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The Complexity of Dentin Hypersensitivity

Dimensions of Dental Hygiene speaks with David H. Pashley, DMD, PhD, about the mechanics, diagnosis, and treatment methods for sensitive teeth.

David H.Pashley, DMD, PhD, is regents’ professor of Oral Biology in the school of Dentistry and professor of Physiology and Endocrinology in the School of Medicine at the Medical College of Georgia, Augusta. He received the Hollenbach Award from the Academy of Operative Dentistry in 1998 and the Wilmer Souder Award in 2001 for his work materials.

Patients don’t always tell us about their sensitive teeth. Dental hygienists are well-versed in deciphering these signals. However, those experiencing dentin hypersensitivity often don’t tell us because of their fear of needing expensive or elaborate dental work. Dentin hypersensitivity is fairly mysterious even to this day. Its etiology is elusive and well-designed clinical trials are difficult to perform. But patients need not suffer. Dental hygienists are posed to be a patient’s first line of defense when it comes to dentin hypersensitivity. Most importantly, hygienists need to rule out other more serious problems that may exhibit the same symptoms as hypersensitivity. If other problems are not the cause of the pain, then the hypersensitivity can be addressed with the many treatments available. Dental hygienists have the perfect opportunity to be pro-active by asking our patients about dentin hypersensitivity. Even small levels of dentin hypersensitivity can lead patients to modify their oral hygiene habits such as avoiding brushing in certain areas or cancelling dental appointments. Understanding what is known about dentin hypersensitivity is the first step toward treating it.
—Dimensions of Dental Hygiene

Describe the mechanics of dentin hypersensitivity.

When dentists first started drilling into teeth, usually without anesthesia, they found that enamel was not sensitive but as soon as they drilled through enamel, they discovered the dentin was very sensitive. They assumed that the dentinal tubules must have nerves that go all the way out the tubules to the enamel. So they asked their anatomy colleagues to stain dentin to reveal the nerves. Instead, at the pulpal ends of the tubules, they found column-shaped cells called odontoblasts. These cells extended a cellular process called the odontoblast process out into the tubule at an unknown distance.

Much later in the 1940s and ’50s, they thought that drilling or root planing activated the odontoblast receptor and that nerves in the pulp then connected to odontoblasts through specialized junctional complexes called synapses. In the nervous system, synapses join two nerves together. Odontoblasts are not nerves. When researchers began to look for synapses between odontoblasts and pulpal nerves, they could not find any. Thus, that theory was rejected.

Immense controversy about the mechanism of sensitivity existed until the 1960s when Martin Brännström, Odont Dr, became interested. He knew that patients were sensitive to air blasts, drilling, scratching with an explorer, hot and cold, and osmotic stimuli. Using freshly extracted human teeth, Brännström removed the end of the root and sealed a glass capillary tube into the pulp chamber. He filled the glass tubule and root with water. He marked the position of the end of the column of water with a marking pen. When pain-producing stimuli, eg, air blasts or ice, were applied to exposed dentin in these extracted teeth, the fluid in the capillary moved toward the crown. Some stimuli caused movement outward, some caused movement inward. Brännström’s experiment showed that the direction of the fluid movement did not matter but rather the quickness of the movement caused the pain. He developed the hydrodynamic theory, which is largely accepted today.1-3

Figure 1. Smear layer (SL) and smear plugs (SP).

The hydrodynamic theory says that anything that causes fluid shifts will cause pain. The corollary of this is if the fluid movements can be stopped, the pain will also cease. At the Medical College of Georgia School of Dentistry, we decided to occlude the tubules to reduce dentin sensitivity. We screened dozens of chemicals that might react with dentin and found several that were very useful. The occluding material has to be smaller than a dental tubule diameter (1 micron), so these crystals must be sub-1 micron. We wanted to use a white precipitate and thus we developed the oxalate type products.

The main predisposing factor for sensitivity is exposed dentin. Attrition, abrasion, abfraction, and chemical exposure can all wear away the cementum, creating exposed dentin. The most common cause is toothbrush abrasion.

Why are some exposed areas of dentin hypersensitive while other areas are not?

Masahiro Yoshiyama, DDS, was very interested in this problem. He isolated the most sensitive area of a tooth and then took a hollow diamond bur about half a millimeter in diameter. He drilled into the root about half a millimeter. He snapped this section off and then looked at it under a scanning electron microscope. He would make the same core over a nonsensitive area and then repair those defects with glass ionomer cement. Using the scanning electron microscope, he showed that the sensitive areas had open tubules and the nonsensitive areas had closed tubules.4,5 This means that not all exposed dentin has open tubules and only open tubules are sensitive. We have found through studying extracted teeth that even though some of the tubules look like they are open on the surface, they are not always open all the way down. They can be closed beneath the surface.

Why is the diagnosis of dentin hypersensitivity difficult?

Dentin hypersensitivity is several conditions and dental professionals can’t always tell the difference. For a patient with mildly sensitive teeth, a desensitizing toothpaste or gel is recommended. Another patient may not let you touch him because of extreme sensitivity. This patient is hypersensitive. Determining this difference is the cause of much debate.

Two variables exist in dentin sensitivity. The first is how conductive the dentin is to fluid movement. The second is how sensitive the nerve is to stimuli. Tubules appear smooth and long but this is misleading. All types of debris are inside, especially collagen fibrils, which cause restriction of fluid flow. There are collagenases in the pulp that can come out to slowly dissolve those intertubule collagen fibrils. If for any reason the body removes the collagen, the tubules become hyperconductive and hypersensitive but this takes a long time. When exposed dentin is present and plaque builds up because the patient won’t brush due to the pain, the bacterial products and plaque diffuse into the pulp and cause very localized, low-grade inflammation. This is not pulpitis but it’s enough inflammation to cause changes in the nerve where it actually becomes hypersensitive.

In a normal patient with mildly sensitive dentin, occluding products reduce permeability by 80%, which is sufficient to desensitize patients with normal nerve thresholds. On the other hand, 80% reduction in permeability is not enough in patients whose nerves are hypersensitive to plaque products. That’s why some products work for some and not others. Nothing completely seals dentin perfectly following one application as they are partial occlusions. Several applications may be necessary.

Does polishing reduce sensitivity?

Anything that contains silica, which most prophy pastes and toothpastes do, will reduce sensitivity. There are very small submicron silicas in most toothpastes and probably prophy pastes that are rather effective in decreasing permeability. Polishing helps reduce sensitivity because it creates a smear layer and possibly forces some of the abrasives from the prophy paste down into the tubules, thus occluding them. The problem is that the smear layer is composed of hydroxy and apatite so when acidic foods like lemons are consumed, it gets removed.

What role does the smear layer play?

A curet has a hardness that is greater than the hardness of dentin so when a curet is used, the dentin is cut and smeared. The dentin becomes sticky, shattered, and sawdust-like and it occludes the tubules, actually forcing some of that debris down inside every tubule. This forms a smear plug and then the smear layer is burnished over on top of it (Figure 1, page 24). This decreases sensitivity and often patients leave the operatory without much sensitivity from the scaling. But over the next 5 to 7 days as they are eating acidic foods and brushing, demineralization occurs. With the smear layer removed, sensitivity is felt. Patients can be more sensitive after their scaling than they were before.

Are topically applied products effective enough that reapplication or home care are not necessary?

No, because these products produce precipitates on and just below the surface. If patients are brushing their teeth incorrectly, they can brush the precipitate off in weeks. With other patients, it can last for months. The goal is to stop the fluid flow enough so with normal salivary secretion, the saliva will remineralize the tubules closed. Toothbrush instruction is critical along with diet and plaque control.

When is a more intensive treatment approach indicated?

I recommend starting with the simplest approach—evaluating the effectiveness of the agent by stimulation using an air blast or explorer before and immediately after topical treatment. The treatment should cause a big change. If nothing happens and the application is repeated and the sensitivity is still not reduced, then another problem exists. This perhaps indicates a beginning pulpitis. Because products that occlude the tubules reduce permeability but don’t seal, a resin-based product is the next step. With resins, filling up the gingival sulcus is a potential hazard that needs to be avoided. Then if it’s still sensitive, a differential diagnosis for pulpal pathology should be followed.

What is the role of tertiary dentin?

When teeth are developing, the crown is formed by primary dentin and then, normally when the root apex closes or when the tooth erupts, there is a slowing down of dentin formation. This is secondary dentin formation. The tubules are still in communication with each other and there is a very slight difference in the rate of formation of dentin, which continues until hardly any pulp chamber is left in old age. Tertiary dentin, or reparative dentin, is formed in response to some kind of severe irritation like a cavity preparation or a carious lesion. Tertiary dentin as a treatment is not reliable because some people make it and some don’t. Young people make it faster than old people and it takes 30 to 60 days.

Reparative dentin forms when odontoblasts receive stimulation that is so profound that it actually kills the odontoblasts and forces the pulp to differentiate new odontoblasts. New dentin is formed. The odontoblast-like cells don’t have a process so they can’t make tubular dentin until they form a cytoplasmic process. Tertiary dentin often begins to be atubular and impermeable, so it is very effective but it takes at least 30 to 60 days. Even if we knew how to turn it on, the patient should not suffer for 60 days. I think we can do a lot to help our patients from the outside of the tooth.

What is the nerve depolarization method?

Milton Hodosh, DDS, is the dentist who developed the first patent on the use of potassium nitrate as a desensitizer. Clinical trials showed that 5% was effective but it takes at least 2 weeks and more typically 4 weeks in an 8 to 12 week study.6,7 Depolarization is an effective follow-up method to a professionally applied treatment.


  1. Brännström M, Linden LA, Astrom A. The hydrodynamics of the dental tubule and of pulp fluid. A discussion of its significance in relation to dentinal sensitivity. Caries Res. 1967;1:310-317.
  2. Brännström M, Linden LA, Johnson G. Movement of dentinal and pulpal fluid caused by clinical procedures. J Dent Res. 1968;47:679-682.
  3. Brännström M. Etiology of dentin hypersensitivity. Proc Finn Dent Soc. 1992;88(suppl 1):7-13.
  4. Yoshiyama M, Masada J, Uchida A, Ishida H. Scanning electron microscopic characterization of sensitive vs insensitivie human radicular dentin. J Dent Res. 1989;68:1498-1502.
  5. Yoshiyama M, Noiri Y, Ozaki K, Uchida A, Ishikawa Y, Ishida H. Transmission electron microscopic characterization of hypersensitive radicular dentin. J Dent Res. 1990;69:1293-1297.
  6. Hodosh M. A superior desensitizer—potassium nitrate. J Am Dent Assoc. 1974;88:831-832.
  7. Kanapka JA. Over-the-counter dentifrices in the treatment of tooth hypersensitivity. Review of clinical studies. Dent Clin North Am. 1990;34:545-560.

From Dimensions of Dental Hygiene. July 2004;2(7):22, 24, 26, 28.

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