Dentin hypersensitivity is consistently a top chief complaint dental hygienists hear from patients. Levels of sensitivity and the underlying causes of this condition can vary widely making it important to create a personalized treatment plan for each patient. Dentin hypersensitivity is characterized by short, sharp pain from exposed dentin in response to thermal, evaporative, tactile, osmotic or chemical stimuli that is not caused by any apparent dental defect or disease.5 It is estimated 45-57% of the population is affected by some level of dentin hypersensitivity, but it is difficult to give a more exact number due to the differences in methods and populations studied.5
Saliva plays a natural role in reducing sensitivity by providing a smear layer containing calcium and phosphate that work to lightly occlude and protect dentin tubules. This layer has been shown to be greatly supported by an alkaline oral environment but is easily disrupted by chemical and physical forces. It is important to note not all exposed dentin is sensitive; hypersensitive dentin displays wide-open, under-calcified tubules. The hydrodynamic theory, the most accepted explanation of dentin hypersensitivity relates to fluid force; it describes a centrifugal fluid movement within dentin tubules that activate nerve endings in the pulp-dentine complex.3
Researchers agree that gingival recession more so than the loss of cervical enamel is the key pre-disposing factor in dentin hypersensitivity.2 Exposed dentin may present with attrition, abrasion, erosion, or abfractions. Prevention of the progression of recession and dentin hypersensitivity begins with identifying causative factors like over-brushing, poor oral hygiene, acidic diet, bruxism, premature contacts, and dry mouth. A higher incidence of dentin hypersensitivity has also been reported by 60-98% of patients who have undergone periodontal therapy.2,3
Steps for patients with dentin hypersensitivity
- Differential diagnosis, to exclude other conditions giving rise to similar pain symptoms such as infection or dental decay.
- Correct diagnosis of dentin hypersensitivity after collection of detailed clinical and dietary history and clinical examination.
- Identification of etiologic and predisposing factors, particularly dietary and oral hygiene habits which may lead to erosion and abrasion.
- Removal or minimization of identifiable etiologic and predisposing factors through nutritional counseling and oral hygiene instruction.
- Recommendation or provision of treatment based upon individual needs followed up with a regular review and emphasis on prevention of the condition.2
There are two main modes of action for desensitizing treatment. Products act by either occluding exposed dentin tubules, or by blocking neural transmission. Desensitizing toothpaste makes up 10% of the global market, and over-the-counter desensitizing gums and mouth rinses are also available. In a study comparing the efficacy of toothpastes and mouth rinses, a 5% potassium nitrate/sodium fluoride/xylitol/triclosan toothpaste was found to be equally effective in reducing sensitivity over a four-week period as a mouth rinse containing 3% potassium nitrate/sodium fluoride/xylitol/triclosan.2,3,5
Potassium salts diffuse along dentinal tubules working to decrease the excitability of intradental nerve fibers by blocking axionic action. Potassium citrate 5%, potassium citrate 5.5%, and potassium chloride 3.75% can be used interchangeably and are more effective than fluoride alone.2 Potassium nitrate 5% is most commonly found in the United States because it is the only ingredient approved by the FDA and validated for the relief of sensitivity by interruption of neural response to pain stimuli.3 Studies show potassium nitrate 5% must be used twice daily for at least two weeks for a measurable reduction in sensitivity, and four to eight weeks for pain reduction.2 The downside of potassium salts is solubility; the ingredient is only effective when potassium ion concentrations remain high.1 If this ingredient is effective in reducing a patient’s dentin hypersensitivity, continued long-term use can be recommended.
Fluoride decreases dentinal permeability by precipitation of calcium fluoride crystals inside dentinal tubules.3 These crystals are partially insoluble in saliva making fluoride a good desensitizing option. Fluoride may be recommended as part of an at-home toothpaste or mouth rinse, or as an in-office varnish application.
Oxalates reduce dentinal permeability and occlude dentinal tubules. Calcium oxalate crystals form inside tubules and on surface dentin after application.
Adhesive materials like glass ionomer and composite form a hybrid layer after smear layer removal to seal tubules. The dentinal surface is etched forming a deep dentinal resin tag inside tubules to occlude them permanently.
Bioglass forms an apatite layer to occlude tubules. Made up of calcium phosphorsilicates, the silica components act as nucleation sites for calcium and phosphate and may have the potential to release calcium and phosphate in an aqueous environment to provide sensitivity relief.2,3
Lasers may coagulate proteins inside dentinal tubules blocking fluid movement. It is not completely clear if Nd-YAG lasers may occlude tubules but GaA1A lasers have shown promise in affecting neural transmission in dentinal tubules.
Casein phosphate-amorphous calcium phosphate (CPP-ACP) can remineralize sub-surface enamel lesions and prevents calcium/phosphate ions from dissolving.
Arginine Calcium Carbonate is found naturally in saliva and reduces dentin fluid flow by occlusion. Arginine is a physiologically positively charged amino acid generally combined with a bicarbonate pH buffer and calcium carbonate as a source of calcium. Higher salivary levels of calcium, phosphate, and carbonate create resistance to normal pulpal pressure and acid challenges.2,4 Arginine calcium carbonate has been shown to show instant relief of sensitivity in some cases and works more quickly than potassium salt and fluoride combination.
Moderate dentin hypersensitivity management typically begins with at-home, over-the-counter desensitizing therapy. If a patient returns after six to eight weeks without relief, in-office treatment options may be initiated from varnish to bonding. In severe cases where patients do not respond to therapy, and individual symptomatic teeth can be identified, endodontic therapy may ultimately need to be considered.3 It is important to determine the underlying cause of dentin hypersensitivity so a personalized treatment plan for each patient can be made to help alleviate their discomfort.
- Charig, A. J., Chapin, C. A., Major, E. E., Thong, S., & Winston, A. E. (2009, October 01). Mechanism of Action of a Desensitizing Fluoride Toothpaste Delivering Calcium and Phosphate Ingredients in the Treatment of Dental Hypersensitivity. Retrieved from https://www.aegisdentalnetwork.com/cced/2009/10/mechanism-of-action-of-a-desensitizing-fluoride-toothpaste-delivering-calcium-and-phosphate-ingredients-in-the-treatment-of-dental-hypersensitivity
- Cummins, D., Ph.D. (2010). Recent advances in dentin hypersensitivity: Clinically proven treatments for instant and lasting sensitivity relief. American Journal of Dentistry,23(A), 1-19. Retrieved from http://www.amjdent.com/Archive/2010/AJOD May Sp Issue Smaller.pdf
- Miglani, S., Aggarwal, V., & Ahuja, B. (2010). Dentin hypersensitivity: Recent trends in management. Journal of Conservative Dentistry : JCD, 13(4), 218–224. Retrieved from http://doi.org/10.4103/0972-0707.73385
- Petrou, I., Heu, R., Stranick, M., Lavender, S., Zaidel, L., Cummins, D., Gimzewski, J. K. (2009). A breakthrough therapy for dentin hypersensitivity: How dental products containing 8% arginine and calcium carbonate work to deliver effective relief of sensitive teeth. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19489189
- Sharma, S., Shetty, N. J., & Uppoor, A. (2012). Evaluation of the clinical efficacy of potassium nitrate desensitizing mouthwash and a toothpaste in the treatment of dentinal hypersensitivity. Journal of Clinical and Experimental Dentistry, 4(1), e28–e33. Retrieved from http://doi.org/10.4317/jced.50665