Dentin Hypersensitivity Full Summary with Clinical and

Theory Q&A
Dentin Hypersensitivity: Etiology, Diagnosis and Treatment; A Literature Review
Davari AR.a, Ataei E.a, Assarzadeh H

Dentin Hypersensitivity: Etiology, Diagnosis and Treatment

1- Definition

• DH is defined as “pain derived from exposed dentin in response to chemical,

thermal, tactile or osmotic stimuli which cannot be explained as arising from any
other dental defect or disease”

• Alternative terms (used interchangeably) include dentin sensitivity, cervical

sensitivity, root sensitivity, and cemental sensitivity. (see Table 1 of original
article). (This formal definition is preserved exactly.)

2- Prevalence and epidemiology

• Prevalence varies widely by study/population: reported rates range from a few

percent up to 85% in adults DH is particularly common in patients aged 30–40
years (overall range 20–50) and more prevalent in females.

• Reporting method affects prevalence: self-reported questionnaires yield higher rates

than clinical exam

• Teeth affected: Canines and premolars (especially buccal surfaces) are most often
involved Dentists estimate ~10–25% of patients have DH, with ~1% experiencing
severe problems

• DH can occur at any age Many patients do not seek treatment, possibly viewing it
as a minor issue

3- Etiopathogenesis

3a- Anatomy of the tooth and dentin-pulp complex

• Dentin is a vital tissue covered by enamel (crown) and cementum (root) It contains
numerous dentinal tubules (filled with odontoblastic processes and ~22% fluid by
volume) This dentin–pulp complex allows transmission of stimuli to the pulp.
3b- Pathogenesis

• Phase 1 – Exposure: DH does not occur while enamel/cementum are intact

• The first step is loss of protective layers (enamel or cementum) from abrasion (hard
brushing), attrition (tooth-to-tooth wear), erosion (acid), or abfraction Gingival
recession commonly exposes root dentin on buccal surfaces of canines/premolars.

• Observation: Sensitive dentin has ~8× more tubules and wider tubules than normal
dentin Thinner calcified smear layers (compared to non-sensitive teeth) allow more
fluid movement.

• Phase 2 – Sensitization: Removal of the smear layer and tubular plugs (by acids,
dietary acids, or vigorous brushing) fully opens the tubules Exposed tubules and pulp
are thus accessible to external stimuli. The smear layer (protein/mineral debris)
normally partially plugs tubules; its loss significantly increases dentin permeability
and pain response.

4- Mechanism

• Direct Innervation (DI) Theory: Nerve fibers extend into dentin carrying stimuli
directly. Evidence: Historically proposed, but largely unsupported because few
nerves reach outer dentin and Rashkov’s plexus matures late

• Odontoblast Receptor (OR) Theory: Odontoblasts act as sensory receptors

transmitting to nerves. Evidence:Largely rejected; odontoblasts lack excitability and
direct links to nerves

• Hydrodynamic Theory: Most accepted. Stimuli (thermal changes, drying, osmotic

shifts) cause fluid movement within open tubules, which mechanically stimulates
nerve endings in the pulp. For example, cold causes outward fluid flow, activating
baroreceptors and producing sharp pain.

• Flowchart of Mechanism (illustrative): Stimulus → fluid shift in tubule → nerve

activation → Pain. This explains clinical DH responses.
5- Clinical treatment of dentin hypersensitivity and Diagnosis

• Diagnosis: Confirm DH by history and exam; first exclude other causes (dental
caries, fractured/chipped enamel, pulpitis, post-bleaching sensitivity) Take a
thorough history (onset, duration, triggers, relieving factors) Perform clinical tests:
apply cold/air/water to suspected teeth to elicit sharp, short pain. Use percussion,
palpation, and transillumination to rule out pulp or periodontal pathology

• Examine all symptomatic teeth; record pain level (qualitatively or via visual
analogue scale)

• Classification of Desensitizing Agents: Can be grouped by administration (at-

home vs in-office) and by mechanism (neural blocker vs tubule occluder)

• At-home agents (e.g. OTC pastes/rinses) vs in-office (varnishes, resins, lasers)

Neural blockers (potassium salts) disrupt nerve depolarization; occluders (fluoride,
oxalates, resins) precipitate minerals to seal tubules

• Grossman’s ideal agent: rapid onset, long-lasting, painless, easy to apply, pulp-safe,
and non-staining

• At-home therapy:

◦ Toothpaste/powders: Early desensitizing pastes used strontium salts and

fluoride to occlude tubules. (Formaldehyde pastes were abandoned due to
toxicity.) Modern formulas typically contain potassium salts (potassium
nitrate/chloride/citrate), which diffuse into tubules and reduce nerve
excitability

◦ Clinical studies show K-nitrate + fluoride pastes significantly reduce DH.

◦ Use with a soft toothbrush and minimal water to maximize contact

◦ Remineralizing pastes (NaF + calcium phosphates) can also dramatically

decrease DH

◦ Newer formulations (8% arginine + calcium carbonate + 1450 ppm F) create

an alkaline environment, precipitating calcium phosphate within tubules

◦ Mnemonics: KAP (Potassium, Arginine, Phosphate) for key paste ingredients.

 ◦ Mouthrinses/gums: Rinses containing potassium nitrate and fluoride help
reduce sensitivity Potassium chloride gums have been studied, but results are
less reliable

◦ Follow-up: Reevaluate after 2–4 weeks of home therapy If sensitivity persists

(especially in severe or limited teeth), proceed to in-office therapy.

• In-office therapy:

◦ Aims for quicker relief, though immediate effect is not always achieved
Choose agents based on their action (nerve vs occlusion)

◦ Neural blockers: Potassium nitrate gels/solutions can be applied in-office to

further depolarize nerves (Lasers also modulate nerve signals.)

◦ Tubule occluders:

▪ Fluorides: Professional APF gel or varnish precipitates calcium

fluoride in tubules (often with acid)

▪ Oxalates: 28% potassium oxalate solution forms insoluble calcium

oxalate crystals in tubules (up to 98% occlusion). Effect is short-lived
unless repeated or aided by etching.

▪ Varnishes: Fluoride varnishes act as a delivery medium; traditional

copal varnish temporarily covers dentin (brief effect)

▪ Adhesive Resins: Dental bonding systems (e.g. Gluma) create a hybrid

layer sealing tubule. Gluma contains HEMA and glutaraldehyde which
coagulate proteins and form resin tags in tubules providing longer-
lasting relief.

▪ CPP-ACP (Tooth Mousse): Casein phosphopeptide-amorphous

calcium phosphate complexes promote remineralization of enamel and
tubule occlusion

▪ Bioglass/Portland cement: Bioactive materials (calcium silicate,

bioglass) can form apatite layers that occlude tubules
 ◦ Laser therapy: Various lasers (diode, Nd:YAG, etc.) can reduce DH (clinical
relief 5–100% depending on parameters)

◦ Proposed actions include protein coagulation inside tubules, partial melting of

dentin (sealing tubules), and desensitizing intradental nerves

◦ Systematic reviews suggest lasers may outperform topical agents no adverse

pulp effects reported

• Management algorithm (summarized):

◦ Confirm diagnosis: exclude other etiologies (pulpitis, caries)

◦ Eliminate contributing factors: e.g. improve brushing technique, reduce

acidic dietary exposure.

◦ Initiate at-home therapy: Soft brush + desensitizing toothpaste (potassium/

fluoride)

◦ Reassess (2–4 weeks): If needed, proceed to in-office treatments (varnish,

resin, laser, etc.)

◦ Escalate care: For severe or localized DH failing above, consider endodontic

treatment on unremitting cases

◦ Follow-up: Schedule periodic reviews to reinforce prevention (fluoride

application, diet counseling)

• Flowchart: (Textual form) Desensitizing agents classify by admin/mech, and the

treatment pathway flows from history/exam → home care → in-office care →
follow-ups.

Discussion

• DH is a chronic, prevalent condition in adults, resulting from loss of enamel/

cementum and tubule exposure Severity varies by individual factors

• Numerous treatments exist (K/F toothpastes, fluoride gels, bonding resins, lasers,
bioglass, etc.)

• These primarily seal dentinal tubules or block nerve signals

• The hydrodynamic (fluid shift) theory best explains DH

 • Conservative management (home care) is first-line, with in-office measures for
refractory cases. Regular follow-up and addressing etiologic factors are emphasized

Exam-Style Questions

Clinical Questions:

1. A 35-year-old woman has sharp tooth pain on cold drinks localized to exposed
root surfaces of her upper premolars. There is no caries or pulpitis. What is the
most likely diagnosis and your initial management plan?

◦ Answer: Likely dentin hypersensitivity. Confirm by stimulus testing (air

blast causing brief sharp pain), ensuring other causes (e.g. pulpitis) are ruled
out Initial management: correct etiology (instruct gentler brushing with a soft
brush), recommend an at-home desensitizing regimen (e.g. potassium nitrate +
fluoride toothpaste used with minimal water)

◦ Advise reevaluation in 4 weeks. If sensitivity persists, plan in-office therapy

(fluoride varnish or Gluma resin)

2. A patient reports generalized sensitivity 24 hours after ultrasonic scaling. All

teeth are vital and have no restorations. On exam, generalized cervical dentin
exposure is noted. How do you distinguish DH from reversible pulpitis, and
what treatments would you consider?

◦ Answer: Elicit pain with stimuli (e.g. air/water) on cervical areas; in DH pain
is sharp and stops when stimulus removed, with no spontaneous pain or
lingering thermal pain (as seen in pulpitis) Vital pulp tests support DH (normal
responses).

◦ Management: reassure patient of transient nature; initiate desensitizing

toothpaste (K/F) and gentle brushing. If still sensitive, apply in-office therapy
to affected teeth: e.g. apply 5% sodium fluoride varnish or bonding resin to
seal tubules

◦ Provide fluoride rinse or GC Tooth Mousse (CPP-ACP) as adjunct Follow-up

in 2–4 weeks to assess improvement.
Theoretical Questions:

1. Define dentin hypersensitivity (DH) as per the Canadian Consensus, and list
synonymous terms.

◦ Answer: DH is defined as “pain derived from exposed dentin in response to

chemical, thermal, tactile or osmotic stimuli which cannot be explained as arising
from any other dental defect or disease”

◦ Synonyms include dentin sensitivity, cervical sensitivity, root sensitivity, and

cemental sensitivity

2. Compare the Direct Innervation (DI) and Odontoblast Receptor (OR) theories of DH
with the Hydrodynamic theory.

◦ Answer: The DI theory posits nerve fibers extend into dentin, directly transmitting
stimuli to the pulp. The OR theory posits odontoblasts themselves sense stimuli and
signal nerves. Both DI and OR lack strong evidence (no free nerve endings in
superficial dentin; odontoblasts can’t fire impulses)

◦ In contrast, the Hydrodynamic theory (Brännström) – the accepted model – holds

that stimuli induce fluid shifts within exposed tubules, mechanically triggering pulp
nerves to cause pain

3. Describe the two phases in the development of dentin hypersensitivity.

◦ Answer: Phase 1 (lesion localization): Exposure of dentin due to loss of enamel or

cementum (abrasion, erosion, attrition, abfraction, gingival recession)

◦ Phase 2 (tubule exposure): Removal of smear layer/tubular plugs (by acids or

vigorous brushing) fully opens the tubules, allowing fluid movement in response to
stimuli

4. Classify desensitizing agents by administration and mechanism, and give one example
each.

◦ Answer: By administration: At-home agents (OTC toothpastes, rinses) vs In-office

agents (varnishes, bonding agents, lasers)

◦ By mechanism: Neural blockers vs Tubule occluders

▪ Neural blocker example: Potassium nitrate toothpaste (at-home) that

depolarizes nerves
 ▪ Tubule occluder example: 5% sodium fluoride varnish (in-office) that
precipitates calcium fluoride in tubules

▪ A helpful mnemonic: KAP – Potassium, Arginine, Phosphate – key

ingredients in many desensitizing pastes.

Dentin Hypersensitivity – Full Summary with

Clinical & Theory Q&A
Dentin Hypersensitivity: Etiology, Diagnosis and Treatment

1. Definition

• DH is defined as:
“pain derived from exposed dentin in response to chemical, thermal, tactile or osmotic
stimuli which cannot be explained as arising from any other dental defect or disease.”

• Alternative terms:
Dentin sensitivity, cervical sensitivity, root sensitivity, cemental sensitivity.

2. Prevalence and Epidemiology

• Prevalence ranges from a few percent up to 85%.

• Common in patients aged 30–40 years (range: 20–50).

• More prevalent in females.

• Self-reported questionnaires report higher prevalence than clinical exams.

• Most affected teeth: Canines and premolars, especially buccal surfaces.

• Dentists estimate ~10–25% of patients have DH; ~1% have severe symptoms.

• May occur at any age.

• Many patients do not seek treatment, viewing it as minor.

3. Etiopathogenesis

3a. Tooth Anatomy and Dentin–Pulp Complex

• Dentin: Vital tissue covered by enamel (crown) and cementum (root).

• Contains numerous dentinal tubules filled with odontoblastic processes and fluid (~22%).

• Enables stimulus transmission to the pulp.

3b. Pathogenesis

Phase 1 – Exposure

• DH doesn’t occur with intact enamel/cementum.

• Caused by:

◦ Abrasion (e.g. hard brushing)

◦ Attrition (tooth-to-tooth wear)

◦ Erosion (acidic sources)

◦ Abfraction (stress lesions)

• Gingival recession exposes root dentin, esp. buccal surfaces of canines/premolars.

• Sensitive dentin shows:

◦ ~8× more tubules

◦ Wider tubules

◦ Thinner smear layers

Phase 2 – Sensitization

• Smear layer/tubular plugs removed by acids or brushing.

• Fully open tubules allow stimuli access to pulp.

• Loss of smear layer ↑ permeability and pain.

4. Mechanism

Direct Innervation Theory (DI):

• Stimuli reach pulp via nerves in dentin.

• Refuted: Few nerves in outer dentin, Rashkov’s plexus matures late.

Odontoblast Receptor Theory (OR):

• Odontoblasts transmit signals to nerves.

• Refuted: Odontoblasts are not excitable and have no direct synapses.

Hydrodynamic Theory (Accepted):

• Fluid movement in open tubules from stimuli (thermal, osmotic, tactile).

• This mechanically stimulates nerve endings in pulp → sharp pain.

• Example: Cold → outward fluid flow → baroreceptor activation → pain.

🧠 Mnemonic:
HYPERSENSITIVE teeth love FLUID FLOW

5. Clinical Diagnosis and Treatment

Diagnosis

• Take thorough history (onset, duration, triggers).

• Clinical tests: Cold/air/water → brief, sharp pain.

• Exclude: Caries, fractures, pulpitis, bleaching-related sensitivity.

• Use: Palpation, percussion, vitality tests, transillumination.

Desensitizing Agents:

Classification:

• By administration:

◦ At-home (toothpastes, rinses)

◦ In-office (varnish, resins, lasers)

• By mechanism:

◦ Neural blockers (e.g. potassium nitrate)

◦ Tubule occluders (e.g. fluoride, oxalates, Gluma)

🧠 Mnemonic: KAP → Key ingredients:

• K – Potassium nitrate

• A – Arginine

• P – Phosphate (calcium phosphates)

At-home Therapy

• Toothpastes:

◦ Early: Strontium, fluoride

◦ Modern: Potassium nitrate/chloride/citrate → reduces nerve excitability

◦ Others: NaF + calcium phosphates; 8% arginine + calcium carbonate + fluoride

• Mouthrinses: K nitrate + fluoride effective

• Reassess after 2–4 weeks

In-office Therapy

Neural Blockers:

• Potassium nitrate gels

• Laser therapy (nerve desensitization)

Tubule Occluders:

• Fluoride varnish/gels: Precipitate CaF₂

• Oxalates: 28% potassium oxalate → calcium oxalate crystals

• Varnishes: Temporary coverage

• Gluma (HEMA + glutaraldehyde): Resin tags + protein coagulation

• CPP-ACP (GC Tooth Mousse): Promotes remineralization

• Bioglass / Portland cement: Forms apatite in tubules

Laser Therapy:

• Diode, Nd:YAG etc.

• Reduces sensitivity by:

◦ Tubule melting/sealing

◦ Coagulating proteins

◦ Desensitizing nerves

Management Algorithm

1. Confirm diagnosis

2. Eliminate causes (brushing, acids)

3. Start at-home care: desensitizing paste + soft brush

4. Reevaluate in 2–4 weeks

5. In-office treatment if symptoms persist

6. Follow-up: fluoride maintenance, hygiene counseling

Discussion

• DH is a chronic and multifactorial condition.

• Most cases respond to conservative therapy.

• The hydrodynamic theory best explains DH.

• Regular follow-ups and preventive care are essential.

🩺 Clinical Case-Based Questions

Q1.
A 35-year-old woman has sharp pain on cold in upper premolars with exposed root surfaces. No
caries or pulpitis.
Diagnosis: Dentin hypersensitivity
Plan:

• Educate on gentle brushing

• Start potassium nitrate + fluoride toothpaste

• Reassess in 2–4 weeks

• If unresolved, apply fluoride varnish or Gluma

Q2.
Generalized sensitivity 24h after ultrasonic scaling. All teeth vital.
Likely cause: DH from dentin exposure
Plan:

• Confirm pain response to air

• Start desensitizing toothpaste

• If persistent, apply 5% NaF varnish or bonding resin

• Adjunct: CPP-ACP (GC Tooth Mousse)

• Reassess in 2–4 weeks

📘 Theoretical Questions

Q1. Define dentin hypersensitivity.

Pain from exposed dentin responding to thermal, tactile, chemical, or osmotic stimuli not due to
other disease.

Q2. Compare DH mechanisms.

Theory Support Explanation

Direct Innervation Weak Few nerves in outer dentin

Odontoblast Receptor Discredited Odontoblasts lack excitability

Hydrodynamic ✅ Strong Fluid movement in tubules → pain

Q3. List systemic causes of pulp calcifications.

• Statins

• Corticosteroids

• Gout

• Hypercalcemia

• End-stage renal disease

• Cardiovascular disease

• Dentinogenesis imperfecta
Q4. Differentiate PCOD vs apical periodontitis.

Feature PCOD Apical Periodontitis

Pulp Vitality Vital Non-vital

Symptoms Asymptomatic Pain, swelling

Radiograph Radiolucent → opaque Radiolucency at apex

Treatment None (follow-up) RCT or surgical intervention

Theoretical Questions:

1. Define dentin hypersensitivity (DH) as per the Canadian Consensus, and list
synonymous terms.

◦ Answer: DH is defined as “pain derived from exposed dentin in response to

chemical, thermal, tactile or osmotic stimuli which cannot be explained as
arising from any other dental defect or disease” Synonyms include dentin
sensitivity, cervical sensitivity, root sensitivity, and cemental sensitivity

2. Compare the Direct Innervation (DI) and Odontoblast Receptor (OR) theories
of DH with the Hydrodynamic theory.

◦ Answer: The DI theory posits nerve fibers extend into dentin, directly
transmitting stimuli to the pulp. The OR theory posits odontoblasts themselves
sense stimuli and signal nerves. Both DI and OR lack strong evidence (no free
nerve endings in superficial dentin; odontoblasts can’t fire impulses)

◦ In contrast, the Hydrodynamic theory (Brännström) – the accepted model –

holds that stimuli induce fluid shifts within exposed tubules, mechanically
triggering pulp nerves to cause pain
3. Describe the two phases in the development of dentin hypersensitivity.

◦ Answer: Phase 1 (lesion localization): Exposure of dentin due to loss of

enamel or cementum (abrasion, erosion, attrition, abfraction, gingival
recession)

◦ Phase 2 (tubule exposure): Removal of smear layer/tubular plugs (by acids

or vigorous brushing) fully opens the tubules, allowing fluid movement in
response to stimuli

4. Classify desensitizing agents by administration and mechanism, and give one

example each.

◦ Answer: By administration: At-home agents (OTC toothpastes, rinses) vs In-

office agents (varnishes, bonding agents, lasers)

◦ By mechanism: Neural blockers vs Tubule occluders

▪ Neural blocker example: Potassium nitrate toothpaste (at-home) that

depolarizes nerves

▪ Tubule occluder example: 5% sodium fluoride varnish (in-office) that

precipitates calcium fluoride in tubules

▪ A helpful mnemonic: KAP – Potassium, Arginine, Phosphate – key

ingredients in many desensitizing pastes.