6: Bleaching Techniques

Bleaching Techniques

Dentistry has changed significantly over the years. The sharp decline in dental caries and increased well-being have led many patients to perceive even the slightest tooth blemish as a “pathologic” condition. Until only a few years ago patients were generally satisfied if they did not experience pain during treatment and/or had a masticatory function that was essentially effective, but now they want invisible restoration and a great smile.

Esthetic requirements have increased substantially in the average population, and the lower third of the face strongly characterizes the personality and revealssometimes dramaticallya person’s sociocultural background. Patients are also deeply conditioned by the examples and articles (often full of nonsense) in popular magazines.

The dental world has responded very well to these demands and can provide good solutions to patients thanks to cutting-edge techniques and constantly evolving materials (Figure 6-1). Modern dentistry has increasingly leaned toward cosmetic, conservative and minimally invasive principles, possibly with direct access to the cavity, to achieve satisfactory results for both the patient and the specialist.

In this new clinical and social picture, bleaching procedures play an important role (Figures 6-2 to 6-7).

In the United States the demand for esthetic treatment occurred much earlier than in Europe. In the mid-1980s the bleaching properties of carbamide peroxide were discovered by accident, as it was used as a mouth disinfectant in patients who underwent maxillofacial surgery with intermaxillary fixation.

Carbamide peroxide was used because of the ban on chlorhexidine; at the time the molecule had not been approved yet by the Food and Drug Administration.

On removal of the fixation, the teeth appeared whiter. Haywood was the first to publish findings regarding the at-home bleaching procedure in 1989.

The Enemies of Dental Esthetics

Pigmentation and Discoloration

Tooth pigmentation (extrinsic stain) occurs when coloring agents of various kinds (chromogenic bacteria, food dyes, beverages, or drugs) are fixed onto the acquired enamel pellicle (AEP) and diffuse through its surface layers (Figure 6-8). The best-known examples of substances containing exogenous pigments are coffee, tea, red wine, tobacco, licorice, chlorhexidine, and stannous fluoride. A high pH in the oral cavity favors the accumulation of pigments.

Tooth discoloration (intrinsic discoloration) instead occurs when the change in shade is caused by internal structural change of the optical properties of dental tissues or by accumulation of color-active agents within the dentin or enamel structure (Figures 6-9 and 6-10).

The following are the most frequent causes of discoloration:

• Aging: Teeth become gray or yellowish owing to deposition of tertiary dentine, tubular sclerosis, or ion exchange between dentin and enamel.

• Amelogenesis imperfecta (there are seven variants): Tooth color ranges from yellow to deep brown owing to disturbances during formation or maturation of the enamel.

• Dentinogenesis imperfecta: Tooth color ranges from red-brown to gray, and the cavum dentis is either obliterated or very reduced by the deposition of a very opalescent dentin.

• Fluorosis: The enamel is hypermineralized and exhibits structural alterations (increased number of pores); the color varies from white-gray (opaque fluorosis) to brown (simple fluorosis, Colorado brown stain) or can be extremely dark (pitting fluorosis).

• Hematologic diseases: Fetal erythroblastosis, thalassemia, sickle cell anemia, and various forms of porphyria may cause discoloration.

• Posttraumatic formation anomalies: Injuries of the deciduous dentition may cause opaque areas on permanent teeth.

• Discolorations caused by silver amalgam fillings, especially in the case of old restoration made with non–gamma-2 amalgam: The release of oxidation products sometimes produces significant color aberrations. For this type of discoloration the only possible treatment is mechanical removal of the hard tissues involved.

• Discoloration may be caused by specific endodontic cements.

• Systemic diseases: Hepatitis may result in discoloration.

• Tetracyclines: Yellow-brown (chlortetracycline) or grayish (demethylchlortetracycline) discolorations are caused by administration of the antibiotic before the eighth year of age. It is common knowledge that tetracyclines have a marked affinity for calcified tissues in formation, to which it binds in the form of orthophosphate. Intensity of discoloration seems to be more dose dependent than time dependent.

• Injuries and pulp necrosis: Although metabolic products resulting from hemorrhagic extravasation or tissue necrosis cause discoloration, the formation of dark ferrous sulfates from hemoglobin seems to play a major role.

The Enemies of Dental Esthetics

Pigmentations Discolorations
Extrinsic stain Intrinsic stain
Extrinsic discoloration Intrinsic discoloration

Pigmentation

Various types of coloring agents (chromogenic bacteria, food dyes, beverages, drugs) become fixed to the AEP and can diffuse onto the surface layers of the enamel.

Discoloration

The change in shade occurs as a result of the structural change in the optical properties of dental tissues or the accumulation of colored substances within the enamel and/or dentin structure.

Bleaching

Bleaching procedures can be classified as follows:

• Internal (or nonvital) bleaching. The active agent is placed within the pulp chamber by the dentist (in-office bleaching) and can also be left in place between sessions (“walking bleach”).

• External (or vital) bleaching. The active agent is placed in contact with the tooth surface. Despite its name, vital bleaching can obviously be performed only on endodontically treated teeth. Vital bleaching can be further divided into at-home bleaching (with self-application of the bleaching agent by the patient as instructed by the dentist) and in-office bleaching (in which the dental team performs the bleaching procedure at the dental chair). The agents used for at-home bleaching are obviously not as concentrated and are thus less powerful (“soft bleaching”) than those used in the office by the dentist (“power bleaching”). For the sake of completeness, I must also mention the microabrasion technique, which can be used in conjunction with bleaching procedures. Microabrasion removes the superficial layers of enamel by means of a strong (inorganic) acid and an abrasive powder and is followed by external bleaching. This procedure can be performed only in the office by a dentist.

At-Home Bleaching

Bleaching Tray

With at-home bleaching the most important aspects of the treatment are proper instruction, patient motivation, and a well-made bleaching tray. The fabrication of the tray is very important, and the dentist should detail to the dental technician all the procedures needed for a well-fitted tray (Figures 6-11 to 6-17).

Two types of bleaching tray are available on the market.

Some are thin and rigidspecific for treating individual teethand probably provide a better seal, as oxygen release by the active agent is diluted by saliva. They seem to be more stable because they engage the tooth equator better. Nevertheless, because they are quite rigid, if they are not properly finished they can irritate the marginal tissues, making them harder to finish, manage, and control.

There are also trays that are supplied as standard with most bleaching systems. They are thicker and softer and can thus be used only for full arch coverage because they are not retentive enough for single-tooth bleaching. They unquestionably do not seal as well and seem more unstable (when empty they tend to fall from the upper arch, although they remain in place when they are filled with the viscous gel). They are less irritating owing to their softness and are thus easier to use for both the dentist and the patient.

Vital Bleaching: Indications and Contraindications

Vital bleaching can be applied to all forms of pigmentation that do not respond to thorough professional cleaning and to less severe forms of discoloration.

Another important indication is pretreatment for the placement of ceramic veneers, as a more esthetic substrate can yield a better clinical outcome or allow more conservative preparation. Like any dental procedure, there are several contraindications to vital bleaching. In fact, tooth bleaching (both at-home and professional) is contraindicated in the following cases:

• Simple pigmentation: One session of oral hygiene, or possibly enamel microabrasion, can solve the problem

• Poorly motivated or uncooperative patients

• Young teeth with large pulp chambers

• Enamel defects (e.g., macroporosity) predisposed to very rapid relapse owing to penetration of exogenous pigments (Figure 6-18)

• Teeth that have been extensively restored have faulty restorations or, worst of all, have caries (Figures 6-19 and 6-20)

• Hypersensitive teeth

• Internal resorption

• Discoloration caused by silver amalgam

Tetracycline Discoloration

Subjects who are currently 40 to 50 years old are the ones who most frequently request bleaching procedures, because they are the ones who in the 1960s experienced the side effects of tetracyclines, which were unknown at the time.

Tetracycline discoloration is classified into three groups according to severity.

In first-degree discoloration there is a decrease in tooth shade value, and the tooth has a darker color at the cervical region. The tooth loses brightness (Figure 6-21). First-degree tetracycline discoloration can be treated with a good degree of predictability. In second-degree discoloration there is a further loss of value and the chroma is darker but fairly uniform. In this case as well, bleaching yields appreciable results (Figure 6-22).

Third-degree discoloration, however, exhibits horizontal banding of different contrasting colors. With this type of discoloration a conservative approach is no longer feasible. More aggressive treatment, such as ceramic veneers or full crowns, is required to achieve esthetic improvement (Figure 6-23).

Side Effects

At the beginning of treatment teeth can become hypersensitive. This hypersensitivity is caused by the good diffusion properties of peroxides. There are no long-term reports on the alleged negative actions of carbamide peroxide. Experiences with in-office bleaching, which is more aggressive, have revealed that pulp damage (necrosis) is a consequence of the application of an excessive heat source, whereby thermal and nonthermal damages are caused by the direct chemical action of peroxides. In some cases deepithelization and gum ulcers have been observed. These problems are often caused by excess gel, extended application time, and incorrect tray design at the sulcular area. Usually these lesions regress spontaneously after a few days.

Peroxides have a negative effect on the adhesion of composite resins to dental tissues owing to oxygen supersaturation in the recently bleached enamel.

As we know, oxygen is a strong inhibitor of composite curing. The excess oxygen, however, is depleted in approximately 2 weeks. The rule of thumb is to wait 3 weeks after completion of at-home bleaching before placing composite restorations.

It should be remembered—and, above all, explained to patients—that peroxide gel can whiten the teeth but has absolutely no effect on preexisting composite restorations or ceramic crowns. Therefore at the end of treatment they will look darker than the surrounding enamel and the patient should thus be willing to bear the cost of their replacement if necessary. The bleaching gel also has a negative effect on microfilled composite resins (e.g., Silus Plus), causing loss of hardness and surface smoothness.

Microfilled hybrid composites, which are now the most widely used, do not seem to encounter significant changes. Peroxides, however, seem to accelerate the aging process of composite resins substantially. Therefore it is always best (not only from the standpoint of color consistency) to perform the bleaching procedure before composite restorations. The cytotoxicity of carbamide peroxide is not an issue and is similar to that of many other materials for dental use, such as eugenol and oxyphosphate temporary cements. Animal studies did not reveal any mutagenic or teratogenic effect for 10% carbamide peroxide. The lethal dose of a 10% solution for a subject weighing 75 kg (165 lb) is 6.5 to 8 L (1.5 to 1.8 gal) (Figure 6-24).

The tray itself can have a slight orthodontic effect or may trigger grinding or clenching mechanisms. No significant effects on the intestinal tract caused by the inevitable ingestion of carbamide peroxide have been reported to date. Salivary pH rises by about half a point in the first 15 to 20 minutes after application. The pH of the gel placed inside the tray rises from about 4.5 (peroxide is acidic) to about 8.0 as the water breaks the peroxide down, first into urea and then into ammonia. The pH remains high for about 2 hours. Regarding orthodontic effects, at night the tray can move the teeth slightly. Therefore in the morning some patients (e.g., those who are “occlusally active”) may experience a different occlusion, but it is a temporary effect that resolves in a matter of hours, if not minutes.

Patients should always be informed about hypersensitivity, because this information may preventor at least minimizethe patient’s grievances.

The presence of finishing imperfections on the tray may cause minor pressure ulcers, which heal very rapidly once the compression area on the tray has been ground down (Figure 6-25).

Chemicals and Modes of Action

Hydrogen peroxide (H2O2) and sodium perborate (NaBO2[OH]2) release oxygen atoms. Carbamide peroxide or derivatives (usually H2N-CO-NH2·H2O2) can be considered a type of peroxide that is chemically unstable. After application (in contact with water) it splits into 3% to 5% hydrogen peroxide and 5% to 7% urea.

Peroxides were once used in dentistry, and occasionally they are still used to treat hard-to-heal ulcers, aphthae, and gingivitis. Longitudinal studies have also demonstrated that the use of carbamide peroxide reduces plaque index and caries incidence significantly during orthodontic treatment. These substances showed tooth whitening as a side effect, and this observation led to the use of carbamide peroxide for this purpose. The mechanism of action is not fully understood, but it is strongly believed that the oxygen released by peroxides penetrates the relatively porous structure of enamel and even dentin, breaking down the complex molecules of pigment nested therein (which are directly responsible for dark tooth pigmentation) into simpler colorless molecules.

Urea is instead directly responsible for the antiplaque effect. In fact, in the oral cavity it breaks down into carbon dioxide and ammonia; the latter causes an increase in pH that hinders the development, metabolism, and maturation of bacterial plaque. The release of oxygen from peroxides (either hydrogen or carbamide) is enhanced by the application of light, heat, or other catalysts.

Sometimes Carbopol is added to at-home bleaching products. This substance is a polymer of polyacrylic acid and it increases gel viscosity, enhances its adhesion to enamel, and slows down and retards the release of oxygen. The various products available on the market differ in pH value, viscosity, the addition of fluoride, and so on. To prolong product shelf life, manufacturers tend to limit the water content and recommend refrigeration. Products containing hydrogen peroxide in concentrations varying from 1% to 10% have recently been put on the market.

Jan 1, 2015 | Posted by in Dental Materials | Comments Off on 6: Bleaching Techniques
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