Dentin hypersensitivity

DEFINITION
THEORIES
• A. Direct Innervation (DI)
Theory
• B. Odontoblast Receptor
(OR) Theory
• C. Fluid
Movement/Hydrodynamic
Theory
DIRECT INNERVATION THEORY
• It has been reported that the nerve’s endings enters dentin through
pulp and extends to DEJ and the mechanical stimuli directly transmit
the pain.
• However, there is little evidence to prove this theory; firstly because
there is little evidence that can support the existence of nerve in the
superficial dentin; where dentin has the most sensitivity; and
secondly because the plexus of Rashkov do not become mature until
complete tooth eruption. However, the newly developed teeth can be
sensitive too
ODONTOBLASTIC RECEPTOR
THEORY
• In the OR theory, odontoblasts act as receptors of pain and transmit
signals to the pulpal nerves.
• But this theory has also been rejected since the cellular matrix of
odontoblasts is not capable of exciting and producing neural impulses.
• Furthermore, no synopsis has been found between odontoblasts and
pulpal nerves
HYDRODYNAMIC THEORY
• First proposed by Brannstorm.
• This theory is the most widely accepted theory for DH.
• The theory has been proposed based on the movement of the fluid inside the
dentinal tubules.
• The theory claims that tubules are open between dentine surface which is
exposed to the environment and pulp
• It is believed that DH is made as the result of movement of the fluid inside the
dentinal tubules, which is further due to the thermal and physical changes, or
as the result of formation of osmotic stimuli near the exposed dentine. The
movement of fluid stimulates a baroreceptor and leads to neural discharge.
The process is called the hydrodynamic theory of pain
Predisposing individuals
•  Overenthusiastic brushers
•  Periodontal treated patients
•  Bulimics
•  People with xerostomia
•  High-acid food/drink consumers
•  Older people exhibiting gingival recession
•  Chewing ‘smokeless’ or ‘snuff’ tobacco
Causes
An initial step for the appearance of dentine hypersensitivity should be
the loss of tissue covering dentine.
• One process may be loss of enamel caused by attrition associated
with over-zealous tooth brushing or by erosion associated with
dietary acidic compounds.
• Another process may be gingival recession caused by periodontal
disease or by over-zealous and/or improper tooth brushing
• Root sensitivity occurs more frequently in the cervical area of the
root, where the cementum is extremely thin.
• Scaling and root planing procedures remove this thin cementum,
thereby inducing the hypersensitivity.
The following information on how to cope with the problem should also
be given to the patient:
• 1. Hypersensitivity appears as a result of the exposure of dentin,
which is inevitable if calculus, biofilm, and their products, which are
buried in the root, are to be removed.
• 2. Hypersensitivity slowly disappears in a few weeks.
• 3. An important factor in reducing hypersensitivity is biofilm control.
• 4. Desensitizing agents do not produce immediate relief and must be
used for several days or even weeks to produce results.
Role of dental plaque

• While there are many factors which can contribute to dentine hypersensitivity, plaque
accumulation has often been cited as an important factor.
• Plaque accumulation on root surfaces may lead to demineralization of tooth structures
which could be associated with patency of dentinal tubule orifices.

• Plaque organisms may shed bacterial products which diffuse across dentin oral
sensitive pulpal nerves. Peritubular dentine was decalcified and thus, the opening of
the dentine tubules increased
• When plaque is removed, it will allow dentin to take minerals from saliva for
mineralisation
• It has been speculated that the inorganic mineral occluded in the dentinal tubules was
derived from the dentinal fluid and/or the saliva (Pashley et al., 1982)
According to Trowbridge and Silver, this can be attained in the following
ways:
• (1) by the formation of a smear layer produced by burnishing the
exposed surface,
• (2) via the topical application of agents that form insoluble
precipitates within the tubules,
• (3) with the impregnation of tubules with plastic resins, or
• (4) by sealing the tubules with plastic resins
• The most common form of management is the placement of a
topically applied agent applied either by a dental professional or by
the patient at home. All currently available treatments appear to work
NERVE DESENSITIZATION
• more likely explanation is that the potassium ions are the active
component and that potassium nitrate reduces dentinal sensory
nerve activity due to the depolarizing activity of the K+ ion, although
this proposal has never been confirmed in intact human teeth
• an oxidizing effect or blocking of tubules by crystallization has been
proposed but not proven
ANTI INFLAMMATORY AGENTS
Corticosteroids
• These agents may induce mineralization leading to tubule occlusion,
this view has yet to be validated and the validity of using such agents
has been questioned
Covering or plugging dentinal
tubules
• Calcium hydroxide
• Sodium fluoride
• Stannous fluoride
• The mode of action appears to be through the induction of a high mineral
content which creates a calcific barrier blocking the tubular openings on the
dentine surface.Alternatively, stannous fluoride may precipitate on the
dentine surface leading to occlusion of the exposed dentinal tubules
• Fluoride iontophoresis
Desensitizing pastes
• The most likely mechanism of action is the reduction of the diameter of the
dentinal tubules to limit the displacement of fluid
• Patients must be aware that their use will not prove to be effective unless they
are used continuously for at least 2 weeks.
• Sensodyne and Thermodent contain strontium chloride
• Certain agents, such as chlorhexidine, decrease the ability of fluoride to bind with
calcium on the root surfaces. Thus it is important to advise patients not to rinse
or eat for 1 hour after a desensitizing treatment
• Potassium oxalate (Protect) and ferric oxalate (Sensodyne Sealant) solutions are
the preferred agents, and special applicators have been developed for their use.
These agents form insoluble calcium oxalate crystals that occlude the dentinal
tubules