Capping exposed pulps is currently an infrequent procedure because of a general lack of confidence in the effectiveness of calcium hydroxide (Ca[OH]2) as an effective agent for this purpose.1 Potassium nitrate (Kno3) is a superior desensitizer for hypersensitive teeth,2,3, and its success has encouraged exploration of its other uses. Used with polycarboxylate (Pca) cement, it serves as an effective liner for deep carious lesions, and as a temporary cement (Kno3/zinc oxide eugenol [ZOE]) to reduce pain following full crown preparation.4 Kno3/Pca cement was used for preserving pulp vitality and diminishing the incidence and severity of post-restoration pain.5 It has been successfully used with tooth bleaching gels and with glass ionomer cement to prevent severe postbleaching and restoration pain.5 Kno3, when combined with tooth bleaching gel and composite, prevents post-procedural pain. It has been combined with dimethyl isosorbide (Dmi) to potentiate its desensitization of hypersensitive teeth,6 and to effectively treat aphthous ulcers.7
This study expands the use of Kno3/polycarboxylate cement by combining it with Dmi8 and examining its effectiveness as a capping agent for carious pulp-exposed teeth.
Some dentists advocate pulp extirpation and endodontic treament of exposed pulps, except in those patients with incompletely closed apices.9 These dentists believe that although there may be no pain with pulp- capped teeth, enough toxic products remain in the pulp to sustain the inflammation.10,11 Connective tissues throughout the body are similar, and it is well documented that they have the ability to heal.10 Pulpal connective tissues should have the same inherent healing capacity as other connective tissues,12 yet no consistent pulp healer had been found.
Factors that are important in promoting pulpal healing are related to the state of health of the pulp and its vitality at the time of treatment. If the pulp exhibits suitable vitality it should be capable of healing when an appropriate medication is administered. Many materials have been selected as pulp- capping agents including antiseptics, anti-inflammatory agents, enzymes, and antibiotics.12 Ca(OH)2 is generally accepted as the material of choice13 for pulp capping.11,14,15 With Ca(OH)2 an area of calcification beneath the exposed pulp often forms,14 but despite this apparently successful bridge formation, the pulp may remain chronically inflammed or become necrotic. Internal resorption is another sequela seen occasionally following capping of pulp-exposed teeth with Ca(OH)2. In other instances dentinal mineralization of the remaining pulpal tissues occurs and occludes the canals, preventing conventional endodontic therapy when this treatment fails.
Capping exposed pulps with Ca(OH)2 in mature permanent teeth appears to be an interim, unreliable procedure. Kno3/Pca cement has been used as a base under deep restorations,5 and subsequently as a capping material for pulpal exposures.16 When placed under deep restorations with less than 1 mm of protective dentin remaining, it was effective in preserving pulpal vitality and it diminished the incidence and severity of post-restoration pain.5 When Kno3 was used in combination with ZOE, it was found to significantly reduce pain following full crown preparation.4 These earlier studies have been monitored and reported.5,16 Kno3 has been combined with Dmi to potentiate Kno3’s desensitization of hypersensitive teeth6 and to effectively treat aphthous ulcers.7 It has also been used in bleaching agents and glass ionomer cements to prevent post-bleaching and/or post-restoration pain.
The goal of this study was to determine if Dmi could potentiate the beneficial effects of Kno3/Pca cement and make pulp capping of vital teeth a reproducible, predictable, successful procedure.
A total of 47 adult male and female patients with pulpal exposures of varying sizes in vital teeth were randomly selected as participants for this study. Persons with the following conditions were excluded: periapical pathosis identifiable radiographically, or allergy to Kno3 and/or zinc polyacrylate. In addition, teeth were excluded if there was pulsating pain of a spontaneous toothache, purulent or serous exudate at the exposure site, or pain created by percussion, as these signs and symptoms are indicative of tooth abscess. Teeth with calcifications of the pulp chamber or root canals were also excluded because they are indicative of previous inflammation or trauma, and the pulps are less responsive to vital therapy.
Patients did not use systemic steroids, antibiotics, antihistamines, or Kno3 dentifrices during the first 3 weeks of this study. The patients were permitted to brush their teeth with their usual toothpaste, but were told to refrain from using mouthwashes and lozenges. Medications for the patients’ well being that did not interfere with the parameters of this study were permitted.
Materials and Methods
Preserve (Healex Products, Inc) is a Kno3/Pca cement. The liquid is 4% Kno3 polyacrylic acid which is mixed with Pca cement powder. For this study the liquids used with the powder were in three bottles, with the liquids released by the drop. Bottle No. 1 contained 7 drops of Dmi per 20 g of 4% Kno3 polyacrylic acid; bottle No. 2 contained 4% Kno3 polyacrylic acid (no Dmi); bottle No. 3 contained only polyacrylic acid (no Dmi or Kno3). Bottle No. 4 contained the cement powder that was mixed with either bottles Nos. 1, 2, or 3. Polyacrylic acid without Kno3 or Dmi (bottle No. 3) served as a negative control. Kno3/Pca cement was used for a comparison (postive control) to determine how the addition of Dmi to Kno3 in a Pca cement effects pulp-capping success.
By the use of a table of random numbers, 47 patients were randomly chosen for the study. Eighteen patients received bottle No. 1 (Kno3/Dmi/Pca cement);17 patients received bottle No. 2 (Kno3/Pca cement); and 12 patients received bottle No. 3 (Pca cement). Envelopes were numbered 1 through 47, and a slip of paper describing the cement was inserted into each envelope. A working list allowed the dentist to use the appropriate pulp-capping agent in serial order. The dentist was unaware which formula was used during placement, because all three liquid bottles appeared identical. The appropriate medication (Nos. 1, 2, or 3) was applied after caries removal without the use of a rubber dam, because it was felt that salivary contamination of the exposed pulp had already occurred. No attempt was made to prevent inadvertent salivary contamination of the pulps, and the exposed area was washed with water and gently air dried.
For posttreatment examinations, patients were identified by their assigned number (Nos. 1 through 47). Patients were examined after 3 months, 1 year, and 2 years. However, if they felt that the pulp capping was not working well, they were seen immediately after contacting the office. At the end of 1 year and 2 years, periapical radiographs were made and compared with a preoperative radiograph. The discovery of periapical pathology, fistulous tracts, or sensitivity to percussion was recorded as a failure to preserve the pulp.
|Figure 1a. Maxillary right second bicuspid (tooth No. 4) with a carious exposure under a full crown.||Figure 1b. Tooth No. 4, 1-year post pulp capped with Kno3/Dmi/Pca cement. The old crown has been replaced with a metal/ceramic crown. Observe the freedom from radiographic pathology.|
|Figure 1c. Tooth No. 4 has remained asymptomatic and free of untoward radiographic or clinical changes.||Figure 2a. Maxillary first molar (tooth No. 14) with carious exposure.|
|Figure 2b. Tooth No. 14, 1-year post pulp capping with Kno3/Dmi/Pca cement and an amalgam restoration. Tooth No. 15 has had a metal/ceramic crown restoration.||Figure 2c. Tooth No. 14, 2-year posttreatment with Kno3/Dmi/Pca pulp-capping cement. It has remained asymptomatic clinically and free of apical pathology radiographically.|
|Figure 3a. Tooth No. 14 with carious pulp exposure.||Figure 3b. Tooth No. 14, 1-year post pulp-capping treatment with Kno3/Dmi/Pca cement and an amalgam restoration. Tooth has remained asymptomatic.|
|Figure 3c. Tooth No. 14, 2-year posttreatment. It has remained asymptomatic and free of apical pathology.||Figure 4a. Tooth No. 31 with carious pulp exposure.|
|Figure 4b. Tooth No. 31, 1-year post pulp capped is asymptomatic and free of periapical pathology.||Figure 4c. Tooth No. 31 has remained asymptomatic and radiographically free of periapical pathology. (Note: Tooth No. 30 is in need of a disto-occlusal restoration which the patient has resisted doing.)|
|Figure 5a. Maxillary left second molar (No. 15) with a very large carious lesion.||Figure 5b. Tooth No. 15, 1-year post pulp capped with Kno3/Dmi/Pca cement and restored with an extremely large amalgam restoration. This tooth has served as a distal abutment for a nesbit partial for 1 year. It has remained asymptomatic and free of radiographic pathology.|
|Figure 5c. Tooth No. 15 has remained asymptomatic and free of untoward radiographic or clinical change. The tooth has continued to serve as a distal abutment for 2 years.|
Eighteen patients were treated with Kno3/Dmi/Pca cement (bottle No. 1) applied over carious pulpal exposures; 17 patients had Kno3/Pca cement (bottle No. 2) over carious pulpal exposures; and 12 patients had Pca cement (bottle No. 3) over carious pulpal exposures. All patients in group No. 1 responded favorably to the medication (Kno3/Dmi/Pca cement). Six patients in group No. 1 experienced slight-moderate pain to cold stimulation that lasted for 3 to 7 days and then completely disappeared. The other 12 patients were asymptomatic and remained that way over the 2-year course of the study. All 18 pulp-exposed teeth appeared normal clinically and radiographically (Figures 1 through 5) for the 2 years of this study. Nine patients in group No. 2 (Kno3/Pca cement), and 10 patients in group No. 3 (Pca cement) developed untoward clinical symptoms. These teeth required either endodontic therapy or extraction. Untoward symptoms included the development of fistulous tracts, reactive lesions identified by radiographs, sensitivity to percussion, swelling, or severe pain. Eight Kno3/Pca cement pulp-capped teeth without Dmi (No. 2) and two pulp-capped teeth with Pca cement (No. 3) were asymptomatic for the length of the study.
A comparision was made for each material’s ability to serve as a pulp-capping agent for carious exposed pulps, to successfully preserve the pulp in acceptable health over a 2-year period of treatment (Tables 1 and 2).
Theoretical Rationale for the use of Dmi with Kno3/Pca Cement for Pulp-Capping Success
The cooperative action of Dmi and Kno3 has been found to desensitize hypersensitive teeth more efficaciously than Kno3 alone.6 Dmi readily penetrates the dentinal tubule orifices and travels rapidly to the pulpal tissue. It enhances Kno3’s effectiveness, causing it to work by a different mode of action than occurs when Kno3 is used alone.6 Kno3 used as a desensitizer without Dmi also travels through the dentinal tubules, but at a slower rate. Bathing the pulpal nerves with potassium ions changes their -85 mvs resting membrane potential to a zero or a positive, thus preventing an action potential from forming. This inhibits nerve conductance and pain emission. In this way, Kno3 desensitizes hypersensitive teeth.
The addition of Dmi to Kno3 dynamically potentiates the desensitizing effects of Kno3 because of its strong osmotic qualities. It travels toward the pulp via the dentinal tubules and overcomes the resistance factors that make up the dentin/pulpal barriers. Dmi helps Kno3 to more rapidly reach the dentinal and pulpal nerves, blood vessels, and embryonic connective tissues. They overcome the tubular constrictions, irregularities, man-made tubular obliterations, dentinal sclerosis, odontoblast process, fluid-containing minerals and immunoglobulins, tubules containing bacteria, antibiotics, antimicrobial agents, odontoblast junctions (tight, intermediate, and gap),17 and intercellular bridges that join cells. These structures restrict and slow the penetration of potassium into pulpal tissue, but the osmotic properties of Dmi open spaces between cells, as well as space through cells. Dmi raises the osmotic pressure of fluid surrounding cells and other membranous structures, drawing water from them and shrinking them in size. The fluid containing Kno3/Dmi flows through the widened bridge spaces, junctions, and enlarged openings between the shrunken odontoblast processes and odontoblasts themselves, enhancing and enabling potassium dentin/pulp permeability. The Kno3/Dmi fluid flows more rapidly and easily through these newly created spaces to reach pulpal nerves and blood vessels.
In the same way as described, dentinal and pulpal nerves shrink significantly because of the increased osmotic pressure caused by the surrounding solution. When cells and membranous structures are caused to shrink osmotically by the Dmi/potassium solution located outside the nerves’ membranes, as well as potassium from the high potassium gradient obtained from Kno3/Dmi desensitizer, the solution flows rapidly into these nerves in quantity. Osmotic cell shrinkage is a strong stimulus for the uptake of potassium. As the captured cellular potassium exceeds equilibrium it begins to leave the inside of nerves. It escapes, leaving negatively hyperpolarized nerves that cannot form an action potential. This inhibits pain production and nerve conduction.
Desensitizing hypersensitive teeth with Kno3/Dmi solution takes place faster, more completely, and lasts longer than with just the use of Kno3 to bathe teeth and nerves. The teeth desensitize faster than with Kno3 alone as the Kno3/Dmi solution travels through the dentinal tubules at a more rapid rate. A major reason for the more profound tooth desensitization is that hyperpolarization is a result of Dmi’s osmotic ability to cause cell shrinkage. It takes place after Kno3 depolarizes the nerves. Dmi/ Kno3 accompishes this without obliterating or diminishing the radius of the dentinal tubules. The dentinal-pulpal circulation and natural defense system remains functionally intact, and is even improved. It may be helped by the nitrate ion, because nitrate salts tend to increase circulation by being converted to nitric oxide. Long-term vitality, pulp health, and longevity of the dentition is dependent on the dentin/pulp’s afferent/efferent circulatory system remaining functional and flowing. This system is an extension of the pulp, and it serves to replenish mineral loss in dentin, keeps teeth nonbrittle, and serves as a barrier to combat the penetration of noxious substances and bacteria, as well as a warning system for untoward influences that could make the pulp unhealthy. It may also accommodate for barometric and atmospheric changes such as those seen with deep sea diving, or air and space travel.
Pulpal nerves so depolarized and hyperpolarized are of two types in that they serve different functions. There are pulpal nerves of the central nervous system that conduct pain, and an abundance of nerves of the autonomic nervous system in the pulp that modulate its microcirculation. The principles and rationale of function are applicable to both types of nerves. The autonomic nerves are inactivated by Kno3/Dmi, and the emission of stimuli to the receptor tissues (mast cells, neutrophiles, and monocytes) that initiate a pulpal inflammatory response is prevented from occurring.
The cooperative action of Kno3/Dmi serves in this way as an anti-inflammatory agent, acting much like corticosteroids, but without the untoward side effects. This is particularly important for the maintenance and preservation of the vital dentition, because it is important that inflammation and its associated swelling be limited in the pulpal tissue. When intrapulpal edema becomes severe it increases intrapulpal pressure and causes the teeth to abscess as the histamines, leukotrienes, bradykinins, prostaglandins, and other inflammatory and edematous components cause pulpal swelling. When severe intrapulpal swelling occurs it pushes the blood vessels and nerves firmly against the unyielding, hard calcific interior walls of the dentin facing the pulp chamber and the canal, promoting loss of vitality, necrosis, abscess, and cellulitis formation. When Kno3/Dmi inactivates pulpal autonomic nerves these untoward sequelae are prevented from occurring, as the stimulus that initiates an inflammatory response cannot take place.
Preventing the inflammatory response from occurring allows the pulpal connective tissues to heal in the same way as do inflamed connective tissues of other parts of the body. For example, swelling of the arm can occur without pressure atrophy resulting as it is not encased in a firm, hard, calcific barrier, and without such a limiting boundary it ultimately subsides and heals. Uniquely, Kno3/Dmi prevents intrapulpal pressures from rising severely, and pulpal atrophy from occurring. Maintaining pulpal vitality keeps the dentinal-pulpal intratubular circulation intact, flowing, and healthy.
The knowledge that Kno3/Dmi desensitizes teeth and maintains pulpal health better than Kno3 alone6 prompted combining Kno3/Dmi with different types of dental cements (Pca, glass ionomer, resin-reinforced glass ionomer, zinc oxyphosphate, ZOE, methacrylate, dimethacrylate, and composite). This report describes its incorporation into Kno3/Dmi/
Pca cement for use as a pulp-capping agent. Pca cement with Kno3/Dmi is especially effective as a pulp- capping agent. Pca cement has a very thin film thickness and it bonds firmly to tooth structure. For this reason, the lining and pulp-capping cement remain where placed, strong and capable of withstanding the overlying pressure of the restoration without cracking or breaking up. It continues to be effective as it releases Kno3 and Dmi into the dentinal tubules over time.
When composites are used to restore teeth, Kno3/Dmi/Pca cement can be safely etched with 37% phosphoric acid. This lining prevents post-composite pain, and for reasons stated previously, a Kno3/Dmi/Pca cement base should be placed under all restorations.5 It is easy to use, hardens quickly, and prevents post-restoration pain. Pulp can be preserved, as it is able to heal like other connective tissues throughout the body. Pulpal inflammatory edema is diminished and/or prevented because the autonomic nerves that control the neurogenic modulation of the pulp’s microcirculation are not able to fire and bring forth this untoward reaction (pulpal pressure atrophy), which invariably leads to loss of tooth vitality. It is for these reasons that Kno3/Dmi/Pca pulp-capping cement appears to be predictably and reliably able to restore the pulpal tissues to normalcy.
Pulp exposure created by dental caries subjects the pulpal tissues to microorganisms from the oral environment.1 Pulp capping generally has been performed with Ca(OH)2 preparations, especially if the pulp was inadvertently exposed during dental procedures. It is used with the desire to resolve inflammation and allow the pulp to return to normal.12,17 Ca(OH)2 stimulates the formation of a dentinal bridge over the exposed pulp, and is a barrier between the pulp and the floor of the cavity preparation that provides protection from chemical and physical trauma.14,18 Ca(OH)2 with a pH of 11.5 to 1315 irritates pulpal tissues, creating a potentially pathologic calcification that may be detrimental to the pulp and its hydrodynamics. Even when modified by six or seven ingredients it does not attain sufficient strength to prevent the dried film from cracking and limiting its ability as a protective base.15
Another limitation is the inability of Ca(OH)2 to bond to tooth structure. The function of a liner or base used with definitive restorations is to promote recovery of the injured pulp and to protect it against trauma.12 Ca(OH)2 is not an anti-inflammatory agent and does not address the problem of intrapulpal edema and pressure atrophy. This is a serious failing. Pulp capping with Ca(OH)2 preparations is an unreliable dental procedure, often leading to pulp extirpation and endodontic therapy or extraction.5,16 Endodontic therapy is effective in removing the pain and infection of diseased teeth, but it necessitates removal of the pulp to the apices of the root canal(s), with subsequent sealing of the apical region and filling of the root canal and pulp chamber with inert materials. The relative vitality of the tooth is maintained by the vasculature of the periodontal ligament, but problems may arise such as brittleness and/or discoloration, and in certain patients periapical disease becomes evident.
The radicular portion of the tooth contains 22% of the tooth’s fluid by volume,12 and this fluid is contained in the 30,000 to 59,000 dentinal tubules per square mm of dentin.17 The fluid travels from the pulp to the dentin and cementum to provide these structures with nutrients, minerals, and immunoglobulins to combat bacterial invaders.2,19 When the pulp is extirpated the fluid source of the roots’ extended circulatory system located in the dentinal tubules abruptly ceases.
The hard root structure loses the fluid that emanates as a transudate from the vital pulp, and the tooth becomes brittle and more susceptible to fracture. The use of Kno3/Dmi/Pca pulp-capping cement preserves the pulp and precludes this sequela because the pulp remains an active source for dentinal tubular fluid. It may offer the alternative of lessening the need for extensive dental procedures, and often makes treatment easier and sometimes more acceptable by the patient.
Kno3/Dmi/Pca cement is especially appropriate for young permanent teeth, because the pulp is necessary for the formation of dentin. If the pulp is lost before the full root length has completely formed, the tooth could have an unfavorable crown/root ratio. Pulpal necrosis before the completion of dentin depositing within the root also leaves a thin root that is more prone to fracture. The use of Kno3/Dmi/Pca cement for capping pulp-exposed teeth will help sustain the vitality of these teeth and allow the development of the full root length. Kno3/Dmi/Pca cement may offer an alternative method for saving teeth that for economic or other reasons would be extracted.
Kno3 in a toothpaste is the safest, most effective desensitizing agent for the treatment of hypersensitive teeth.2,18 It has other important uses in dentistry, as well. It uniquely maintains pulp vitality and diminishes the incidence and severity of post-restorative pain when used in a cavity liner under deep restorations.5,16 It is potentiated by Dmi, and their effectiveness appears to be optimized by their cooperative action.3 This study adds to its growing list of uses by demonstrating that a Kno3/Dmi/Pca cement is an effective capping agent for carious exposed vital pulps.
1. Seltzer S, Bender IB. Pulp capping and pulpotomy. In: Seltzer S, Bender IB, eds. The Dental Pulp, Biologic Considerations in Dental Proedures. 2nd ed. Philadelphia, Pa: JP Lipincott Co: 1975.
2. Hodosh M. A superior desensitizer: potassium nitrate. J Am Dent Assoc. 1974;88:831.
3. Tarbet WI, Siverman Q, Stolman JM, et al. Clinical evaluation of a new treatment for dentinal hypersensitivity. J Periodontal. 1980;51:535-50.
4. Hodosh, AJ, Hodosh S, Hodosh M, Potassium nitrate-zinc oxide eugenol temporary cement for provisional crowns to diminish post preparation tooth pain. J Prosthet Dent. 1993;70:493-495.
5. Hodosh M, Hodosh S, Hodosh AJ. Maintenance of pulpal vitality using potassium nitrate-polycarboxylate cement cavity liner. Quintessence Int. 1991;22:495-502.
6. Hodosh M. Potentiating potassium nitrate’s desensitization of hypersensitive teeth with dimethyl iosorbide. J Gen Dent. 2001;45(5):521-536.
7. Hodosh M. The treatment of aphthous stomatitis lesions with saturated Kno3/Dmi (in press).
8. Clariant LSM (UK) Lmtd, Prince William Ave, Sandycroft Deeside, Flintshire CH52PX.
9. Langeland K, Dowder WE, Tronstad L, et al. Human pulp changes of iatragenic origin. Oral Surg. 1971;32:943.
10. Orban B. Contributions to the histology of the dental pulp and periodontal membrane with special reference to the cells of defense of these tissuers. J Amer Dent Assoc. 1929;16:965.
11. Cvek, M. A clinical report on pulpotomy and capping with calcium hydroxide in permanent incisors with compalicated crown fractures. J Endod. 1978;4.232.
12. Cohen S, Burns R. Pathways to the Pulp. St. Louis, Mo, Toronto, Canada: The CV Mosby Co; 1984:335.
13. Eidelman E, Finn SB, Knoulourides T. Remineralization of carious dentin treated with calcium hydroxide. J Dent Child. 1965;32:218.
14. Jones MD, Gibbs GH. Direct pulp capping with dycal. J Can Dent Assoc. 1969;35:384-387.
15. Phillips RW. Skinner’s Science of Dental Materials. 7th ed. Philadelphia, Pa: EB Saunders Co; 1973:492-496.
16. Hodosh M, Hodosh S, Shklar G, et al. Potassium nitrate: an effective treatment for pulpitis. Oral Surg. 1983;33:419-420.
17. Garberoglio R, Brannstrom M. Scanning elecron microscopical investigation of human dentinal tubules. Arch Oral Biol. 1976;21:355.
18. Berk H, Stanley HR. Pulp healing following capping in human sound and carious teeth. J Dent Res. 1958;37:66.
19. Olgart L, Brannstrom M, Johnson G. Invasion of bacteria into dentinal tubules. Experiments in vivo and in vitro. Acta Odontol Scand. 1974;32:61.
Dr. Milton Hodosh has maintained a private practice since 1955 and is the recipient of 11 National Institute of Dental Research grants (principal investigator). He has promoted Kno3 as a superior desensitizer and introduced its use in dental cements, composites, and bleaching gels. He was adjunct assistant research professor of oral pathology at Tufts University School of Dental Medicine from 1969 to 1974; adjunct clinical professor of dental surgery, Biomedical School, Brown University from 1974 to 1991; and associate clinical professor of oral pathology at Harvard University School of Dental Medicine from 1974 to 1991. He has written numerous original articles and holds patents pertaining to the dental and medical fields.
Dr. Steven Hodosh has been in private practice since 1980 and has a major interest in restorative dentistry. He has published numerous original manuscripts.
Dr. Alex Hodosh has been in private practice since 1987. His special interests include dental implantology and periodontology. He has published numerous original manuscripts.