The developing dentition can be affected by a number of systemic factors, including metabolic and genetic diseases that cause intrinsic tooth discoloration (Plotino et al. 2008). Systemic factors also include drug-induced discolorations, including those from the intake of antibiotics and excess fluoride. In the case of fluoride its source can be either iatrogenic or from natural sources, such as drinking water.

Although most publications refer to aging as a local cause of intrinsic discoloration, the physiological continuous deposition of secondary dentin throughout the life of an individual may be considered both a systemic and a local cause of intrinsic discoloration, as reactionary tertiary dentin forms in response to external stimuli, such as tooth attrition and bacteria from caries lesions. The deposition of both secondary dentin and tertiary dentin results is a narrower pulp space with time. Thicker dentin affects the light-transmitting properties of teeth, resulting in a gradual darkening of the tooth and increased opacity. In addition, the chemical structure and physical properties of dental hard tissues change over time.

Local causes of posteruptive intrinsic stains include intrapulpal hemorrhage, residual pulpal tissue after endodontic therapy, calcific metamorphosis, endodontic materials, restorative materials such as amalgam, and root resorption. Other less frequent causes are trauma to developing teeth and periapical infection of primary teeth (Hattab et al. 1999). Besides being responsible for posteruptive pigmentation of vital teeth (Chap. 6), the antibiotic minocycline also causes discoloration of nonvital teeth. In one case, minocycline was utilized in the root canal as a component of antibiotic paste resulting in blue discoloration of immature necrotic permanent teeth in children (Dabbagh et al. 2002). In another case, minocycline was applied as a component of a triple antibiotic mixture inside a root canal of a tooth with a necrotic pulp, as an attempt to disinfect the root canal system for revascularization. Minocycline resulted in tooth discoloration 6 weeks after the triple antibiotic paste had been applied (Kim et al. 2010).

Necrotic pulps may cause tooth discoloration as a result of the decomposition of the pulpal tissues producing colored byproducts that infiltrate the dentinal tubules. Discoloration related to improper endodontic treatment may be caused by trauma inflicted during pulp extirpation or obturation materials left in the pulp chamber. Another cause of discoloration in endodontically treated teeth is the residual pulp tissue left in the pulp horns when the access to the pulp chamber is under-prepared (Brown 1965; Faunce 1983). Evidence suggests that stains in endodontically treated teeth are not just confined to the pulp chamber, but they penetrate into the dentin substrate showing through dentin and enamel (van der Burgt and Plasschaert 1986).

Fitch (1861) stated, “the disintegration of the red corpuscles of the blood is another source of discoloration. The hematine, or iron, which is supposed to constitute the pigment of these globules, passes readily into the tubules of the dentine from the pulp chamber of the tooth, whenever the red disks are disintegrated, and the discoloration becomes more or less permanent. These red globules may be dissolved or broken up.” Spasser (1961) reported that “in many cases, the hemolysis of red blood cells with the release of hemoglobin, especially when associated with hemorrhage following pulp extirpation or trauma” was responsible for the discoloration of endodontically treated teeth. More recently other authors have corroborated this theory. Diffusion of blood components into the dentinal tubules caused by pulp extirpation or traumatically induced internal pulp bleeding is one of the causes for discoloration of nonvital teeth (Arens 1989). Products of blood (erythrocytes) decomposition, such as hemosiderin, release iron. The iron can be transformed to ferric sulfide with hydrogen sulfide produced by bacteria, which causes a dark brownish discoloration of the tooth (Brown 1965; Glockner et al. 1999; Attin et al. 2003). Other end products of hemoglobin decomposition, biliverdin and bilirubin, are themselves known causes of color alteration in the skin and mucosae, being responsible for jaundice in some systemic diseases (Shibahara et al. 2002; Leuschner 2003).

Coronal discoloration of endodontically treated teeth may also be caused by endodontic sealers (Fig. 8.2), such as Grossman’s cement and AH26 silverfree (Dentsply Caulk) (van der Burgt and Plasschaert 1985; van der Burgt et al. 1986). Temporary restorative materials, such as classical ZOE, Cavit (3M ESPE), and I.R.M. (Dentsply Caulk), also result in discoloration of endodontically treated teeth (van der Burgt et al. 1986). Two mineral trioxide aggregate (MTA)-based endodontic materials, ProRoot MTA (Dentsply Tulsa Dental Specialties) and MTA Angelus (Angelus Indústria de Produtos Odontológicos), have also been reported to cause tooth discoloration when used over a period of 12 weeks (Jang et al. 2013). The discoloration was observed at the MTA-dentin interface and intracoronal dentin surface. Removal of the discolored MTA resolved the discoloration.

When referring to whitening of nonvital teeth, Salvas (1938) wrote, “bleaching teeth is, at best, more or less of an unsatisfactory operation. Although we may succeed in restoring the color of a tooth, it is seldom permanent.” The unpredictability of intracoronal whitening has not changed considerably since Salvas wrote these statements in 1938.

Taking into consideration that the treatment outcome as well as the durability of the treatment varies for each clinical situation, the patient must be informed of these inherent limitations of intracoronal whitening. Another detail that the patient must be aware of is that root dentin does not respond well to bleaching, either external or internal (Kwon 2011). This is especially significant in case there is gingival recession that has resulted in exposed root surface.

The indications and contraindications for intracoronal whitening are displayed in Table 8.1. Prior to starting an internal whitening procedure to lighten single or multiple teeth, it is crucial to understand all treatment options available for each specific clinical case. The prognosis of internal whitening depends on several factors, including the etiology and the duration of the discoloration. Additionally, a history of traumatic injury to the tooth or teeth may be associated with subsequent external cervical resorption. It is also important to understand that the intrinsic discoloration in endodontically treated teeth affects dentin but not enamel (van der Burgt et al. 1986). A precise diagnosis relies on accurate clinical and radiographic exams. The presence of craze lines on the enamel structure and marginal microgaps in existing restorations may result in seepage of the intracoronal bleaching agents to the surrounding tissues. For this reason, the use of transillumination to diagnose microgaps and craze lines is extremely important. The treatment plan must be based on existing evidence to improve the chance of clinical success.

Intraoral photographs are essential to document the baseline color. Although the color of darkened endodontically treated teeth is not usually within the range of universal shade guides, the clinician may still take a photograph with a tooth tab from the Vita Classical A1-D4 shade guide (VITA Zahnfabrik H. Rauter GmbH & Co. KG) next to the darkened tooth. This will provide an excellent comparative reference for the postoperative versus the preoperative color.

Superoxol used to be the most commonly used intracoronal bleaching material. More recently, water has been used (instead of hydrogen peroxide) mixed with sodium perborate (Ari and Ungör 2002; Plotino et al. 2008). Sodium perborate (NaBO₃) is a white crystalline powder that contains about 95 % of the perborate corresponding to 9.9 % available oxygen (Rotstein and Friedman 1991). In contact with water, sodium perborate decomposes with the liberation of hydrogen peroxide and later of oxygen. Sodium perborate is, therefore, a hydrogen peroxide precursor (Ari and Ungör 2002). Warm air and acidic solutions also initiate the decomposition of sodium perborate. A thick creamy paste of sodium perborate with water is currently recommended, left in the pulp chamber for varying periods of time.

Two techniques for bleaching endodontically treated teeth have been used through the years, namely, the thermocatalytic technique and the walking bleach technique. Other bleaching techniques include combined thermocatalytic and walking bleach techniques (Freccia et al. 1982).

Hydrogen peroxide is the main toxic substance that has been used for internal bleaching (Chaps. 4 and 5). Hydrogen peroxide is a reactive oxygen species (ROS) (Bax et al. 1992) with oxidative ability (Kashima-Tanaka et al. 2003), as seen in Chap. 3. It is well known that free radicals and ROS exert biological actions such as inflammation, carcinogenesis, aging, and mutation (Valko et al. 2007). ROS also play an important role in tissue injury at sites of inflammation in various diseases (Valko et al. 2007).