Managing Dentin Hypersensitivity

Tooth sensitivity has been linked to many causes, including a fractured cusp, dental caries, toothbrush abrasion, abfraction or erosion from gastric acids. Other sources can stem from food and drinks, such as wine, soda and energy drinks. During the 20th Century, populations in developing countries have experienced a drastic increase in cases of decayed, filled or missing teeth, all of which can contribute to tooth sensitivity. Leaky or broken restorations, cracked tooth syndrome and pulpitis are additional sources that can cause pain in patients. If the above prove to be absent, however, then sensitivity may be linked to dentin hypersensitivity.

A diagnosis of dentin hypersensitivity is made through a process of elimination of other factors. The condition has been defined as, “a 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 other form of dental defect or pathology.”¹ Many people avoid the things that can cause this pain, including breathing in cold air, hot or cold drinks or certain foods that may stimulate the pain. The prevalence of dentin hypersensitivity can range from 8 to 57% in the general population and, among periodontal patients, its frequency is considerably higher (60 to 98%).^{2- 8}

‘LARGE AND SMALL STRAWS’

Teeth are set up with a series of hollow tubes (called dentinal tubules) that extend from the pulp laterally to the dentino enamel or cemento enamel junction and are occluded with enamel or cementum (Figure 1). Some authors and instructors have described the tubules as a handful of straws with openings of various diameters, some small and some large. On the pulpal side is a cell called an odontoblast that has a process extending into the tubule. Some tubules also contain a nerve. The tubule is filled with fluid that surrounds the nerve axon and odontoblastic process, and when fluid moves within the dentinal tubules it causes pain. This is known as the hydrodynamic theory and is accepted by most dental health professionals as the most logical expla- nation of why pain is felt.

In a healthy patient, the dentinal tubules in the root are covered by cementum and gingival mucosa. In time, however, the gingiva can move apically due to poor hygiene technique such as improper tooth brushing. Once the soft, thin cementum layer is exposed at the cementoenamel junction, acids can erode or abrasives in toothpaste can remove the protective covering that the cementum provides, and the dentinal tubules are no longer occluded. Thus, air, fluid, acid, heat, cold, touch and other factors cause the fluid within the tubule to move outwardly or inwardly. This exerts pressure (or stimulation) on the nerve, resulting in a pain response.

In order for patients to develop dentin hypersensitivity, two processes must be in place: First, the dentin has to be exposed (lesion localization). Second, the dentinal tubule system has to be opened and be patent to the pulp (lesion initiation).⁹ Usually these tubules are occluded with calculus or cementum, and during routine periodontal therapy the calculus and sometimes cementum is removed—resulting in the tubules no longer being occluded, causing patients to be more sensitive postoperatively.

PREVENTIVE MEASURES

What can patients do to prevent or reduce the loss of the protective covering? It is best to use preventive measures that would reduce the exposure of the tubules (for example, by recommending that patients avoid aggressive brushing with a medium- or hard-bristle toothbrush). Most toothpaste contributes little to hard-tissue loss if used in the typical twice-a-day manner—however, many dentin hypersensitivity sufferers will brush their teeth in excess, up to five times a day.^{10, 11}

Once other factors for tooth pain have been eliminated, it is necessary to follow a systematic approach to treating dentin hypersensitivity. One of the first things to suggest to patients is the least invasive method or product that they can use, such as one of the desensitizing types of toothpaste available today. These toothpastes can either reduce dentinal tubule flow, or block the nerve response— or combination of both.

Both potassium nitrate and potassium chloride have been used to perform this task in at-home application, and with great success.^9,12 Fluid flow reduction has been accomplished with many agents that create a new smear layer or are surface blockers.

TREATING HYPERSENSITIVITY

Desensitizing toothpaste should be one of the first choices of treatment because these products are inexpensive, non-invasive, easy to use and readily available. The most common dentifrices add either a potassium salt, such as potassium nitrate, or strontium salt, such as strontium chloride. The exact mechanism of action of the potassium ions (chloride, citrate, nitrate or oxalate) is still uncertain, but it is speculated that high concentrations of potassium close to the dental surface could lead to a depolarization of the membrane of the nerve fibers, preventing their repolarization and thus inhibiting the sensation of pain.^13,14 Strontium-type dentifrices (acetate and chloride) are thought to reduce sensitivity by actually plugging or occluding the tubules.

When considering in-office therapy, it should be determined if the patient has general sensitivity or localized sensitivity. The clinical procedures chosen should be different for the two types. An isolated, inoffice approach can be adopted for the localized form, whereas the use of homecare products by the patient can be a viable alternative for generalized forms of sensitivity.¹⁴

Generalized tooth sensitivity treatment requires patient compliance because success hinges on the patient following the treatment plan. Patients should reduce or eliminate risk factors and adopt practices that minimize dentin hypersensitivity, examples include:

• Aggressive brushing
• Avoid foods or drinks that are acidic, including energy drinks and winE
• If acidic foods or drinks are ingested, it is recommended that patients rinse with water soon afterward, or use a fluoride type rinse.
• After eating or drinking, it is advisable to delay brushing so as to allow tooth enamel to remineralize naturally after meals

FOLLOW-UP APPOINTMENTS

It is important to follow up regularly with your patients to re-evaluate their sensitivity and compliance with prescribed treatment. If they are still experiencing hypersensitivity after three or four weeks, and report having been compliant with treatment, then a prescription of high concentrated fluorides, usually 5,000 ppm, should be considered as an adjunct.

DESENSITIZING AGENTS

If the patient still complains of either generalized or localized dentin sensitivity, then a licensed oral healthcare professional can apply a desensitizing agent directly to the teeth. Agents that block or occlude the tubules include fluoride varnishes, dentin bonding agents, glass ionomer cements and, if needed, composite resins or periodontal graft surgery.

As mentioned earlier, calculus can often occlude the dentinal tubules and, when removed, result in postoperative sensitivity. New anti-sensitivity agents have recently been introduced. Sensitive ProRelief (Colgate Oral Pharmaceuticals, Canton, Mass.) contains ProArgin technology consisting of arginine and an insoluble calcium carbonate that effectively forms crystals to block the tubules with two three-second applications (this product was previously available as ProClude). NUPRO NUSolutions (DENTSPLY, York, PA) polishing paste contains NovaMin, and its formulation allows for the blockage of tubules to immediately relieve sensitivity. A normal prophylaxis using these new polishing pastes for relief of dentin hypersensitivity transforms a routine procedure into one that is now therapeutic.¹⁵

By following these simple steps, oral healthcare professionals can aid patients suffering from dentin hypersensitivity and help them reduce or even eliminate pain, thus improving the quality of life.

REFERENCES

1. HollandGR, Narhi MN, Addy M, Gangarosa L, Orchardson R. Guidelines for the design and conduct of clinical trials on dentine hypersensitivity. J Clin Periodontal . 1997;24(11):808-13.
2. Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity-an enigma? A review of terminology, epidemiology, mechanisms, aetiology and management. Br Dent J. 1999;187(11):606-11
3. Addy M. Dentine hypersensitivity; definition, prevalence, distribution and aetiology. In: Addy M, Embery G, Edgar WM, Orchardson R, editors. Tooth wear and sensitivity. Clinical advances in restorative dentistry. London: Martin Dunitz; 2000;239-48.
4. Jackson R. Potential treatment modalities for dentine hypersensitivity home use products In: Addy M, Embery G, Edgar WM, Orchardson R, editiors. Clinical advances in restorative dentistry. Tooth wear and sensitivity. London: Martin Dunitz; 2000;326-338.
5. Canadian Advisory Board on Dentin Hypersensitivity. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity, J Can Dent Assoc. 2003;69:221-226.
6. Chabanski MB, Gillam DG, Bulman JS, et al. Prevalence of cervical dentine sensitivity in a population of patients referred to a specialist periodontology department. J Clin Periodontal 2002;52:375-376
7. von Troil B, Needleman E, Sanz M. A systematic review of the prevalence of root sensitivity following periodontal therapy. J Clin Periodontal. 2002;29(Suppl) 3:173-177.
8. Strassler HE, Serio FG. Dentinal Hypersensitivity: Eitlogy, diagnosis and management Available at: www.ineedce.com. Accessed March 9, 2010.
9. Kelsch N, Dentinal Sensitivity: Cause and Treatment. Journal of the California Dental Hygienists Association. 22:14-19.
10. West NX. Dentin hypersensitivity; clinical and laboratory studies of toothpastes, their ingredients and acids. [dissertation] Cardiff, United Kingdom, University of Wales, 1995.
11. West NX. Dentin hypersensitivity: preventive and therapeutic approaches to treatment, Periodontology. 2000. 2008;48:31-41.
12. Touyz LZG, Stern J. Hypersensitivity dentinal pain attenuation with potassium nitrate. Gen Gent. 1999;47:42-45.
13. Kim S. Hypersensitive teeth: desensitization of pulpal sensory nerves. J Endod. October 1986;12(10):482-485.
14. Rosing CK, Fiorini T, Liberman DN, Cavagni J. Dentine hypersensitivity: analysis of self-care products. Braz Oral Res. 2009;23 (Special Issue):56-63.
15. Duran I, Sengun A. The long term effectiveness of five current desensitizing products on cervical dentin sensitivity. Journal of Oral Rehabilitation. 2004;31;351-356.

From Dimensions of Dental Hygiene. June 2010; 8(6): 56, 58, 60, 62.