Dentin Hypersensitivity

 Dentin Hypersensitivity/ Sensitivity

 Dentinal Hypersensitivity/ Sensitivity
 Cervical Hypersensitivity/ Sensitivity
 Root Hypersensitivity/ Sensitivity
 Cemental Hypersensitivity/ Sensitivity

Definition
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.
Pain is described as unpleasant sensory and emotional experience associated with actual or
potential tissue damage, clinically/ classically short, sharp, of rapid onset in character and of the
duration of the applied suitability
dictates choices of foods and drinks, pain may be dull/ sharp, vague/ specific, intermittent/ constant
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 form of dental defect or pathology.

Prevalence
non-carious cervical lesions (NCCLs) and DH in adult populations, with prevalence rates ranging
from 5% to 85% and 2-8% to 78%
age range of 20-50 years. more prevalent with the age range of 30-40 and more prevalent in female
individuals that would probably be related to their dental hygiene and dietary, older  gingival
recession and loss of enamel and cementum
2 methods of determining:
(1) through asking some questions from the patient and (2) through clinical examination.
Occur on canines and premolars, buccal surface. Upper premolars  upper molars  incisors
Periodontitis
Old people with root exposure, usually do not show painful sensitivity d/t:
 Mineral deposition inside the tubules (dentinal sclerosis)
 Reduction in the number of tubules
 Pulp chamber reduction due to an increase of reparative dentin
 A reduction in cellularity, vascularity and nerve fibers in the pulp.
Theories for Dentinal Hypersensitivity
Odontoblastic Transduction Theory
Odontoblastic processes are exposed on the dentine surface  be excited by a variety of chemical
and mechanical stimuli.  release of neurotransmitters and transmission of impulses towards
nerve endings. (outdated)
Neural Theory
From the odontoblastic theory, thermal or mechanical stimuli directly affect nerve ending in dentin
tubules (via direct comm with pulp nerve endings (d/t unmyelinated nerve fibres in the outer layer
of root dentine and presence of putative neurogenic peptides)
Hydrodynamic Theory
By Brannstrom et.al., fluids within the dentinal tubules are disturbed by temperature, physical or
osmotic changes  fluid changes and movements stimulate baroreceptor  neural discharge.
(Dentin tubules are filled with fluid are opened to the oral cavity, dentine surface to within pulp)
The theory states that sensitive dentin is based on the stimulus-induced fluid flow in the dentinal
tubules and consequent nociceptor activation in the pulp/dentin border area. Intradental
myelinated A-β and some A-δfibres are thought to respond to stimuli that displace the fluid in the
dentinal tubules  characteristic short, sharp pain of dentin hypersensitivity
i. Dehydration (desiccation from air movement): outward movement of fluid to dehydrated
surface
ii. Thermal changes: expansion or contraction of dentinal tubules  changes in dentinal fluid
flow
iii. High osmotic stimuli (sugar, acid, and salt): fluid flow within dentinal tubules
iv. compression of the surface / “stiletto heel effect”: compress the surface tissue and on
release cause expansion  increased outward fluid flow
odontoblasts are closely related to the nerve endings, and biological signals are probably
transduced from them to the axons and vice versa.

A. Direct Innervation (DI) Theory

B. Odontoblast Receptor (OR) Theory
C. Fluid Movement/ Hydrodynamic Theory
Aetiology
Average diameter of tubules in sensitive teeth was almost 2 times greater than that of tubules in nonsensitive
teeth (0.83 µm vs. 0.4 µm). According to Poiseuille’s law, which states that fluid flow is proportional to the fourth
power of the radius, diameter differences alone would indicate that the fluid flow in tubules of hypersensitive teeth
should be 16 (i.e, 24) times greater than that of fluid in nonsensitive teeth. Combining the increased number of open
tubules with the increased diameter of the tubules in sensitive teeth, it can be postulated that the fluid flow in sensitive
teeth is approximately 100 times greater than in nonsensitive teeth. The number of tubules increases toward the pulp,
and this may not only increase the probability of dentin hypersensitivity but also help explain any increase in
symptoms as tooth wear advances toward the pulp.

dentin surface of a tooth must be exposed (lesion localisation) by: (1) loss of covering of perio
struct (ging. recession) or (2) loss of enamel
a number of dentin tubules in close proximity to each other must be patent from the pulp to the
oral environment (lesion initiation).
Factors of ging. recession:
1. Inadq attached gingiva
2. Prominent roots
3. Oral habits causing gingival laceration
4. Excessive tooth cleaning
5. Excessive flossing
6. Overzealous tooth cleaning habits
7. Secondary to diseases (NUG, periodontitis, HGS)
8. Crown preparation
Gingival recession  with/ without bone loss  exposed more dentin
 cementum is abraded/ eroded  expose underlying dentin
Root exposure d/t lack of antagonist tooth  extrusion
Reasons of continued dentin exposure: Cause of enamel loss (GERD, Xerostomia)
1. Poor plaque ctrl 1. Attrition
2. Excess oral acids 2. Abrasion
3. Cervical decay 3. Abfraction
4. Toothbrush abrasion 4. Erosion
Factors: Diameter, Patency status, # of open tubules

Pathogenesis
Based on the studies, DH is developed in two phases:
lesion localization: dentin must become exposed
lesion initiation: through either loss of enamel or gingival recession, and the dentin tubules must
be open to both the oral cavity and the pulp
Diagnosis
Investigating the medical history of the patient and examination.
In investigating the medical history ask questions about:
 the time of the start of DH
 the intensity of the pain
 the stability of the pain
 the factors that reduce or increase the intensification of the disease.
1. Which tooth or teeth is/are sensitive and on which aspect?
2. On a scale from one to 10, how much does it hurt, with 10 being the most painful?
3. How long does the pain last?
4. Can the pain be characterized as sharp, dull, shooting, throbbing, persistent, constant, pressure, burning,
intermittent?
5. Does it hurt when you bite down (pressure)?
6. Does the discomfort linger or stop immediately after a stimulus such as cold water is removed?
7. On a scale from one to 10, how much does the pain impact your daily life?
8. Is the pain stimulated by certain foods: Sweet? Sour? Acidic?
9. Does sensitivity result from hot or cold food or beverages?
10. Does discomfort stop immediately upon removal of the painful stimuli, such as cold food or beverage?
11. How effectively are you managing the stress in your life?

In examination, some techniques such as pure air, pure water, and sounds are used in order to
reconstruct the stimulating factors and to determine the degree of pain of the patient.
Some other diagnostic tests are as follows: palpitation for diagnosing pulpitis or periodontal
involvement, pushing a wood stick or transillumination for diagnosing a fracture or cracked tooth.
The degree of pain should be described through qualitative parameters such as slight, medium, and
severe pain or through using quantitative parameters such as visual analogue scale (VAS).
Using a verbal rating scale and the use of a short, intermittent "air blast" to quantify the subjective
level of pain as follows:
0—No discomfort/pain; no discomfort/pain but aware of stimulus
1—Mild discomfort/pain—described as mild discomfort during but not following the air blast
2—Marked discomfort/pain—described as definitive discomfort during the air blast
3—Marked discomfort/pain lasting more than 10 seconds following exposure to air.

Management
2 main methods:
 tubular occlusion
 block nerve activity (direct ionic diffusion, increasing concentration of K+ ions on the pulp)
Ideal properties of desensitizing agent:
 rapidly acting with long-term effects,
 non-irritant to pulp,
 painless and easy to apply,
 should not stain

Mode of administration
 At home desensitizing agents
 Readily available but longer remission time (2-4 weeks)
 In-office treatment
 Not readily available, but provide immediate relief

On the basis of mechanism of action

 Nerve desensitization
 Protein precipitation
 Plugging dentinal tubules
 Dentine adhesive sealers
 Lasers
 Homeopathic medication
Content: strontium chloride, potassium nitrate; dibasic sodium citrate formaldehyde, sodium
fluoride, sodium monofluorphosphate and stannous fluoride
MOA: precipitation of calcium phosphate on the dentin surface and calcium  obliteration of
dentinal tubules
Home use:
1. Silver nitrate  fast coagulation of the Tomes processes forming silver albuminate, which turns
dark when exposed to light  blackening the tooth surface
2. Potassium salts  diffusion along the dentinal tubules  blocking the axonic action 
decreasing the excitability of the intradental nerve fibers
3. Strontium chloride & zinc chloride (protein precipitants)  organic precipitation and
odontoblast denaturation  form sealing film  prevents fluid movement and has an occlusive
action
In office use:
1. Fluorides: precipitation of CaF2 vcrystals inside the dentinal tubules  decrease the dentinal
permeability
Forms: sodium fluoride 2% (acidulated form can form crystal deep in tubules), stannous
fluoride, sodium monofluorophosphate, fluorosilicates (Ammonium hexafluorosilicate) and
fluoride combined with iontophoresis.
2. Oxalate: reacts with the dentin calcium & promotes deposition of calcium oxalate crystals on
the dentin surface & tubules  reducing hydraulic conductivity, sealing the tubules more
effectively than the intact smear layer. May be pre-etched for deeper penetration into tubules
3. Varnish: remove smear layer  apply fluoride (acidulated for improved ion penetration)/
copal varnish  short term relief
4. Adhesive materials: Resin-based dental adhesive systems  seal the dentinal tubules by
forming a hybrid layer (combined dentine-resin layer)  more durable and long-lasting
dentine desensitizing effect
5. Bioglass: silica  acts as a nucleation site for precipitation of calcium and phosphate 
promote infiltration and remineralization of dentinal tubules  forms an apatite layer 
occludes the dentinal tubules
6. Portland cement (calcium silicate cement)  occlude the dentinal tubules by remineralization.
7. Casein phosphopeptide (CPP)–amorphous calcium phosphate (ACP): CPP contains
phosphoseryl sequences which get attached and stabilized with ACP  stabilized CPP–ACP
 prevents dissolution of calcium and phosphate ions  maintains a supersaturated solution
of bioavailable calcium and phosphates
8. Glutaraldehyde (combination of an aqueous solution of 5% glutaraldehyde and 35%
hydroxyethyl methacrylate): reaction with serum albumin in dentinal fluid (protein
coagulation)  precipitate formation  subsequent narrowing or blocking of the tubule 
counteracting the hydrodynamic mechanism effect up to 7 to 9 months
9. Arginine and calcium carbonate formulations: natural biological process of tubule occlusion
by salivary glycoproteins under alkaline pH
10. Periodontal surgery: Mucogingival surgery  root coverage  minimize areas of exposed
dentin
11. Lasers: cause melting of dentine  closure of exposed dentinal surface without causing
cracking (4mm center, 3μm along the lateral margin)  reduction of permeability and
hydraulic conductance
Low-output lasers (diode type)  analgesic effect controlled by decreasing nerve transmission.

Higher output lasers (Nd:YAG and CO2 laser) 

Nd:YAG laser effects on DH is thought to be the laser-induced blocking or contraction of

dentinal tubules and/or analgesia.;

CO2 laser  occluding or narrowing the dentinal tubules

Toothpaste/ dentifrices: contains potassium salts, bioactive glass, combination of fluoride,
hydroxyapaptite and xylitol and 15% n-HA crystals.
Pepsodent Pro-sensitive relief and repair (Hindustan Unilever Limited, India) contains
potassium citrate as an active ingredient along with hydroxyapatite, zinc citrate, and fluoride.
(Potassium ions released from toothpastes diffuse along the dentinal tubules to inactivate
intradental nerves and act by blocking synapses between nerve cells, thereby reducing nerve
excitation and the associated pain.)
NovaMin (bioactive glass) is an inorganic amorphous calcium sodium phosphosilicate (CSPS)
material containing 45% SiO2, 24.5% Na2O, 24.5% CaO, and 6% P2O5. Sensodyne repair and
protect (Glaxo SmithKline, India) is NovaMin (5%) containing desensitizing dentifrices. CSPS in
NovaMin has a strong attraction to collagen as well as physically occludes dentin tubules. Initial
reactivity of the NovaMin particles is associated with the development of a surface negative charge
which facilitates binding to side groups on Type I collagen fibers. NovaMin can quickly occlude
dentin tubules to form a protective layer on the dentin surface but effect takes several weeks.
Remin Pro (VOCO GmbH, Germany) is a water-based desensitizing paste. sodium fluoride (1450
ppm), hydroxyapatite, and xylitol, thus making it effective against demineralization and erosion.
On the tooth surface, fluoride is converted to fluorapatite when it comes in contact with saliva.
Once the fluorapatite layer is formed, the tooth surface becomes more resistant to acid attacks. The
hydroxyapatite contained in Remin Pro fills superficial enamel lesions and the tiniest irregularities
that arise from erosion. Cariostatic properties of xylitol prevent it from being converted into
harmful lactic acid by cariogenic bacteria thus allowing the mouth to naturally remineralize
damaged teeth with less interruption.
nano-Hydroxyapatite toothpaste (Japan) can be easily integrated into the dental tubules thus
enhancing their occlusion and reducing DH. n-HA also facilitates its binding to the dentin apatite
and tooth enamel due to higher surface area, biological activity, and chemical reactivity.
Gingival Recession

Aetiology:

 direct mechanical or physical influence on the gingival tissues

 indirectly due to an inflammatory reaction in the gingival tissue
 calculus, tooth brushing, high frenal attachment (impede plaqueremoval by causing pull on the marginal
gingival), tooth position, tooth movement by orthodontic forces, improperly designed partial dentures,
smoking, restorations, chemicals

Consequences: Aesthetics, gingival bleeding and plaque retention, hypersensitivity, caries

Tx:

 Restoration, crowns, veneers

 Construction of gingival mask (silicone flexible ging veneer)
 Root conditioning (Application of tetracycline HCL or citric acid to root surface before placement of soft
tissue graft)
 Frenectomy
 Surgical root coverage (free epithelial ging graft, subepi . CT graft, semilunar flap., coronally advanced flap,
guided tissue regeneration)

Class Symptoms Treatment Success

Class I Recession that does not extend to the mucogingival Complete root coverage 100%
junction with no periodontal bone loss in the interdental
areas
Class II Recession that extends to or beyond the mucovingival Complete root coverage 100%
junction, with no interdental bone loss
Class III Recession that extends to or beyond the mucogingival Only partial root coverage 50-70%
junction, with some periodontal attachment loss in the to the height of the contour
interdental area or malpositioning of the teeth of interproximal tissue
Class IV Recession that extends to or beyond the mucogingival Root coverage is <10%
junction, with severe bone and/or soft-tissue loss in the unpredictable and requires
interdental area and/or severe malpositioning of the teeth adjunctive treatment (ie
orthodontics)