Dentine hypersensitivity:

preventive and therapeutic

approaches to treatment
NI COLA X. WEST
Many individuals are affected by the oral pain
condition of dentine hypersensitivity. For the
majority of suffers the pain is episodic and, although
sharp in nature, is short in duration and hence
annoying, but bearable. Measures such as avoiding
cold running water when tooth cleaning and taking
care when breathing in air on cold, frosty winter
mornings, are often adopted. For less fortunate
individuals the pain is far more severe, lasts for hours
or days and interferes with day-to-day activities and
pleasures.
One of the earliest citings of dentine hypersensi-
tivity dates back to Blum in 1530 (11). However, it
was not until 1700 that this oral pain condition was
more extensively investigated (23). Data docu-
mented in the UK Adult Dental Health Survey of
1998 showed that there is an increasing life expec-
tancy of the western population who have a func-
tional natural dentition (64), which will be prone to
toothwear. It is not unreasonable to suggest that the
incidence of dentine hypersensitivity is therefore
likely to become a more frequent dental nding in
the future. This is supported by Zero & Lussi (98),
who state that following the decline of tooth loss in
the 20th century, the increasing longevity of the
teeth with tooth wear in the 21st century will be far
more demanding on the preventive and restorative
skills of the dental professionals. Similarly, the
continued high prevalence of periodontal disease in
a population retaining their teeth for longer is likely
to lead to greater numbers of teeth with recession as
a result of both disease and treatment. Thus, it
would not be surprising if general dental practioners
noted an increase in cases of dentine hypersensi-
tivity and a rise in requests for treatment in the
foreseeable future.
Denition and prevalence
Characteristic pain arises from exposed dentine typ-
ically in response to a variety of stimuli, for example,
thermal, evaporative, tactile, osmotic or chemical,
which cannot be ascribed to any other form of dental
defect or pathology (19). A modication to this de-
nition was suggested by the Canadian Advisory Board
on Dentine Hypersensitivity in 2003, who suggested
that disease shouldbe substitutedfor pathology (13).
When dental professionals examine patients for
dentine hypersensitivity, the most consistent gure
documented is 15% (24). However, the reported
prevalence for dentine hypersensitivity varies from 3
to 57% (25, 29, 45, 44, 54, 61, 73). Dentine hypersen-
sitivity can present from early to old age, with the
majority of sufferers aged between 20 to 40 years (29).
Later in life, age-related changes in pulpal processes
result in a reduction of sensitivity owing to reparative
processes, such as secondary dentine and tertiary
dentine, brosis in the pulp and sclerosis of the tu-
bules, whichwill decrease permeability andreduce the
hydraulic conductance of dentine. Women are more
frequently affected and at a younger mean age (25, 4),
although with any medical condition more women
tend to present than men. Different professionals also
report different perceived levels of dentine hypersen-
sitivity in their patients, with hygienists reporting
twice the level perceived by dentists (Canadian Advi-
sory Board on Dentine Hypersensitivity 2003) (13).
Pain mechanisms
A number of theories have been proposed over the
years to explain the pain mechanism of dentinal
31
Periodontology 2000, Vol. 48, 2008, 3141
Printed in Singapore. All rights reserved
2008 The Author.
Journal compilation 2008 Blackwell Munksgaard
PERIODONTOLOGY 2000
hypersensitivity. An early hypothesis was the dentinal
receptor mechanism theory, which suggests that
dentine hypersensitivity is caused by the direct
stimulation of sensory nerve endings in dentine. On
the basis of microscopic and experimental data, it
seems unlikely that neural cells exist in the sensory
portion of the outer dentine (42). This theory is not
well accepted. The odontoblast transducer mecha-
nism proposed by Rapp et al. (72) suggested that
odontoblasts act as receptor cells, mediating changes
in the membrane potential of the odontoblasts via
synaptic junctions with nerves. This could result in
the sensation of pain from the nerve endings located
in the pulpodentinal border; however, the evidence
for the odontoblast transducer mechanism theory is
generally lacking and inconclusive.
The currently accepted hypothesis is the hydrody-
namic theory. Brannstrom (12), working on Gysis
hypothesis (34) that dentine hypersensitivity may be
caused by movement of the dentinal tubule contents,
suggested the hydrodynamic theory of sensitivity. An
increased outward uid ow causes a pressure
change across the dentine, distorting the A-d bres by
a mechanoreceptor action, causing sharp, shooting
pain (90). There may also be another process
involved, because when uid ow changes rate in
a tubule there is an electrical discharge called
streaming potential across the dentine. This may be
able to stimulate nerves electrically.
The width of the tubule is very important, as the
rate of uid ow is dependent on the fourth power of
the radius. If the tubule diameter doubles, a 16-fold
increase in uid ow results (33). Sensitive teeth have
many more (8) and wider (2) tubules at the buccal
cervical area compared with nonsensitive teeth (2). A
higher velocity of uid ow also occurs in tubules of
smaller diameter, possibly provoking pain sensations.
Dentine will only be sensitive if the tubules are patent
from the pulp to the oral environment, and this pa-
tency will change with production and removal of the
smear, hence resulting in an episodic condition (2).
The trigeminal nerve supplies the pulp, with
innervation from myelinated bres (A-b and A-d) and
nonmylinated C bres (58). It is proposed that the
larger myelinated bres (A-b and some A-d) can re-
spond to stimuli that displace the uid in the dentinal
tubule through a hydrodynamic mechanism, such as
tactile, evaporative, osmotic or thermal challenges, to
elicit short, sharp, stabbing pain that typically lasts
for only a few seconds.
The classical pain experienced with dentine
hypersensitivity can persist as a dull, throbbing ache
for variable periods of time (88). Dentine hypersen-
sitivity sufferers can readily be divided into two
groups: those who just have the sharp, shooting pain
and those who have the subsequent dull, aching pain.
The poorly localized, dull, burning ache is thought to
be caused by unmyelinated nerves, C-bres and some
of the slowest A-d bres (63). Vasoactive polypeptides,
such as plasma kinins, calcitonin-gene-related pep-
tide, neurokinins and substance P, are found in, for
example, C bres. After possible injurious stimuli to
the odontoblasts, it is possible that polypeptides may
be involved in the regulation of neural transmission
mediated by the C-bres (62), triggering inamma-
tory reactions (66), termed neurogenic inammation
(51). This pain is a dull, throbbing, aching pain that
typically lasts for hours. These nerves are not excited
by the hydrodynamic mechanism.
The status of the pulp in dentine hypersensitivity
is not known, although symptoms would suggest
minor inammation as a result of the length of time
that symptoms persist without developing into a true
pulpitis. It has been suggested that when the pain
continues as a throbbing ache then a true pulpitis is
present. Another term, root sensitivity, has been
suggested by the 2002 Workshop of the European
Federation of Periodontology (78) for dentine hyper-
sensitivity arising from gingival recession in perio-
dontal disease and following periodontal treatment.
This group of patients may have microorganisms
invading the root dentinal tubules of periodontally
involved teeth (7), with pain often occurring inter-
dentally, coinciding with recession in these areas.
Hence, this condition may be of different etiology but
results in similar pain symptoms.
Preventive management strategies
for dentine hypersensitivity
Dentine hypersensitivity results from dentine ex-
posed from either coronal or radicular regions of the
tooth. Preventive measures must therefore be pri-
marily aimed at reducing the risk of exposing dentine
either as a result of the removal of enamel, usually
caused by erosion, or the removal of cementum,
most often attributed to either overzealous tooth-
brushing in a healthy mouth or periodontal disease
and or treatment.
Exposure of dentine as a result of loss of
cementum: gingival recession
Marginal tissue recession is the displacement of the
soft tissues apical to the cementoenamel junction to
32
West
expose the radicular tissue. Gingival recession is a
common nding both in populations with high
standards of oral hygiene (79, 81), as well as in pop-
ulations with poor oral hygiene (9, 52). The former
type of recession can be attributed to overzealous
toothbrushing and is predominantly found on the
buccal surfaces of teeth (78). The latter type of
recession is seen in periodontal patients both exhib-
iting the disease and following treatment. These le-
sions can be found anywhere around the root (97).
Dentine hypersensitivity can be attributed to both
types of recession but is most frequently associated
with recession of the healthy gingiva. The two etiol-
ogies result in the same pain condition; however,
they should be treated differently in terms of pre-
vention, etiology and research. Recession linked to
periodontal disease is often termed root sensitivity.
There are few data on gingival recession identifying
toothbrushing as an etiological factor (47), making
the evidence circumstantial rather than factual.
Healthy gingival recession shows side, site and tooth
number distributions that coincide with toothbrush-
ing habits and handedness (5). Furthermore, teeth
and tooth surfaces that receive most brushing during
the brushing cycle overall show the highest predi-
lection for recession with a more common incidence
on the left side where a high majority of subjects are
right handed (5). Plaque scores derived from epide-
miological and clinical studies also correlate with
sites of gingival recession and dentine hypersensi-
tivity, coinciding with the lowest plaque scores (5). To
conrm this etiology of gingival recession, a ran-
domized controlled clinical trial is needed.
It has been suggested that recession will increase
over time with the use of abrasive toothpastes, to-
bacco and frequent brushing with or without a
toothpaste; however, the data are limited (86).
Interestingly, the evidence for tobacco as an etiolog-
ical agent is mixed (32, 60).
Toothbrushing appears to be intimately linked to
recession associated with dentine hypersensitivity.
Further work in needed to investigate the relationship
between toothbrushing habits, force, duration of
brushing, frequency, lament characteristics and the
role of the toothpaste. Prevention should thus focus
on improving toothbrushing skills and possibly
investigating the toothpastes particularly the abra-
sivity characteristics and other constituents that may
play a role in the etiology of recession. Prevention,
early recognition and treatment of periodontal dis-
ease should also be a priority, and stringent efforts
ought to be made to control periodontal diseases that
are still commonplace amongst adults in the UK (59).
Exposure of dentine as a result of loss of
enamel
Tooth wear has attracted much attention in the dental
literature over the last decade. Tooth wear is usually
multifactorial with one type of wear dominating; in-
deed, it is highly likely that there is an interaction
between at least two of these processes which leads to
the wear of hard tissue. Erosive tooth wear, in partic-
ular, is becoming increasingly signicant to the lon-
gevity of the dentition. Lifestyles have dramatically
changed the consumption characteristics of soft
acidic drinks, and healthy (often acidic) diets are
prominent in the media. Emphasis on preventive
dentistry has also increased, with the population
spending more effort on oral hygiene practices, which
can result in the increased prevalence of tooth wear.
Enamel is highly susceptible to acid erosion, which
is probably the most aggressive type of wear com-
pared with abrasion and attrition. The acid may be
derived from intrinsic, gastric, or more often, extrin-
sic, sources that are dietary in origin. Evidence drawn
from studies in situ reveal that individuals who
consume 1 l of soft drinks per day, which is not
uncommon, can lose 1 mm of enamel over 2
20 years (37). The wide range of enamel loss is the
result of individual susceptibility to acid erosion.
When an acid comes into contact with the tooth, not
only is there bulk loss of the hard tissue but also
softening of the remaining surface (21). In vitro re-
search has shown that surface softening can extend
35 microns and be susceptible to loss after a few
brush strokes (22). So, if the erosive challenge is fol-
lowed soon after with the abrasive challenge, the
softened hard tissue will be easily removed and has
no chance to reharden. This scenario is depicted well
in an individual having a grapefruit for breakfast
followed by brushing their teeth with brush and
toothpaste. So, an important message for these pa-
tients is do not brush your teeth straight after an
acidic challenge. How long to wait is a debatable
issue, but at least half an hour would seem prudent.
The in vitro studies indicate that for optimal pro-
tective effects against erosion, a salivary pellicle
should be allowed to form for 1 h for enamel and
possibly less than 1 h for dentine (95). Saliva from
different sources offers differing protection against
acid erosion of enamel and dentine (95). An erosive
challenge preceding the action of the oral muscula-
ture must also not be underestimated. An in situ
study (31) demonstrated the abrasive nature of the
tongue on both softened enamel and dentine
following exposure to soft acidic drink.
33
Dentine hypersensitivity
Dentine is more susceptible to erosion than
enamel and shows the same irreversible loss and
surface softening (89, 90). Acidic drinks, including
carbonated drinks, wine and herbal teas, will
remove the smear layer and expose tubules (1).
Acidic mouthrinses have also been shown to cause
erosion (70), as have toothpaste detergents in vitro
(94).
The role of abrasion alone, with and without
toothpaste, has been studied particularly in in vitro
work. A toothbrush alone has no measurable effects
on enamel loss and has minimal loss on dentine if a
normal twice-a-day regimen is followed (38). Tooth-
pastes have to comply to relative enamel abrasivity
and relative dentine abrasivity values for the market
place, which are determined by the International
Standards Organizations Standard for toothpaste
methodology (43). Most toothpaste will contribute
little to hard tissue loss if used in a twice-a-day
manner. However, many dentine hypersensitivity
suffers will brush their teeth in excess, up to ve
times a day (92). For these individuals, brushing
instruction is necessary, and a low abrasive paste
may be advocated.
Attrition may result in colossal sensitivity as a
result of parafunctional activity. Interestingly, an
in vitro study showed that enamel attrition was
markedly reduced in an acid environment, as a result
of the smoothness of the contacting surface (22). The
combination of abrasion and attrition has been the
subject of case report data which infer that an indi-
vidual with attrition habits, who chews a coarse diet,
may enhance tooth wear (22).
In summary, evidence strongly suggests that den-
tine hypersensitivity lesions can be localized through
dentine exposure by the effects of toothbrushing and
gingival recession, by erosion alone, or by combined
erosion abrasion.
The episodic condition of dentine
hypersensitivity
For dentine hypersensitivity to occur, not only does
the dentine need to become exposed (lesion locali-
zation) and but the tubules need to be patent to the
pulp (lesion initiation). Many people have dentine
exposed to the oral environment owing to loss of
cementum and or enamel, but clinical experience
indicates that only a proportion of those people suffer
from dentine hypersensitivity (5). In vitro studies
indicate that erosion from acidic soft drinks causes
rapid loss of the smear layer resulting in the wide
opening of tubules (1), and similarly most tooth-
pastes readily remove the smear layer to expose
tubules (1, 92). However, toothbrushing can also re-
place the smear layer (1), creating a dynamic envi-
ronment.
Preventive management strategy
summary
prevention needs to be aimed at reducing the risks
of etiological factors for dentine hypersensitivity.
regular advice on toothbrushing techniques and
oral healthcare products should be given.
periodontal disease screening should be a pre-
requisite of dental examinations.
periodontal treatment should be instigated swiftly,
when needed, followed by regular supportive
periodontal therapy.
sufferers should be advised to limit the frequency
of soft acidic drinks and not brush their teeth
directly after an acidic intake.
a diet history over three nonconsecutive days
needs to be recorded and careful note made in the
medical history when extrinsic erosion is sus-
pected.
night-time splints can be worn to limit wear from
parafunctional habits.
Therapeutic management
strategies for dentine
hypersensitivity
Clinical experience suggests that the professional
approach to treating dentine hypersensitivity has
been based on results of treatment rather than
addressing the etiological and predisposing factors
that created the problem. Hence, an array of products
is available to professionals formulated to treat
dentine hypersensitivity, many showing equivocal
efcacy.
Reviewing clinical trials of dentine hypersensitiv-
ity helps to explain this conundrum. Although the
majority of recently published clinical trials conform
to Good Clinical Practice (40), the protocols for
comparing different agents are not standardized,
resulting in numerous variables to be compared. A
paste with an active agent may be tested against its
base paste, a conventional uoride paste or another
paste with an active agent. Treatments rarely take
into account etiological factors, and the measure-
ment of pain is difcult to standardize between
individuals owing to its subjective nature. Further-
34
West
more, complicating factors, such as the placebo
effect, Hawthorn effect, regression to the mode and
control product effect, compound the interpretation
of clinical ndings and hide the true effect of the
treatment. In a study by West et al. (93), the pla-
cebo effect was shown to be 40%, reducing the
symptom range available to show signicance for
the agent tested. The clinical efcacy of many of the
current products tested also appears to be at the
lower end of the therapeutic range. This may be a
result of the low success rate of the agent reaching
the target site, a lack of sensitivity of the clinical
trial, a lack of understanding of the patients inter-
pretation of the pain-evoking stimuli, the recovery
time between repeated stimulations, clinician
patient relationship or indeed the potency of the
active agent (16). A recent study showed than when
assessing subjects response to pain-evoking stimuli,
perception of pain appeared to be altered by sen-
sory factors, prompting a heightened pain response
(3), which compounds analysis of pain interpreta-
tion further.
Differential diagnosis
Prior to advocating treatment regimens it is impor-
tant to consider conrmation of the correct diagnosis
and exclude the differential diagnosis. A number of
other dental conditions can give rise to pain symp-
toms similar to those of dentine hypersensitivity.
Indeed, a denitive diagnosis of dentine hypersensi-
tivity is reached through exclusion of the following
conditions, which need a variety of treatment options
for resolution.
cracked tooth syndrome, often in heavily restored
teeth.
incorrect placement of dentine adhesives in
restorative dentistry, leading to nanoleakage.
fractured restorations and incorrectly placed den-
tine pins.
pulpal response to caries and to restorative treat-
ment.
inappropriate application of various medicaments
during cavity oor preparation.
lack of care while contouring restorations so the
tooth is left in traumatic occlusion.
palatogingival groove and other enamel invagin-
ations.
chipped teeth causing exposed dentine.
vital bleaching.
Great care must be given in diagnosis of the condi-
tion to exclude all other dental defects and pathology,
as these can give rise to a similar pain (18).
Clinical examination for dentine hypersensitivity
would include objective assessments, such as
mechanical tactile stimuli, for example running a
sharp explorer over the area of exposed dentine; and
thermal stimuli, for example using a hot or cold
stimulus or an evaporative stimulus, such as a blast of
cold air from the triple syringe. The teeth on either
side of the tooth under investigation should be iso-
lated so that no referred pain is detected. The out-
come for the stimulus to aid diagnosis is a short,
sharp pain for the duration of stimulus application. If
a few stimuli are used to help to achieve a diagnosis,
the order of application should be that which causes
the least to the most amount of pain. Often individ-
uals will not respond to all types of stimulus, but
classically clinicians will use the evaporative stimulus
only. Repeated testing should be avoided as it is not
known how long it takes to reach threshold evalua-
tion.
One of the common pain conditions that can be
confused with dentine hypersensitivity is the cracked
tooth syndrome. It can be extremely difcult to see
the early crack, and the pain symptoms of a cracked
tooth and of dentine hypersensitivity are very similar.
Transillumination and the aid of a microscope mag-
nication can be of great value, but vitality testing
will not separate the pain conditions; both should
yield positive responses. Radiographs should be ta-
ken of the teeth in question and all other types of
pathology excluded. However, unless the crack is
perpendicular to the radiograph lm, again it is dif-
cult to separate the two conditions. A determining
factor for differential diagnosis is that the pain of
cracked tooth syndrome tends to be on the release of
pressure rather than with increased occlusal pressure.
A tooth sleuth can be employed for this purpose.
Furthermore, the history of other teeth and the
number of teeth affected is valuable information for
the clinician. Dentine hypersensitivity rarely affects
one tooth, unlike the cracked tooth syndrome.
For dentine hypersensitivity to occur, dentine must
be exposed and a number of tubules need to be
patent from the oral environment to the pulp. Clini-
cally exposed dentine is often clearly visible. How-
ever, occasionally teeth with this condition show
minimal or no obvious signs of exposed dentine. For
conrmation of open tubules, a silicone-based
impression can be taken and the replica examined
under the electron microscope.
If the pain persists after all other pathology is
diagnosed and treated, dentine hypersensitivity can
be conrmed and the second line of treatment
strategy embarked upon.
35
Dentine hypersensitivity
Professional and home-use treatment
Two treatment modalities are used in the treatment
of dentine hypersensitivity: alteration of uid ow in
the tubules, and modication or blocking of the
pulpal nerve response. Toothpaste constituents, such
as silica abrasives (6) or active agents, have been
proposed to occlude tubules. Surface barriers, such
as varnishes, dentine-bonding agents, composite
resins, glass ionomer cements and compomers, can
also be professionally applied. The effectiveness of
the tubular occluding agents will depend on their
resistance to removal. In vitro results demonstrate
that a number of agents can occlude tubules, but this
does not necessarily correlate with the in vivo situa-
tion when there must be resistance to the oral chal-
lenges of day-to-day activity. Occluding materials can
be washed from the tubule, or may be acid labile.
Wear can also occur, abrading the surface of, for
example, a dentine-bonding agent or a glass ionomer
after a couple of months.
Desensitizing agents, such as potassium ions, may
reduce intradental nerve excitability by diffusion
along the tubules, thereby raising the concentration
of local extracellular potassium ions and hence
blocking intradental nerve function (55). This
hypothesis is based on animal experiments and has
not been conrmed on human teeth where the dif-
fusion distances are greater (67) and where there is a
continual outward ow of dentinal uid to the oral
environment (90), which tends to oppose any inward
diffusion (65). Physical methods, such as endodontic
treatment or extraction, are obviously methods that
are permanently effective at stopping pain from
dentine hypersensitivity.
Conclusive evidence of superiority claims for suc-
cessful treatment regimens still eludes the dental
profession, despite the fact that a multitude of
products are available for treatment. This is a result
of the complexity of pain assessment and the nature
of the episodic disease process, which prevent iden-
tication of a superior treatment regimen.
Treatment for dentine hypersensitivity can be
administered professionally, or for use at home,
depending on the degree of the problem and the
dentist patient preference. Home treatment usually
involves toothpastes and mouthwashes and is by far
the easiest method of administering treatment. It is
also fairly inexpensive. A wide range of commercially
available products are manufactured for self-treat-
ment. Current products in the marketplace include
potassium, strontium, oxalate and uoride salts
combined in toothpastes, gels and mouthrinses.
Toothpastes
The mode of action of toothpaste can be either tubule
occlusion or nerve stabilization. Potassium salts are
now the most commonly used agents in pastes; other
salts frequently used are nitrates, chloride, citrates
and oxalates. Studies on potassium toothpastes by a
number of authors have demonstrated a signicant
benet of a potassium-based paste over a control
paste (77, 83, 80, 91, 14), although other studies failed
to show these benecial effects (26, 93). The impli-
cation of the placebo effect must not be underesti-
mated, with the control product showing efcacy,
clearly demonstrated in the study of Yates et al. (96).
Strontium salts have dominated the market of
desensitizing pastes for the last 30 years and have
therefore been subjected to most methods of testing
for efcacy (46). Overall, the studies demonstrated an
improvement in patients perception of pain; how-
ever, it is important to compare intergroup differ-
ences, not intragroup differences (27, 68, 26, 82, 93).
In conclusion, analyses of these studies demonstrate
that strontium salts have equivocal benecial effects
at reducing dentine hypersensitivity under these trial
designs. The theory behind incorporating strontium
salts in toothpastes derives from the ability of the salt
to have a considerable afnity for dentine owing to
the high permeability and possibility for absorption
into or onto the organic connective tissues and the
odontoblast processes (75). Work in vitro with the
strontium acetate toothpaste has been very promis-
ing, the silica abrasive achieving good tubule occlu-
sion of etched dentine as a result of the silica abrasive
(4, 92, 10). Even more exciting was the nding that
the silica layer was not removed on rinsing (10).
Unfortunately, these properties have not been
demonstrated clinically with the same success in the
treatment of dentine hypersensitivity.
The mode of action of oxalates has been proposed
as tubule occlusion by oxalate ions reacting with
calcium ions in the dentinal uid to form insoluble
calcium oxalate crystals (30). A recent in vitro study
by Suge et al. (85) evaluated the effects of pre-appli-
cation or post-application of calcium chloride on
enhancing the occluding ability of potassium oxalate.
However, the results showed no signicant treatment
effect as a result of calcium-enhanced uptake. In vitro
work has shown that while oxalates result in good
tubule occlusion, they are acid labile and can be
easily washed from the surface of dentine (6).
It has been suggested that uoride may eventually
mechanically block the tubules, or that labile uoride
36
West
in the organic matrix of the dentine could block the
transmission of stimuli. The former view would
support Brannstroms hydrodynamic theory (12) and
was also favoured by Greenhill & Pashley (80). More
recent ndings suggest that sodium uoride is
superior to sodium monouorophosphate regarding
uoride deposition on the teeth (20). It is interesting
to note that dentine hypersensitivity is still a large
problem where populations use uoridated tooth-
paste and live in uoridated water regions. This may
be a result of a problem with the delivery system (19)
or failure of the tooth to take up uoride.
Particular attention has been focused on the
toothpastes containing potassium nitrate. However, a
Cochrane review (71) concluded that there was no
strong evidence available to support the efcacy of
potassium nitrate for the treatment of dentine
hypersensitivity.
Mouthrinses
Few studies have evaluated active agents in mouth-
rinses. Of these, two have both been potassium salts
(26, 96). Neither of these well-designed studies
demonstrated efcacy of the potassium nitrate or the
citrate agent, respectively.
Professionally applied products in
the management of dentine
hypersensitivity
Again, a wide range of commercially available prod-
ucts are available for professional treatment. In-ofce
treatments tend to be reserved for the individuals
who have received preventive advice and have tried
at-home products but found them to be ineffective.
Professionally applied sodium uoride has been
used to treat dentine hypersensitivity (15). A varnish
can set by releasing ethanol and taking up moisture. In
this way the insoluble resins, in the shape of a sticky-
plastic congealing lm, gradually fall out and, for
example, sodium uoride is thought to then dissolve
and deposit on the tooth. Although several authors
demonstrate a distinct enrichment of the surface en-
amel with such a varnish (69), it may be that the var-
nish is effective as a result of occlusion of the tubules
by the resin, rather than because of the effect of the
uoride. Observation shows that this approach re-
duces the painof dentine hypersensitivity for as long as
the varnish is on the tooth. Oxalates such as uoride
have also been professionally applied; however, the
success rates for efcacy are equivocal. A cal-
cium uoride solution that also contains silica is
currently marketed, giving good clinical results.
Alternative treatment regimens include those of
Chinese traditional medicine, which are becoming
more and more popular in the western world, par-
ticularly when treatment fails by orthodox methods.
Dentine hypersensitivity has been treated success-
fully in China by brushing teeth with a mixture of
root Dahurian, angelica, the root of Chinese wild
ginger, puncture vine, the rhizome of davallia, pep-
permint and gallnut (99). Unfortunately no clinical
trials have yet been undertaken.
Glass ionomer, resin-reinforced glass ionomer
compomers, adhesive resin primers and adhesive
resin-bonding systems have been used successfully
for the treatment of dentine hypersensitivity. Treat-
ment can be problematic if there has been little tissue
loss, and overcontouring can lead to plaque-retentive
sites and gingival inammation (87). Furthermore,
suffers of dentine hypersensitivity tend to be metic-
ulous at cleaning their teeth, often using excessive
brushing force on frequent occasions. Unless the
toothbrushing habits are corrected, materials can be
abraded and may require replacement. Low (53)
evaluated glass ionomers in the treatment of this
condition and observed a good success rate; however,
evaluation of pain was not described. Hansen (36)
has also reported success using resin-reinforced glass
ionomer. Cavity varnish can give temporary relief of
symptoms when applied in a thin lm on open
dentinal tubules (35); however, the smear layer must
be modied or removed before application, in order
to occlude the tubules and be stable to acidic attack.
The use of adhesive resin primer products is docu-
mented in vitro to occlude tubules (84) and clinically
by Ianzano et al. (39); however, there were no un-
treated control teeth in the trial. Other groups (8)
could not demonstrate efcacy clinically. In theory
the concept is clear and practical, with the thin lms
occluding the tubules. However, occasionally failure
of polymerization occurs and the lms can be easily
abraded. Dondi dallOrologio et al. (17) concluded,
following analysis of a primer and a conditioner, that
both were highly effective at reducing or eliminating
dentine sensitivity for periods of up to 6 months. A
study by Martens (56) agreed with these ndings.
However, if the seal between the material and the
root surface breaks down, dentine sensitivity may
re-occur. The systems incorporating the primer
and adhesive components together produce a thicker
lm and have been used with success (76). A well-
controlled study by Ide et al. (41), using another
37
Dentine hypersensitivity
commercially available system, again gave good
efcacy, the surface not being etched prior to the
application of material. In conclusion, these materi-
als are frequently used by clinicians for the treatment
of dentine hypersensitivity. There are few well-con-
trolled trials to support their efcacy. Those which
have been reported, together with clinical experience,
would support the use of these materials after
employment of preventive advice and home-use
treatment, particularly for isolated teeth that have not
responded.
Neodymium-doped yttrium aluminium garnet
(Nd:YAG) laser irradiation has been advocated for the
alleviation of symptoms from dentine hypersensitiv-
ity. It is thought to work by coagulation of proteins in
the dentinal uid, hence reducing permeability (28).
It is also believed to create an amorphous sealed
layer on the dentine surface that appears to be the
result of partial meltdown of the surface (57). How-
ever, there is a possibility that peripheral tubules are
opened, negating any benet. The Nd:YAG laser has
been used with encouraging results (74, 48). Other
clinical studies do not support this nding (49), with
the laser treatment reducing the pain sensation but
not signicantly more than that of the placebo
treatment. In summary, the clinical results obtained
from laser therapy are equivocal and do not seem to
justify the high expenditure of the equipment for this
purpose.
Coronally repositioning periodontal aps to cover
areas of exposed dentine have been advocated as a
treatment regimen for dentine hypersensitivity (50).
Compared with the other modalities of treatment for
this condition, this is an invasive procedure. How-
ever, the results can be very pleasing, both estheti-
cally and therapeutically. As a last resort these
treatment procedures have been used to alleviate the
pain of dentine hypersensitivity when all other
methods of pain relief fail.
Summary on therapeutic management
strategies for dentine hypersensitivity
preventive measures should be followed as indi-
cated.
clinically there are many treatment modalities for
dentine hypersensitivity that the clinician nds
successful in alleviating the pain of dentine
hypersensitivity.
the rst line of treatment should be the least
invasive, such as a low abrasive strontium-based or
potassium-based toothpaste.
high uoride products can be utilized.
if these treatment modalities fail, varnishes resins
can be used followed by conventional restorative
procedures.
unfortunately, no single treatment seems to suit all.
The least invasive treatments are usually advocated
rst followed by the professionally led treatment.
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