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NIOM-Scandinavian Institute of Dental Materials, Kirkeveien 71B, PO Box 70, N-1305 Haslum, Norway;
Institute of Odontology, Faculty of Health Sciences, University of Copenhagen, Denmark
* corresponding author, jon.dahl{at}niom.no
Abstract (I) Introduction (II) History of Bleaching (III) Medicaments (IV) Non-vital Tooth Bleaching (IV-1) METHODS (IV-2) EFFICACY (IV-3) ESTHETIC RESULTS (IV-4) ADVERSE EFFECTS (V) External Tooth Bleaching (V-1) METHODS (V-2) EFFICACY AND ESTHETIC RESULTS (V-3) LOCAL SIDE-EFFECTS Tooth sensitivity Mucosal irritation Alteration of enamel surface Effects on restorations (V-4) GENERAL SIDE-EFFECTS (V-5) GENOTOXICITY AND CARCINOGENICITY OF BLEACHING AGENTS (V-6) TOXICITY OF HYDROGEN PEROXIDE AND CARBAMIDE PEROXIDE Case reports of human exposure Animal studies (V-7) RISK ASSESSMENT OF EXTERNAL TOOTH BLEACHING (V-8) LEGAL AND ETHICAL ASPECTS OF EXTERNAL TOOTH BLEACHING (VI) Concluding Remarks Acknowledgments REFERENCES
| Abstract |
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Key words. Enamel, esthetics, ethics, toxicology
| (I) Introduction |
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Scaling and polishing of the teeth remove many extrinsic stains. For more stubborn extrinsic discoloration and intrinsic stain, various bleaching techniques may be attempted. Tooth bleaching can be performed externally, termed night guard vital bleaching or vital tooth bleaching, or intracoronally in root-filled teeth, called non-vital tooth bleaching. The aims of the present paper are to review critically the literature on the biological aspects of tooth bleaching, including efficacy and side-effects of such treatments. In addition, the safety of vital tooth bleaching is especially addressed.
| (II) History of Bleaching |
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| (III) Medicaments |
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). Hydrogen peroxide acts as a strong oxidizing agent through the formation of free radicals (Gregus and Klaassen, 1995), reactive oxygen molecules, and hydrogen peroxide anions (Cotton and Wilkinson, 1972) (Fig. 1). These reactive molecules attack the long-chained, dark-colored chromophore molecules and split them into smaller, less colored, and more diffusible molecules. Carbamide peroxide also yields urea (Budavari et al., 1989) that theoretically can be further decomposed to carbon dioxide and ammonia. It is unclear, however, how much ammonia is formed during tooth bleaching with carbamide peroxide. The high pH of ammonia facilitates the bleaching procedure (Sun, 2000). This can be explained by the fact that, in a basic solution, lower activation energy is required for the formation of free radicals from hydrogen peroxide, and the reaction rate is higher, resulting in an improved yield compared with an acidic environment (Cotton and Wilkinson, 1972). The outcome of the bleaching procedure depends mainly on the concentration of the bleaching agent, the ability of the agent to reach the chromophore molecules, and the duration and number of times the agent is in contact with chromophore molecules.
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| (IV) Non-vital Tooth Bleaching |
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). A modification of the method that reduces the number of in-office appointments has been suggested (Liebenberg, 1997; Caughman et al., 1999). Access to the pulp chamber is gained by removal of the coronal restoration and the coronal part of the root filling. The remaining root filling is sealed off with glass-ionomer cement. The patient places the bleaching agent, usually 10% carbamide peroxide, intracoronally at regular intervals and covers the lingual aspect of the tooth with a plastic splint. In this method, the pulp chamber is left unsealed during the weeks of treatment. If the seal of the root-filling leaks, contamination of the periapical tissue may lead to endodontic treatment failure, the residual bleaching agent will be ingested due to insufficient rinse of the sticky gel, and intracoronal dentin will be subject to discoloration from pigments in foods or beverages. The chair time saved with this bleaching method does not compensate for the adverse biological consequences.
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(IV-3) ESTHETIC RESULTS
The evaluation of the esthetic outcome of a bleaching treatment is subjective, and the patient’s opinion may differ from that of the dental surgeon (Glockner et al., 1999). In addition, different terms and definitions of the outcomes have been applied which make comparisons between studies difficult (Friedman et al., 1988; Holmstrup et al., 1988; Glockner et al., 1999). Immediate treatment success has usually been defined as no or slight deviation in color between the treated and non-treated teeth. More than 90% immediate success has been reported with the thermo-catalytic method (Howell, 1980) or the conventional "walking bleach" procedure (Holmstrup et al., 1988). The failure rate may be useful in determing the long-term esthetic results of internal bleaching. Failure, however, has not been defined in the different long-term studies (Brown, 1965; Friedman et al., 1988; Holmstrup et al., 1988; Glockner et al., 1999), but the intuitive definition is "teeth that need to be re-treated". The need for re-treatment increased with the observation time, i.e., 10% after 1 to 2 years (Friedman et al., 1988), 20–25% after 3 to 5 years (Brown, 1965; Holmstrup et al., 1988), and 40% failure in teeth observed up to 8 years (Friedman et al., 1988). In a more recent study, a 7% failure rate was reported after 5 years, but the majority of cases in this study were defined as ideal for bleaching (no other filling than the palatinal endodontic opening) (Glockner et al., 1999). A study of endodontically treated, internally bleached tetracycline-stained teeth that were followed for 3–15 years showed that four out of 20 patients needed re-treatment (Abou-Rass, 1998). At present, no study has provided a good predictor for the long-term outcome of internal bleaching. It appears that teeth with multiple fillings are not ideal candidates for the procedure (Howell, 1980; Glockner et al., 1999).
(IV-4) ADVERSE EFFECTS
Cervical root resorption (Fig. 3) is an inflammatory-mediated external resorption of the root, which can be seen after trauma and following intracoronal bleaching (Friedman et al., 1988). A review of published case reports on cervical root resorption revealed 22 such cases following intracoronal bleaching (Table 1). Table 1 summarizes the results of 4 follow-up studies. Fifty-eight bleached (30% H2O2 and heated) pulpless teeth were followed for 1–8 years, and 4 cases (7%) of external root resorption were observed (Friedman et al., 1988). Another 95 teeth examined three years after treatment by the "walking bleach" technique (sodium perborate in water) revealed no cervical resorption (Holmstrup et al., 1988). In a four-year follow-up of 250 teeth with severe tetracycline discoloration, with sodium perborate in oxygen-water as the bleaching agent, no evidence of external resorption was found (Anitua et al., 1990). An analogous study comprised of 112 teeth bleached with a paste of sodium perborate in 30% hydrogen peroxide and observed for 3–15 years reported no external root resorption (Abou-Rass, 1998).
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Tooth crown fracture has also been observed after intracoronal bleaching (Grevstad, 1981), most probably due to extensive removal of the intracoronal dentin. In addition, intracoronal bleaching with 30% hydrogen peroxide has been found to reduce the micro-hardness of dentin and enamel (Lewinstein et al., 1994) and weaken the mechanical properties of the dentin (Chng et al., 2002).
| (V) External Tooth Bleaching |
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(V-2) EFFICACY AND ESTHETIC RESULTS
Data on the efficacy and duration of external tooth bleaching are mostly related to case presentations, and only a few clinical studies are available for review. It is generally advocated that most teeth are susceptible to bleaching (Figs. 4, 5), provided that the treatment is carried out for a sufficiently long time (Haywood, 1996; Goldstein, 1997; Heymann, 1997; Dunn, 1998; Leonard, 1998). The first subjective change in tooth color was observed after 2–4 nights of tooth bleaching with 10% carbamide peroxide (Tam, 1999a). In a clinical study of night-guard vital bleaching for 6 wks (10% carbamide peroxide), 92% of the 38 patients experienced some lightening of the treated teeth (Haywood et al., 1994). The patients were followed up by mailed questionnaires, and 74% of the 26 respondents and 62% of the 23 respondents experienced no or slight reversal in color after 1.5 and 3 years, respectively. A follow-up of 30 patients whose teeth were bleached with 10% carbamide peroxide revealed that 43% perceived their tooth color as stable 10 yrs after bleaching (Ritter et al., 2002). Another clinical trial examined the effects of the use of 10% carbamide peroxide nightly for 2 wks, and found, on an average, that the teeth were eight shade units lighter on the Vita shade guide, calibrated according to lightness value (Swift et al., 1999). Two years’ follow-up revealed that the teeth, on average, darkened two units on this shade guide, and that the regression occurred during the first 6 months after bleaching. No patients found it necessary to re-bleach their teeth. Use of 20% carbamide peroxide resulted in lighter teeth than with 7.5% hydrogen peroxide when evaluated immediately after termination of a 14-day at-home bleaching procedure (Mokhlis et al., 2000). However, no difference between the two treatments with regard to tooth lightness was observed 10 wks later. In a small study which compared bleaching strips and 10% carbamide peroxide in trays, it was claimed that the bleaching strips were more efficient (Sagel et al., 2002), but others have not confirmed this finding, and there are no long-term follow-up data on this issue.
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). Data from various studies of 10% carbamide peroxide indicate that from 15 to 65% of the patients reported increased tooth sensitivity (Haywood et al., 1994; Schulte et al., 1994; Leonard et al., 1997; Tam, 1999a). Higher incidence of tooth sensitivity (from 67 to 78%) was reported after in-office bleaching with hydrogen peroxide in combination with heat (Cohen and Chase, 1979; Nathanson and Parra, 1987). Tooth sensitivity normally persists for up to 4 days after the cessation of bleaching treatment (Cohen and Chase, 1979; Schulte et al., 1994), but a longer duration of up to 39 days has been reported (Leonard et al., 1997; Tam, 1999a). In a clinical study that compared two different brands of 10% carbamide peroxide bleaching agent, 55% of the 64 patients reported tooth sensitivity and/or gingival irritation, and 20% of those who experienced side-effects terminated the treatment due to discomfort (Leonard et al., 1997).
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An in vivo study in dogs indicated that hydrogen peroxide alone or in combination with heat caused alterations in odontoblasts and deposition of dentin (Seale et al., 1981). Hemorrhage and inflammation were observed in teeth 3 and 15 days after bleaching, and the pulpal changes were reversed 60 days after the treatment (Seale et al., 1981). In another study, 15-, 30-, and 45-minute treatments with hydrogen peroxide and heat were applied 4 times at two-week intervals, and the dogs were killed at 13, 62, and 92 days following the last treatment (Seale and Wilson, 1985). Histological examination of the pulp of the bleached teeth revealed pathological changes in odontoblast morphology and dentinogenesis at both the 13- and 62-day time points, and the severity of the changes was related to the length of each treatment. Repair of the lesions was observed 92 days after the last treatment (Seale and Wilson, 1985). Tooth sensitivity was also a common symptom in patients who had not bleached their teeth, and their symptom was correlated with gingival recession (Jorgensen and Carroll, 2002). Patients with a previous history of tooth sensitivity may thus have a higher risk for such an adverse effect from external tooth bleaching, and this should be taken into account before treatment begins.
Mucosal irritation
A high concentration of hydrogen peroxide (from 30 to 35%) is caustic to mucous membranes and may cause burns and bleaching of the gingiva. In animal experiments, exposure of the gingiva to 1% H2O2 for 6 to 48 hrs resulted in epithelial damage and acute inflammation in the subepithelial connective tissue (Martin et al., 1968). Long-term application of 3% or 30% hydrogen peroxide in the hamster cheek pouch twice weekly resulted in inflammatory changes (Weitzman et al., 1986). In clinical trials that used 10% carbamide peroxide in custom-made trays, from 25 to 40% of the patients reported gingival irritation during treatment (Leonard et al., 1997; Tam, 1999a). It is therefore advisable that the tray be designed to prevent gingival exposure by the use of a firm tray that has contact with solely the teeth. In this respect, the newly introduced bleaching strips may be unfavorable, since the bleaching gel will come into contact with the gingiva.
Alteration of enamel surface
Morphological alteration of the enamel following tooth bleaching (Fig. 6) has been addressed in several studies. Enamel slabs were subjected to different bleaching agents containing 10% carbamide peroxide for 15 hrs a day, for two- and four-week periods, and evaluated by scanning electron microscopy (Shannon et al., 1993). During the remaining 9 hrs every day, the slabs were exposed to human saliva in vivo. Significant surface alterations in enamel topography were observed in slabs treated with the bleaching solutions for 4 wks (Shannon et al., 1993). This finding was confirmed in a study with 30% hydrogen peroxide and 30% hydrogen peroxide mixed with sodium perborate (Ernst et al., 1996). Compared with the untreated control surfaces, the enamel surface exposed to the bleaching agents underwent slight morphologic alterations. Teeth that were bleached in vivo with 35% carbamide peroxide (30 min/day for 14 days) lost the aprismatic enamel layer, and the damage was not repaired after 90 days (Bitter, 1998). By infrared spectroscopic analysis, it was found that in vitro treatment of extracted teeth with 35% carbamide peroxide for 30 min/day for 4 days changed the inorganic composition of the enamel, whereas 10% and 16% concentrations did not (Oltu and Gürgan, 2000). Evaluation of casts made from impressions of teeth bleached with 10% carbamide peroxide for 8–10 hrs/day for 14 days revealed no or minimal changes in the enamel surface (Leonard et al., 2001), which may be due to inadequate reproduction of the minor enamel alterations in the impression. A high concentration of carbamide peroxide was detrimental to enamel surface integrity, but the damage was less than that seen after phosphoric acid etch (Ernst et al., 1996). A clinical implication of these findings may be that the teeth are more susceptible to extrinsic discoloration after bleaching due to increased surface roughness.
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(V-4) GENERAL SIDE-EFFECTS
The risk of adverse effects has not been the main focus in the design of clinical studies of external tooth bleaching. For example, for a case-reference study that detects a doubling of the risk for an adverse effect that occurs at a level of 1:1000 in the reference group, the study group must have at least 1000 people, and for detection of a 10% increase in the risk, more than 10,000 people must be enrolled in the study (Bjerre and LeLorier, 2000). In the clinical studies published on tooth bleaching that address adverse effects (Cohen and Chase, 1979; Nathanson and Parra, 1987; Haywood et al., 1994; Schulte et al., 1994; Leonard et al., 1997; Tam, 1999a,b), the number of participants has been small compared with the above numbers, and many studies did not have control groups. Therefore, the potential general adverse effects of external tooth bleaching cannot be assessed at this time.
(V-5) GENOTOXICITY AND CARCINOGENICITY OF BLEACHING AGENTS
The genotoxicity of hydrogen peroxide and of tooth whiteners containing carbamide peroxide has been evaluated (IARC, 1985; ECETOX, 1996; Li, 1996). The consensus arising from these evaluations was that direct contact with hydrogen peroxide induced genotoxic effects in bacteria and cultured cells. When hydrogen peroxide was administered to bacteria or cultured cells in the presence of catalase or other metabolizing enzymes, the effect was reduced or abolished. Testing of hydrogen peroxide for systemic genotoxic effects in animals revealed no evidence of in vivo mutagenicity. Since hydroxy radicals, perhydroxyl ions, and superoxide anions formed from hydrogen peroxide are capable of attacking DNA, the genotoxic potential of hydrogen peroxide is dependent on the accessibility of free radicals to target DNA. This may explain why hydrogen peroxide induces genotoxicity in the presence of metabolizing enzymes neither in vitro nor in vivo. Tooth whiteners containing carbamide peroxide were mutagenic in certain bacterial strains and non-mutagenic in the presence of additional activating enzymes. Several in vivo studies addressing the formation of micronuclei in bone marrow cells and sister chromatide exchange after exposure to carbamide-peroxide-containing products revealed no genotoxic effects.
Data on animal experiments evaluating long-term effects of the oral administration of hydrogen peroxide are given in Table 3. A dose-dependent increased incidence of duodenal hyperplasia was observed in a study where 0.1% and 0.4% hydrogen peroxide was administered to mice via drinking water for 100 days (Ito et al., 1981). In addition, the number of adenomas and carcinomas increased in the duodenum of the exposed groups, but not in a dose-related manner (Ito et al., 1981). In another study, mice were given 0.4% hydrogen peroxide in the drinking water for up to 700 days. Benign and malignant lesions were found in the stomach and duodenum after 90 days’ exposure (Ito et al., 1982). The incidence did not increase with exposure time, but more severe lesions were observed later in the experiment. The stomach lesions regressed completely after an exposure-free period of 10–30 days, but some of the duodenal lesions persisted. Strains with different catalase activity and provided to mice with 0.4% hydrogen peroxide in the drinking water resulted in tumor incidence inversely related to the catalase activity (Ito et al., 1984). In mice, topical application of 15% hydrogen peroxide in acetone on the skin for 25 wks resulted in an increased number of papillomas in the treated group, but no malignant changes were observed in mice followed for 50 wks (Klein-Szanto and Slaga, 1982).
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Based on the aforementioned studies, hydrogen peroxide was shown to have a weak local carcinogenic-inducing potential. The mechanism is unclear, but a genotoxic action cannot be excluded, since free radicals formed from hydrogen peroxide are capable of attacking DNA. Several studies of DMBA carcinogenesis in mice skin and hamster cheek pouch indicate that hydrogen peroxide may act as a tumor-promoter (Klein-Szanto and Slaga, 1982; Weitzman et al., 1986).
The International Agency for Research on Cancer (IARC) concluded that there is limited evidence in experimental animals and inadequate evidence in humans for the carcinogeni-city of hydrogen peroxide and classified the chemical into Group 3: Unclassifiable as to carcinogenicity to humans (IARC, 1999). Recently, the genotoxic potential of hydrogen peroxide in oral health products has been evaluated (SCCNFP, 1999). It appears unlikely that oral health products containing or releasing hydrogen peroxide up to 3.6% H2O2 will enhance cancer risk in individuals except in those who have an increased risk of oral cancer due to tobacco use, alcohol abuse, or genetic predisposition (SCCNFP, 1999). To evaluate higher concentrations of hydrogen peroxide was not the task of the committee.
(V-6) TOXICITY OF HYDROGEN PEROXIDE AND CARBAMIDE PEROXIDE
Case reports of human exposure
The acute effects of hydrogen peroxide ingestion are dependent on the amount ingested and the concentration of the hydrogen peroxide solution. The outcomes of accidental ingestion, or intentional ingestion for suicide, of solutions of 10% hydrogen peroxide and higher were more severe than those seen at lower concentrations (Dickson and Caravati, 1994). Accidental ingestion of 35% hydrogen peroxide has resulted in several fatal or near-fatal poisonings (Giusti, 1973; Giberson et al., 1989; Humberston et al., 1990; Christensen et al., 1992; Sherman et al., 1994; Litovitz et al., 1995; Ijichi et al., 1997). These individuals vomited, were cyanotic, and experienced convulsions and respiratory failure (Giberson et al., 1989). Cerebral infarction and ischemic changes of the heart due to gas embolism have also been observed (Rackoff and Merton, 1990; Christensen et al., 1992; Luu et al., 1992; Cina et al., 1994; Sherman et al., 1994; Ijichi et al., 1997). Young children are at high risk for accidental ingestion. A two-year-old child died after drinking 100 mL of a 35% hydrogen peroxide solution, which corresponds to a dose of 290 mg hydrogen peroxide/kg BW (Christensen et al., 1992). Also, ingestion of a lower concentration of hydrogen peroxide has resulted in serious injury. Lung edema and diffuse intestinal emphysema were found on autopsy of a 16-month-old child who had swallowed approximately 600 mg hydrogen peroxide/kg BW of a 3% hydrogen peroxide solution. When the child was first seen, white foam emerged from the child’s mouth and nose, and the child died 10 hrs later (Cina et al., 1994). Portal venous gas embolism was observed in a two-year-old child after unintentional ingestion of 3% hydrogen peroxide solution (Rackoff and Merton, 1990).
One syringe (3.5 g) of 18% carbamide peroxide yields 210 mg of hydrogen peroxide. Fatal poisoning is therefore not likely even if a two-year-old child (body weight approximately 12 kg) ingests one syringe of bleaching agent. Ulceration of the oral mucosa, esophagus, and stomach is more likely to occur in such a case, accompanied by symptoms such as nausea, vomiting, abdominal distention, and sore throat, as have been reported for other hydrogen peroxide-containing preparations (Dickson and Caravati, 1994). It is therefore important to keep syringes with bleaching agents out of the reach of children, to prevent any possible accident.
Animal studies
Oral LD50 determination is a crude estimate of the toxicity of a compound (van den Heuvel et al., 1990), but such data are often provided and used for toxicological assessment. The single-dose LD50 values for non-carbopol-containing 10% carbamide peroxide solutions and a carbopol-containing 10% carbamide peroxide solution in mice were found to be 143 mg/kg and 87 mg/kg, respectively (Woolverton et al., 1993). This corresponds to 15 and 9 mg carbamide peroxide per kg BW. For hydrogen peroxide, the oral LD50 value was found to be approximately 1600 mg/kg (Ito et al., 1976), but no other studies have confirmed the above findings. In rats, a single oral dose of 5 g/kg BW of proprietary solutions of 10%, 15%, and 35% carbamide peroxide induced a concentration-dependent acute toxicity, and the rats showed respiratory depression, reduced weight gain and water consumption, changes in estrous cycle, and, at necropsy, histological abnormalities of the stomach, including necrotic mucosa and disrupted gastric glands (Cherry et al., 1993). In the highest-concentration group, 3 animals died of gastric hemorrhage and bloating. Six of 36 rats died within 2 hrs after receiving, orally, 5 g/kg BW of a tooth whitener containing 6% hydrogen peroxide (Redmond et al., 1997). After 15 min, the stomach was grossly bloated with gas, and after 2 hrs the blood hematocrit was elevated, and histology revealed injury to the gastric mucosa. The gastric mucosa appeared normal one week later, and the blood chemistry normalized 2 wks after the exposure. In rats, stomach gavage of 15 and 50 mg carbamide peroxide per kg BW or 150 and 500 mg of tooth whitener containing 10% carbamide peroxide per kg BW resulted in ulceration of the gastric mucosa after 1 hr; the lesions started to heal after 24 hrs (Dahl and Becher, 1995). The ulcerations from the exposure to the tooth-bleaching agent were more pronounced than those observed after a comparable dose of carbamide peroxide. This may be attributed to the hydrophobic nature of the gel and the content of carbopol in the bleaching agent, which likely increases tissue adherence and retards the decomposition of hydrogen peroxide (Dahl and Becher, 1995).
In catalase-deficient mice that were given 100 ppm, 300 ppm, 1000 ppm, or 3000 ppm hydrogen peroxide in distilled water for 13 wks, the "no observed adverse effect level" (NOAEL) was 100 ppm, corresponding to 26 and 37 mg/kg BW/day for males and females, respectively (Weiner et al., 2000). In the 1000- and 3000-ppm groups, small duodenal mucosal hyperplasias were observed; the lesions appeared reversible during a six-week recovery period. In a study of rats given 50 mg/mL hydrogen peroxide by oral gavage 6 times a wk for three months, the NOAEL was found to be 56 mg/kg BW/day (Ito et al., 1976). Deleterious localized effects on the gastric mucosa, decreased food consumption, reduced weight-gain, and blood chemistry changes were observed in the affected animals. Rats exposed daily, by oral gastric tube, to 0.06%-0.6% hydrogen peroxide solutions for 40–100 days, and to doses above the NOAEL (30 mg/kg BW/day), exhibited significant reduction in plasma catalase levels, and, in the highest-dose group, reduced weight-gain and blood chemistry changes were found (Kawasaki et al., 1969).
(V-7) RISK ASSESSMENT OF EXTERNAL TOOTH BLEACHING
Risk assessment is traditionally considered to consist of four steps: the hazard identification, the dose-response relationship, the exposure assessment, and the risk characterization (IPCS, 1999). The risk characterization is founded on a critical comparison of the data on exposure and the dose-response relationship.
The important ingredient in tooth whitening today is hydrogen peroxide. The NOAEL values based on repeated-dose studies with hydrogen peroxide per os have been estimated to be from 26 to 56 mg/kg BW/day (Kawasaki et al., 1969; Ito et al., 1976; Weiner et al., 2000). These three studies are consistent in their findings of the "no adverse effect" level, and we have selected 26 mg/kg BW/day for the following risk assessment.
The amount of bleaching agent used for bleaching one arch of teeth has been calculated to be 900 mg per application when administered according to the manufacturer’s instruction (Dahl and Becher, 1995), and an average of 500 mg per application based on clinical experiments (Li, 1996). At least 25% of the bleaching agent administered in bleaching trays is ingested during 2 hrs of bleaching (Matis et al., 2002). We have calculated the exposure to hydrogen peroxide from tooth bleaching and the safety factor using different concentrations of the bleaching agent (Fig. 7). The results are given in Table 4. The safety factor (= NOAEL/exposure) varies between 350 and 55. In risk assessment based on toxicity data derived from animal studies, the minimum accepted safety factor is 100 (Woodward, 1996). This safety factor is not reached in preparations that deliver or contain more than 12.6% H2O2 when 500 mg of bleaching agent is used for bleaching one arch. Longer bleaching periods per day, multiple applications, bleaching maxillary and mandibular teeth at the same time, and overfilling the tray increase the exposure and reduce the safety factor. For example, if both maxillary and mandibular teeth are bleached at the same time, the minimum required safety factor will not be reached for preparations that contain or deliver more than 7.9% H2O2, which corresponds to 22% carbamide peroxide (Budavari et al., 1989). According to the exposure data from a previous evaluation (900 mg/application) (Dahl and Becher, 1995), the concentration of H2O2 should not exceed 3.5%, which corresponds to 10% carbamide peroxide (Table 4). Based on the risk assessment, it must be concluded that selection of preparations with a low concentration of carbamide peroxide is recommended for the optimum safety of the patient. In addition, overfilling the tray without removing excess material, biting on the tray, and bleaching both maxillary and mandibular teeth at the same time are not advisable.
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Tooth whiteners are generally regarded in Europe as cosmetic products (EU Commission, 1996). According to the cosmetic regulation, the maximum authorized content or release of hydrogen peroxide in such oral hygiene products is 0.1% (EU Commission, 1992). Tooth-whitening products can also be claimed to be medical devices, and evaluated according to the medical device regulation (EU Commission, 1993). Products granted the EU certification, i.e., the CE marking (CE = Communauté Europeén), could be used for tooth bleaching provided that the claims of the manufacturer and the definition of a medical device according to the European regulation are followed. The definition of a medical device includes "material or other article intended by the manufacturer to be used for the purpose of treatment or alleviation of disease, or for the purpose of treatment, alleviation of or compensation for a handicap". At least in Europe, the use of bleaching agents containing more than 0.1% hydrogen peroxide requires a proper professional diagnosis of a disease or a handicap. Bleaching must therefore be regarded as an alternative to other dental procedures such as laminates and full crown therapy.
| (VI) Concluding Remarks |
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| Acknowledgments |
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