Dentin hypersensitivity is characterized by short, sharp pain from exposed dentin in response to stimuli like heat, cold, sweet foods, or toothbrushing. It occurs when gums recede or enamel is lost, exposing open dentin tubules. The hydrodynamic theory explains that stimuli cause fluid movement in dentin tubules, activating nerve endings and causing pain. Treatment focuses on desensitizing nerves with potassium nitrate toothpaste or occluding tubules with agents like fluoride, CPP-ACP, or resins to block fluid flow and pain signals.

1. DENTIN HYPERSENSITIVITY
READER
DR PANKAJ PRIYADARSHI
DEPARTMENT OF CONSERVATIVE
DENTISTRY AND ENDODONTICS

2. Definition
According to Holland et al, dentin
hypersensitivity is characterized by short,
sharp pain arising from exposed dentin in
response to stimuli typically thermal,
evaporative, tactile, osmotic or chemical and
which cannot be ascribed to any other form of
dental defect or pathology.

3. Etiology
Dentin hypersensitivity is a multifactorial
condition and is not fully understood.
However, there is a definite change in the
structure of dentin in the affected area. These
areas contain a larger number of patent
dentinal tubules with a larger tubular
diameter than the normal unaffected areas.

4. The following three theories have been
proposed to explain this condition:
1. Direct Innervation Theory-
This theory postulates that direct mechanical
stimulation of exposed nerve endings at the
dentinoenamel junction (DEJ) is responsible
for dentinal hypersensitivity.
The major shortcoming of this theory is that
there is insufficient evidence to prove that
the outer dentin that is most prone to be
sensitive is well innervated.

5. 2. Odontoblast Receptor Theory-
This theory proposes that the odontoblasts
themselves act as neural receptors and relay
the signal to the nerve terminal.
The major shortcoming of this theory is that
there is no evidence to demonstrate synapses
between odontoblasts and nerve terminals.

6. 3. Hydrodynamic Theory-
This is the most accepted theory to explain
the mechanism behind dentin
hypersensitivity.
The hydrodynamic theory proposed by
Brannstorm suggests that dentin
hypersensitivity is due to the hydrodynamic
fluid movements occuring across exposed
dentin with open tubules which in turn
mechanically activates the nerves present at
the inner ends of the dentin tubules or in the
outer layers of the pulp.

8. The dentinal tubules, which are open an wide,
contain fluid. Various stimuli (i.e. thermal,
tactile, chemical or osmotic changes) displaces
the fluid in the dentinal tubules in either an
inwardly or outwardly direction. The
movement of this liquid stimulates the
odontoblastic processes, and the subsequent
mechanical disturbances stimulates
baroreceptors (a nerve receptor sensitive to
pressure) that leads to neural discharges
(depolarization). This neural pulpal activation
is perceived as pain by the patient.

9. Stimulus
Fluid flow in exposed open dentinal tubules
Stimulation of intra-tubular baroreceptors
Pain

11. Etiological and predisposing factors associated with
dentin hypersensitivity:
- Loss of enamel
- Gingival recession
- Attrition
- Erosion (intrinsic and extrinsic)
- Tooth malposition
- Denudation of cementum
- Thinning, fenestration, absent buccal alveolar bone
plate
- Abrasion
- Abfraction
- Periodontal disease and its treatment
- Periodontal surgery
- Patient habits

12. Clinical Features
1. Pain is the most common clinical feature
associated with dentin hypersensitivity.
2. The intensity of pain varies from mild
discomfort to severe sensitivity.
3. The pain is typically rapid in onset, sharp in
character and is of short duration.
4. External stimuli which can elicit the
expression of this condition include:

13. i. Thermal stimuli
a. Hot/cold food and beverages
b. Cold blast of air
ii. Osmotic stimuli
a. Sweet food
iii. Acidic stimuli
a. Citrus fruits
b. Acidic beverages
c. Medicines
iv. Mechanical stimuli
a. Toothbrush
b. Dental instruments
5. The most commonly involved teeth are
i. Buccal surfaces of premolars
ii. Facial surfaces of incisors

14. Management of
Dentin Hypersensitivity

15. Diagnosis:
1. A thorough patient history and clinical
examination
2. Diagnosis is confirmed by using a jet of air or
by using a diagnostic probe on dentin in a
mesiodistal direction in the area where the
patient complains of pain.

16. Clinical Management:
Removal of Etiological Factors-
The removal of the following etiological
factors can prevent dentin hypersensitivity
from recurring
1. Improper tooth brushing technique
2. Poor oral hygiene
3. Premature contacts
4. Gingival recession
5. Endogenous and Exogenous acids

17. Treatment Strategies-
The various clinical methods of management
of dentin hypersensitivity are:
1.Desensitizing the nerve
Daily use of 5% potassium nitrate containing
toothpaste for 4 weeks is an effective way to
desensitize dentin.
Potassium nitrate increases the extracellular
potassium ion concentration and thus
depolarizes the nerve. This prevents the
transmission of pain signals to the brain.

18. 2. Occluding the dentinal tubules
Occluding the distal terminal ends of exposed
dentinal tubules is another method of
managing dentin hypersensitivity.
i. Salts or ions
a. 0.4% Stannous fluoride
b. 2% Sodium fluoride
c. Potassium oxalate
d. Strontium chloride
e. Calcium carbonate

19. ii. Protein precipitates
a. CPP-ACP
b. Silver nitrate
c. Glutaraldehyde
d. Zinc chloride
3. Dentin adhesives
i. Dentin bonding agents
ii. Composites
iii. Glass ionomers
4. Crown placement
5. Periodontal grafting
6. Lasers
Nd- YAG lasers have shown to effectively occlude
dentinal tubules.