Dentin hypersensitivity/orthodontics courses

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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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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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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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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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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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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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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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
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900 micrometer near
the D.E.J
1.2 micrometer in the
middle
2.5 micrometer near
the pulp

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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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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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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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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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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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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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
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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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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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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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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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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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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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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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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.
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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.
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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.
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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

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

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

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

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

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

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
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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

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

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

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

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

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.
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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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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