 1981). The C fibers include both afferents and
sympathetic postganglionic axons.
The role of Adelta and C fibers in dental pain perception was studied by
recording from previously identified fibers while sudden cold stimuli were applied
to the teeth (Jyväsjärvi and Kniffki, 1987). Stimuli were used which were known
to cause pain sensations in human teeth. When the mean rating of the subjective
pain vs. time was plotted, it was correlated very closely with the time-course of
firing of the Ad fibers. The C fiber discharge was much slower and uncorrelated
with the pain from cooling. This suggested a strong role for Ad fibers in
transmission of pain induced by cold stimulation.
In a study of pulpal C fibers (Jyväsjärvi et al., 1988), it was found that they
typically responded to thermal, mechanical, and chemical stimulation. Thus, they
appeared to be polymodal nociceptive fibers.
CENTRAL PATHWAY OF DENTAL PAIN
Afferents from the mandibular and maxillary divisions of the trigeminal
nerve relay in the spinal sensory nucleus of V. From this region fibers cross the
pons and many relay in the pontine reticular formation; ultimately they project to
the intralaminar and ventroposterior thalamic nuclei, and thence diffusely to the
cortex.
The projections of sensory axons innervating a tooth may be traced with the
use of horseradish peroxidase (HRP, Furstman et al., 1975). HRP is injected into a
pulp cavity, from where it is transported in sensory axons to their terminations.
23

24. Following a 1-2 day period for transport to occur, label was found in the trigeminal
ganglion. Later studies (e.g Arvidsson and Gobel, 1981) used this technique to
show that a single pulp nerve projected to the dorsomedial parts of the main
sensory nucleus of V as well as the subnuclei oralis and interpolaris.
24

25. CHEMICAL THEORY OF DENTAL PAIN
A variety of chemicals including substance P, histamine, 5-hydroxytryptamine,
bradykinin and prostaglandins may contribute to sensitization and hyperalgesia
around an injury. This situation is also likely to exist in the dental pulp, where
nerve endings are known to be sensitive to applied chemicals and where certain
neurotransmitters and peptides have been shown to occur.
Olgart (1985) reported on some studies where the the activity of nerve endings
in the pulp was recorded using a similar method to that of Scott and Tempel
(1963). The effects of applying various factors to the exposed dentin and pulp were
observed, such as: (1) ammonia excited nerve responses as long as it was present in
the dentinal cavity, (2) several amino acids could excite the nerves, (3) lactic acid
and other organic acids failed to excite the nerves, (4) sucrose applied to dentinal
cavities produced an immediate burst of nerve activity.
Immunohistological studies in which distinct compounds can be identified in
tissues have also been applied to the dental pulp. Olgart et al. (1977) found
substance P-like immunoreactivity in small nerve fibers in the pulp, and the
calcitonin gene-related peptide has also been identified in thin sensory axons of the
pulp (Silverman and Kruger, 1987).
CGRP is calcitonin gene-related peptide. Remember that calcitonin is a
hypocalcemic hormone, which causes calcium deposition and removal from the
circulation. Calcitonin is secreted by parafollicular cells from the thyroid, and from
neural tissue. It is a single-chain peptide of 32 amino acid residues.
CGRP is made in nervous tissue and consists of 37 amino acids. CGRP mimics
the action of calcitonin in some species, causing deposition of calcium, but not in
others. CGRP and its binding sites are widely distributed in the CNS, where it is
believed to serve as a neurotransmitter. CGRP is found in many bipolar neurons in
sensory ganglia and produces marked vasodilatation.
25

26. Cohen et al. (1985) showed that pulps from diagnosed painful teeth had as much
as 20 times as much prostaglandin E2 and F2a as pulps from asymptomatic teeth.
The phosphonucleotide Adenosine triphosphate has recently been shown to act
as a neurotransmitter in the nervous system (Ralevic and Burnstock, 1998). This
compound activates ATP receptors or purinoceptors. There are ligand-gated ion-
channel purinoceptors called P2X and G-protein coupled receptors called P2Y. In
2001 Alavi, Dubyak and Burnstock published evidence of P2X receptors in human
dental pulp (Alavi et al., 2001). The slides of the pulp were stained with antibodies
against the receptor P2X3 and against neurofilament proteins, which serve as a
marker of nerve fibers. The results showed the presence of P2X3 receptor protein
in the same location as nerve fibers.
Thus, although the story is not as complete as for cutaneous nociceptors, we
should be mindful that chemical intermediates undoubtedly play a role in dental
pain perception. Research in this area will perhaps help in forming strategies to
alleviate dental pain and inflammation.
MECHANISMS OF DENTINE SENSITIVITY
Historically, dentists have been impressed with the sensitivity of newly
exposed dentin even at the dentino-enamel junction (DEJ). Several hypotheses
have been put forward over more than a century to explain the sensitivity of
dentine. They logically concluded that the stimuli must have been directly exciting
nerves that traveled to the dentin surface. However, histological studies using
special stains for nerves failed to identify such pathways at either the DEJ or
cemento-enamel junction (CEJ). Rather, their distribution was limited to the pulp
or, at most, extended only 0.1 mm into the dentinal tubules. Furthermore, topical
application of local anesthetics to peripheral dentin did not produce the desired
effect. Similarly, topical application of agents that normally activated nerve fibers
(potassium salts acetylcholine) did not produce pain. Thus, the notion that dentin
sensitivity was due to direct stimulation of dentinal nerves had to be rejected.
In the 1960’s a new hypothesis was developed, suggesting that dentin
sensitivity was due to stimulation of odontoblast process in the exposed dentin.
This theory was based on the idea that odontoblasts could serve as receptors and
26

27. that there must be synapses between pulpal nerves and odontoblasts. Further work,
however, failed to marshall much evidence to support this theory. Most authorities
now believe that there are no synaptic junctions between odontoblasts and pulpal
nerves.
Circumstantial and direct evidence disproved the theory of ‘innervation of
dentine’ and ‘odontoblast transducer’ mechanisms. This left the hydrodynamic
hypothesis first proposed by Gysi in 1900, and for which significant evidence
accrued in the 1950s and 1960s, as the most widely accepted theory to date.
Brannstrom and his colleagues, by combining clinical and laboratory experiments,
developed support for what is now called the hydrodynamic theory of dentin
sensitivity. In essence, they observed that in extracted teeth a wide variety of pain
-producing stimuli induced fluid movement, in both inward and outward
directions, through dentin. They reasoned that this fluid movement through dentin
excited mechanoreceptors nerves near and pulp. A corollary to this theory is that
anything that interferes with fluid movement through dentinal tubules, or which
lowers nerve excitability, would decrease dentin sensitivity. This theory can also
explain most causes of sensitivity under restorations.
The hydrodynamic theory postulates that most pain evoking stimuli
increase the outward flow of fluid in the tubules. This increased flow, in turn,
causes a pressure change across the dentine, which activates A - δ intradental
nerves at the pulp dentine border or within the dentinal tubules. The stimulation is
thought to occur via a mechanoreceptor response, which occurs when gentle
pressure is applied to skin hair. In Addition, when fluid moves in tubules, an
electrical discharge known as steaming potential occurs; this is directly
proportional to pressure. Whether this discharge reaches levels sufficient to
stimulate nerves has not been established, although it is theoretically possible. In
vivo studies (Linden and Brannstrom, 1967; Pashley et al., 1981a; 1981b; Maita et
al., 1991) have reported that dentinal fluid can slowly seep to exposed dentin;
surfaces as it flows down a hydrostatic pressure gradient from the pulp.
Apparently, this spontaneous rate of fluid movement is too slow (Vongsavan and
Mathews, 1993) to activate mechanoreceptors which may be more responsive to
the rate of change of fluid movement (Ahlquist et al., 1988; Linden and Millar,
1988) rather than the absolute rate.
27

28. In dentine hypersensitivity, the definition highlights different stimuli
inducing pain. Of these, cold or evaporative stimuli are usually identified as the
most problematic for sufferers. Heat is not commonly reported perhaps because it
is the exception to stimuli evoking pain causing relatively slow inward movement
of dentinal fluid.
The hydrodynamic theory of dentin sensitivity implicates both dentin and nerves as
important elements. It allows, then, that one could have “dentin hypersensitivity”
or nerve hypersensitivity or both (table 2).
Mechanism creating hypersensitive dentin
1. Increases in the hydraulic conductance of dentin
a. Dissolution of smear layer
b. Loss of smear plugs
c. Loss of mineralized plaque
2. Decreases in A delta nerve threshold (i.e. nerve hypersensitivity)
a. Elevations in local pulpal pressure due to inflammation
b. Direct effect of neurogenic peptides on local tissues pressure and/or neural
membranes
c. Direct effect of bacterial products on the conductance channels
DENTIN PERMEABILITY
The hydrodynamic theory of dentin sensitivity is based on the premise that
sensitive dentin is permeable throughout the length of the tubules (Brannstrom,
1981), that is lesions must have dentinal tubules open at the dentine surface and
patent to the pulp.
The notion that all sensitive dentin must have open tubules has not been proven
although there is some experimental support for that hypothesis. Scanning
electron microscopic and dye penetration studies provided such evidence,
demonstrating the presence of a greater number (8 times) and wider tubules (2
times diameter) on ‘hypersensitive dentine compared to ‘non sensitive’ dentine.
Absi et al (1987) identified the sensitive areas on exposed dentin in teeth scheduled
28

29. for extraction. They then compared the number of open dentinal tubules, by SEM,
of these areas compared to similar locations on nonsensitive control teeth. The
sensitive teeth had an average of 17751 open tubules per unit area compared to
2210 open tubules in the same area of nonsensitive teeth. The average diameter of
the sensitive tubules was 0.83 µ m (table1).
Tubule density and diameter in sensitive vs nonsensitive dentin
Tubule Characteristics Sensitive Nonsensitive
Tubule density
(number/mm2, x ± SD) 17751 ± 12719(6) 2210 ± 2074(6)
Tubule diameter (µm) 0.83± 0.39 (26) 0.43 ± 0.19 (22)
Recalculated from Absi et al, 1989. Number in parentheses indicates number of
samples
The tubule density in sensitive areas is close to the maximum possible
tubule diameter and density of root dentin (Fogel et al., 1988). Thus, the sensitive
areas have tubules that are nearly as open as they can be. These authors also
placed in teeth in methylene blue dye for 1 hr to determine if the areas of exposed
cervical dentin were open from the dentin surface to the pulp surface. After
sectioning the teeth longitudinally, they found that both the depth and intensity of
the dye penetration was greatest in the sensitive relative to the nonsensitive dentin.
They indicated that the permeable dentin was not uniform but seemed to be
clustered into discrete regions. This is consistent with clinical observations of
dentin sensitivity which are often much localized.
Recently, Absi et al (1989) reported the development of a replica
technique that permits miniature impressions to be made of sensitive root surfaces
using silicone impression material. Epoxy resin casts were made of these
impressions which were then examined by SEM and compared to organelle tooth
surfaces in vitro and in vivo. They obtained a good correlation between original
tooth surfaces in vitro and in vivo. They obtained a good acceleration between
original versus epoxy casts of sensitive root surfaces that permitted sufficient
resolution to measure tubule number and diameter. Others have had less success
29

30. with this method. It relies on the ability to clean plague from tooth surfaces
without creating a smear layer.
Another approach to identifying whether sensitive root surfaces have
exposed, patent dentinal tubules was reported by Yoshiyama et al. (1989, 1990)
and involved dentin biopsies. They identified regions of high sensitivity clinically
and then biopsied the sensitive dentin using a hollow (1 mm inside diameter), core
producing diamond bur. Examination of the surface of cylindrical specimens by
SEM revealed that 75% of the tubules were open in contrast to only 24% in the
insensitive dentin biopsies. They also fractured the biopsies to examine the
contents of the tubules below the surface. Hypersensitive dentin exhibited
relatively open tubule lumens, while the tubules of insensitive, exposed dentin
were partially occluded with mineral deposits. In a TEM study, they reported that
81% of the total tubules in insensitive dentin were occluded but only 15% of the
total tubules of hypersensitive dentin were occluded. They also showed that some
exposed but insensitive dentin was insensitive because the tubules were totally
occluded with peritubular dentin.
Specifically, the hydrodynamic theory assumes that the hydraulic
conductance of sensitive dentin permits sufficient fluid flow within tubules to
activate mechanoreceptors near the pulp. Thus according to the theory, dentin
sensitivity should be proportional to the hydraulic conductance of dentin. Standard
texts on dentinal tubules indicate that tubule numbers and diameters increase from
the outer dentine towards the pulp. That is, as dentin becomes thinner its hydraulic
conductance increases. This raises the possibility that fluid flow, and therefore
hypersensitivity, may increase as dentine is lost through tooth wear processes or
multiple root planings – assuming such wear does not induce reparative process in
dentine. The difference in tubule diameter may be the more important variable
since fluid flow is proportional to the fourth power of the radius (i.e., doubling the
tubule diameter results in a 16-fold increase in fluid flow). This information has
important implications for treatment strategies.
However, the most important variable is the condition of the tubule apertures
(Hirvonen et al., 1984). Tubule orifices plugged with smear plugs have a much
lower hydraulic conductance than those same tubules devoid of smear plugs and
30

31. smear layers. Thus, relative to open tubules, dentin covered with a smear layer is
less sensitive than dentin with open tubules (Johnson and Brannstrom, 1974). As
dentin loses its smear layer, it becomes hyperconductive and hence
“hypersensitive” relative to what it was when it was covered with a smear layer,
especially from the patient’s perspective.
Conditions of hypersensitivity could develop if mildly sensitive root dentin
that was covered by a smear layer (created during root planning) becomes more
sensitive because of dissolution of the smear layer by acidogenic plaque organisms
(Kerns et al., 1991). In this case, the amount of fluid movements in response to the
same stimulus (that is, tooth brushing) would be much greater after solubilization
of the smear layer, making the sensitivity seem to the patient, to be hypersensitive
with respect to what it had been before. This should all occur without any change
in the excitability of the nerve and could be considered as dentin hypersensitivity.
Nerve excitability
The number of tubules innervated by pulpal nerves is approximately 40%
in coronal dentin over pulp horns, but falls off rapidly to 8% to 10% in mid coronal
dentin and only 1% at or below the CEJ. This makes coronal dentin more sensitive
than root dentin and more difficult to treat because one needs to seal most of the
tubules to prevent sensitivity. On root dentin, since only 1% of the tubules are
innervated, one need not seal every tubule. However, each nerve fiber branches
and innervates a number of tubules, which make random pattern of innervated
dentin. If is unknown whether these patterns or innervation fields change with age
or inflammation.
Alternatively, changes may occur in nerve sensitivity. One might argue
that the sensitivity of exposed dentin is not normal because the microenvironment
of intradental nerves is probably not normal. The ionic environment around
intradental nerves may change as dentinal fluid flows through dentin. Certainly,
bacterial products have the potential for modifying nerve excitability (Panopoulos,
1992).
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
31

32. firing. These peptides have been implicated in neurogenic inflammation. They
increase local blood flow and increase capillary permeability. Extravasation of
plasma tends to cause local elevations in pulpal tissue pressure that may lower the
excitatory threshold of mechanoreceptors nerves, thereby contributing to a true
hypersensitivity of that dentin.
Convective transport or fluid filtration appears to be the critical stimulus to
activate A delta nerves in the pulp (Narhi et al., 1982; Ahlquist et al., 1988). That
is, diffusion of few solutes has been shown to produce Ad nerve activity.
Exceptions include serotonin (Narhi et al., 1989) and potassium ions (Narhi and
Haegerstam 1983; Markowitz et al., 1991). Intradental C-fibers respond to
bradykinin and histamine (Narhi et al., 1984; Narhi, 1985). Experimentally, these
agents are placed topically in very deep cavities to determine if they activate
specific pulpal nerves. Clinically, these agents may be released within the pulp
during the development of an inflammatory response. This might be initiated by
mechanical, thermal or immunologic stimuli. If one accepts the hypothesis that the
sharp, well localized pain associated with activation of Ad fibers requires rapid
fluid shifts within dentin, then it limits Adequate stimuli to those that cause
convective transport across dentin (Pashley, 1989). A corollary of that theory is
that diffusive transport should not activate Ad fibers and hence should not cause
sharp, well-localized pain. As both convective and diffusive transport occurs
within the same open dentinal tubules, it means that considerable diffusion of
potentially toxic materials can diffuse across sensitive dentin into the pulp.
Further, as diffusion through capillary tubes varies with the square of their radius
rather than with the radius raised to the 4th
power (as is true to convective transport,
Pashley, 1989), partially occluded tubules may have too low a hydraulic
conductance to respond to hydrodynamic stimuli but would still permit
considerable diffusion of materials across dentin to the pulp where they could
trigger an inflammatory response.
However, even in patent tubules, the inward diffusion of potentially
cytotoxic bacterial products is opposed by the outward convective movement of
dentinal fluid. This tends to flush the tubules free of irritants and presumably
would increase if the underlying pulpal tissue pressure increased during
inflammation (Van Hassel, 1971; Heyeraas 1985; Kim et al., 1989). Vongsavan
32

33. and Matthews (1991) recently reported that Evan’s Blue dye failed to penetrate
into fractured cat dentin in vivo, but did so if the tooth was extracted. They
postulated that outward fluid flow in the vital tooth was sufficient to modify the
inward diffusion of solutes. While this was only a qualitative study, it was one of
the first such reports that discussed the potential implications of the balance
between the inward diffusion of exogenous solutes and the outward movement of
endogenous dentinal fluid (Sena, 1990).
Presumably, the bacterial residing in plaque continuously shed products
into patent tubules. These potentially cytotoxic substances may diffuse to the pulp
where, depending upon their concentration and potency, they may initiate an
inflammatory reaction. Part of the inflammatory reaction is an increase in the
permeability of local blood vessels and vasodilatation of resistance vessels. There
reactions combine to increase the rate of transudation of plasma across pulpal
blood vessels. This leads to a localized increase in pulpal tissue fluid pressure
(Heyeraas, 1989; Kim et al., 1989) which produces more fluid movement across
dentin to the surface. While this increase in fluid flow may be protective in that it
flushes cytotoxic materials from the tubules, it may also lower the pain threshold
by increasing the rate of spontaneous fluid flow across dentin. That is, what was
previously an inadequate stimulus before the development of inflammation, may
become a threshold stimulus. This was recently tested in vivo by isolating single
sensory units that innervate exposed dentin in anesthetized cats (Vongsavan and
Mathews, 1993). By sealing a fluid filled system to the exposed dentin, electrical
thresholds can be measured under spontaneous dentinal fluid flow and after
applying enough exogenous negative pressure to double to triple the outward fluid
movement. This theoretical increase in receptor sensitivity in exposed dentin due
to elevated tissue pressure is in Addition to any direct influences that bacterial
products may have on neural membrane ionic channel conductance that could also
lower the pain threshold. These mechanisms of altered pain thresholds can only
occur in permeable dentin. To the extent the dentin becomes less permeable; they
would exert less of an influence.
Similarly, if one postulates that the active ingredient in a desensitizing
formulation exert therapeutic effects on intradental nerves, then the effects would
be expected to be greater in dentin with a high permeability (i.e. very sensitive
33

34. dentin) than in dentin with a low permeability (i.e. little sensitivity, Sena, 1990).
However, dentin with a high permeability may flush the tubules with dentinal fluid
at a rate that slows the inward diffusion of the active ingredient. The same
rationale can be applied to desensitizing agents that act by decreasing tubule
dimensions. Tubules that are wide open (i.e. very sensitive dentin), should be
more easily occluded than tubules that are partially occluded.
Thus, there is a growing weight of evidence that supports the
hydrodynamic theory of dentin sensitivity and its corollary, that sensitive dentin is
permeable throughout its thickness. Any treatment that decreases dentin
permeability should decrease dentin sensitivity. This provides an opportunity to
use relatively simple in vitro experiments as screening methods for evaluation of
the potential of new desensitizing products (Greenhill and Pashley, 1981;
Takahashi, 1986). This technique is not useful for agents that may desensitize by
acting on neurovascular elements of the dental pulp) Pashley, 1986). Such agents
must be evaluated using neurophysiology techniques. In the past, several authors
have attempted to evaluate the effects of various ions such as potassium, by
prepared deep cavities in cat teeth to within 50-100 µ m of the pulp. They
measured intradental nerve activity to osmotic stimuli before and after treatment
with potassium (Markowitz et al., 1991). However, it is unlikely that the active
ingredients in many desensitizing products could diffuse across 2-3000 µm (2-3
mm) of dentin that exists in human dentin and reach high enough concentrations to
modify the activity of intradental nerves. This can be tested by isolating single Ad
nerve from the mandibular nerve of anesthetized cats and then apply the putative
desensitizing agent to exposed dentin that is thick enough to impose a clinically
relevant diffusion barrier.
Now that we understand the central role that dentin permeability plays in
the phenomenon of dentin sensitivity, we can screen potential therapeutic agents
for their ability to occlude dentin. This has brought an objective; quantitative
approach to problem solving that was missing in the past. The use of such simple
in vitro systems should accelerate the development of new, improved agents that
can acutely lower dentin permeability and dentin sensitivity.
34

35. ETIOLOGY & PREDISPOSING FACTORS
By virtue of its relation with the pulp, dentine is naturally sensitive, but for
this sensitivity to manifest clinically the dentine must be exposed which can
influence its sensitivity. Dentine freshly exposed by cutting or root planning may
not be particularly sensitive because of the presence of a smear layer. In
hypersensitive dentine, the smear layer is generally absent and the tubules are
patent. There is still some debate about the origins of hypersensitive dentine. One
school of thought is that dental plaque control is important in preventing its
development. It is suggested that discomfort on brushing promote plaque
accumulation, with further increases in sensitivity. In contrast, others report that
the highest incidence of hypersensitive dentine is found in areas that are almost
plaque-free which may be associated with over-zealous tooth brushing or attrition.
This tends to produce a smear layer, but a tooth may become hypersensitive if the
smear layer is removed by localized acid erosion, due to dietary acids such as fruit
drinks or reduced salivary buffering. It is also noteworthy that hypersensitive
dentine is seldom found on lingual surfaces even in the presence of plaque. These
two disparate positions can be reconciled by recognizing that small amounts of
acidogenic plaque could demineralize exposed dentine as effectively as dietary
acids. Brushing of these softened surfaces will accelerate loss of dentine and may
lead to sensitivity. It is agreed that plaque alone is insufficient to cause
hypersensitive dentine in the absence of brushing.
Two-process need to occur for dentine hypersensitivity to arise: dentine has
to become exposed (lesion localization), and the dentine tubule system has to be
opened and be patent to the pulp (lesion initiation). Lesion localization and lesion
initiation require both differing and similar etiological agents in order to occur:
1. Lesion localization
Normal dentin, which is sealed peripherally by enamel or cementum, is not
sensitive to osmotic or tactile stimuli. It will respond to thermal stimuli because
these move dentinal fluid enough to deform pulpal mechano-receptors. However,
the degree of thermal sensitivity increases when dentin becomes exposed.
Exposure of dentine may occur by loss of either enamel or periodontal tissues, the
latter of which is often termed gingival recession.
35

36. Loss of enamel
Loss of enamel is generally considered under the heading of tooth wear,
which encompasses attrition, abrasion and erosion. None of these physical and
chemical processes probably ever acts alone to produce tooth wear; depending on
the tooth surface concerned, all three could interact. For example, at contacting
enamel surfaces or non-contacting surfaces, abrasion and erosion are likely to
collaborate in enamel loss. Indeed, given the site of predilection for dentine
hypersensitivity, namely buccal cervical areas, exposure of dentine through enamel
loss is almost certainly due to an interaction of erosion with abrasion. In certain
teeth, abfraction may act as a predisposing or co-destructive factor. This
theoretical process, modeled in finite element analysis studies, suggests that
eccentric occlusal loading leads to cusp flexure setting up cervical stress lesions,
which, in turn, increase the susceptibility of enamel to abrasion and/or erosion.
Attrition occurs due to tooth-to-tooth contact. Tooth wear due to attrition can
reach pathological levels with parafunctional habits such as bruxism. As a result,
occlusal dentine hypersensitivity may ensue. The interaction of abrasion and
erosion with attrition has not been researched to any great degree. Recent studies
in vitro demonstrated that enamel attrition was markedly reduced in an acid
environment. An explanation for this somewhat surprising finding was the
maintenance of very smooth contacting enamel surfaces due to the acid erosion,
which reduces friction.
Interaction between abrasion and attrition, such as from the chewing of
coarse diets or abrasive materials, has been the subject of only anecdote or case
reports.
Such cases suggest that some abrasive materials regularly introduced into
the mouth and chewed, either as a habit or from an occupational environment, can
cause marked enamel loss on contacting surfaces. Moreover, if combined in an
acid medium, such as chewing fibrous acidic fruits like apples, tooth wears
escalates dramatically. A model in vitro stimulating the chewing of abrasive acid
foods confirmed the potential for rapid enamel loss
Most interest in abrasion has centered on the effects of tooth brushing with
toothpaste, with the majority of studies conducted in vitro and on dentine. As
such, they are more relevant to the initiation of dentine hypersensitivity. A
36

37. toothbrush alone has no measurable effects on enamel. Indeed, most toothpastes
have very low relative enamel abrasivity (REA) values, as determined using the
International Standards Organization’s Standard for toothpastes methodology.
Most toothpastes alone contribute little to enamel loss even over a lifetime of use.
Erosion causes significant tooth wear and thereby dentine exposure at all sites on
the anatomical crowns of teeth and, particularly, in the cervical area, where the
enamel is very thin. Acids are usually classified as intrinsic or extrinsic: the
former is hydrochloric acid from the stomach; the latter originates from the diet or
the environment particularly in certain occupation. Dentine hypersensitivity has
been reported in association with erosion caused by acids from both intrinsic and
extrinsic sources.
However, with respect to the buccal cervical site of predilection for dentine
hypersensitivity, lesion localization due to enamel loss is almost certainly the result
of extrinsic acid erosion alone or, more likely, combined with tooth brushing with
toothpaste. Thus, when acids come into contact with enamel, not only is there bulk
loss of tissue but surface softening as well. Studies in vitro suggest that the surface
softening can extend to 3-5 microns and that the tissue is highly susceptible to
physical insults: a few strokes with a tooth brush and toothpaste, even a toothbrush
alone can remove this fragile layer. Re-hardening can occur; however, evidence in
vitro suggests that this may take hours, thus emphasizing the need to avoid
brushing teeth after food and/or drink. Indeed, the preventive potential of most
toothpastes supports recommending brushing teeth before meals rather than the
often-cited Advice to brush after meals.
The potentially serious nature of erosion was highlighted by a review of
prevalence figures. In the 1993 UK Child Dental Health Survey, dentine exposure
on deciduous teeth was found in a quarter of 5-6 year – olds and was even present
on permanent teeth in 2 per cent of 11-year olds. A review of the literature
suggests the relevance of soft drink consumption from a very early age as
important to tooth wear. Studies in situ confirm the role of such drinks in enamel
erosion and highlight a tenfold difference of individual susceptibility to erosion by
acidic drinks
The data from such studies indicated that, depending on susceptibility, and
without the synergistic effects of other tooth wear factors, such as abrasions,
37

38. individuals consuming one litre of soft drinks per day could lose one millimeter of
enamel in 2 to 20 years. Recently, some drinks have been modified successfully to
minimize erosion and surface softening of enamel
Such modifications have thus far centered on Adding calcium to drinks and
making changes to titratable acidity and pH. Interest has also focused on
polyphosphates; however, unpublished data from our laboratory studies indicate
that, while these compounds may minimize surface loss of enamel, they may cause
quite deep subsurface demineralized lesions.
Gingival recession
Gingival recession and its etiology have been reviewed. Recently, one
author has described the condition as an enigma, a description that now seems
more aptly attributable to gingival recession than to dentine hypersensitivity. The
etiology of gingival recession appears to be multi factorial and is made more
complex by suggested predisposing factors. With few exceptions, etiological and
predisposing factors are implicated on the basis of circumstantial evidence and/or
epidemiological association data. This applies, in particular, to tooth brushing,
which has long been associated with gingival recession. Numerous factors ranging
from filament stiffness and end rounding, to tooth brushing force, duration and
frequency, have been considered relevant. Interestingly, tooth paste, and not the
brush, is felt to produce abrasion to hard tissues, yet its role in soft tissue damage
and gingival recession has never been considered. Other etiological agents in
gingival recession include acute ulcerative gingivitis (periodontitis), self-inflicted
injury, periodontal disease, and periodontal non-surgical and surgical procedures
with buccal or lingual alveolar bone dehiscence or fenestration acting as
predisposing factors.
Patients with gingival recession and a good deal of supra and gingival
calculus are generally unaware of how inflamed their gingiva’s are when Adjacent
to such calculus deposits. The patients may have had dentin sensitivity years ago,
but that “exposed” dentin is now well sealed by calculus, hence they are
asymptomatic. After removal of the calculus and planing of their root surfaces, the
patients again experience dentin sensitivity.
38

39. Another unresolved question is whether the traditional hypersensitive
dentine is different from that occurring after periodontal surgery. During root
planning, although cementum and some root dentin are removed, the dentinal
tubules remain occluded by smear plugs and a smear layer created during
manipulation of the root surface. The smear layer would also restrict the diffusion
of any bacterial products that might be shed from any plaque that might be
developing on the root surfaces. These smear layers are only 1-2 µ m thick and are
acid labile. Only after removal of the periodontal packs would the smear layer be
directly exposed to the solubilizing effects of saliva, dietary liquids, acidic
components of the diet, and uninhibited plaque development. Bacterial plaque
colonizes on the treated surfaces within 24 hours, and begins to solubilize the
smear layer over the next few days. Although the longevity of “periodontal” smear
layers is unknown, it is quite probable that, under acidogenic conditions, it may
last only 5 to 7 days. As smear layers and smear plugs dissolve, the rate of
permeation of bacterial products (from developing plaque) across dentin into the
pulp may increase. With the underlying nerves exposed to bacterial products, the
open dentinal tubules might become hyperexcitable owing to the direct effects of
bacterial products diffusing from plaque through the permeable dentin to the
nerves.
Alternatively, the effect may be indirect, via induction of an inflammatory
response that, in turn, might produce endogenous substances such as leukotriene
B4, which has been shown to excite intradental nerves (Madison et al., 1989).
Increases in local pulpal tissue pressure may produce sufficient outward fluid flow
through open tubules to bring mechanoreceptors closer to threshold, thereby
increasing dentin “sensitivity”. Thus, dentin sensitivity increases 5-7 days
following root planing and then spontaneously decreases over the next 2-4 week.
How does this state of hypersensitivity resolve or “heal” without any therapeutic
intervention? Several explanations are possible. 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 (Pashley, 1986). This may lower the hydraulic conductance of the exposed
dentin below levels that permit activation of mechanoreceptors hydrodynamically.
39

40. The transudation of plasma and the macromolecules that is 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
and hence the rate of permeation of bacterial products from plaque to the pulp.
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.
A more perplexing question is why do 10-15% of patients who develop dentin
sensitivity fail to “heal” over-time? One would have to conclude that their dentin
remains permeable for months to years. The reasons for failure of the normal
protective mechanisms in these patients is unknown, but may be related to local
factors such as salivary composition or flow or perhaps they have more active
fibrinolytic systems (Sindet-Pedersen et al., 1990) than most patients.
They may use anti tartar dentifrices that may inhibit remineralization as well as
calculus formation. Some investigators have made anecdotal observations that anti-
tartar dentifrices may cause dentin sensitivity, yet laboratory studies fail to identify
any demineralization of treated root surfaces. What probably occurs is that
asymptomatic patients have their teeth cleaned of calculus and are told to brush
with an anti tartar dentifrice. The patient develops dentin sensitivity a few days
later because of the removal of the calculus during the prophylaxis, but incorrectly
associates the sensitivity with the use of the anti tartar dentifrice. Their teeth may
remain sensitive for a longer period of time than usual, because the anti tartar
dentifrice does indeed interfere with the formation of new calculus which would
seal the sensitive dentin, thereby elimination their discomfort. Thus, while the anti
tartar dentifrice may prolong dentin sensitivity created by the clinician, it does not
cause it.
Older patients generally exhibit more gingival recession, placing them at higher
risk for the development of root caries and dentin sensitivity, both of which are
due, in part, to demineralization of dentin. These patients often take medications
for a variety of systemic conditions. Many of these drugs interfere with salivary
function, causing decreased salivary flow rate and buffer capacity which may
reduce the remineralization potential of saliva.
40

41. Turesky et al reported that patients over the age of 65 taking beta blockers,
diuretics, anticholinergics, thyroid, or anti-gout medications had significantly less
calculus formation despite higher plaque scores. While these authors did not
measure dentin sensitivity, their results indicate a reduced ability to remineralize
tooth surfaces (e.g., calculus formation). Thus, one might expect more dentin
sensitivity in such patients, and potentially higher decay rates.
Attempts to draw a sharp distinction between spontaneously hypersensitive dentine
and hypersensitive dentine following periodontal therapy seem arbitrary. It patients
who have had periodontal surgery remain sensitive after 3 months, they should be
regarded as having chronic sensitivity. Persistent dentin sensitivity signals a state
of persistent high dentin permeability. It reminds us of the two phenomena having
a common denominator, the patency of dentinal tubules.
In conclusion, it is perhaps not surprising that the buccal cervical areas is
predisposed to dentine hypersensitivity since erosive and abrasive factors alone or
in combination are most likely to impact at this site to expose dentine. Although
not studied, clinical experience suggests that gingival recession rather than loss of
cervical enamel would account for the majority of exposed dentine. However,
erosion alone or combined with abrasion and/or attrition may expose dentine
through enamel loss at other sites on the anatomical crown
2. Lesion initiation
Evidence already presented indicated that the lesions of dentine
hypersensitivity have many more and wider open tubules than do non-sensitive
dentine. Replica studies demonstrated that cementum at the cervical area of teeth
is rapidly lost and is never seen to cover the dentine once recession has occurred.
This observation suggests that the layer is easily removed by physical and/or
chemical influences. Dentine is thought to be covered by a smear layer or the
tubules occluded by calcium phosphate deposits derived from saliva. Removal of
these occluding materials could also occur as a result of physical or chemical
agents that open the dentinal tubules. Most research on and, therefore, conclusion
about lesion initiation are based on studies in vitro.
In view of the manufacturers’ and standards organizations’ interest in the
abrasivity of toothpaste to dentine, the influence of tooth brushing with toothpaste
41

42. has attracted some interest by researchers. The toothbrush alone has little effect on
dentine: it takes several hours of constant brushing in vitro to either remove the
smear layer or recreate a smear layer (these experiments represent years of normal
tooth brushing). Toothpastes, their abrasives and, to some degree, the common
toothpaste detergent, sodium lauryl sulphate, all cause wear to dentine. Based on
laboratory data, an associated review concluded that, under normal circumstances,
tooth brushing with most toothpaste has little or no effect on enamel and clinically
insignificant effects on dentine. Studies in situ, however, suggest that excessive or
abusive tooth brushing habits could cause pathological dentine loss.
In dentine hypersensitivity, however, the following question begs to be
asked: what effects does brushing teeth with toothpaste have on the dentine surface
and, in particular, the smear layer and the tubules? Several scenarios can be
envisaged, including: abrasive removal of the smear layer, abrasive creating of a
smear layer, detergent removal of the smear layer, occlusion of tubules by abrasive
particles, or occlusion of tubules by active desensitizing ingredients. Again,
studies in vitro indicate that most toothpastes readily remove the dentine smear
layer to expose tubules.
Erosion of dentine appears to bring about rapid loss of the smear layer and
the opening of the smear layer and the opening of dentinal tubules. Most soft
drinks, some alcoholic beverages and yoghurt all readily remove the dentine smear
layer after a few minutes exposure. Moreover, these sources of extrinsic acid
dramatically reduce the resistance of the smear layer to gentle force such as a
nylon toothbrush used without toothpaste. Interestingly, some mouth rinses with
pH values below 5 also readily dissolved the smear layer, and were even shown to
erode enamel both in vitro and in situ. Like enamel, erosion causes bulk loss of
dentine and surface softening, the softened dentine being similarly very susceptible
to physical insults. Moreover, what little evidence is available throws into
question the ability of softened dentine to reharden.
In conclusion, available evidence suggests that lesion initiation in dentine
hypersensitivity can be induced by abrasive and erosive agents, whereas erosion
alone is probably the more dominant factor, in synergy with abrasion, it may bring
about dentine wear and tubule opening.
42

43. FACTORS AFFECTING DENTINAL HYPERSENSITIVITY
A. Factors affecting dentinal permeability
1. Structure of dentine and odontoblasts
The dentinal tubule is the portal through which stimuli gain access to the
pulp. However, dentine can be regarded as a barrier to bidirectional diffusive
transport between the mouth and the underlying pulp. Its barrier properties depend
on a number of factors, such as the presence or absence of a smear layer, the
thickness of the remaining dentine, the exposed surface area, whether it is root or
coronal dentine, whether it is normal or sclerotic, and the molecular size of the
permeating agent.
All of these could alter the sensitivity of dentine by affecting the fluid flow
from the pulp and diffusion of substances along tubules. It has been shown that
tubules in hypersensitive dentine surfaces are wider and more numerous than in
non-sensitive dentine. As only a small fraction of exposed dentine is usually
sensitive, this restricted permeability tends to limit the diffusive flux of exogenous
substances into the pulp. Although the outward movement of dentinal fluid can
mitigate the inward diffusion of exogenous substances (Matthews et al. 1993) it
can not prevent them from diffusing across dentine. However, open tubules have
also been demonstrated on non-sensitive surfaces, and so even if tubules are open
on the surface they may be occluded deeper in dentine. Factors such as increased
formation of peritubular dentine and deposition of tertiary dentine will tend to
reduce the overall permeability of the dentine and may account for the lower
incidence of hypersensitive dentine in older people.
The precise functions of the odontoblasts remain uncertain; the extent of
the odontoblast process appears to vary in different regions of the tooth but the
significance of this finding is not known. A primary function is likely to be in the
formation of peritubular and secondary or tertiary dentine, but the odontoblast may
also play a part in sensory transduction although at present there is no direct
evidence for this and it is clear that more detailed investigation is required of the
biophysical properties of odontoblasts and their relations to intradental nerve
43

44. terminals. The permeability of the layer is likely to be a factor in regulating fluid
movement and diffusion of substances between the dentinal tubules and the pulp.
This in turn will be governed by the interodontoblastic junctions. Cavity
preparation disrupts the junctional complexes between odontoblasts (Turner,
Marfurt and Satteberg, 1983), but what happens to this potential permeability
barrier (Bishop, 1992) in cases of dentine sensitivity is unknown. To the extent
that this barrier is lost, the probability of increased leakage of plasma proteins and
fluid is higher than if the junctional complexes reform. Perhaps those who exhibit
chronic dentine sensitivity cannot reform these junctional complexes because of
local pulpal inflammation. Alternatively, the outward flow of dentinal fluid might
prevent the formation of junctional complexes. The incidence of nerve sprouting
also correlates with; persistent inflammation (Kimberly and Byers, 1988) and may
be driven more by inflammation than by changes in connections within the within
the odontoblast layer. This may lead to a loss of cell to cell communication that
may be necessary to inhibit nerve sprouting. That is, there may be more nerve
sprouting in the absence of odontoblast junctional complexes than in their presence
(Taylor, Byers and Redd, 1988; Swift and Byers, 1992). Apparently, what is
important in the production of dentinal pain is the innervation density and the rate
of fluid flow of dentinal fluid through the tubules or Adjacent to
mechanoreceptors.
If odontoblasts are injured by inflammation, bacterial substances or
excessive fluid flow (e.g. shear stress), they may die and be replaced by newly
differentiated mesenchymal cells. These primitive odontoblasts tend to take less
tubular and more atubular reparative dentine, which can decrease the hydraulic
conductance of dentine, making it less sensitive. This mechanism does not seem to
operative in patients who remain sensitive for years.
At the peripheral end of the dentinal tubules a number of physicochemical
forces act to occlude the open tubules (Pashley, 1986) and change the barrier
properties of dentine. At normal pH, salivary calcium and phosphate levels are
generally supersaturated with respect to many forms of calcium phosphates with
respect to many forms of calcium phosphates including apatite. This tends to
mineralize previously demineralized dentin, form calculus and close open tubules
(Brannstrom and Garberoglio, 1980; Kerns et al., 1991). Tooth brushing can form
44

45. smear layers over tubule orifices and dentifrices contain silica, which can bind to
dentine (Addy et al., 1985) resulting in decrease in dentine permeability (Pashley
et al., 1984a) and sensitivity. These mechanisms can be thwarted by acid foods,
drinks or acidogenic observe that an individual’s dentine sensitivity waxes and
wanes over weeks to months. Acids probably dissolve surface deposits, thereby
reopening tubules and changing the hydraulic conductance of the dentine.
Dentine hypersensitivity, then, can be due to hyperconductive dentine as a
result of increases in the diameter of the tubules at their peripheral surface and/or
by loss of junctional complexes at their pulpal ends. Individuals who have
presented with dentine sensitivity and who have had their degree of sensitivity
measured carefully have suddenly become ‘hypersensitivity and who have and
their dentine hyperconductive relative to what it was when they came in for
evaluation. Just as hyperconductive dentine is hypersensitive, one can decrease
dentine sensitivity by making dentine hypoconductive. This is most easily
accomplished by modifying the condition of the tubule apertures (Hirvonen et al.,
1984) using topical agents such as oxalates or restorative materials.
The composition of dentinal fluid is not uncertain, nor is it known how
this may alter under different conditions, for example in pulp inflammation. The
ionic content could influence the excitability of intratubular nerve terminals, and
any protein content could have a profound effect on the hydrodynamics of fluid
flow.
2. Pulp haemodynamics
An Adequate blood supply is important for the health of any tissue, and
techniques such as laser doppler flowmetry have provided valuable information
about the control of pulp blood vessels are subject to essentially the same neural
and humoral controlling influences as those in other tissues. Stimulation of the
sympathetic fibres to the pulp causes vasoconstriction and reduced pulp blood
flow. Vasoconstriction such as noradrenalin applied directly to the exposed pulp
decrease pulp blood flow, whilst drugs such as acetylcholine, bradykinin and
substance P increase pulp blood flow. Although the pulp contains both α and β –
Adrenoreceptors, the effects of the β –receptors seem to be limited and they are
probably of lesser physiological importance in regulating pulp blood flow.
45

46. The magnitude of pulpal blood flow (0.4ml min-1
.g-1
; Kim, 1985) is high
relative to the metabolic requirements of the pulp and relative to other tissues.
That is, pulpal blood flow is equivalent to that of the brain. One Advantage of a
high blood flow is that it can rapidly clear the pulp chamber of any irritating
bacterial products that might reach the pulp through exposed sensitive dentine,
even in the face of an outward movement of dentinal fluid. Pashley (1979)
performed in vivo experiments in dogs in which dentine were exposed on both the
buccal and lingual surfaces of mandibular molars. Fluid filled chambers were
cemented on to both dentine surfaces. The lingual chamber was perfused with
isotonic saline via a syringe pump into a fraction collector. After allowing the
system to reach a steAdy state, radioactive iodide was added to the buccal chamber
to determine if any radioactivity would reach the lingual chamber. For this to
occur, the iodide would have to diffuse across the buccal dentine, the buccal
subodontoblastic capillary network, the central pulp, the lingual subodontoblastic
capillary network and the lingual dentine. Little radioactive iodide reached the
lingual chamber over the next several hours, even though frequent sampling
revealed that iodide was appearing rapidly in the systemic blood. This indicated
that the buccal subodontoblastic capillaries were very efficient at clearing iodide as
soon as it reached the capillaries. When pulpal blood flow was severely restricted
by adding adrenaline to the buccal chamber or by killing the dog, there was no
further accumulation of iodide in systemic blood (because there was no additional
pulpal clearance of isotope). However, the iodide began appearing rapidly in the
lingual chamber, which reflected increases in its concentration in pulpal the buccal
dentine but was no longer cleared from the pulp chamber by a functioning pulpal
circulation. Thus, it is clear that reduction in pulpal blood flow can lead to
increases in the concentration of exogenous substances in pulpal interstitial fluid.
Similarly, increases in pulpal blood flow should decrease the interstitial fluid
concentration of exogenous substances.
A relatively recent concept is the role of oxygen- derived free radicals, such
as the superoxide ion (O2) and its derivative the hydroxyl radical (OH2), in the
vascular control. Oxygen- derived free radicals produce complex vascular effects,
depending on circumstances, can cause either vasoconstriction or vasodilation.
Free radicals may act directly on the blood vessels, or they may act directly on the
46

47. blood vessels, or they may modify the effects of other endogenous mediators such
as noradrenaline and the endothelium- derived relaxing factor (nitric oxide).
Although some effects of oxygen- derived free radicals and nitric oxide have been
demonstrated in the pulp, it is not known to what extent these actions occur
naturally. This is to be an area of vigorous research in the future.
3. Outward Fluid Movement
The outward fluid movement noted first by Brannstrom (1966) and, more
recently, by Vongsavan and Matthews (1992a), can serve a protective role by
flushing exogenous, potentially irritating bacterial substances out of the tubules.
Vongsavan and Mathews (1991) demonstrated that the rate of outward fluid
movement in cat canine dentine in vivo was sufficient to prevent the inward
diffusion of Evans blue dye, although this could be overcome by applying external
pressure or by making the tooth non vital. They later tried several different sized
molecules in a microscopic study designed to examine where in dentine
permeation of dyes occurred. In that study, horseradish peroxidase penetrated the
peripheral but not the central tubules of cat canine dentine when 30cm H2O was
applied to a chamber cemented to the dentine surface in vivo. Lucifer yellow, a
fluorescent dye, penetrated peripheral dentine even in the absence of the extrinsic
pressure (De Francesco and Mathews, 1991). Thus, although there are some
conflicting data, there may be a protective role for the slow, outward movement of
dentinal fluid. Under some circumstances, the concentration of inwardly diffusing
substances can be significantly lowered by outward fluid flow. In a recent, simple
in vitro experiment, Pashley and Mathews (1993) measured the inward flux of I in
the presence and absence of a smear layer and in the presence and absence of a
stimulated pulpal pressure of 15cm H2O. In the presence of a smear layer, raising
the pulpal pressure from 0 to 15cm H2O reduced the inward flux of iodide by about
10%. When this maneuver was repeated after removal of the smear layer, the
reduction in inward iodide flux was about 50%. These findings support those of
Vongsavan and Mathews (1992a) and indicate the outward rinsing action of
dentinal fluid might protect the pulp from irritating plaque products in sensitive
dentine. This rinsing depends upon the hydraulic conductance of dentine and on
the magnitude of pulpal tissue pressure. Pulpal pressure probably increases in
47

48. teeth with dentine sensitivity due to inflammation caused by bacterial by products
or simply by neurogenic inflammation created by painful stimuli. Local pulpal
tissue pressure could easily double or triple (Heyeraas and Kvinnsland, 1992) in
sensitive dentine that is stimulated. The rate of inward diffusion of potential
irritants depends upon their concentration and their diffusion coefficient.
Fortunately, the concentration of bacterial substances is relatively low, as are their
diffusion co-efficient. Bacterial endotoxin is certainly very cytotoxic, but its
molecular weight is over 1 million, hence its diffusion coefficient is very low,
making its diffusion very slow.
Radicular dentine tubules have smaller diameters than coronal dentine
(Fogel, Marshall and Pashley, 1988). If the rate of transudation of fluid from the
microcirculation under radicular dentine is similar to that under coronal dentine,
then one would expect higher velocities of outward dentinal fluid flow in radicular
than coronal dentine. Thus, the flushing action of dentinal fluid in radicular
dentine may exceed that in coronal dentine. As most hypersensitivity is found in
radicular dentine, the outward fluid flow in such open tubules may interfere with
the inward diffusion of therapeutic agents. Clearly more research is needed to
explore the protective effects of outward dentinal fluid flow and all the factors that
can influence the fluid flow. There must be a balance reached between the rate of
inward diffusion of exogenous substances and the rate of flushing of the tubules by
outward dentinal fluid flow
B. Factors affecting nerve excitability
1. Morphology of intradental nerves
The pulp contains both somatic and autonomic nerves. The patterns of
innervation vary in different parts of the tooth, and it has been shown that
individual nerves contain a range of peptides and neuromodulators, including
substance P and calcitonin gene-related peptide. Neuromodulators released from
nerve terminals could influence the local microvasculature and also the responses
of the nerve themselves. It is possible that changes in the local state of the nerves
and pulp could account for the variations in tooth sensitivity that may occur with
time.
48

49. The responses of the nerves and odontoblasts to injury have generated
much interest. The nerves display plastic changes in response to injuries, such as
those caused by dental operative procedures. The severity of the changes increases
with the degree of trauma and in relation to how the dentine surface is
subsequently treated. In some types of localized injury, where the primary
odontoblasts are replaced by secondary odontoblasts, the innervation of the
repaired area is greatly reduced. Another feature associated with dentinal injury is
the presence of nerve terminal sprouting. Nerve sprouting seems to correlate with
inflammation, but this does not establish a casual relation. The sprouting does not
begin until 18-24 h after injury, some time after the painful symptoms have
appeared. It could be due to increased levels of growth factors in the pulp, but
bacterial toxins and / or fluid movement could affect sensitivity. There is some
limited evidence of increased terminal sprouting in pulps of hypersensitive teeth,
but this needs confirmation.
2. Intradental nerve properties
The two types of myelinated afferent pulp nerves (A β and A δ fibres)
appear to be excited by a variety of stimuli acting through a hydrodynamic
mechanism and the similarities in their properties suggest that belong to the same
functional group. Some pulpal afferents have receptive fields in both coronal and
radicular dentine. Also, there are differences in the responsiveness of nerves
innervating different areas of dentine, which may correlate with the reported
differences in the sensations elicited from dentine in different regions of the tooth.
The effectiveness of many dentinal stimuli is increased following acid etching,
which will increase the size and numbers of patent tubules. Oxalate treatment
reduces the nerve response, presumably by occluding tubules. In man, there is a
correlation between the numbers of exposed tubules and subjective pain ratings. In
contrast, unmyelinated C fibers generally do not respond to dentinal stimulation,
and seem to react to conditions that cause pulp damage or after damage role of
fluid movement in stimulating intradental nerve terminals and on the nature of the
transducer mechanism responsible for converting fluid movements into receptor
potentials.
49

50. 3. Neurogenic inflammation
It is now clear that the tooth pulp can longer be regarded as a passive
recipient of stimuli, but rather reacts to them in a way that can modify its own
responsiveness. Stimulation of dentine causes the release of a host of transmitters
and modulators that can affect both blood vessels and afferent and efferent nerves.
These effects constitute neurogenic inflammation. In Addition to exciting afferent
nerves through hydrodynamic mechanisms, physiological stimulation of dentine
generally causes an increase in pulp blood flow and increased permeability of
micro vessels. Even relatively mild tactile stimuli can increase pulp blood flow.
Subsequent changes in tissue fluid pressures may further affect pulp blood flow.
Blood flow changes do not appear to be due to a direct action on vasomotor nerves
but are mediated by axon reflexes initiated by activation of the myelinated afferent
nerves. These reactions can be further influenced by vasomotor nerves, which now
appear to act only on the blood vessels, but may also modify the responsibilities of
afferent nerve terminals.
It is possible that sustained, low-grade stimulation of the pulp could
produce neurogenic inflammation, and this may be responsible for the
characteristic spontaneous changes in the degree of clinical ‘sensitivity’ that occur
with time. But as yet, very little is known about that nature of any neuropharma-
cological differences between the pulps of normal and hypersensitive teeth.
Because neurogenic inflammation might be present in hypersensitive teeth, it has
been suggested that anti-inflammatory drugs such as aspirin could reduce dentinal
hypersensitivity, but this does not appear to have been fully investigated.
There is still considerable debate about whether bacterial substances
permeating across dentine can alter nerve excitability directly (Panopoulos, Mejare
and Edwall, 1983), or whether they exert their effects indirectly by releasing
endogenous mediators of inflammation or neuropeptides from pulpal nerves. A
third way in which the activity of mechanoreceptors can be altered is by fluid flow
around them. That is, local changes in pulpal pressure brought about by the release
of neuropeptides or inflammatory mediators acting on pulpal blood vessels could
bring pulpal nerves closer to threshold, indirectly, by increasing the rate of outward
fluid flow.
50

51. 4. Ionic composition of extracellular environment
Nerve excitability is affected by the ionic composition of the local
extracellular environment. This environment can be affected by the state of the
pulp and also by substances diffusing inwards from the mouth. Laboratory studies
of the effects on nerve conduction and therapeutic potential of potassium and
divalent cations in reducing intradental nerve activity have identified the local
concentrations that are required to modify nerve activity. However, it is not certain
if substance supplied to the outer dentine in vivo can diffuse along the tubules in
sufficient amounts to affect the excitability of intradental nerves.
5. Pain perception and psychology
Pain is more than a mere sensation. It does not always occur in direct
proportion to the intensity of a noxious stimulus or the extent of tissue damage.
The nociceptive system is not a passive relay mechanism, but actively modulates
the sensations and perceptions resulting from tissue damage or injury. The amount
of pain felt is influenced by many things, such as the individual’s sex and age, the
circumstances and present context, previous experiences and current expectations.
Personality characteristics also influence how the individual how the individual
reacts to noxious stimuli. The emotive reactions differ in acute and chronic pains;
the former often cause depression. All of these factors that can affect pain
experience and perception may also affect the response to treatment. The effects of
these variables are recognized in systemic pain management, but they are not
always considered when dealing with conditions such as dentinal hypersensitivity.
Hypersensitive dentine tends to be regarded as a purely peripheral phenomenon,
but the role of central factors can no longer be ignored.
In Addition to the peripheral changes in the pulp and dentine, it is possible
that the heightened sensitivity of hypersensitivity dentine may involve changes in
the central nervous system. Immuno-chemical studies suggest that change in the
central nervous system following peripheral injuries. One example is the rapid
expression of the proto-oncogene c-fos in central nervous neurons following
peripheral noxious stimulation. The presence of c-fibers suggests that neurons in
the nociceptive pathways may display considerable plasticity of their connections
and responses. Thus, far from being exclusively a peripheral problem,
51

52. hypersensitive dentine may involve increased excitation of second and higher order
projection neurons, and may turn out to have some similarities to other
hyperalgesic states. It is pertinent to consider to what extent expectations and
emotional factors contribute to dental pain.
52

53. PROTECTIVE ROLE OF PAINFUL STIMULI AND THE
DYNAMIC REACTIONS OF THE PULP DENTINE COMPLEX:
A HYPOTHESIS
The barrier properties of dentine are not constant but change in response to
external and internal modifications. When first exposed, dentine permeability is
relatively high, permitting painful stimuli to induce sufficient fluid shifts across
dentine to activate pulp nerves, both directly and via axon reflexes (Olgart, 1992;
Vongsavan and Matthews, 1992b). These nerves not only provide sensory
information but also release peptides that have a variety of local effects, including
increases in vascular permeability fluid and plasma proteins and increases in local
pulpal blood flow. This neurovascular response probably greatly increases the
turnover of local extracellular fluid volumes, thereby clearing the tissue of any
exogenous bacterial products that might promote inflammation. The increased rate
of local pulpal blood flow, and transudation of large plasma proteins such as – ∝2
macroglobulin, fibrinogen, growth factors and gamma globulins across pulpal
capillaries and venules, increases the outward flow of dentinal fluid, which is
highest in the most open (and presumably most sensitive) tubules. Not only does
the outward fluid lower the inward diffusion of bacterial substances, but the large
proteins also tend to lower the permeability of the pulp-dentine complex.
Fibrinogen can be converted to fibrin anywhere from the perivascular tissue
spaces, to interodontoblast spaces, to peri-odontoblast process spaces to
intratubular spaces. All of these spaces contribute to the resistance to fluid
movement that is fundamental to hydrodynamic activation of this neurovascular
reaction depends upon the magnitude of its stimulation by bacterial substances and/
or painful agents. If these are sufficient to cause sprouting of pulpal nerves, then
presumably the neurovascular reactions will be enhanced. Ultimately, these
intrapulpal- intradentinal reactions should make hypersensitive dentine less
conductive and hence less sensitive. Thus the intrinsic barrier properties of dentine
can decrease, under ideal circumstances, making it less permeable. These reactions
may occur in days to weeks under ideal conditions. Increased production of
reparative dentine requires months and sometimes does not happen in
hypersensitive teeth. Creation of smear layers and mineral precipitates within
53

54. tubule orifices can also make dentine hypoconductive but these reactions can be
reversed by acidic foods or acidogenic plaque micro- organisms.
In older people or in individuals who have had many episodes of localized
pulpal inflammation under sensitive tubules, the pulpal tissues may heal by scar
formation. This generally leads to a reduction in the number of capillaries in the
tissue and may result in less fluid transudation across these vessels for any given
intravascular tissue pressure or release of neurotransmitter. There may also be a
reduction in the density of nerves in the pulp, which would also interfere with the
proposed reactions. This may reduce the efficacy of the protective mechanism
outlined above and may explain why some suffer from dentine hypersensitivity for
years. The hypothesized changes in the neurovascular compartment of the pulp
need to be tested determine their relative contributions to the protection of the
pulp- dentine complex. Once identified, the various components will be available
for therapeutic manipulation.
MEASUREMENT OF DENTINAL PAIN
Most methods for studying dentinal sensitivity use thermal, mechanical,
osmotic, evaporative or electrical stimuli, all of which can elicit dental pain.
However, not all of these are equally suitable or sufficiently quantifiable for use in
clinical assessments. Ideally, the stimuli chosen for evaluation ought to be
measurable and reproducible, but should also be clinically relevant and take
account of the pain experience of the individual. In practice, dentine sensitivity
can be measured either as pain thresholds to graded stimuli or by using one of the
various forms of subjective rating scales. However, there are few standard
methods and stimulators are often custom made, although this is not necessarily a
problem as long as the specifications are clearly defined. In order to obtain a more
comprehensive picture, clinical studies often employ more than one form of
stimulus. Some, but not all, studies report good correlations between the degree of
sensitivity measured by different methods.
Electrical stimuli differ from most other dentinal stimuli in that they bypass
the normal receptor mechanisms and excite nerves directly in the pulp. The
relative merits of constant current and constant voltage stimulators generated
54

55. intense debate. Nerve thresholds are defined in terms of current, but most
electrical stimulators vary the applied voltage, so that any changes in voltage
threshold could arise from alterations to the resistance or impedance of the
combined tooth electrode system. Impedance changes could also reflect changes
in the dentine structure, such as deposition of peritubular dentine or tertiary dentine
that might underlie a change in tooth sensitivity. The use of electrical stimulation
method can be defended by observations that teeth classed as hypersensitive on the
basis of air or tactile stimuli are consistently found to have lower thresholds to
electrical stimuli than non -sensitive teeth. Although the stimulating electrodes are
placed on enamel rather than on the exposed root surface, hypersensitive teeth
show lower threshold to electrical stimuli than non-sensitive contra lateral controls.
These findings might suggest lowered pulp thresholds, but this has not been
confirmed. As yet, there is no direct evidence that nerves in inflamed pulps have
lowered threshold or that pulp thresholds correlate with the pathological state of
the pulp. Hence one might need to consider the possibility that changes in the
response to electrical stimulation may be due to altered processing in the central
nervous system, rather than in the periphery. However, one can argue that this
may not be important, provided the method used is capable of detecting any
change in the responsiveness of the nociceptive system as a whole.
MEASUREMENT OF HYDRAULIC CONDUCTANCE
As fluid movements across dentine are thought to provide the stimulus
response coupling mechanism involved in dentine sensitivity, the factors that
regulate fluid distribution across the pulp dentine complex require careful study.
Measurement of hydraulic conductance in vitro has provided important basic
information about the physical factor governing tubular fluid movement and
dentine permeability as well as showing how these are affected by clinical
procedures and the chemicals present in desensitizing preparations. These methods
can be applied in vivo to study pulpal pressures and outward fluid flows. Several
new concepts were introduced that require more study. Evaporative water loss in
response to air blasts can now be accurately measured in vitro.
55

56. Measurement of diffusion in dentine can pose technical difficulties, and
mathematical modeling may provide an alternative method for studying diffusion.
Computer models can be used to predict the time course of ion accumulation at
different points along the tubules under a variety of conditions, including
concentration gradients, assumed diffusion coefficients, dentine thickness, tubular
dimensions, hydraulic conductance, pulpal pressure presence or absence of
odontoblasts and the permeability of the cell junctions. Such models necessarily
require certain assumption to be made, but the predictions can be tested
experimentally to assess the validity of the model.
INTERACTIONS BETWEEN FLUID FLOW AND NERVE
ACTIVITY
Novel techniques for measuring fluid flow across cat dentine in vivo have
established that the resting outward fluid flow is around 13 pl/s. The mean flow
per tubule is 0.6 ft/s, which corresponds to a mean tubular fluid velocity of
1.4µm/s near the outer dentine surface. The rate of outward fluid flow is increased
by pulpal vasodilatation produced by stimulation of the inferior alveolar nerve,
whilst constriction of pulp blood vessels by stimulating the sympathetic supply
reduces dentinal fluid flow, or causes it to reverse and go towards the pulp.
Recently devised techniques allow simultaneous recordings to be made of
dentinal fluid flow and activity in intradental and pulp afferent nerves. The
experiments show that the direction and magnitude of dentinal fluid flow produced
by positive or negative hydrostatic pressure stimuli is correlated with intradental
and single unit nerve activity. Spontaneous outward fluid flow is well below the
threshold for nerve activation. The lowest threshold for initiating action potentials
in intradental nerves is approx. 50 times greater than resting flow rates. Threshold
for nerve activation are lower for negative pressures (causing outward fluid
movements) than for positive pressures (causing outward fluid movements) than
for positive pressures (causing inward fluid movement). For units that respond to
both inward and outward flows, the neural responses are greater with outward than
inward flows of the same rate. It is now necessary to investigate the transducer
56

57. mechanism in greater detail to establish why outward fluid movement is a more
effective stimulus than inward.
Stimulation of dentine sufficient to activate A fiber also causes an increase
in pulpal blood flow and outward fluid flow via axon reflex activity. It is
suggested that one function of intradental nerves is to detect open dentinal tubules.
Increased activity in intradental nerves may bring about pulp changes that result in
increased outward fluid flow, which may provide a defense against the ingress of
possible toxic agents along tubules.
PREVENTION OF DENTINE HYPERSENSITIVITY
Suggestions for patients
• Avoid gingival recession due to poor plaque by practicing good oral
hygiene techniques
• Avoid using large amounts of dentifrice, or reapplying Additional
dentifrice during brushing.
• Avoid hard bristled toothbrushes without end rounded bristles
• Avoid brushing teeth immediately following ingestion of acidic food
or beverages
• Avoid over brushing with excessive pressure for prolonged periods of
time
• Avoid excessive flossing or incorrect use of other interproximal
cleaning devices
• Avoid ‘pecking’ at the gyms or using toothpicks inappropriately
Suggestions for professionals
• Avoid over instrumenting the root surfaces during calculus removal
and scaling and root planning
• Avoid over polishing the exposed roots during stain removal
• Avoid violating the biologic width when placing crown margins
causing subsequent recession
57

58. • Avoid ‘burning’ the gingival tissue during in-office tooth whitening
or bleaching procedures
MANAGEMENT STRATEGIES
In clinical experience, the professional approach to dentine hypersensitivity
has been heavily treatment based with little regard for the control of the etiological
and predisposing factors, which created the problem. This is perhaps not
surprising since the practitioner and the sufferer are virtually bombarded with a
vast array of products formulated to treat dentine hypersensitivity. The Canadian
consensus board, previously referred to, conducted surveys of dental professionals
and indicated that there was confidence about diagnosing but not about managing
dentine hypersensitivity. Nevertheless, it should be noted that the literature
contains evidence, albeit often equivocal, for the apparent efficacy of a wide range
of quite different, if not downright bizarre, agents for the treatment of dentine
hypersensitivity. Few other human conditions or diseases, with the possible
exception of hemorrhoids, appear treatable by such a diverse range of compounds.
As with all conditions or diseases, management strategies, which include
treatment, are usually more successful than treatment alone. Failure to consider
causation in the management of dentine hypersensitivity, as with caries and
periodontal disease, may result least in recurrence or, at worst, failure of treatment.
Unfortunately, unlike caries and periodontal disease management, strategies for
dentine hypersensitivity are not data driven but rather are based on logic derived
from an understanding of the nature of the etiology of and the predisposition to the
condition.
Accepting that logic and biologic are often not the same, the following
management strategy is proposed:
1. Ensure the correct diagnosis of dentine hypersensitivity is based on a
history and examination, and is compatible with the definition’s clinical
descriptor.
2. Consider a differential diagnosis, as suggested by the definition of dentine
hypersensitivity, which alone may explain the symptoms or identify the
presence of other conditions contributing to the pain of dentine
hypersensitivity.
58

59. 3. Treat any and all secondary conditions that induce symptoms similar to
dentine hypersensitivity.
4. Identify etiological and predisposing factors, particularly with respect to
erosion and abrasion. Consider detailed, written dietary histories and oral
hygiene habits (frequency, duration and timing of brushing of brush
change, and appearance of brush at change). Some of these aspects of
tooth brushing behavior are best apprised by observing the patient brushing
in the dental practice.
5. Remove or modify identified etiological or predisposing factors. Offer
dietary Advice to minimize erosion and oral hygiene instruction to
minimize abrasion and to divorce abrasion from erosion.
6. Recommend or provide treatments appropriate to the individual needs of
the sufferer. The number of teeth involved and the severity of the pain are
important variables, and should influence the treatment options.
DIAGNOSTIC CONSIDERATIONS
For this purpose, the clinician has to evaluate the patient’s dietary
recollection data very carefully; enjoying fruit drinks such as orange juice or
other acidic beverages very frequently, as well as the abuse of modern life style
drinks (which often contain high amounts of titratable acid), or diets high in
vegetables may contribute to erosive effects removing dentine and/or dentinal
smear layer, thereby opening the tubules. Moreover, exploring the medical
history very cautiously can provide valuable information on intrinsic (e.g.
vomiting, regurgitation, rumination; eating disorders like anorexia and bulimia
nervosa) and extrinsic erosive factors (e.g. acidic occupational/environmental
reasons or the excessive use of acidic medicaments such as vitamin C or aspirin
as fluids).
For many years, clinicians have focused on physical factors like tooth
brushing abrasion when trying to eliminate extrinsic factors of DH. Indeed.
Mechanical tooth wear can be caused by abrasive dentifrices when used with a
brush excessively. However, evidence from the literature seems to be
inconsistent, since toothpastes can block the dentinal tubules by producing a
59

60. smear layer or are able to occlude the orifices with some of their (primarily
abrasive) ingredients, depending on the type of action. Therefore, it seems to be
reasonable to suppose a combination of erosive and abrasive influence on DH;
the effects of intrinsic/extrinsic acids will be particularly enhanced by tooth
brushing with abrasives. This erosion-abrasive effect will be responsible for
cervical enamel loss; moreover, with respect to dentine, these insults will cause a
ready opening of the dentinal tubules, accompanied by an accelerated dentin
loss.
With regard to tooth surface loss, another factor initiating DH might be
involved. While to date it seems unclear why the cervical region of the tooth is
particularly prone to wear, producing an angular lesion (horizontal to the dentine
and acute at the enamel margin), this kind of class V cavity is localized very
frequently at the facial surfaces of the upper canines and premolars.
Interestingly, these teeth are most commonly affected with DH as well, thus
suggesting a similar etiology. At least theoretically, abfraction could weaken the
tooth by forming stress concentrations near to the gingival margin; subsequently,
this would render the apatite crystals more susceptible to chemical attack
(erosion) or further mechanical deterioration of both. Again this phenomenon
would result in opened dentinal tubules being responsible for DH.
Moreover, with regard to the more pronounced notch-shaped cervical
lesions, a wider diameter of the tapered dentinal tubules can be found near the
pulp; at the same time, more tubules per unit area are present. While in the
coronal dentine the tubule density increases four-fold (in superficial dentine the
area occupied by tubule lumina is approximately 1 pr cent of the total surface
area, and their value will increase up to 22 per cent at the pulp), in the root
dentine this consequently means that with a preceding cervical lesion the extent
of the discomfort is likely to increase.
Tooth surface loss caused by either abfractive, abrasive, or erosive effects
is assumed to be a relative slowly progressing but cumulative life time process
which is extremely difficult to diagnose in early stages; sometimes no obvious
changes can be observed on the teeth for many years. However, it seems evident
that every single factor mentioned above (or presumably all of them in
combination) can be considered to be capable of opening the dentinal tubules.
60

61. Thus, with the exception of periodontal surgery (where the dental professional
will produce DH by removing cementum and dentine), the patients themselves
seem to be ‘responsible’ for opening the dentinal tubules in most cases. For this
reason, albeit DH can be diagnosed clinically, the basic causative factors can
only be evaluated by a concise screening and extrinsic influences.
FACTORS TO CONSIDER IN THE DIFFERENTIAL
DIAGNOSIS OF DENTIN HYPERSENSITIVITY
1. Abscessed or non-vital tooth: With periapical radiolucency of draining
fistula; necrotic with sensitivity to occlusion partially necrotic in one
canal, with vital tissue elsewhere (in which case tooth tests vital to
stimuli). Pain typically occurs spontaneously or upon occlusion or
tapping
2. Cracked tooth. Vertical fracture or single cusp partial fracture. Pain
typically occurs on release of biting or tapping of a single cusp
3. Dental caries. Greatest degree of sensitivity experienced when dental
decay passes the dentine enamel junction. As caries penetrates further
into the tooth, sensitivity lessens until pulp becomes involved.
4. Gingival recession. Often occurs post-periodontal surgery, when a large
portion of the root is exposed, or due to ageing, mechanical trauma,
frenum attachment pulls or occlusal trauma.
5. Toothbrush abrasion. Caused by use of a hard toothbrush or a soft
toothbrush with abrasive toothpaste or by aggressive brushing, and
generally located on the side opposite the dominant hand. Abrasion may
either instigate gingival recession or stem from greater accessibility to
softer root surfaces from recession.
6. Abfraction lesions. Generally associated with occlusal trauma where the
anatomic crown of the tooth has flexure. Although non-carious, these
lesions can become very sensitive and even progress into the pulp. They
may be multifactorial where abrasion and erosive forces combine to
produce tooth surface loss.
61

62. 7. Erosive lesions. Associated with acid reflux, hiatus hernia, purging,
bulimia (intrinsic causes), and diet (extrinsic causes). Intrinsic acid
lesions typically occur on the palatal surfaces, while extrinsic acid lesions
tend to occur on the buccal surfaces. Consuming large quantities of
carbonated cola drinks and fruit drinks, which have a very low pH, causes
tooth surface loss, as does tooth brushing following an acidic assault,
which removes the acid softened enamel or dentine
8. Diet sensitivity. Generally associated with a low pH material, such as
fresh tomatoes, orange juice, cola drinks. Areas with exposed dentine are
etched, causing sudden sensitivity. Diet choices may aggravate
sensitivity for erosion
9. Genetic sensitivity. Patients reporting history of sensitive teeth. It is not
known whether sensitivity correlates to the 10 percent of teeth that do not
have cementum covering all the dentine at the DEJ, or is a factor of lower
overall patient pain threshold values.
10. Restorative sensitivity. Dentin sensitivity develops under restorative
materials for a number of different reasons. Far more dentin is removed
during cavity preparations than occurs during root planing. Generally,
larger surface areas of dentin are exposed to thermal, vibratory and
evaporative insults associated with cutting cavity preparations. It can be
triggered following placement of a restoration for several possible
reasons: certain amalgams (such as Tytin) having a history of 24-48 hours
sensitivity due to shrinkage, rather than the usual expansion, during
setting; contamination of composites during placement or improper
etching of the tooth on composites, which results in micro leakage;
improper tooth drying technique; incorrect preparation of glass ionomer
or zinc phosphate cements; general pulpal insult from cavity preparation
technique; the thermal or occlusal causes; galvanic reaction to dissimilar
metals that creates a sudden shock or ‘tin foil’ taste in the mouth. Many
currently marketed dentin bonding systems acid etch the dentin which
removes the smear layer and increases dentin permeability. Hypertonic
reagents are then placed on dentin as primers, followed by the application
of Adhesive resin which flow into the open tubules to form resin tags of
62

63. varying lengths. These resins do not completely polymerize and may
leach unpolymerized monomers which can diffuse into the pulp and cause
irritation. Thus, there may be some neurogenic inflammation associated
with cavity preparation, plus chemical irritation due to bonding resins that
could contribute to increased dentin sensitivity following many
restorative procedures. Class II restorations, involving proximal boxes
which terminate below the CEJ, develop sufficient forces during
polymerization to allow the composite resin to dislodge the weakest bond
and thereby open a margin. The weakest bond is often the gingival floor
of the proximal box, because of the type dentin present and because it has
often been contaminated by blood or gingival fluid. These solutions
contain more protein than saliva and can lead to lower than normal bond
strengths. The clinical consequences of a lack of bonding in this case are
due to the open gingival margin. This permits bacterial contamination of
the internal dentin walls of the proximal box, leading to bacterial
irritation of the pulp, which can cause pulpal inflammation.
Some patients complain of dentin sensitivity on teeth covered with a full
crown restoration. The sensitivity could be on the root surface at or
slightly below the gingival margin, or it could be due to leakage under the
crown due to the loss of luting cement. These two conditions can be
differentiated by use of an explorer, air blasts, and hypertonic solution.
An explorer will elicit pain when passed over exposed, sensitive cervical
dentin, but will not be able to stimulate exposed dentin under the casting.
Air blasts will usually cause pain when directed at exposed root dentin,
but do not cause pain under castings. If the suspected margin is painted
with a hypertonic solution such as saturated calcium chloride, the
hypertonic solution such as saturated calcium chloride, the hypertonic
calcium chloride solution will diffuse into the marginal gap within 10-20
seconds and osmotically pull dentinal fluid across the “exposed” dentin,
thereby hydrodynamically causing dentinal pain and identifying the open
margin. If the exposed dentin is not sensitive to an explorer or air blasts,
but is sensitive to hypertonic solutions, it suggests that the sensitivity is
beneath the casting, not on the root surface.
63

64. 11. Medication sensitivity. Due to medications that dry the mouth (e.g.
antihistamines, high blood pressure medication) thereby compromising
the protective effects of saliva and aggravating diet related trauma or
proliferating plaque. Even a reduction in salivary flow due to ageing or
medications can lower the pH of the saliva below the level at which
caries occurs (6.0-6.8 for Dentine caries; < 5.5 for enamel caries) and
increase erosive lesions to exposed dentine.
12. Bleaching sensitivity. Commonly associated with carbamide peroxide
vital tooth bleaching and thought to be due to the by products of 10 per
cent carbamide peroxide ( 3 percent hydrogen peroxide and 7 per cent
urea) readily passing through the enamel and dentine into the pulp in a
matter of minutes. Sensitivity takes the form of reversible pulpitis caused
from the dentine fluid flow and pulpal contact of the material, which
changes osmolarity, without apparent harm caused from the dentine fluid
flow and pulpal contact of the material, which changes osmolarity,
without apparent harm to the pulp. Sensitivity is caused by all other
forms of bleaching (in office, with or without light activation, and new,
over the counter) and depends on peroxide concentration.
TREATMENT CONSIDERATIONS
Patient Management
According to Trowbridge et al. (1990), “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 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 dentin
sensitivity is no exception. Periodontal therapy and certain restorative procedures
can result in gingival recession, exposed dentin, and subsequently hypersensitive
64

65. roots. Properly informed patients with newly exposed dentin often proceed
towards spontaneous remission with minimal intervention.” This is extremely
important in reinforcing practitioners’ credibility in the eyes of their patients.
Honesty, empathy and patient education by the practitioner, not an auxiliary, are
paramount to successful patient management of any clinical problem including
dentin sensitivity.
Ideally, one should use an in office treatment design to significantly reduce
the magnitude of their sensitivity, which is then followed up using a desensitizing
dentifrice and a soft toothbrush. However, the patient should be made aware that
there is an escalating series of treatments available for dentin sensitivity that can be
employed to control any discomfort that they develop. It is vital that practitioners
develop a plane of escalating therapy that they feel comfortable with so that they
can react appropriately and decisively in the treatment of this common condition.
Ideal treatments of sensitivity should begin with scoring the patient’s
degree of dentin sensitivity using a 1 second air blasts 5 cm from the sensitive
surface while covering adjacent teeth with fingers; the desensitizing treatment
should then be attempted. At the end of one or more treatments, the sensitive areas
should be re evaluated.
Once the size, location and magnitude of the patient dentin sensitivity is
identified, one needs to explain the problem to the patient in lay terms, using
whatever aids that are appropriate for the patient and enlist their participation in the
treatment of the condition. If the etiology of their condition can be explained to
them they will be less likely to continue to contribute to the development of this
painful condition.
Overall there are two treatment approaches: to occlude dentinal tubules,
thereby blocking the hydrodynamic mechanism; to block neural transmission at the
pulp. The majority of treatments, whether home use or applied in office, are
formulated to occlude tubules. Blockage of neural transmission to the pulp
theoretically can be achieved using topically applied potassium salts and
completely by endodontics or tooth extraction. It is worth remembering that
clinical trials on professionally applied and, more particularly, home use treatments
show a significant improvement in symptoms due to either or both, a placebo
response or/and regression to the mode (natural improvement). Such studies even
65

66. suggest that the mere recommendation o a home use desensitizing product, or the
professional application of anything to exposed dentine, results in, on average, a 40
percent and even greater improvement, irrespective of the specific treatment.
If only one or two teeth are severely sensitive, then one might consider
restorative procedures. However, if the patient presents with 10-20 sensitive teeth,
then other options should be exercised before committing them to extensive and
expensive restorative procedures. In the treatment of dentinal sensitivity, one
needs to develop an escalating plan of treatment that is appropriate to each patient.
For instance, if a patient has such severe sensitivity that they cannot breathe
through their mouth or if they cannot brush their teeth, it would be inappropriate to
recommend that they begin using a desensitizing dentifrice. Rather, their acute
sensitivity must be treated immediately. This should begin with simple treatment
first, reserving more complex treatments for more intractable conditions.
Patient compliance with instructions on the use of desensitizing dentifrices
will be greater if practitioners are honest and tell them that brushing the sensitive
sites will be uncomfortable for a few days but that if is absolutely essential that
they do so if they wish to resolve the condition. If the level of sensitivity is very
high, it is unrealistic to expect a patient to comply with instructions regarding the
use of a desensitizing dentifrice. For such patients, their level of sensitivity must
be reduced by a professional treatment before they can be expected to maintain
proper oral hygiene.
Authorities agree that the hydrodynamic theory of dentinal sensitivity
explains most experimental observations associated with this condition. In
essence, the history postulates that all painful stimuli (hot, cold, osmotic tactile,
etc.) cause pain by inducing minute shifts in dentinal fluid contained within
tubules. The fluid movement activates mechanoreceptor nerves near the pulp
thereby, causing pain. There are to different approaches to the topical treatment of
dentinal sensitivity that are based on the hydrodynamic theory. The first attempts
to interfere with hydrodynamics by occluding the tubules. The second tries to
decrease the sensitivity of the mechanoreceptors themselves. Most treatment falls
into the first category.
66

67. DESENSITIZING DENTIFRICES
Over the counter remedies for dentinal sensitivity are limited to
desensitizing dentifrices. Some of these dentifrices occlude dentinal tubules better
than others (Addy et al., 1985). The most popular dentin desensitizing dentifrices
include 5% potassium nitrate as the active ingredient (Table 3, Denquel, Promise,
Sensodyne-F). The success of dentifrices depends on the frequency of use
(morning and evening use preferred), length of time of use and on whether they
brush the sensitive areas. Patients with recurring sensitivity should probably
remain on desensitizing dentifrices indefinitely. Some manufacturers have
included fluoride in the formulation of their dentifrices as an anticaries measure
although fluorides may be marginally effective at reducing dentin sensitivity as
well. Those dentifrices containing potassium salts seem to provide more relief
than other desensitizing dentifrices.
The improvement of dentin sensitivity over time (the waning phase) may be
due to remineralization phenomenon and even calculus formation. While one
should not encourage calculus formation, remineralization of previously
demineralized dentin surfaces involves many of the same physiochemical
phenomenons as occurs in the mineralization of dental plaque. As most anti tartar
dentifrices are designed to interfere with crystal growth, which is important in
remineralization of dentin, patients may find their dentin sensitivity increases when
they use such products. Although no definitive studies of the influence of anti
tartar dentifrices on dentin sensitivity have been published, it seems prudent to
Advise patients with sensitivity to avoid anti tartar dentifrices.
TOPICAL DESENSITIZING AGENTS
The next simplest therapy is the topical use of any of a number of
professionally applies agents such as calcium hydroxide, sodium or stannous
fluoride solutions, gels, varnishes, potassium oxalate, ferric oxalate, (table 3).
These are all designed to occlude the orifices of the dentinal tubules and thereby
block hydrodynamic reactions from causing pain. None of these agents are
permanent and they may require reapplication. Potassium and ferric oxalate seems
to be more effective immediately but such clinical studies are always complicated
67

68. by significant placebo effects. However, these agents may provide temporary
relief to dentin sensitivity and can be applied by dental hygienists as well as by
dentists. It is worth mentioning that patients with moderate to severe sensitivity
scores should be given special consideration during such treatment. Whatever
solutions are used should be warmed between 34-37°C to avoid thermally induced
pain with room temperature solutions. A practitioner may begin with the
application of a topical solution of potassium oxalate (Protect, John O. Butler Co.),
or Sensodyne Sealant, (Block Drug Co. Inc.), an acidic solution of ferric oxalate.
Dentin Desensitizing agents
Active Ingredient
A. Over-the-counter remedies
Potassium Nitrate (5%)
Strontium Chloride (10%)
Citrate/Pluronic Gel
(0.5% citric acid, 1.5% sodium
citrate, 20% pluronic F-127)
Brand name
Denquel
Promise
Sensodyne-F
Sensodyne
Protect
Source
Procter & Gamble Co
Block drug company Inc
Jersy City, NJ
Block Drug Company, Inc
Jersey City, NJ
John O. Butler Company
Chicago, IL
B. Professional Products
Potassium Oxalate
Ferric Oxalate
Topical Fluorides
Stannous Fluoride (0.4%)
Neutral NaF (1.1%)
Acidulate NaF (1.2%)
Sodium Fluoride Pase
(331/3% NaF)
Protect Dentin
Desensitizer
Senosodyne
Sealant
Omni-Gel
Gel-kam
Luride
Luride
Dentin
Desensitizing
Paste
John O. Butler Company
Chicago, IL
Block Drug Company Inc.
Jersy City, NJ
Dunhall Pharmaceuticals
Inc.
Stratford, TX
Scherer Laboratories, Inc,
Dallas, TX
Lorvic Corporation
St. Louis, MO
Colagate-Hoyt
Laboratories
68

69. Needham, MA
Sultan Dental Products,
Engle wood, NJ
The soluble oxalate salts react with calcium in dentinal fluid to form
microscopic crystals of insoluble calcium oxalate in the orifices of the tubules. By
estimating the patient’s sensitivity immediately before (using short air blast or
gentle use of explorer) and after treatment, one can evaluate the efficacy of a
treatment. While the use of acidic oxalates is often very effective in decreasing
dentin sensitivity, these products do demineralize the dentin surface. Normal
remineralization mechanisms should restore these surfaces within a few days.
Topical fluorides form crystals that are smaller than those of the oxalates, and
therefore do not occlude dentinal tubules as quickly. However, fluoride treatment
reduces the acid solubility of dentin, promotes remineralization, and has
antibacterial effects. Thus, there is no contraindication to the use of stannous
fluoride, for example, immediately after topical oxalate treatments. Additionally
fluoride treatment may contribute to tubule occlusion and may make the dentin less
susceptible to future sensitivity caused bye erosion of root structure. The
maintenance of dentin desensitization can be promoted by such fluoride treatments
at home. Following topical application, these treatments should offer significant
reduction in dentin sensitivity for several weeks to months, until the natural
desensitizing mechanisms express their full potential. These topical treatments
should be done on unanesthetized patients. If they are not effective immediately,
the treatment should be repeated.
If oxalate treatment does not provide sufficient relief, or if it is not
available, the sodium fluoride containing varnish Duraflor or Duraphat can be
applied to the affected surface. Duraphat is used in Europe for application of
topical fluorides. In Canada, it is called Duraflor. It remains on teeth much longer
than our fluoride gels which seem to be much less effective at desensitizing dentin.
They contain 2.2% sodium fluoride which can react with calcium in dentinal fluid
to form crystals of calcium fluoride. Another mechanism may be physical
occlusion of the surfaces with the heavy varnish that constitutes the bulk of these
preparations.
69

70. If the patient has many sensitive teeth, an alternate approach would be the
fabrication of a vinyl mouthguard that extends over the sensitive surfaces. These
devices can be used by the patients to hold materials such as calcium hydroxide
paste, 1.23% neutral sodium fluoride gel or 0.5% dexamethasone ophthalmic
ointment on the sensitive surfaces overnight. Only after these patients obtain relief
should they be placed on a desensitizing dentifrice. Of course, patients with only
mild dentinal sensitivity can be Advised to switch from their usual dentifrice to a
desensitizing dentifrice.
If topical treatments are not successful in controlling dentin sensitivity, then
the clinician should consider escalating the treatment to include restorative
procedures (Gayton et al., 1984). All that is required is that the dentin be cleaned
with a rubber cup and wet pumice to remove any plaque or calculus. Etching the
dentin is not necessary prior to the use of glass ionomer cements. The use of the
capsulated glass ionomers that are mixed in an amalgam titrator and delivered in a
“gun” are very convenient. However, the new light cured glass ionomers have
good flow characteristics and give excellent control. If a more esthetic result is
desired, the use of third generation dentin bonding systems should be considered
(Gluma, Columbus Dental, Scotchbond Multipurpose, 3M Dental products;
Tenure, Den Mat; Prisma Universal Bond 3, L.D. Caulk, etc). These should be
covered with a thin veneer of composite resin to protect the bonded surface. If the
sensitivity is close to the free gingival margin, the clinician may have more control
over light cured glass ionomer cements which are also more forgiving in a moist
environment than are most dentin bonding agents. The resins have a tendency to
spread or flow beyond their intended limits which often leads to their accumulation
subgingivally. Attempts to finish restorative materials at gingival margins can lead
to removal of cementum and exposure of previously unexposed dentin leading to
new sensitivity. If the patient’s sensitivity is not severe, if is desirable to restore
these areas without anesthesia so that one can determine how successful the
treatment has been immediately. If the patient has severe sensitivity, one should
use local anesthesia during the restorative procedure but re evaluate their
sensitivity on subsequent visits to determine if further treatment is required.
It is clear that restorative treatment is more time consuming and will be
more expensive than more conservative treatments. However, such definitive
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71. treatment may be preferred if only a few teeth are involved or if patients have only
limited access to dental treatment.
71

72. POTENTIAL TREATMENT MODALITIES FOR DENTINE
HYPERSENSITIVITY: HOME USE PRODUCTS
Introduction
The incidence of dentine hypersensitivity has been reported to range from 8 to 35%
in ‘normal’ populations (Addy 1990, Gillam 1992, Fischer et al. 1992, Murray and
Roberts 1994). The condition is much more frequently encountered in certain
specific populations, e.g. in those patients attending periodontal clinics (Gillam et
al. 1994, Chabanski et al. 1996). A wide range of commercial products is available
for self-treatment. The products include agents such as potassium salts, strontium
salts and fluoride salts in toothpaste, mouthwash and gel formulations.
These agents are believed to reduce the symptoms of dentine
hypersensitivity by both occluding dentine tubules and thus blocking the neural
stimulus and response (Pashley et al. 1978a, 1978b), and/or intercepting the neural
response by chemical intervention (Bilotto et al. 1978, 1988, Markowitz et al.
1991). Tooth brushing rarely lasts more than a minute (Duke and Forward 1982),
neither does a mouthwash treatment: therefore, the effect of the agent in a
toothpaste or mouthwash must either be rapid or else the agent must be substantive
to the teeth and mucosa. Alternatively the effect of an agent could build up over
the period of use of the product.
The effectiveness of self-applied products for the treatment of dentine
hypersensitivity is often reduced by the lifestyle of the patient. Acid foods and
drinks have been shown to soften dentin and may remove deposits on the dentine
surface (Absi 1989). Brushing has been shown to exacerbate the removal of any
surface deposits (Absi et al. 1995). These deposits may be performing the
desirable function of blocking tubules and reducing dentine hypersensitivity. The
effectiveness of these self-treatment products that occlude dentine tubules could
perhaps be improved by counseling patients on their diet and brushing habits.
Strontium salts
Five studies have been reported since the review by Zappa (1994) that examined
the effect of toothpastes containing strontium salts, either as the chloride or the
72

73. acetate, on patients with dentine hypersensitivity. It is not possible to make an
exact comparison of the results of these studies because the period of use of the
toothpastes was not consistent, the placebo or control toothpaste was not the same
in all of the studies and the formulations of the test products were also different.
However, a number of generalizations can be made.
All the studies demonstrated an improvement in patients’ perception of
their dentine hypersensitivity. The effectiveness of the toothpastes in reducing the
symptoms increased with the period of use of the products. One study (Gillam et
al 1992) reported no difference in the effect on dentine hypersensitivity to two
toothpastes both of which contained strontium chloride but with different silica
abrasive systems. A later study (Pearce et al. 1994) reported that toothpastes
containing either strontium chloride or strontium acetate provided comparable
benefits for the relief of dentine hypersensitivity. In the latter study (Pearce et al.
1994) and also a number of others (Gillam et al 1996, Silverman et al 1996, West
et al. 1997) the negative control toothpaste reduced the symptoms of dentine
hypersensitivity; this effect also increased with the duration of the treatment. In
none of these studies was a consistent significant improvement in patients’
symptoms of dentine hypersensitivity observed for the strontium containing
products compared with the negative control toothpaste. It may therefore be
concluded that strontium salts appear to have only a minimal effect in reducing the
symptoms of dentine hypersensitivity.
Potassium salts
Potassium salts are now the most commonly used agents incorporated into
toothpastes and mouthwashes for the self-applied treatment of dentine
hypersensitivity. All these studies demonstrated an improvement in the patients’
perceived symptoms of dentine hypersensitivity after use of the products
containing potassium salts with that of a control product. All these studies
demonstrated an improvement in the patients’ perceived symptoms of dentine
hypersensitivity after use of the products containing either potassium nitrate or
potassium chloride. The effect of the product increased with time. The placebo
effect (Yates et al. 1998) is also very apparent in these studies, with the beneficial
effect of the control toothpaste or mouthwash also increasing with time. Studies
73

74. on tooth pastes reported by a number of authors (Salvato et al. 1992, AyAd et al.
1994, Nagata et al. 1994, Silverman et al. 1994, 1996, Schiff et al 1994) all
demonstrated a significant benefit for the tooth paste containing a potassium salt
compared with the control toothpaste. However, other studies (Gillam et al. 1996,
West et al. 1997) failed to show any benefit for toothpaste containing the
potassium salt compared with conventional fluoride toothpaste.
Only two studies (Fillam et al. 1996b, Yates et al. 1998) have been reported
which evaluated the effect of mouthwashes on dentin hypersensitivity.
Other agents
The effects of different fluorides and of a mouthrinse containing aluminium lactate
on dentine hypersensitivity have been reported in two studies (Higuchi et al. 1996,
Plagmann et al. 1997); Plagmann et al. (1997) concluded that both sodium fluoride
and amine fluoride reduced dentine hypersensitivity over a period of 8 weeks,
although neither agent was more effective than a control toothpaste. Higuchi et al.
(1996) reported that the daily use of a mouthrinse containing aluminium lactate
significantly reduced the symptoms of dentine hypersensitivity compared with a
control rinse. No other recent studies have been reported which confirm these
results.
Conclusion
There appears to be little doubt that, under the controlled conditions of clinical
trial, toothpastes, whether or not they contain potential active agents such as
strontium salts or potassium salts appear to reduce the symptoms of effects is not
clear. The effect could be attributed to a ‘placebo’ or ‘Hawthorne’ effect (Yates et
al. 1998) which has been observed in many clinical studies. Alternatively, the
control products may have activity in their own right. Many tooth- pastes contain
silica, either as a polishing agent or as a thickener. It is well documented that these
particles can effectively occlude dentine tubules and that the deposit is resistant to
mild abrasion or an erosive challenge (Jackson et al 1990, Absi et al. 1995).
Sodium monoflurophosphate has also been reported in the past to reduce dentine
hypersensitivity (Bolden et al 1968, Hazen et al. 1968, Kanouse and Ash 1969) and
this may also contribute to the activity of conventional toothpastes
74

75. There is little convincing clinical evidence for the activity of strontium
salts. Deposits from toothpastes that contain strontium salts consist mainly of the
polishing agent or thickener, which are often insoluble silicas, or a combination of
these. There is no reported evidence for strontium slats enhancing the deposition
of material or increasing the longevity of the deposit. The evidence for the activity
of potassium salts is also inconclusive. If the effect of potassium ions in reducing
dentine hypersensitivity is dependent on the diffusion of the ions along the dentine
tubules to the neural receptors, the probability of this occurring during the short
period of use of a tooth paste or mouthwash is very low (SteAd et al. 1994,
Vongsavan and Mathews 1992). This may mean that some other mechanism must
exist.
If any of these agents-strontium or potassium salts – are effective in
reducing dentine hypersensitivity, then studies on simple aqueous their activity.
No studies have been reported in the literature, which has evaluated the effect of
such simple treatments.
POTENTIAL TREATMENT MODALITIES FOR DENTINE
HYPERSENSITIVITY: IN OFFICE PRODUCTS
Introduction
The prevalence of dentine hypersensitivity is high enough (Chabanski et al
1996) to warrant the development of effective in office treatments. Patients who
suffer from dentine hypersensitivity expect their dentists to have an effective
treatment. Indeed, if the treatment is not effective, the patients may question the
professional competence of their dentists. This chapter will attempt to survey the
wide range of materials that has become available for the in office treatment of
hypersensitive dentine in recent years (Trowbridge and Silver 1990, Gangarosa
1994).
After diagnosing dentine hypersensitivity, it is important to explain the
multi-faceted causes of the condition to patients. Dietary evaluation should be
carried out as well as instruction and demonstrated proficiency in proper tooth
brushing. Patients should be provided with an ultra soft toothbrush and perhaps
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76. encouraged to brush without a dentifrice (Kuroiwa et al 1994). Patients need to
become involved in the resolution of their condition.
In office treatments for hypersensitive dentine
I. Treatment agents that do not polymerize
A. Varnishes/precipitants
1. Shellacs
2. 5% sodium fluoride varnish
3. 1% NaF, 0.4% SnF2, 0.14% HF solutions
4. 3% mono potassium –monohydrogen oxalate
5. 6% acidic ferric oxalate
6. Calcium phosphate preparations
7. Calcium hydroxide
B. Primers containing HEMA
1. 5% glutaraldehyde, 35% HEMA in water
2. 35% HEMA in water
II. Treatment agents that undergo setting or polymerization reactions
A. Conventional glass ionomer cement
B. Resin reinforced glass ionomer/compomers
C. Adhesive resin primers
D. Adhesive resin bonding systems
III. Use of mouthguards
IV. Iontophoresis
V. Lasers
76

77. I. Treatment agents that do not polymerize
A. Varnishes, precipitants
The use of 5% sodium fluoride (NaF) in a thick varnish as a dentine
desensitizer has been reported by Clark et al. (1985). The varnish does temporarily
occlude dentinal tubules but the material is readily lost over time. The varnish was
found to be effective for the relief of dentine hypersensitivity, Hansen (1992)
reported an interesting cross over study, where patients with dentine
hypersensitivity were treated first with dentine hypersensitivity were treated first
with fluoride varnish and if that failed, with a light- cured glass ionomer.
Treatment with the fluoride varnish produced 22% failures within 1 weak, and a 1-
year cumulative success rate of 44%. With the glass ionomer 2% of the treatments
failed within the first week and the 1-year success rate was 79%. This is a good
example of escalating therapy. If the simple therapy did not work, a more complex
but more effective therapy was carried out.
A number of treatments for hypersensitive cervical dentine are based upon
occlusion of open dentinal tubules. For instance, burnishing sensitive root surfaces
with a paste made up of 33% NaF, 33% kaolin and 33% glycerine has been used
for over 50 years. The only clinical trial that used blinded conditions and placebo
controls was done by Tarbet et al. (1979). They burnished the paste into affected
dentine (or enamel in controls) with an orangewood stick for 30s. When sensitivity
was scored with cold air at 15 min and at 3, 7, 10 and 14 days after treatment, there
was a significant (P<0.001) immediate desensitizing effect of the treatment. The
effect was lost between the seventh and tenth day of evaluation. Ho9wever, the
placebo paste burnished on enamel was also effective at reducing sensitivity when
tested immediately, but not at the longer time periods. It was unclear whether the
desensitizing result was due to the presence of NaF, kaolin or burnishing, as none
of these variables were tested separately.
The clinical evidence for the efficacy of oxalate- containing solutions is
mixed. Muzzin and Johnson (1989) conducted a clinical trial over 1- 4 weeks using
cold water as a stimulus. That study revealed that potassium oxalate was effective
immediately after treatment and after 4 weeks, but not at 1 or 2 weeks. The
significance level in this study (P= 0.005) may have been overly rigorous. Cold
water was used rather than air blasts or tactile stimuli. However, another more
77

78. recent clinical trial failed to objectively demonstrate the efficacy of a similar
oxalate dentine desensitizer, or of an Adhesive primer, although the patient’s
subjective impression was that both systems were effective (Gillam et al. 1997).
Air blasts failed to show any severe a stimulus. In vitro studies have confirmed that
oxalates tend to solubilize over time (Pashley, unpublished observations), which
may explain why they lost their effect at the 2- month evaluation period. Another
clinical study by Russel et al. (1997) indicated that an oxalate solution was only
marginally effective.
Imai and Akimoto (1990) demonstrated the effectiveness of a two- step
procedure in which the dentine was saturated with 5% disodium phosphate solution
followed by a sequential application of 10% calcium chloride.
The precipitation of calcium phosphate that is of a particle size small
enough to enter dentinal tubules depends upon the concentration of the reactants,
and especially on their pH (Tung et al.1993). This sequential, two- step approach
to occluding tubules with calcium phosphate has been expanded by the work of
Ishikawa et al. (1994) and Suge et al. (1995a, 1995b). That group has recently
added small amounts of NaF to the solutions to promote conversion of dicalcium
phosphate to apatitic crystals.
Calcium hydroxide paste has long been used to treat hypersensitive dentine.
A clinical trial by Green et al. in 1977 obtained significant desensitization to
thermal stimuli (using a Peltier device) and mechanical stimulation following a 5-
min treatment with calcium hydroxide paste. The desensitizing effect lasted for the
3- month study. Similar results were reported, more recently by Kono et al. (1996).
B. Primers containing HEMA
The use of HEMA- containing primers is gaining popularity. However, few
controlled clinical trials have been done to demonstrate their efficacy. Using a
HEMA primer versus water treated controls, Felton et al. (1991) measured the
sensitivity of the facial surfaces of full crown preparations to tactile, air blast and
osmotic stimuli. The primer, composed of 5% glutaralde-hyde and 35% HEMA in
water, was very effective in reducing dentine sensitivity both in the presence or
absence of the smear layer (P< 0.01). The sensitivity evaluation was measured only
once, 14 days after crown preparation. Similar significant results were obtained by
78

79. Dondi dall ‘Orologio and Malferrari (1993) in a comparison of the desensitizing
effects of 5% glutaraldehyde- 35% HEMA primer with an aluminum nitrate /
glycine (pH 2.5) conditioner. These authors evaluated the degree of
hypersensitivity of cervical roots with air blasts and a dental explorer. The
reductions in sensitivity (P< 0.05 compared with untreated control teeth) lasted for
the entire 6- month trial. However, this excellent result could not be confirmed by
Quarnstrom et al. (1998).
II. Treatment agents that undergo setting or polymerization reactions
A. Conventional glass ionomer cements
One of the first clinical evaluations of the use of glass ionomers for the
treatment of hypersensitive dentine in cervical abrasion lesions was reported by
Low (1981). The cervical lesions were etched with 50% citric acid for 30- 45 s,
then rinsed and dried prior to placement of the glass ionomer cement. Although the
method of evaluating sensitivity was not described and no controls were used, the
author reported complete loss of hypersensitivity in 89.7% of all patients.
B. Resin- reinforced glass ionomers
Hansen (1992) obtained a 1- year success rate of 79% using a resin –
reinforced glass ionomer to treat hypersensitive dentine. This study was discussed
above in the section on varnishes because the comparison was with a fluoride
varnish. These materials should be successful in treating hypersensitive dentine if
they cover the affected area.
C. Adhesive resin primers
Theoretically, the use of Adhesive primers to occlude the open tubules of
hypersensitive dentine looks very thin residual film thickness. The use of Adhesive
resin primer products has been shown to decrease dentine permeability in- vitro
(Simpson et al. 1993). The first clinical trial of the use of primers was done by
Ianzano et al. (1993). In a small pilot study, they treated seven patients with 42
teeth sensitive to air blasts and explorer. Using a no-tech, moist- bonding
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80. technique, six to eight coats of primer were applied in anaesthetized patients. After
evaporating the acetone, the treated surfaces were light- cured for 20 s. Sensitivity
was scored before and immediately after treatment. The patients were asked about
their sensitivity by telephone 1 month after treatment. About one half of the
patients had less sensitivity immediately after treatment. At 9 months, six of the
seven patients were free of pain (P<0.001). There were no untreated control teeth
used in the study. In another small clinical trial, Cagdiaco et al. (1996) covered
dentine exposed during preparations for laminate veneers with one of two primer
products. Postoperative sensitivity was evaluated immediately and 4 days later,
compared with untreated controls, using an air blast. Both primers eliminated
dentine sensitivity in this short study. The dentine was acid- etched prior to
application of one of the primers. However, a full clinical trial of the use of the
acid – etched primer product, done by a different group, could not demonstrate
efficacy at reducing dentine hypersensitivity (Anderson and Powell 1994). One
problem with resins that produce thin films is that atmospheric oxygen may diffuse
into the thin films and interfere with free radical polymerization reactions
(Erickson, 1989). After light curing, unprotected resin films less than 20 µm thick
may remain unpolymerized and would be quickly lost. If thin films of resins are to
be used to treat dentine hypersensitivity, there is a need to develop polymerization
initiators and reactions that are insensitive to oxygen. Thicker resin films are
created using a more recently developed primer system in which the primer and
Adhesive components are mixed together into a single bottle. Russell et al. (1997)
reported some success in using this system to treat cervical hypersensitivity
dentine.
An alternative resin desensitizer has been introduced recently. It is a two-
bottle system; equal volumes of primers A and B are mixed and gently rubbed on
the hypersensitive dentine for 30 s, followed by air – drying. The system contains
oxalic acid and an emulsion of polymethyl- methacrylate copolymerized with p-
styrenesul-fonic acid. The treated surface becomes covered with a layer of polymer
about 5-10 µm thick and some primitive resin tags are formed within open tubules.
The long-term effectiveness of this resin product may be limited by the inability of
the resin tags to bond the walls of the peritubular dentine matrix lining most
dentinal tubules. Only if the peritubular dentine is removed by acid etching to
80

81. expose the collagen fibrils of the surrounding intertubular dentine matrix can liquid
resin infiltrate into the demineralized matrix and hybridize with it.
D. Adhesive resin bonding systems
Jensen and Doering (1987) used a light- cured system to treat root surface
hypersensitivity; the treatment was successful in eliminating sensitivity to air blasts
and explorer in 89% of patients with extreme sensitivity, and in 97% of moderately
sensitive teeth immediately after treatment. Even after 6 months, the treatments
gave 75% and 94% reductions in dentine hypersensitivity, respectively.
In a 6- week study, Javid et al. (1987) evaluated a single application of
cyanoacrylate to hypersensitive root surfaces, and found a significant (P< 0.01)
immediate reduction in sensitivity to air blasts that slowly returned toward
pretreatment values (40% loss of effect) over the subsequent 6 weeks.
Several Japanese papers reported that the use of resin Adhesives reduced
radicular hypersensitivity (Suda et al. 1990, Yoshimine et al. 1991, Yoshiyama et
al. 1991). Although they obtained good results, the investigators did not utilize
statistical analyses or untreated control groups. An important morphological study
was conducted by Yoshiyama et al. (1992) using a hard tissue biopsy technique to
evaluate the long term effects of resin treatment for hypersensitive dentine. Using
a hollow cylindrical diamond bur, the authors biopsy several regions from resin
treated root surfaces 6 months after treatment. Treated regions that exhibited a
recurrence of hypersensitivity were identified and biopsied, as were Adjacent
treated regions that remained insensitive to air blasts. In the regions exhibiting
recurrence of hypersensitivity, 60% of the tubules were patent and free of resin
tags. In contrast, in regions where the treatment had remained effective, over 75%
of the tubules were occluded. However, in all the treated teeth, no resin coating
remained on the surface, indicating that resin desensitization is due to the presence
of resin tags in the tubules (Yoshiyama et al. 1993).
The use of fluoride containing Adhesive resins has been tried as a treatment
for hypersensitive dentine. Orchardson et al. (1993) used multiple applications
(twice weekly for 4 weeks) of a fluoride-containing, light cured resin following
pretreatment of the teeth with a paste containing fine (0.8µm) quartz particles.
They reported no consistent changes in treatment teeth compared to the controls
81

82. over the 4week study. Several patients had some desensitization, which returned
when the resin became detached. The use of the pretreatment paste may have
occluded the tubules with smear layer debris, thereby preventing resin penetration.
Better clinical success was achieved by Tavares et al. (1994) using another fluoride
containing Adhesive resin. Although these authors cleaned the surfaces with a
rubber prophy cup, they acid etched the adjacent cervical enamel with phosphoric
acid. When rinsing the enamel, it is likely that the adjacent dentine was
inadvertently lightly etched as well (Erickson et al. 1992). They used a primer,
followed by the fluoride containing resin. In-group A, sufficient loss of tooth
structure permitted placement of a layer of resin composite over the Adhesive. In
group B, less tooth structure was lost, so no resin composite was placed over the
Adhesive resin layer. Sensitivity was scored with cold (0°C) water before,
immediately after treatment and at 3, 6 and 12 months. Control teeth remained
sensitive. The results revealed highly significant reduction (P<0.0001) in cervical
sensitivity to cold water in the resin treated teeth at all time periods through 6
months, with group A showing lower sensitivity than group B. By 12 months, the
treatment effect was no longer statistically significant due to a rise in the sensitivity
of the control groups and a fall in the efficacy of the treatment groups. Resin
retention was excellent in group A (nearly 100%), but by 6 resin layer. Yet, fewer
than 20% of the subjects in group B reported increased sensitivity levels. The
authors suggested that resin tags may have remained in the tubules even after loss
of surface resin. There is no evidence in favor of the use of fluoride containing
Adhesive resins over fluoride free resins, as these studies did not include the use of
such controls.
In a less well controlled study, Calamia et al. (1996) scored sensitivity to
air blast and explorer prior to and immediately after placement of an Adhesive
system. Postcard replies were used to assess the patients’ subjective sensitivity at
1 and 7 days, but they were objectively evaluated on recall, at 1 and 6 months.
Immediately after treatment, all resin bonded teeth showed much less sensitivity
compared with control teeth (no statistical analyses were done). After 7 days, 29
of 31 treated teeth were less sensitive than controls. After 6 months, 19 of 21 teeth
available at recall showed decreased sensitivity when tested.
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83. Using a recently marketed Adhesive system, Russell et al. (1997) reported
moderate success in desensitizing cervical hypersensitive dentine, using cool water
from a three way dental syringe as a stimulus. They rescored sensitivity at 1 week
and 1 month and reported that 76% of the Adhesive treated patients experienced
improvements in their symptoms over the 1-month study.
In a recent, well controlled study, Ide et al. (1998) evaluated the
desensitizing effects of another Adhesive system. They evaluated sensitivity with
both restricted and unrestricted air stimuli, a Yeaple probe and with cold (10 º C)
water. Subjective response was recorded on a visual analog scale (VAS) and the
short form of the McGill pain questionnaire prior to and 1week after treatment.
Control teeth had bonding agent applied to the middle third of the enamel on the
sensitive control teeth. Their results indicated that the resin treatment of sensitive
root surfaces produced a significant (P> 0.02-0.05) reduction in tactile sensitivity,
subjective sensitivity (McGill questionnaire) and sensitivity to both air stimuli, but
not to cold water. The authors were so impressed with the effectiveness of the
resin treatment that they suggested that it be regarded as the gold standard both for
assessing techniques for estimating cervical sensitivity, and or investigating the
efficacy of professionally applied topical desensitizing agents. It is important to
point out that they did not acid etch the dentine surface prior to application of the
resin, as pilot experiments had shown that this treatment increased dentine
sensitivity.
Other materials that have good potential for treating dentine
hypersensitivity are the self -etching/ self- priming bonding systems. They are
usually two-bottle systems where one drop of primer A is mixed with a drop of
primer B and the mixture is painted on the sensitive surface for 30 s, followed by
gentle air- drying to remove volatile solvent. The surface is then covered with a
thin layer of Adhesive and light cured for 20 s. Re-evaluation of the resin-covered
surface should only be done with air or cold water, as the use of an explorer may
tear the resin and re-expose tubules. Adhesive systems that utilize a separate acid
etching step may open up some tubules that are not covered by the second resin
application step, leaving some tubules open and sensitive. The self-etching
Adhesive systems use an acidic methacrylate monomer dissolved in HEMA that
both etches and primes the surface so that the subsequently applied Adhesive is
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84. more likely to cover the primed surface and occlude all tubules. The disadvantage
of the Adhesive systems is that their polymerization is inhibited by atmospheric
oxygen to a depth of 10-15µ m. If they are over thinned with an air cure even
though Adequate light irradiation is done. This is normally not a problem in
conservative dental treatment where these thin Adhesive layers are covered with
resin composites that exclude atmospheric oxygen and provide additional free
radicals for polymerization. Although the latest generation of Adhesive bonding
systems are hydrophilic and provide better bonds in wet environments, the wetness
should be water, not blood or protein-rich ceveicular fluid which may lower bond
strengths (Xie et al. 1993)
In summary, the effectiveness of Adhesive resins in reducing dentine
sensitivity has improved as bonding techniques and formulations have improved
(Nakabayashi and Pashley, 1998). These materials are somewhat technique
sensitive and care must be taken to avoid creating a rough ledge of resin in the
gingival crevice. Few well-controlled long-term studies have been performed, but
most clinical trials have shown good short term success.
III. Use of mouthguards
The use of a mouth guard-type appliance to deliver potassium nitrate
desensitizing agent was first reported by Reinhart et al. (1990). They had only
partial success in that they obtained a significant reduction in sensitivity only after
2 weeks of treatment, but not 1, 3 or 4 weeks of treatment with 10% KNO3 gel. The
lack of effectiveness of 10% of KNO3 may have been due to the short daily
treatment time of 5 min. They used glycerin to give the KNO3 a gel- like
consistency. These solutions are very hygroscopic and hypertonic. Had the KNO3
been made up as an aqueous solution that was subsequently gelled, the results
might have been better. In an interesting case report by Jerome (1995), a patient
with severe bruxism had developed dentinal hypersensitivity in almost all of his
teeth as a result of loss of enamel and much dentine. To make the patient more
comfortable, a vacuum-formed mouthguard appliance was made and the patient
was instructed to place small amounts of a desensitizing dentifrice containing 5%
KNO3 in the mouthguard for almost 24 hours each day. Within 1 week, the patient
could drink room temperature liquids without wearing the appliance, a feat that had
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85. been impossible prior to treatment. Many clinicians who are bleaching patients
teeth with the ‘mouthguard’ technique report that the sensitivity that sometimes
develops after a few days of bleaching can be successfully treated with 5% KNO3
toothpaste or gel in the same tray (Haywood, 1996). These treatments are usually
done overnight. No controlled clinical trials have been done to confirm the efficacy
of this technique, but it is something that should be considered for patients who
have multiple sensitive teeth that do not respond to conventional treatments.
Controlled clinical trials should be done to test the efficacy of potassium nitrate
gels or pastes when used overnight.
IV. Iontophoresis
SThe in- office use of iontophoresis of NaF to treat hypersensitive dentine
has been Advocated by Gangarosa (1983, 1994) and others (Kerns et al. 1989,
Christiansen 1998). It is a technique- sensitive method that requires the purchase of
an apparatus. Reports of lack of efficacy (Brough et al. 1985) may be due to
inadvertent passage of current through adjacent gingival tissue rather than through
cervical dentine. However, clinicians skilled in iontophoresis are strong Advocates
of its use for this purpose.
Principles: Iontophoresis is the process of introducing ionic drugs in to body
surfaces for therapeutic purposes, and is highly suited to therapy of conditions at or
near body surface. High concentrations of drugs can be placed precisely where
they are needed, rather than depending upon diffusion or systemic Administration.
Iontophoresis requires that: (a) a charged drug be delivered t the electrode of the
same polarity, (b) the condition or disease under treatment be delivered at the
electrode of the same polarity, (b) the condition or disease under treatment be at or
near the surface and (c) a modern, sophisticated source of direct current, with
appropriate means of application, be used. This current source must have features
that make it not only effective but also safe (Gangarosa and Jeske, 1992)
Medical and dental uses: Iontophoresis has a long history of use, having been
suggested for various therapies for many years in medicine, physical therapy and
dentistry. The reader is referred to reviews of the extensive literature on
iontophoresis (Harris, 1959; Gangarosa, 1983; Sloan and Soltani, 1986; Tyle,
1986.
85

86. Use of iontophoresis in desensitization: Iontophoresis with sodium fluoride
solutions was proposed as a method of treating hypersensitive dentine by research
from the 1950s to 1970s (reviewed by Murthy, Talim and Singh, 1973; Gangarosa,
1983). Murthy et al. (1973) reported the effectiveness of fluoride iontophoresis in
a double blind, controlled clinical trial. They compared iontophoresis of sodium
fluoride to a placebo (iontophoresis of the patient’s saliva) and concluded that 1%
fluoride iontophoresis provided a statistically (p<0.01) more effective treatment
than placebo or topical applications; the desensitization occurred immediately after
iontophoresis in most patients, whereas the placebo was ineffective. Also the
burnishing of 33% topical fluoride paste was only modestly effective.
Gangarosa and Park (1978) demonstrated highly consistent desensitization
using 2% neutral sodium fluoride iontophoresis. The study compared cathodal (-)
fluoride application as a positive control, and also to cathodal fluoride
iontophoresis was effective (defined as no retreatments required) for all teeth
classified as having severe, dentine exposure; however, 35% of teeth with
intolerable sensitivity (pain lasting up to 15 s after the stimulus) required
retreatments. Anodal fluoride iontophoresis produced an immediate reduction in
the sensitivity score in 80% of the teeth, but this was short- lived and required
retreatment. Cathodal saline iontophoresis caused increased sensitivity in three
subjects; this required discontinuation of the saline control in the study but the
increased sensitivity could be reversed with fluoride iontophoresis.
Later, Lutins, Greco and McFall (1984) investigated whether fluoride
iontophoresis as specified by Gangarosa (1983) would be effective in a controlled
clinical trial using a quantifiable testing method (a thermal probe0. Two treatments
with 2% neutral sodium fluoride iontophoresis were given 1 month apart. The
control was two topical treatments with the same solutions and procedures but with
no current applied. Teeth that were treated with fluoride iontophoresis showed
80% desensitization, which was statistically better than the 50% improvement in
topically, treated teeth. In a more recent, double-blind evaluation at 4 months and
14 months after treatment, Gangarosa et al. (1989) made a longitudinal study of
teeth treated by dental by dental students at their first practice session (see also
Chen, Morihana and Gangarosa, 1994; this issue). The desensitization effect was
not only immediate, but the teeth showed continuing desensitization at both
86

87. double- blind evaluations. A few of the severe and intolerable hypersensitivities
had to be retreated after the 4-month evaluation in order to achieve continuous,
long lasting desensitization. Another double- blind controlled clinical trial of
fluoride iontophoresis (Kern et al. 1989) was on teeth that were still sensitive 6
months after periodontal surgery. The teeth were stimulated with controlled tactile
pressure (Vine probe) and a controlled air-blast and the patient’s subjective
response was also recorded. They controlled that iontophoresis was statistically
better (p> 0.0005) than the placebo in reducing all three measured variables.
In the scheme of gradually increasing complexity of therapies for
hypersensitivity, iontophoresis represents an intermediate stage between topical
agents and resin bonding, since the sensitivity may be effectively treated without
the necessity of a restoration. Like composite use, however, iontophoresis
techniques are operator sensitive. Since almost all dentists are well versed in
composite application, and iontophoresis has not been routinely taught by dental
schools nor, as yet, Adopted by a significant number of dentists, it appears that the
third generation resin systems offer the best method of choice for generalized in
office treatment if topical treatment fail.
V. Lasers
Another in office management for hypersensitive dentine is the use of
lasers. Although there are a number of anecdotal reports of the efficacy of lasers
for treating hypersensitive dentine, only two clinical trials have been published.
Renton –Harper and Midda (1992) evaluated an Nd:YAG laser to treat patients
with cervical sensitivity to cold air. Treated roots were lased for 2 min at 10
pulses/s at increasing power levels until the patient detected the laser energy or
until a maximum of 100mJ was reached. Although they included sensitive control
teeth in the study, the treatment was not blinded to the clinician or the patient,
although assessment of sensitivity on recalls blinded. Treated to air ( P=0.05)
immediately after treatment and at 3, 7 and 14 day recalls. The second study was
less well controlled and reported desensitization by a very low power helium-neon
laser that was used for aiming the Nd:YAG laser ( Gelskey et al.1993), as well as
by the Nd:YAG laser. The presumed mechanism of action is the coagulation and
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88. precipitation of plasma proteins in dentinal fluid. It is also possible for the thermal
energy to alter intradental nerve activity (Orchardson et al.1988).
TREATMENT CONSIDERATIONS FOR CERVICAL DENTIN
SENSITIVITY IN ASSOCIATION WITH LOST TOOTH
STRUCTURE
If, however, the patient has lost tooth structure at the cervical area and
presents with dentin sensitivity, the best treatment is the use of restorative
materials. Restorative treatment of cervical dentinal sensitivity can be successfully
accomplished using any currently marketed third generation dentin bonding agent
or glass ionomer cement. The newer light cured glass ionomer cements are easy to
work with and have been used to successfully treat dentin sensitivity, although the
esthetics are not as good as can be achieved with dentin bonding resins followed
by a veneer of composite resin. These newer products are technically more
difficult to place and finish without inadvertently exposing more sensitive. If one
performs the restorative procedure on an unanesthetized patient (which is desirable
because one can immediately evaluate the desensitizing effectiveness of the
restoration), the patient may complain of a “stinging pain” when the bonding
agents are applied in sequence, as most of them are hypertonic. This stinging will
disappear after bonding.
The use of restorative materials to treat dentin sensitivity requires more
time and is more expensive, but it is also more long lasting and predictable. If
patients have moderate to severe sensitivity in multiple teeth with minimal loss of
tooth structure, clinicians should consider the use of topical agents such as oxalates
or fluorides. If one or two teeth remain sensitive after such treatment, they can
then be treated with restorative resin materials. The easiest materials to use are
those resins designed to flow into and occlude dentinal tubules without
accumulating on the surface. This approach was popularized by a number of
investigators.
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89. TREATMENT CONSIDERATIONS FOR BLEACHING
ASSOCIATED SENSITIVITY
If the patient has previously bleached their teeth with the nightguard vital
bleaching technique, then the custom-fitted tray can be used as the carrier for the
anti sensitivity toothpaste. If the patient is not a candidate for bleaching but has a
history of chronic sensitivity, then non-scalloped, no reservoir designed tray can be
fabricated. If it is unclear whether this approach will benefit the patient, a less
involved technique may be tried that uses a direct thermoplastic tray made directly
in the patient’s mouth without an alginate impression, stone cast and laboratory
exercise. While this tray is more rigid, it is a quick means for determining the
efficacy of a tray-applied medicament such as toothpaste or fluoride gels.
Much has been learned about tooth sensitivity with the Advent of at home
bleaching. Nightguard vital bleaching applies a 10 percent carbamide peroxide
material in custom fitted tray overnight for 2 to 6 weeks. Although some claims
have been made for nightguard bleaching products that do not induce sensitivity,
double blind clinical studies have shown that sensitivity occurs in 55 percent to 75
percent of treatment groups with placebo groups experiencing sensitivity in 20 to
30 percent of subjects. One study even reported tooth sensitivity of about 15
percent in subjects wearing only the bleaching tray. Therefore, it appears that this
kind of sensitivity is a multi factorial event that cannot be totally avoided because
it is not exclusively related to the peroxide whitening materials.
One option to address this type of sensitivity is to try to predict which
patients will become sensitive. However, the only significant predictors
determined thus far are a previous history of sensitive teeth and a regimen of more
than one application of the bleaching solution per day. Moreover, the 2-6 month
treatment time for the complete management of tetracycline stained teeth has
demonstrated just how sporadic the sensitivity is some patients.
Since tooth sensitivity during bleaching is common, yet unpredictable, it
must be addressed clinically when it occurs. Often the sensitivity experienced is
‘mild’ and required no alteration in the treatment protocol. In cases where it
cannot be ignored, the dentist may have to instruct the patient to decrease the
frequency (typically, to every other day) and duration of treatments. When this
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90. protocol fails, some practitioners advocate the use of topical fluorides in
conjunction with the beaching treatments. Others recommend using desensitizing
toothpaste for 2-3 weeks prior to initiating as well as during bleaching. Persons
experiencing nighttime sensitivity may switch to daytime wear and reduce contact
time of the peroxide to 2-4 hours. In severe cases patients may have to stop
bleaching for a few weeks or even altogether.
The advent of tray delivered desensitizing agents containing potassium has
greatly aided the dentist in taking a more active approach to managing sensitivity
and affords patients a simple effective means to control their treatment. The
bleaching study demonstrates the efficacy of 10-30 minute applications of the
desensitizing material, used as needed (one time only, once a week, continuous
before each bleaching treatment, or alternated with bleaching treatments.
Patient complains of tooth sensitivity
Evaluate factors which influence treatment
Age Diet
Previous dental history Radiographic findings
Habits
Test for sensitivity
1. Explorer
2. One sec. Blast of air
3. Ethyl chloride on cotton pellet
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91. TREATMENT PLAN
Objective: Relieve discomfort/Prevent decay
Cervical sensitivity
1. Potassium or ferric oxalates
2. F1 dentifrice Recent filling
3. 0.4% SnF2 gel 1. 0.4% SnF2 gel
4. Iontophoresis 2% NaF 2. Line cavity and
5. Glass ionomers and/or composites Replace filling
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92. SUMMARY AND CONCLUSION
Up to 90% of patients suffering from Dentin Hypersensitivity claim that in
particular a cold stimulus causes the painful condition, whereas a tactile stimulus
affects up to10 per cent of patients
Assisting the patient with educational advice, including the role of
desensitizing dentifrices containing either strontium salts (chloride or acetate) or
potassium salts (chloride or nitrate) will be of valuable help in all cases of slight
to mild sensitivity, although the actual mode of action remains unclear, and there
are some conflicting results if compared to control tooth-pastes. These
preparations can also be used with mouth guards (e.g. for treatment of multiple
hypersensitive teeth or DH developing after vital bleaching therapy) to occlude
dentinal tubules (strontium salts) or modulate nerve excitability (potassium
salts).
With moderate severity, varnishes or lacquers containing highly
concentrated fluorides can be used successfully. Follow –up care, accompanied
by re instruction and continued home-use of desensitizing toothpastes meeting
the patient’s general demands (e.g. fluoride prophylaxis, whitening, tartar
control, flavor), will keep the patient free of pain. Moreover, in these cases
presumably sclerotic dentine will be stimulated, thus rendering the tooth in a
more or less natural state. The described treatment regimens can be classified as
‘reversible’ or ‘non-invasive’; if this simple therapy does not succeed; a more
complex but more effective and escalating therapy should bi preferred19.
This is also true in cases of severe hypersensitivity in particular if DH is altering
the patient’s lifestyle (e.g. changes in eating/ drinking behavior, or hampering
sport activities). Then the treatment should be (‘semi-) invasive’ including the
use of agents that set (e.g. glass ionomers) or polymerize (e.g.
photopolymerising sealants, or Adhesive resin bonding systems) to occlude the
dentinal tubules. In a few cases of pronounced severity and gross substance loss,
‘invasive’ therapy by means of crowns may be indicated; thus endodontic or
even exodontics can be avoided.
It is clear that there are a number of in-office treatments available for
hypersensitive cervical dentine. The use of restorative materials is more effective
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93. than the use of topical agents, but they require the loss of some tooth structure
and they require more treatment time. Self-etching, self-priming resin Adhesives
are the simplest resin systems to use, but there have been no published clinical
trials of their efficacy for that application.
Clinicians are urged to become familiar with these in -office products so
that they can develop escalating in -office treatment approaches that are effective
for mild, moderate and severe cases of hypersensitive dentine.
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