Dentin hypersensitivity is dental pain which is sharp in character and of short
duration, arising from exposed dentin surfaces in response to stimuli,
typically thermal, evaporative, tactile, osmotic, chemical or electrical; and
which cannot be ascribed to any other dental disease.
A degree of dentin sensitivity is normal, but pain is not usually
experienced in everyday activities like drinking a cooled drink. Therefore,
although the terms dentin sensitivity and sensitive dentin are used
interchangeably to refer to dental hypersensitivity, the latter term is the
most accurate. Symptoms
The pain is sharp and sudden, in response to an external stimulus. The
most common trigger is cold, with 75% of people with hypersensitivity reporting
pain upon application of a cold stimulus. Other types of stimuli may
also trigger pain in dentin hypersensitivity, including:
Thermal – hot and cold drinks and foods, cold air, coolant water jet from a
dental instrument. Electrical – electric pulp testers.
Mechanical–tactile – dental probe during dental examination, periodontal scaling
and root planing, toothbrushing. Osmotic – hypertonic solutions such as
sugars. Evaporation – air blast from a dental
instrument. Chemical – acids, e.g. dietary, gastric,
acid etch during dental treatments. The frequency and severity with which
the pain occurs are variable. Causes
The main cause of DH is gingival recession with exposure of root
surfaces, loss of the cementum layer and smear layer, and tooth wear. Receding
gums can be a sign of long-term trauma from excessive or forceful
toothbrushing, or brushing with an abrasive toothpaste, or a sign of
chronic periodontitis. Other less common causes are acid erosion, and periodontal
root planing. Dental bleaching is another known cause of hypersensitivity.
Other causes include smoking tobacco, which can wear down enamel and gum
tissue, cracked teeth or grinding of teeth.
Dentine contains many thousands of microscopic tubular structures that
radiate outwards from the pulp; these dentinal tubules are typically 0.5–2
micrometres in diameter. Changes in the flow of the plasma-like biological fluid
present in the dentinal tubules can trigger mechanoreceptors present on
nerves located at the pulpal aspect, thereby eliciting a pain response. This
hydrodynamic flow can be increased by cold, air pressure, drying, sugar, sour,
or forces acting onto the tooth. Hot or cold food or drinks, and physical
pressure are typical triggers in those individuals with teeth sensitivity.
Most experts on this topic state that the pain of DH is in reality a normal,
physiologic response of the nerves in a healthy, non-inflamed dental pulp in the
situation where the insulating layers of gingiva and cementum have been lost;
i.e., dentin hypersensitivity is not a true form of allodynia or hyperalgesia.
To contradict this view, not all exposed dentin surfaces cause DH. Others suggest
that due to the presence of patent dentinal tubules in areas of
hypersensitive dentin, there may be increased irritation to the pulp,
causing a degree of reversible inflammation.
Diagnosis The diagnosis of DH may be challenging.
It is a diagnosis of exclusion, reached once all other possible explanations for
the pain have been ruled out. A thorough patient history and clinical examination
are required. The examination includes a pain provocation test by blasting air
from a dental instrument onto the sensitive area, or gentle scratching
with a dental probe. If a negative result for the pain provocation test
occurs, no treatment for dentinal hypersensitivity is indicated and
another diagnosis should be sought, such as other causes of orofacial pain.
Inflammation of the dental pulp, termed pulpitis, produces true hypersensitivity
of the nerves in the dental pulp. Pulpitis is classified as irreversible
when pulpal inflammation will irreversibly progress to pulpal necrosis
due to compression of the venous microcirculation and tissue ischemia,
and reversible when the pulp is still capable of returning to a healthy,
non-inflamed state, although usually dental treatment is required for this.
Irreversible pulpitis is readily distinguishable from DH. There is poorly
localized, severe pain which is aggravated by thermal stimuli, and which
continues after the stimulus is removed. There also is typically spontaneous pain
without any stimulus. Reversible pulpitis may not be so readily
distinguishable from DH, however usually there will be some obvious sign such as
a carious cavity, crack, etc. which indicates pulpitis. In contrast to
pulpitis, the pain of DH is short and sharp.
Epidemiology Dentin hypersensitivity is a relatively
common condition. Due to differences in populations studied and methods of
detection, the reported incidence ranges from 4-74%. Dentists may under-report
dentin hypersensitivity due to difficulty in diagnosing and managing
the condition. When questionnaires are used, the reported incidence is usually
higher than when clinical examination is used. Overall, it is estimated to affect
about 15% of the general population to some degree.
It can affect people of any age, although those aged 20–50 years are more
likely to be affected. Females are slightly more likely to develop dentin
hypersensitivity compared to males. The condition is most commonly associated
with the maxillary and mandibular canine and bicuspid teeth on the facial aspect,
especially in areas of periodontal attachment loss.
Prognosis Dentin hypersensitivity may affect
individuals' quality of life. Over time, the dentin-pulp complex may adapt to the
decreased insulation by laying down tertiary dentin, thereby increasing the
thickness between the pulp and the exposed dentin surface and lessening the
symptoms of hypersensitivity. Similar process such as formation of a smear
layer and dentin sclerosis. These physiologic repair mechanisms are likely
to occur with or without any form of treatment, but they take time.
Treatment There is no universally accepted,
gold-standard treatment which reliably relieves the pain of dental
hypersensitivity in the long term, and consequently many treatments have been
suggested which have varying degrees of efficacy when scientifically studied.
Generally, they can be divided into in-office, or treatments which can be
carried out at home, available over-the-counter or by prescription. OTC
products are more suited for generalized, mild to moderate dentin
hypersensitivity associated with several teeth, and in-office treatments for
localized, severe DH associated with one or two teeth. Non-invasive, simple
treatments which can be carried out at home should be attempted before
in-office procedures are carried out. The purported mechanism of action of
these treatments is either occlusion of dentin tubules or desensitization of
nerve fibres/blocking the neural transmission.
= Prevention = Gingival recession and cervical tooth
wear can be avoided by healthy dietary and oral hygiene practices. By using a
non-traumatic toothbrushing technique will help prevent receding gums and
tooth wear around the cervical margin of teeth. Non-abrasive toothpaste should be
used, and brushing should be carried out no more than twice per day for two
minutes on each occasion. Excessive use of acidic conditions around the teeth
should be avoided by limiting consumption of acidic foods and drinks,
and seeking medical treatment for any cause of regurgitation/reflux of stomach
acid. Importantly, the teeth should not be brushed immediately after acidic
foods or drinks. A non-abrasive diet will also help to prevent tooth wear.
Flossing each day also helps to prevent gum recession caused by gum disease.
= Home treatment = At-home treatments include desensitizing
toothpastes or dentifrices, potassium salts, mouthwashes and chewing gums.
A variety of toothpastes are marketed for dentin hypersensitivity, including
compounds such as strontium chloride, strontium acetate, arginine, calcium
carbonate, hydroxyapatite and calcium sodium phosphosilicate. Desensitizing
chewing gums and mouthwashes are also marketed.
Potassium-containing toothpastes are common; however, the mechanism by which
they may reduce hypersensitivity is unclear. Animal research has
demonstrated that potassium ions placed in deep dentin cavities cause nerve
depolarization and prevent re-polarization. It is not known if this
effect would occur with the twice-daily, transient and small increase in
potassium ions in saliva that brushing with potassium-containing toothpaste
creates. In individuals with dentin hypersensitivity associated with exposed
root surfaces, brushing twice daily with toothpaste containing 5% potassium
nitrate for six to eight weeks reduces reported sensitivity to tactile, thermal
and air blast stimuli. However, meta analysis reported that these
individuals' subjective report of sensitivity did not significantly change
after six to eight weeks of using the potassium nitrate toothpaste.
Desensitizing toothpastes containing potassium nitrate have been used since
the 1980s while toothpastes with potassium chloride or potassium citrate
have been available since at least 2000. It is believed that potassium ions
diffuse along the dentinal tubules to inactivate intradental nerves. However,
as of 2000, this has not been confirmed in intact human teeth and the
desensitizing mechanism of potassium-containing toothpastes remains
uncertain. Since 2000, several trials have shown that potassium-containing
toothpastes can be effective in reducing dentin hypersensitivity, although
rinsing the mouth after brushing may reduce their efficacy.
Studies have found that mouthwashes containing potassium salts and fluorides
can reduce dentine hypersensitivity, although rarely to any significant
degree. As of 2006, no controlled study of the effects of chewing gum containing
potassium chloride has been made, although it has been reported as
significantly reducing dentine hypersensitivity.
Nano-hydroxyapatite is considered one of the most biocompatible and bioactive
materials, and has gained wide acceptance in dentistry in recent years.
An increasing number of reports have shown that nano-hydroxyapatite shares
characteristics with the natural building blocks of enamel having the
potential, due to its particle size, to occlude exposed dentinal tubules helping
to reduce hypersensitivity and enhancing teeth remineralization. For this
reason, the number of toothpastes and mouthwashes that already incorporate
nano-hydroxyapatite as a desensitizing agent is increasing.
= In-office treatment = In-office treatments may be much more
complex and they may include the application of dental sealants, having
fillings put over the exposed root that is causing the sensitivity, or a
recommendation to wear a specially made night guard or retainer if the problems
are a result of teeth grinding. Other possible treatments include
fluorides are also used because they decrease permeability of dentin in
vitro. Also, potassium nitrate can be applied topically in an aqueous solution
or an adhesive gel. Oxalate products are also used because they reduce dentin
permeability and occlude tubules more consistently. However, while some
studies have showed that oxalates reduced sensitivity, others reported
that their effects did not differ significantly from those of a placebo.
Nowadays, dentin hypersensitivity treatments use adhesives, which include
varnishes, bonding agents and restorative materials because these
materials offer improved desensitization.
Low-output lasers are also suggested for dentin hypersensitivity, including
GaAlAs lasers and Nd:YAG laser. They are thought to act by producing a transient
reduction in action potential in C-fibers in the pulp, but Aδ-fibers are
not affected. See also
Remineralization of teeth References