Bleaching:
Is it safe and effective?
Gary R. Goldstein, DDS,” and L. Kiremidjian-Schumacher,
PhD”
Kriser Dental Center, New York University, New York, N.Y. It has been well documented that bleaching whitens teeth, but has its safety been documented? This paper reviews bleaching’s predictability, esthetics, longevity, and side effects. A discussion of the bleaching reaction on teeth and soft tissue raises concerns over the safety of the procedure. (J PROSTHET DENT 1993;69:325-8.)
I
t has been well-documented that teeth can be bleached.‘-7 The in-office techniques using 30% to 35% hydrogen peroxide (HP) have been advocated for many years, but their popularity has been limited because of the caustic nature of the solution and the need for meticulous rubber dam placement. The new at-home mouthguard applied procedures with carbamide peroxide (urea hydrogen peroxide, perhydrit, hyperol, or perhydrol-urea) are easier to use and do not require placement of a rubber dam.s In a 1990 Clinical Research Associates (CRA) survey,g 52 % of the 9846 respondents were using the technique, which was first published by Haywood and Heyman,a g or a modification of it. The CRA newsletter reviewed seven products in July 1989 and 10 in December 1989.‘O,I1 Today, the number of products being marketed directly to patients or through the dentist to the patient is growing daily. Late night and cable television, lay magazines, and newspapers all promot.e regionally and nationally marketed brands.
Is bleaching
predictable?
The literature indicates that bleaching is not predictable. In a study by Nathanson and Panna” only a third of the subjects showed marked changes. Goldstein’ stated that the exact shade can’t be predicted. In the CRA survey,9 14% of those who used the at-home technique were not satisfied with the results. The number one reason for dissatisfaction was that the profoundness of the bleach was unpredictable. Studies by the authors were unable to predict to what degree a tooth could be bleached.12 The patient’s teeth in Figs. 1 and 2 were successfully bleached with the same technique and for the same length of time as the patient’s teeth in Figs. 3 and 4. With the exception of the dull appearance of the enamel as a result of preetching, little whitening is evident in the second patient’s teeth. This unpredictability is undesirable in a fee-for-service
situation, because the patient might decide that the result did not justify the fee.
Is bleaching
esthetic?
In most patients, where superficial stains are removed, the answer is yes (Figs. 1 and 2). But in stains requiring prolonged treatment, the answer is not always clear. The teeth appear whiter but are chalky and dull (Figs. 3 and 4), and consequently the patient’s stain problem has been traded for a flat, dull, and unrealistic look.
Does it last:? Indications are that it probably does not. Most authors conclude that retreatment is necessary! with Goldstein’ and Feinman et ali3 recommending retreat,ment in 1 to 3 years.‘, I;3 Holmstrup et a1.14 reported that 20.3”;~ of bleached teeth showed an unacceptable recurrence of discoloration after 3 years and Friedman et al.‘” had a 21”; esthetic failure. Walton et al.‘” reported a return of discoloration as early as 1 week. Meyers et al.‘:’ reported a return of color in 4 days.
Are there si.de effects? The occurren’ce of external cervical resorption associated with bleaching of nonvital teeth has been well documented.‘“, ‘sSz6Pulpal responses to bleaching have been studied and found to be extensive but most likely reversible.“, 27-31 Most investigators
report
some posttreatment
sensitivi-
ty, l, 6.g,S. 28which dissipates with time. All of these studies were performed with 30 % to 35 “; HP for approximately 20 minutes with a once-a-week exposure. No studies have been done with 3c; HP with a 3- to 8-holrr daily exposure
for several weeks. A study by Ledoux et alYs showed bleaching with 30% HP causes extensive structural changes in rat dentin and enamel. Titley et a1.s’ used a 30-minute exposure of 35% HP on human d.entin and found an intact, smear layer with
aProfessor and Director of Prosthodontic Research, Division of Restorative and Prosthodontic Sciences. bProfessor, Department of Oral Medicine and Pathology. Copyright ‘6 1993 by The Editorial Council of THE JOURNAL OF PROSTHETICDENTISTRY. OOZZ-3913/93/$1.00+.10. 10/l/43228
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a dense amorphous precipitate. Ruse et ai.“:’ demonstrated that other than increasing the nitrogen content, there were no other sign&cant changes in the elemental composition of the bovine enamel studied. Torneck et a1.s” showed a
decrease in the bond strength of composite resin bonded to bovine enamel bleached with 30 “r HP. They hypothesized
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Fig. Fig.
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1. Preoperative photo of stained teeth.
2. Postoperative photo of in-office bleached teeth after three sessions shows positive results. Fig. 3. Preoperative photo of stained teeth. Fig. 4. Postoperative photo of in-office bleached teeth after three sessions shows chalky white appearance of teeth.
that this was the result of the presence of residual peroxide or peroxide-related substances at or near the enamel surface. Responses of soft tissue to exposure to HP have been reported. g-11*35-3sRees and Orth36 reported two patients who had oral ulcerations after using 3% HP for 1 to 2 minutes, three to five times daily. Martin et al.37 used 1% HP dropped continuously onto dog gingiva and showed edema in the epithelial layer after 6 hours, vacuolization after 24 hours, and destruction and sloughing of the cornified layers after 48 hours. Dorman and Bishop3* produced edema in dog tongues with a dilute HP (3 % ) solution after a single 30-minute exposure. How
does it work?
The exact mechanism is unclear. Bleaching is an oxidation reaction whereby the substance to be bleached donates electrons to the bleaching agent, and it can be performed to a degree by any oxidizing agent. Dental bleaching procedures use HP because it is unstable and will easily decompose to water and oxygen. The at-home procedure
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employs carhamide peroxide as a vehicle for the delivery of HP (10 % carbamide peroxide in the presence of water releases 3.5% HP). A low concentration of HP requires an increase in exposure time. The rate of the reaction: 2H202 > 2H20 + O2 is dependent on the HP concentration and the levels of salivary peroxidase. If a large amount of HP is present where a zero-order reaction occurs, the time required to clear the HP is proportional to its concentration. The longer it takes to clear the HP, the greater the exposure time to reactive oxygen species. Although it is possible that 02, which has two unpaired electrons in its outer shell, can pick up two electrons simultaneously, the more likely scenario calls for consecutive one-electron transfers involving free radical (Os-, superoxide) intermediates. 3g-41The superoxide then reacts with HP in the Haber-Weiss Reaction, Os- + HsOs > 0s + OH- + . OH, producing the hydroxyl ( . OH) radical.40s41 This reaction occurs slowly at physiologic PH.~’ HP can penetrate enamel and dentin.‘> 3oIt is also mobile and can
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diffuse through the soft tissue to vulnerable parts of a ce11.42 The slow breakdown of HP in an environment containing ferric and ferrous ions will produce strongly reactive intermediary ions and oxygen, with both probably contributing to the bleaching process. Is it safe? In a January 1991 literature search, we found 246 citations in cross-referencing HP with toxicity. Oxygen has toxic effects.40,43It has been known to damage plants, animals, and aerobic bacteria in concentrations greater than in normal air. Even 21% oxygen has damaging effects.*O The oxygen paradox is that while it is essential for higher life forms, it is toxic to all aerobes.** Free radicals interact with and can destroy whatever is near them,*“, 45-4gand they are known carcinogens.40v*I, 43,5o The superoxide radical plays a major role in the toxic effects of oxygen. 51Fridovich has stated that Oz- is a commonly encountered intermediate of oxygen reduction in both biotic and abiotic systems and that this free radical constitutes a threat to the chemical integrity of living cells.:” Weitzman et a1.35stated that hydrogen peroxide can, by itself, induce pathologic changes frequently associated with neoplastic lesions; it may also augment carcinogenesis associated with 9,10-dimethyl 1,2 benzanthracene (DMBA). DMBA is a known carcinogen analogous to the polycyclic aromatic hydrocarbons found in tobacco.34Their study used hamsters with the buccal pouches painted with 3”:’ HP or 305 HP twice weekly for 19 to 22 weeks. A 0.25 “0 DMBA solution was also painted on selected groups twice weekly on days other than when the HP was applied. What would the results have been if the HP was allowed to contact the tissues for 3 to 8 hours every day as is currently advocated in the at-home technique? Smokers are the most likely candidates for successful bleaching. Telling them to stop smoking during the bleaching exposure probably will not reverse the previous damage. Dyskeratosis and carcinoma in situ are the precursors of malignancy. They will not be reversed in a short period of time after the cessation of smoking. What is the effect of the HP exposure on these highly susceptible cells? SUMMARY Bleaching is an effective method of whitening teeth. It is not predictable and has a sufficient history of adverse effects to warrant concern by the profession. Above all, procedures used in dental practice should preserve and protect the oral tissues environment. To date the clinical safety of bleaching has not been demonstrated. Most of the published research indicates that there should be concern for its safety when used in prolonged treatment. CONCLUSIONS To justify bleaching on the grounds that it is cosmetic and not therapeutic, and as such does not need to meet
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Food and Drug Administration (FDA) standards, is turning a blind eye to its prolonged contact wit,h oral tissues and to the possible aspiration and inhalation of HP and its byproducts. The FDA has not accepted that argument and has requested safety studies for the at-home products. If the possibility of harm exists, it is dentistry’s obligation to explore it first, not react to the problem if and when it occurs. Chakwan Siew, PhD, head of the ADA Research Institute’s Department of Toxicology said, “These products work, but at what cost down the road?““2 Wisely, the ADA Council of Dental Therapeutics has not granted acceptance to any of the whiteners. REFERENCES 1 Goldstein R. Bleaching teeth. New materials-- new role. J Am Dent Assot (Special issue) 1987;443-523. 2 Goldstein CE, Goldstein RE, Feinmsn RA, Garber DA. Bleaching vital teeth: the state of the art. Quintessence Int 198%20:729-37. 3. Nathanson D, Panna C. Bleaching vital teeth: a review and clinical study. Compendium 1987;7:496-8. 4. JordanRE, Boksman L. Conservative vital bleaching treatment of discolored dentition. Compendium 19&1;5:893-8. 5. Cohen S, Parkins FM. Bleaching tetracycline-stained teeth. Oral Surg Oral Med Oral Pathol 1970;29:465-71. 6. Wilson CFG, SeaIe SN. Color change following vital bleaching of tetracycline-stained teeth. Pediatr Dent 1985$205.8 I. Fisher NL, Radford JR. Internal bleaching of discoloured teet,h. Dent Update 1990;17:110-1;113-4. 8. Haywood VB, Heymann HO. Nightguard vital bleaching. Quintessence Int 1989;20:1’73 -6. 9. Clinical Research Associates Newsletter. Provo. I ‘tab: Clinical Research Associates, Dee 1990. 10. Clinical Research Associates Newsletter. Provo. l.‘raft: Clinical Research Associates, July 1989. 11. Clinical Research AssociatesNewsletter. Provo. I ‘tab: Clinical Research Associates, Dee 1989. 12. Goldstein GR. Kiremidjiar-Schumacher L. Clmical evaluation of a non-heat technique for vital bleaching [Abstracr] .J Dent Res 1991; 70:376. 13. Feinman RA, Goldstein RE, Garber DA. Bleat.hing teeth. Chicago: Quintessence Publ, 1987;13. 14. Holmstrup G, Palm AM, Lambjerg-Hansen H. Bleaching of discolored root-filled teeth. Endodont Dent Traumatol 1988;4:197-201. 15. Friedman S, Rothstein I, Libfeld H, Stabholz A, Heling I. Incidence of external resorption and esthetic results in 58 hlrnched pulpless teeth. Endodont Dent Traumatol 198&4:23-6. 16. Walton RE, O’Dell NL, Myers DL, Lake FT, Shimp KG. External bleaching of tet racycline stained teeth in dogs. ,I Endodont 1982;8:53642. 17. Meyers DR, O’Dell NL, Lake FT, Bell RA, Barenie JT. The effectiveness of bleaching for the removal of tetracycline from rat incisors. J Pedod 1980;4:227-‘35. II treatment of bleaching-related ex18. Friedman S. Surgical-restorative ternal root resorption. Endodont Dent Traumatol 1989;5:63-7. 19. Cvek M, Lindvall AM. External root resorption Lbliowing bleaching of pulpless teeth with oxygen peroxide. Endodont Dent Traumatol 1985;1:56-60. failure following bleaching. Gen Dent 20. Snyder DE. Findodontic 1977;25:54-5. 21. Lado EA. Bleaching of endodontically treated teeth: an update on cervical resorption. Gen Dent 1988;36:500-1. 22. Lado EA, Stanley HR, Weisman MI. Cervical resorption in bleached teeth. Oral Surg Oral Med Oral Pathol 1983;55:?8-80. 23. Harrington GW, Natkin E. External resorption associated with bleaching of pulpless teeth. J Endodont 19795344-8. cervical root resorption 24. Goon WW, Cohen S, Borer RF. External following bleaching. J Endodont 1986;12:414-8. cervical resorptio.!. .I Endodont 1986: 25. Latcham NL. l’ostbleaching 12:262-4.
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26. Montgomery S. External cervical resorption after bleaching a pulpless tooth. Oral Surg Oral Med Oral Patholol 1984;57:203-6. 27. Ledoux WR, Malloy RB, Hurst RW, Mc-Innes-Ledoux P, Weinberg R. Structural effects of bleaching on tetracycline stained vital teeth. J PROSTHET DENT 1985;54:55-9. 28. Cohen SC. Human pulpal response to bleaching procedures on vital teeth. J Endodont 1979;5:134-8. 29. Robertson WD, Mel6 RC. Pulpal response to vital bleaching procedures. J Endodont 1980$?645-9. 30. Scale SN, McIntosh JE, Taylor AN. Pulpal reaction to bleaching of teeth in dogs. J Dent Res 1981;60:948-53. 31. Se& SN, Wilson CFG. Pulpal response to bleaching teeth in dogs. Pediatr Dent 1985;7:209-14. 32. Titley K, Torneck CD, Smith DC. Effect of concentrated hydrogen peroxide solution of the surface morphology of cut human dentin. Endodont Dent Traumatol 1988;4:32-6. 33. Ruse ND, Smith DC, Torneck CD, Titley KC. Preliminary surface analysis of etched, bleached, and normal bovine enamel. J Dent Res 1990;69:1610-3. 34. Torneck CD, Titley KC, Smith DC, Adibfar A. The influence of time of hydrogen peroxide exposure on the adhesion of composite resin to bleached bovine enamel. J Endodont 1990;16:123-8. 35. Weitzman SA, Weitberg AB, Stossel TP, Schwartz J, Shklar G. Effects of hydrogen peroxide on oral carcinogenesis in hamsters. J Periodont 1986;57:685-8. 36. Rees TD, Orth CF. Oral ulcerations with the use of hydrogen peroxide. J Periodont 1986;57:689-92. 37. Martin JH, Bishop JG, Guentherman RH, Dorman HL. Cellular response of gingiva to prolonged application of dilute hydrogen peroxide. J Periodont 1968:39:208-10. 38. Dorman HL, Bishop JG. Production of experimental edema in dog tongue with dilute hydrogen peroxide. Oral Surg 1970;29:38-43. 39. Bayer PD, Lardy H, Myrback K. Th e enzymes. 2nd ed. New York: Academic Press; 1963:147-56. 40. Halliwell B, Gutteridge MC. Oxygen toxicity, oxygen radicals, transition metals and disease. Biochem J 1984;219:1-14.
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41. Rubin E, Farber JL. Pathology. Philadelphia: JB Lippincott, 19BB56. 42. Florence TM. The production of hydroxyl radical from hydrogen peroxide. J Inorg Biochem 1984;22:221-30. 43. LeGrande CE. Free radicals and tissue culture: Part I. Art to Science. 1990;9:1-17. 44. Shogi A, Oxawa E. Necessity of transferrin for RNA synthesis in chick myotubes. J Cell Physiol 1986;127:349-56. 45. Starke PE, Farber JL. Ferric ion and superoxide ions are required for the killing of cultured hepatocytes by hydrogen peroxide. Evidence for the participation of hydroxyl radicals formed by the iron-catalyzed Haber-Weiss reaction. J Biol Chem 1985;260:10099-104. 46. Starke PE, Farber JL. Endogenous defenses against the cytotoxicity of hydrogen peroxide in cultured rat hepatocytes. JBiol Chem 1985;260:&92. 47. Rubin R, Farber JL. Mechanisms of the killing of cultured hepatocytes by hydrogen peroxide. Arch Biochem Biophys 19&1,228:450-9. 48. Imlay JA, Linn S. Mutagenesis and stress responses induced in Escherichia coli by hydrogen peroxide. J Bacterial 1987;169:2967-76. 49. Peterkofsky B, Prather W. Cytotoxicity of ascorbate and other reducing agents towards cultured flbroblssts as a result of hydrogen peroxide formation. J Cell Physiol 1977;90:61-70. 50. Hsie AW, Recio L, Katz DS, Lee CQ, Wagner M, Schenley RI,. Evidence for reactive oxygen species inducing mutations in mammalian cells. USA: Proc Nat1 Acad Sci 1986;83:9616-20. 51. Fridovich I. Superoxide radical: an endogenous toxicant. Ann Rev Pharmacol Toxic01 1983;23:239-57. 52. Berry JH. What about whiteners? Safety concerns explored. J Am Dent Assoc 1990;121:223-5. Reprint
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