SensiStat: A New Saliva-Based Composition for Simple and Effective Treatment of Dentinal Sensitivity Pain

Dentistry Today


It has been estimated that approximately 30 million American adults suffer from short, sharp, and frequent episodes of dental pain at one time or another from: (1) cold items such as ice cream or ice cubes; (2) a metal object such as a fork; (3) air on a cold day or a dentist’s air syringe; or (4) very sweet foods or liquids that come in contact with their teeth. This painful condition is usually referred to as dentinal sensitivity or dentinal hypersensitivity. If left untreated, it can sometimes lead to necrosis and, ultimately, tooth loss.1


The sensitive tooth process starts when the cementum or enamel covering dentin is removed or breached, and the fluid within the exposed dentinal tubules is able to transmit pain-producing stimuli. Dentinal fluid is a serum-like liquid that is derived from the tissue fluid of the dental pulp. The rigid nonyielding walls of the tubules that it fills ensure that the slightest change in the movement of fluid within open tubules will be transmitted throughout their lengths as a disturbance (Figure 1). For example, cold causes slight dentinal fluid shrinkage, touch causes a minute pressure change, air causes some dentinal fluid evaporation, and sweets cause osmotic movement.2-4 Fluid disturbances such as these reach mechano-receptors of pulpal nerve fibers that are attached to odontoblasts that protrude into the pulpal end of the dentinal tubules and are interpreted as pain (Figure 1). The cementum and enamel covering the dentin have no such tubules, no innervation, and hence no involvement in pain sensation other than protecting the dentin and keeping its fluid-filled tubules inactive as a pain sensor.

The concept of hydrodynamic transmission or transduction in dentinal pain causation was first formulated by Gysi6 at the turn of the twentieth century, and mainly expanded upon by Brännström2,3 and Brännström et al,5 and thereafter by Pashley4,7 and others. It is now generally accepted by most researchers in this field as being central to the problem of dentinal sensitivity.

Dentinal fluid arises from the tissue fluid that permeates the pulp of the tooth. It is only subject to movement and leakage out of open dentinal tubules when the cementum covering the cervical part of the dentin is breached by acid or abrasion, or the enamel covering the crown part of the dentin is breached, for example by restorative procedures or crown fracture. When this happens, dentinal fluid ceases to be immobile and becomes a slowly leaking fluid pushed out of the tubules by hydrostatic pressure derived from the blood and tissue fluid of the pulp.


About 80% of sensitive teeth are premolars and cuspids.8-10 Affected are mainly the facial rather than the lingual surfaces of these teeth near the gingival margin. Prevalence is more on the left side of the mouth in right-handed people and the converse for left-handed people because of their respective manipulative abilities in brushing their teeth.9 Women have a higher prevalence rate than men, and this is attributed partly to more frequent tooth brushing by women.11 Sensitive teeth begin to appear when an individual reaches about 25 to 30 years of age, and are most prevalent in approximately 30- to 50-year-olds. This is the age when gingival recession develops and when the roots of the teeth and the thin covering of cementum, become exposed to the oral environment.


Cementum is easier to breach following contact with acid than enamel, because cementum is thinner and solubilized easier by certain foods (eg, fruit juices and diet and nondiet sodas, which are generally very acidic). Cementum is also more easily lost than enamel as a result of toothbrush abrasion.9 In essence, it is dietary acids and abrasive brushing of the teeth that are the major reasons for loss of cementum.

Another means of cementum removal and a cause of dentinal sensitivity is scaling and root planing performed to remove calculus.4,12 This appears to be especially true when done in conjunction with periodontal surgery where root exposure is more pronounced. Toothpastes with anti-calculus agents and other oral products such as some mouthwashes and bleaching agents13 may also contribute to this process either by contributing to acid erosion or interfering with the natural remineralization function performed by saliva. The latter involves replacement of mineral lost from cementum or enamel with salivary calcium and phosphate.


Cutting into the crowns of teeth when restorative procedures are carried out usually results in open dentinal tubules,14 often with postoperative pain. This is because such procedures result in removal of enamel and reduced thermal insulation. Placement of a restoration can result in microscopic spaces and microleakage between restorations and tooth walls. As a consequence of the latter, pain-causing stimuli are able to affect any fluid between the restoration and tooth that forms a continuum with open dentinal tubules. Materials applied as linings of cavity preparation walls are frequently used in anticipation of this problem, but often are less than satisfactory.


Because loss of cementum leads to open dentinal tubules, it logically follows that plugging or sealing these tubules will stop the leaking and ability of fluid movement in these tubules to elicit pain. Saliva with its remineralizing ability can gradually plug such open tubules, but this usually involves considerable time during which pain can still be elicited. Saliva does this by more than one means. One is by supplying calcium and phosphate ions that are carried by the saliva into the open tubules and gradually bring about tubule plugging. This is slow and occurs in the presence of dentinal fluid outflow.

A second means by which saliva can help seal open dentinal tubules is by forming a precipitable aggregate consisting of calcium phosphate in combination with salivary glycoproteins. This aggregation process is favored by a more alkaline salivary pH. The composition of the aggregates formed and the relation of their formation to the pH was discovered in the 1970s and named salivary precipitin.10,15 However, salivary precipitin formation, while helpful in plugging tubules, when excessive can also lead to formation and accumulation of dental calculus on the teeth. This may provide a good covering material for open dentinal tubules, but when removed during scaling and root planing (often with some cementum), teeth that were not previously sensitive can become sensitive.4

The effectiveness of saliva in plugging dentinal tubules may be inadequate if ingestion of acidic foods,  improper toothbrushing, and use of acidic oral products continue as before. This is often the case when individuals develop chronic dentinal sensitivity, not only because of excessive intake of acidic foods and improper brushing but also because the protective capacity of saliva in these individuals is deficient in remineralization and plugging capability, and/or if the amount of saliva secreted, and its pH, is below normal.


Figure 1. Pulp – Dentine – Plaque – Oral Fluid – Diet


In their efforts to treat dentinal hypersensitivity, many scientists have tried different ways of plugging open dentinal tubules. A major effort in this regard has been to shut off the dentinal tubule transduction system (Figure 1) by plugging open tubules. The main approach has been to form a poorly soluble calcium phosphate deposit within the orifice of open tubules by, for example, bringing together soluble calcium and soluble phosphate salts or applying a more soluble acidic calcium phosphate salt first and following this by alkali.16 Neither is easy to do in the oral cavity where everything is dynamic. Because strontium behaves like calcium, strontium salts have also been tried as dentinal tubule occluding agents. In addition, formation of a calcium oxalate deposit has been attempted, and this has met with better success.17,18


Another approach to eliminating tooth sensitivity (other than use of veneers or restorations) is to use potassium ions, generally provided in the form of potassium nitrate, to reduce the ability of the pulp nerve fibers to transmit pain stimuli.19 Most of the present-day desensitizing toothpastes rely on this approach, but appear to have had much less success than originally anticipated.18 Perhaps this is because nerve fiber depolarization and inactivation by ions would involve these ions diffusing upstream through the whole length of the narrow dentinal tubules in human teeth to reach the target nerve fibers in the pulp involved in pain elicitation, and then maintaining their continued depolarization. Perpetual depolarization is not likely to be physiological.


Figure 2. Scanning electron micrographs of dentin slices with open tubules before (bottom) and after (top) exposure to SensiStat containing prophy paste (ProClude) and subsequent rinsing six times with distilled water. Magnification 4,000X. Figure 3. Scanning electron micrographs of dentin slices with open tubules before (bottom) and after (top) exposure to a flour of pumice containing prophy paste (Preppies) and subsequent rinsing six times with distilled water. Magnification 4,000X.
Figure 4. Effect of ProClude and Preppies flour of pumice prophy pastes on the hydraulic conductance of dentin slices. One application of ProClude or Preppies flour of pumice was applied with a prophylaxis cup, rinsed six times with deionized water (400 µL each time) and hydraulic conductance was then measured for 90 minutes.

Hydraulic conductance

(mL cm-1 min-1 cm H2O-1 

After many years of work to determine how saliva can affect open dentinal tubules, our research group has developed a simple and effective new approach to the plugging and sealing of dentinal tubules. The method uses an arginine bicarbonate/calcium carbonate complex called SensiStat applied in a prophylaxis paste (ProClude, Ortek Therapeutics) to plug and seal open dentinal tubules. This can be applied while polishing the teeth. The procedure is painless and reduction of tooth sensitivity is usually immediate. Figures 2 and 3, respectively, show results obtained when dentin slices with widely open dentinal tubules are treated with ProClude prophy paste containing SensiStat or a flour of pumice control prophy paste. Similar tubule filling was observed. However, when tested by the method of Greenhill and Pashley,17 which tests whether the tubules are sealed, ie, measuring level of fluid conductance, the results are different (Figure 4). In other words, both pastes fill the open tubules. However, the ProClude paste actually seals and thus shuts off access to the fluid in the dentinal tubules and its ability to transmit pain stimuli.

Although the method is simple, the mechanisms are several and complex. A number of chemical and physical reactions act in concert. This information was gathered from studying the repair properties of saliva.10,20 A prime reaction is that the highly soluble arginine bicarbonate component of SensiStat surrounds, or is surrounded by, particles of the poorly soluble calcium carbonate component, and because of the adhesive properties of the composition forms a paste-like plug that not only fills the open tubules but also adheres to the dentinal tubule walls. Because of its alkalinity, the SensiStat also reacts with the calcium and phosphate ions of the dentinal fluid to make the plug chemically contiguous with the dentinal walls and therefore more secure. Subsequent testing of the plug by exposure to strong external acids has confirmed that it is firm. For example, the plug remains intact and resists removal even after exposure in vitro to hydrochloric acid for 24 hours.

Ingestion of ice cream and having ice in one’s drinks is a pleasure that returns almost immediately to many patients following a single application by the dentist or hygienist. The plug is poorly soluble in water. It also has reactive qualities. Specifically, if acid dissolves any calcium carbonate in the plug, arginine is released. This amino acid can be used by bacteria in the region to produce an alkaline environment. This is another means of counteracting any acid present or produced by the plaque bacteria when sugars enter the oral cavity.20

Clinical testing has proven effectiveness, and sensitive-tooth treatment with this composition has received US FDA approval (number K002989). In one study,21 when used as a single application in conjunction with scaling and root planing of 290 sensitive teeth in 88 subjects, sensitivity reduction was 58.8% when tested for pain response to a brief blast of air from a dental air syringe, and 64.6% for pain upon scratching.10

In a follow-up 28-day investigation to be presented at the forthcoming meeting of the American Association for Dental Research in March 2003 in San Antonio, a single application gave immediate sensitivity reduction of 71.7% evaluated by air and 84.2% by scratch with no reduction in effectiveness by the end of the study period. Of the 253 teeth that were sensitive at the start of the study, two thirds became completely nonsensitive to either sensitivity testing method.

In subjects who still show sensitivity after a single application, repeat application will usually stop or reduce sensitivity further. When it does not, one should suspect pulpal involvement.


Studies are underway to determine whether SensiStat can be used to treat early surface demineralizations, and halt development to frank caries that requires restoration. Development of dental caries, as in the development of tooth sensitivity, involves tooth demineralization by acid, but the two conditions differ in at least one respect. In the case of caries, the acid comes from metabolism of fermentable carbohydrate by the bacteria in dental plaque20 whereas, in the case of dentinal sensitivity, the acid comes largely from acidic foods, especially beverages and excessive or improper use of acidic oral products. Many alcoholic and nonalcoholic drinks (eg, beer, cocktails, diet and nondiet sodas) and acidic foods (eg, grapefruit) are highly acidic, and few individuals realize how their frequent use can lead to the development of sensitive teeth. This painful condition can significantly reduce the quality of life.


Finally, reduction in saliva flow, especially associated with many medications,22 results in substantial reduction in the protection against development of sensitive teeth afforded by saliva. Because of the dry mouth discomfort arising from hyposalivation,23,24 greater use of acidic beverages can ensue, resulting in a greater likelihood of development of sensitive teeth. In treating dentinal sensitivity, managing hyposalivation may be necessary.25


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2. Brännström M. Sensory Mechanisms in Dentine. London, England: Pergamon Press; 1962:73-79.

3. Brännström M. Sensitivity of dentine. Oral Surg Oral Med Oral Pathol. 1966;21:517-526.

4. Pashley DH. Theory of dentin sensitivity. J Clin Dent. 1994;5:65-67.

5. Gysi A. An attempt to explain the sensitiveness of dentine. Br J Dent Sci. 1900;43:865-868.

6. Brännström M, Lindén LA, Aström A. The hydro-dynamics of the dental tubule and of pulp fluid. Caries Res. 1967;1:310-312.

7. Pashley DH. Dentin permeability and its role in the pathobiology of dentine sensitivity. Arch Oral Biol. 1994;39(suppl):73S-80S.

8. Graf H, Galasse R. Morbidity, prevalence and intra-oral distribution of hypersensitive teeth. J Dent Res. 1977;(Spec Iss A)56:162.

9. Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity: the distribution of recession, sensitivity and plaque. J Dent Res. 1987;15:242-248.

10. Kleinberg I, Kaufman H, Wolff M. Measurement of tooth hypersensitivity and oral factors involved in its development. Archs Oral Biol. 1994;39:63-71.

11. Buckley LA. The relationships between malocclusion, gingival inflammation, plaque and calculus. J Periodontol. 1981;52:35-40.

12. Philstrom BL, Hargreaves KM, Bouwsma OJ, et al. Pain after periodontal scaling and root planing. J Am Dent Assoc. 1999;130:801-807.

13. Pontefract H, Hughes J, Kemp, et al. The erosive effects of some mouthrinses on enamel. A study in situ. J Clin Periodontol. 2001;28:319-324.

14. Pashley EL, Talman R, Horner JA, et al. Permeability of normal versus carious dentin. Endodont Dent Traumatol. 1991;7:207-211.

15. Chatterjee, R, Kleinberg I. Aggregation of salivary proteins. In: Kleinberg I, Ellison SA, Mandel ID, eds. Saliva and Dental Caries. Washington, DC: Information Retrieval, Inc; 1979:155-173.

16. Ishikawa K, Suge T, Yoshiyama M, et al. Occlusion of dentinal tubules with calcium phosphate using acidic calcium phosphate solution followed by neutralization. J Dent Res. 1993;73:1197-1204.

17. Greenhill JD, Pashley DH. The effects of desensitizing agents on the hydraulic conductance of human dentin in vitro. J Dent Res. 1981;60:686-698.

18. Pashley DH, O’Meara JA, Kepher EE, et al. Dentin permeability. Effects of desensitizing dentifrices in vitro. J Periodontol. 1984;55:522-525.

19. Anderson DJ, Hannam AG, Matthews B. Sensory mechanisms in mammalian teeth and their supporting structures. Physiol Rev. 1970;50:171-195.

20. Kleinberg I. A mixed-bacteria ecological approach to understanding the role of the oral bacteria in dental caries causation: an alternative to Streptococcus mutans and the specific-plaque hypothesis. Crit Rev Oral Biol Med. 2002;13:108-125.

21. Wolff MS, Kaufman, Kleinberg I. Dentinal hypersensitivity following scaling and root planing (SRP) and dental prophylaxis. J Dent Res. 2002;80:191(Abstract).

22. Sreebny LM, Schwartz S. A reference guide to drugs and dry mouth. Gerontol. 1997;4:33-47.

23. Wolff MS, Kleinberg I. Oral mucosa wetness levels in hypo- and normo-salivators. Archs Oral Biol. 1998;43:455-462.

24. Wolff MS, Kleinberg I. The effect of ammonium glycopyrrolate (Robinul) induced xerostomia on oral mucosal wetness and flow of gingival crevicular fluid in humans. Archs Oral Biol. 1999;44:97-102.

25. Sreebny LM. Recognition and treatment of salivary induced conditions. Internat Dent J. 1989; 39:1977-204.

Dr. Kleinberg is professor and chairman of the Department of Oral Biology and Pathology at the State University of New York at Stony Brook.

Disclosure: Patents for SensiStat have been assigned to and are owned by the Research Foundation of the State University of New York at Stony Brook and licensed to Ortek Therapeutics, in which Dr. Kleinberg is a director.