CHAPTER (3)

DENTIN HYPERSENSITIVITY

By the end of this chapter, the student will be able to:

1. Define post operative pain and hypersensitivity
2. Know the difference between pain and hypersensitivity
3. Identify the etiological factors responsible for post
operative pain
4. Detect the problem by proper diagnosis and patient
examination
5. Correlate between patient complain and clinical findings
6. Understand how to prevent problem

Definition
Dentin hypersensitivity is defined as "sharp, short pain "arising from exposed
dentin in response to stimuli (thermal, chemical; tactile or osmotic) and which
cannot be ascribed to any other form of dental defect or disease (Holland et al.,
1997, Kim and Karastathis,2010)
Prevalence:
• 60-98% in patients with periodontitis.
• Transient hypersensitivity after deep scaling, root planning and gingival
surgery.
• Hypersensitivity after teeth bleaching and restorative procedures.
• Peak age 20-40 years.
Mechanism of dentin sensitivity:

(1) Neural theory: Stimulus applied to dentin causes direct excitation of the
nerve fibers.

(2) Odontoblastic transduction theory: Stimulus is transmitted along the

odontoblast and passes to the sensory nerve endings through synapse.

(3) Hydrodynamic theory (1979).

Stimulus causes displacement of fluid present in dentinal tubules which further

excite nerve fibers.

Currently most investigators accept that dentin sensitivity is due to the

hydrodynamic theory.
 Figure 1: Theories of dentin hypersensitivity

Lesion localization and incidence:

• More than 90% of hypersensitive surfaces are at the cervical margin of buccal
or labial surfaces.
• Age: 20-40 years.
• Female > male.
• Buccal cervical surfaces.
• Canines, first premolars, incisors, second premolars and molars.
• Right handed tooth brushes - left side.
• 8-30% of adults.

Etiology of Dentin Hypersensitivity:

1. Loss of Enamel
2. Gingival Recession
3. Bleaching Consideration
1. Loss of Enamel
▪ Both enamel and cementum may be lost from tooth surface either gradually
or suddenly, exposing dentin which elicit acute hypersensitivity.
▪ At Cemento enamel junction CEJ area, there may be only a thin layer of
enamel, making it susceptible to enamel loss.
▪ Cementum is thin and not highly mineralized, it can be easily abraded or
eroded.
▪ Enamel and cementum don’t meet in 10% of teeth.
▪ Abrasion, erosion, abfraction or attrition leads to enamel loss.

2. Gingival Recession:
The occurrence of gingival recession is a
precursor to the loss of cementum and exposure
of dentin.
Causes of gingival recession:
1. By age
2. Tooth brush type and technique---Toothbrush
abrasion.
3. Excessive use of oral hygiene devices
4. Oral habits: traumatic tooth picking, excessive Figure 2: Loss of Enamel
flossing.
5. Faulty crown preparation
6. Gingival recession secondary to specific diseases, i.e. NUG periodontitis,
herpetic gingivostomatitis"
7. Surgical and nonsurgical periodontal treatment
 Figure 3: Gingival recession Figure 4: Power bleaching

3. Bleaching Consideration:

- Bleaching agents can potentially cause or increase dentin sensitivity.

- 25% of people develop hypersensitivity after bleaching.
Recommendation after Bleaching:
▪ Desensitizers: potassium nitrate.
▪ High concentration desensitizing gel using tray delivery method.
▪ Reducing bleaching time and using fluoride after bleaching.
▪ Lower concentration of peroxide 10-15%.

Lesion initiation:
• Not all exposed dentin is sensitive
• It occurs when smear layer or tubular plugs are removed
• Abrasion and erosion may be involved, but acid erosion is the predominant
factor
• Plaque is not significant factor, patient with dentin hypersensitivity tend to
have good plaque control.
Diagnosis and Assessment of Dentin Hypersensitivity:
Effective treatment must be precede by proper diagnosis, established after
exclusion of any other possible causes of pain (Porto et al, 2009)
1- Proper History.
2- Clinical Evaluation.

1- Proper history including:

❖ Medical history:
➢ Excessive vomiting
➢ Gastroesophageal reflux disease
➢ Frequent use of antacids and acidic medications
➢ Alcoholism
➢ Autoimmune diseases (SJogren’s syndrome), oral & eye dryness
➢ Radiation of head and neck
➢ Medication that cause salivary hypo function
❖ Dental history:
➢ History of bruxism
➢ Use of occlusal guard
➢ History of previous dental procedures
❖ Dietary history
➢ Acidic food and beverage frequency
❖ Oral hygiene methods
➢ Tooth brushing methods and frequency
➢ Type of dentifrice
➢ Use of mouth rinse
➢ Use of topical fluorides
2- Clinical Evaluation: Useful diagnostic tools:
❖ Dental explorer& periodontal probe
❖ Air jet
❖ Pulp vitality test
❖ Percussion test
❖ Assessment of occlusion
❖ Radiograph
Pain assessment:
The severity or degree of pain can be quantified according to either:
- Categorical scale (slight, moderate, sever)
- Visual analogue scale (VAS) (Orchardsonet al, 2006)
1) Stimulus based assessment
According to type of stimulus mechanical, thermal, chemical, electrical and
evaporation
2) Response based assessment:
Estimates pain severity by:
❖ Verbal rating scale:
4 scale grading pain as
Slight---- Moderate----Sever ----- Agonizing
 ❖ Verbal analogue scale:

Line of 10 cm the extremities of the line represent from no pain to the most
severe pain

Figure 5: Pain scale

Differential diagnosis of dentin hypersensitivity of dentin:

• Diagnostic aids: include history of pain, percussion, palpation, pulp testing
and radiographic examination
• Etiology of the pain is the first consideration
• Patients are usually capable of accurate localizing the pain
• Dental pain can be intensified by thermal changes, sweet and sour, all of
which could elicit hyper sensitivity.
• Pulpal pain can be differentiated from dentin pain since it is often described
as severe, intermittent and thropping.
• Pain of pulpitis often occurs without provocation and occurs after thermal
irritation and may persist after removal of stimulus. While dentin
hypersensitivity subsides after removal of the stimulus.
• Pain on biting diagnosed together with lights and dyes, the presence of a
fracture line in the tooth.
• Fractured restoration can be diagnosed by careful visual examination and
magnification.

Prevention of dentin hypersensitivity:

❑ Dietary modification
▪ Dietary counseling
▪ Control consumption of acidic foods and carbonated beverages
▪ Avoid brushing immediately after acidic foods
▪ Drinking acidic beverages through a straw
▪ Drinking alkaline or neutral beverages (water or milk) after acidic ones
❑ Reduce or eliminates parafunctional habits
▪ Parafunctional habits such as bruxism, clenching may lead to tooth flexure
and abfraction
▪ Using night guards can reduce the effects of such unconscious habits
Management of dentin hypersensitivity:
Treatment plan of dentin hypersensitivity should include identifying and
elimination of predisposing factors
1) Natural desensitization: includes:
➢ sclerosis of dentin
➢ deposition of reparative and tertiary dentin
➢ formation of smear layer
➢ calculus formation
2) Clinical desensitization
1- Nerve desensitization: (Denervation)
Using Potassium nitrate, potassium ions diffuse through dentinal tubules and
decrease the excitability of intra dental nerves
2- Cover or plugging of dentinal tubules
a) Ions or salts:
➢ Fluoride
➢ Strontium salts
➢ Oxalates
➢ Glutaraldehyde
➢ Calcium phosphates
➢ Casein phosphopeptides
➢ Hydroxyapatite (HA)
b) Dentin sealers
➢ Glass ionomer
➢ Resin composite
➢ Varnishes
c) Bioactive glass
d) Propolis
e) Periodontal soft tissue grafting
f) Crown placement / restoration
g) Lasers
 Figure 6: Nerve desensitization

Figure 7: Top and side view of dentinal tubules plugging

Treatment modes:
A. At home treatments:
➢ Desensitizing toothpaste
➢ Tooth paste application: practitioners should educate patients about proper brushing
techniques.
➢ Mouth washes and chewing gums: containing potassium nitrates and fluorides help
reducing hypersensitivity
➢ Bleaching trays containing desensitizing agents

B. In office treatments:
➢ Topically applied desensitizing agent
Criteria of successful desensitizing agent
▪ Nonirritant to the pulp
▪ Painless on application
▪ Easily applied
▪ Rapid action
▪ Affective for a long time
▪ Without staining effect
➢ Fluoride:
▪ Sodium fluoride and stannous fluoride can reduce sensitivity
▪ Fluorides reduce dentin permeability by precipitation of calcium fluoride salts
within the dentinal tubules
➢ Potassium nitrate:
▪ reduce nerve excitability
▪ Applied in gel, varnish or paint –on forms
➢ Oxalate:
Potassium oxalates cause 98% reduction in dentin hypersensitivity
➢ Calcium phosphate
Reduces dentin permeability
➢ Adhesives and resins
➢ Ionotophresis:
This procedure uses electricity to enhance diffusion of ions into tissues
➢ Lasers
➢ Miscellaneous treatments:
e.g.: coronally positioned flap

Management of bleaching sensitivity:

1. Passive management:
• Reduce treatment time
• Reduce treatment frequency
• Alter peroxide concentrations
2. Active management
• Apply neutral fluoride
• Apply 3-5% potassium nitrate in the tray
• Pretreatment with fluoride or potassium nitrate

Figure 8: Ionotophresis
Figure 9: Coronally positioned flap