Oral Health Group
Feature

Dentin Hypersensitivity: Simplified

December 1, 2010
by Fay Goldstep, DDS, FACD, FADFE


All dental practices have patients with dentin hypersensitivity. Many patients avoid dental treatment because of the hypersensitivity. Surprisingly, most practices do not have a systematic approach for diagnosing and treating this condition. This is simply because it seems too complicated. There are a multitude of products. What works? Why does it work? Many practitioners have had poor success in the past with sensitivity treatments and are reluctant to try again. Today’s products are effective and easy to use. The following discussion will attempt to bring simplicity and clarity to the subject of diagnosis and treatment of dentin hypersensitivity.

Definition
Dentin Hypersensitivity is defined as a short sharp pain arising from exposed dentin in response to:

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  •  Thermal change
  •  Evaporation of air
  •  Tactile stimulus
  •  Osmotic pressure
  •  Chemical stimulus

and cannot be ascribed to any defect or pathology.1
The three essential components of dentin hypersensitivity are:2

  •  exposed dentin surfaces
  •  open tubule orifices on the exposed dentin surfaces
  •  patent tubules leading to a vital pulp (Figure 1)

Dentin hypersensitivity has been reported to affect up to 57% of the general population.3-10 It occurs most frequently in patients 30 to 40 years of age.11 All teeth are susceptible but canines and premolars are the most affected.12, 13

A 2002 international survey of 11,000 adults revealed that only half of the affected individuals had talked to their dentist about their sensitivity and only half of this group actually received treatment recommendations.14 Many patients do not wish to burden the dentist with this problem or they may feel that it may not be taken seriously.

Mechanism of Action
The most widely accepted theory for the mechanism causing dentin hyper sensitivity is the hydrodynamic theory first proposed by Brannstrom in 1963.15 When dentinal tubules in vital teeth are exposed and open, the fluid in the tubules flows in an inward or outward direction depending on pressure differences in the surrounding tissue. This fluid shift activates pain receptors in the intratubular nerves or superficial pulp and the patient feels pain.2. (Figure 2)

Diagnosis
Prior to establishing the diagnosis of dentin hypersensitivity, one must first rule out other conditions which exhibit similar symptoms:2

  •  Caries
  •  Pulpitis
  •  Marginal Leakage
  •  Restoration fracture
  •  Cracked tooth
  •  Polymerization shrinkage

It is important to use specific clinical descriptors with the patient (like brief, sharp, localized) to differentiate dentin hypersensitivity from pulpal pain (which is prolonged, dull, aching, poorly localized and longer lasting).2

Risk factors for dentin hypersensitivity include:16

  •  Periodontal disease
  •  Gingival recession
  •  Parafunction (abfractions)
  •  Acidic diet
  •  Xerostomia
  •  Bleaching

These factors predispose the patient to the essential components of dentin hypersensitivity: exposed, open and patent dentinal tubules leading to a vital pulp. There may also be passage of fluids through the enamel. The enamel may be thought of as a semi-permeable membrane that allows passage of fluids and small molecule through the organic defects between the enamel crystals. With time, the organic channels become plugged due to the formation of organic biofilm. When this occurs, the bidirectional flow of fluids stops and so does the pain. During bleaching the organic plugs may be dissolved, reopening the enamel channels and causing sensitivity.17

Treatment
The first line of treatment for dentin hypersensitivity, is of course, prevention. Any and all of the predisposing factors must be dealt with first. This may not be an easy task. Periodontal disease, recession, occlusal forces and diet present many challenges. The treatment of sensitivity is much simpler in comparison.
If we review the mechanism of action of dentin hypersensitivity, it is easy to understand the wide range of products available for treatment. The product must either block the movement of fluid in the tubules or stop the transmission of the pain response to the pulp. For added simplification, it is important to focus on the active ingredient, and not on the multitude of products.

Products are available for in- office or at-home applications. Treatment should not be restricted to one option only. This is not a one-size-fits-all solution. Different treatments may be tried and modified based on the patient’s response.

The first group of products works by occluding the open tubules and decreasing pulpal fluid flow. This group includes: fluorides, fluoride varnishes, tissue fixatives, oxalates, remineralizing agents, and Pro-Argin technology.

The second group of products works by depolarizing the nerve so that it cannot transmit the pain response. These products contain potassium nitrate

Occlusion of Dentinal Tubules
Fluorides
Fluoride application is believed to work through a reaction between the fluoride ion and ionized calcium in the tubular fluid. This reaction forms an insoluble calcium fluoride precipitate in the tubule.18 Different fluorides show differing efficacies. Stannous fluoride is more effective than sodium fluoride in concentrations used for toothpaste formulations. (Figure 3)

Fluoride Varnishes
Fluoride varnishes may be used for sensitivity relief but are chiefly indicated for caries control and remineralization. The desensitization effect is transient since the material is abraded soon after placement. Many applications may be necessary for increased efficacy. It is thought that the benefit comes from the physical blockage of the tubules by the varnish base rather than the fluoride itself.18

Tissue Fixatives
Tissue fixative desensitizing products contain agents such as glutaraldehyde or HEMA. These agents bind to tissue fluid proteins in the dentinal tubules and the superficial cells of the subadjacent pulp and denature (coagulate) these proteins. These products cannot be placed near the gingival epithelium since they may cause necrosis of the gingiva as well as the loss of the biological attachment.17

Oxalates
Desensitizers containing metallic salts, predominantly oxalates, form insoluble chemical precipitates in the peritubular dentin. No acid etch or light curing is needed. They cause no irritation of the gingival tissues. One example is Super Seal by Phoenix Dental. Super Seal forms a complex with the calcium rich zone of the peritublar dentin to create a crystal plug. This effectively shuts down dentin sensitivity at near 100% levels.19 (Figure 4)

Remineralizing Pastes
Remineralizing pastes are used in- office or at-home to restore the minerals that have leached out of patients’ teeth due to caries, diet etc. These pastes have the added advantage of reducing sensitivity, through tubule occlusion. Two active ingredients have been shown to be the most effective for this purpose:

Novamin (calcium sodium phosphosilicate bioactive glass) and Amorphous Calcium Phosphate.

Novamin containing toothpastes have been shown to significantly reduce dentin hypersensitivity, with continued home use.20,21 The effect is cumulative for up to about six weeks and then stabilizes.

ACP forms a protective mineral barrier of hydroxy
apatite which occludes the exposed dentinal tubules.22 (Figure 5)

ACP is most effective in the form called Recaldent (casein phosphopeptide-amorphous calcium phosphate) where the casein portion (derived from milk) binds the ACP to the tooth surface, where it can do its job.

Recaldent containing pastes are placed on the affected areas after regular brushing.

Pro-Argin Technology
In healthy patients, saliva is normally very effective in reducing dentin hypersensitivity. Saliva provides calcium and phosphate which over time occlude open dentin tubules. Pro-Argin technology was developed based on this role that saliva plays in naturally reducing hypersensitivity.23,24

The Pro-Argin formula contains arginine, an amino acid found in saliva. The positively charged arginine binds to the negatively charged dentin surface. This attracts a calcium rich layer from the saliva to infiltrate and block the dentinal tubules16. (Figure 6)

This technology is available for in-office application, through a paste, which is delivered by prophylaxis cup. There is also a toothpaste for at-home use. The in office paste has been found to provide immediate and lasting relief of hypersensitivity for four weeks when it is applied as the final polishing step of a professional cleaning.25 It has also been found to decrease dental prophylaxis discomfort when used prior to the procedure.26

Depolarization of the Nerve
The second major group of desensitization products works by depolarizing the nerve that transmits the pain response. After the nerve is depolarized, it cannot re-polarize and this diminishes its excitability. The ingredient that produces this effect is potassium nitrate.27 According to the FDA, for a potassium nitrate toothpaste to claim to be desensitizing it must contain 5% of the ingredient. Potassium nitrate penetrates the enamel and dentin to travel to the pulp and creates a calming effect on the nerve. This effect can be thought of as “anesthetic-like”.28

Potassium nitrate products are Ideal for whitening sensitivity. Whitening sensitivity occurs due to the easy passage of peroxide through the enamel (a semi permeable membrane) and dentin to the pulp. Desensitization products that work by occluding the dentinal tubules are ineffective in preventing the passage of the tiny peroxide molecule, which can travel in the interstitial spaces between the tubules.28

Potassium nitrate can be delivered in several effective ways to counteract whitening sensitivity:

1. Pre-brushing with a 5% potassium nitrate containing toothpaste for 2 weeks pre-whitening and during whitening. It takes approximately 2 weeks for the potassium nitrate to be at peak desensitization efficacy.29

2. Whitening tray delivery of a potassium nitrate toothpaste for 10 to 30 minutes during whitening treatment. This seems to be very effective for more acute sensitivity.28 It is preferable to use a toothpaste without sodium laurel sulfate (SLS) which is the primary ingredient in most toothpastes, and creates the effect of foaming. SLS has been associated with increased gingival irritation, especially on prolonged contact.

3. Syringe delivery of potassium nitrate and fluoride. The material is applied as needed for specific areas of sensitivity.
4. Potassium nitrate incorporation into the whitening gel itself. Bleaching efficacy does not seem to be affected by this addition30.

Conclusion
Treatment of dentin hypersensitivity is a simple, clear process. It starts with a differential diagnosis ruling out other possible
etiologies like caries, pulpitis, cracks, marginal leakage etc. Next, an attempt is made to eliminate predisposing factors such as periodontal disease, parafunction, acidic diet, and xerostomia.

At the same time, the patient is evaluated with respect to the potpourri of potential desensitization ingredients and the products which contain them. It is essential for the dental practitioner to know these ingredients, their mechanisms of action, benefits and indications. Some patients may require more than one type of treatment. The treatment is fine tuned until a successful solution is found. There is no longer a reason for any patient to endure dentin hypersensitivity. Simple answers have been found to this longtime problem. And the dentist has created a patient for life.    OH

Dr. Fay Goldstep sits on the Oral Health Editorial Board (Healing/Preventive Dentistry), has served on the teaching faculties of the Post-graduate Programs in Esthetic Dentistry at SUNY Buffalo, the universities of Florida (Gainesville) and Minnesota (Minneapolis). She has lectured nationally and internationally on healing dentistry, innovations in hygiene, dentist health issues and office design. Dr. Goldstep is a consultant to a number of dental companies, and maintains a private practice in Markham, ON, Canada and can be reached at goldstep@epdot.com.

Oral Health welcomes this original article.
References available upon request.