INTRODUCTION
Tooth discoloration is a common problem leading patients to seek treatment to have the discoloration removed. People of various ages may be affected, and it can occur in both primary and secondary teeth. The etiology of dental discoloration is multifactorial, and different parts of the tooth can take up different stains. This effect is a result of the anatomy of the tooth. Intrinsic discoloration increases with increasing age and is more common in men (Eriksen and Nordbo 1978). It may affect 31% of men and 21% of women (Ness et al. 1977). The result is a complex of physical and chemical interactions with the tooth surface. The aim of this chapter is to assess the etiology of tooth discoloration and the mechanisms by which teeth stain. It is the intention of this chapter to explain the complexity of tooth discoloration.
COLOR OF NATURAL HEALTHY TEETH
Teeth are polychromatic (Louka 1989). The color varies among the gingival, incisal, and cervical areas according to the thickness, reflectance of different colors, and translucency in enamel and dentin (see Figure 1.2). The color of healthy teeth is primarily determined by the dentin and is modified by the following:
• The color of the enamel covering the crown.
• The translucency of the enamel, which varies with different degrees of calcification.
• The thickness of the enamel, which is greater at the occlusal or incisal edge of the tooth and thinner at the cervical third (Dayan et al. 1983).
• The intensity, thickness, structure of the dentin.
• Presence of secondary or tertiary dentin trauma.
• Existing restorations.
CLASSIFICATION OF DISCOLORATION
Many researchers classify staining as either extrinsic or intrinsic (Dayan et al. 1983, Hayes et al. 1986, Teo 1989). There is confusion concerning the exact definitions of these terms. Feinman et al. (1987) described extrinsic discoloration as that occurring when an agent stains or damages the enamel surface of the teeth, and intrinsic staining as occurring when internal tooth structure is penetrated by a discoloring agent. According to these definitions, the terms staining and discoloration are used synonymously. However, extrinsic staining will be defined here as staining that can be easily removed by a normal prophylactic cleaning (Dayan et al. 1983). Intrinsic staining is defined here as endogenous staining that has been incorporated into the tooth matrix and thus cannot be removed by prophylaxis.
Some discoloration is a combination of both types of staining and may be multifactorial. For example, nicotine staining on teeth is extrinsic staining that becomes intrinsic staining. The modified classification of Dzierzak (1991), Hayes et al. (1986), and Nathoo (1997) will be used as a guide. See Table 1.1.
STAINS DURING ODONTOGENESIS (PRE-ERUPTIVE)
These alter the development and appearance of the enamel and dentin on permanent teeth.
Developmentally defective enamel and dentin
Defects of enamel development (Figures 1.6A and 1.6B) can be caused by, for example, amelogenesis imperfecta (Figure 1.5), dentinogenesis imperfecta, and enamel hypoplasia. The defects in enamel are either hypocalcific or hypoplastic (Rotstein 1998). Enamel hypocalcification is a distinct brownish or whitish area found on the buccal aspects of teeth (see Figure 1.5). The enamel is well formed and the surface is intact. Many of these white and brown discolorations can be removed with whitening in combination with microabrasion (see Chapter 10). Enamel hypoplasia is developmental defective enamel. The surface of the tooth is defective and porous and may be readily discolored by materials in the oral cavity. Depending on the severity and extent of the dysplasia, the enamel surface may be whitened with varying degrees of success. Some enamel white hypoplastic lesions are due to exposure of chemicals (such as bisphenol a) peri- or postnatally (Jedeon et al. 2013).
Fluorosis
This staining is caused by excessive fluoride uptake with the developing enamel layers. The fluoride source can be from the ingestion of excessive fluoride in the drinking water or from overuse of fluoride supplements (Ismail and Hasson 2008) or fluoride toothpastes (Shannon 1978). It occurs within the superficial enamel and appears as white or brown patches of irregular shape and form (Figure 1.7A). The acquisition of stain, however, is posteruptive. The teeth are not discolored on eruption, but because the surface is porous they gradually absorb the colored chemicals present in the oral cavity (Rotstein 1998). Staining caused by fluorosis manifests in three different ways: as simple fluorosis, opaque fluorosis, or fluorosis with pitting (Nathoo and Gaffar 1995). Simple fluorosis appears as brown pigmentation on a smooth enamel surface, whereas opaque fluorosis appears as gray or white flecks on the tooth surface (Figure 1.7B). Fluorosis with pitting occurs as defects in the enamel surface, and the color appears to be darker.
Table 1.1 Etiology of tooth discoloration
|
Extrinsic stains • Plaque (Figure 1.26), chromogenic bacteria, surface protein denaturation • Mouthwashes (e.g., chlorhexidine) • Beverages (tea [Figure 1.28], coffee [Figures 1.27 and 1.31], red wine, cola) • Foods (curry, cooking oils and fried foods [Figure 1.33], foods with colorings, berries, beetroot) • Illness • Antibiotics (erythromycin [Figure 1.29], amoxicillins [Figures 1.6A and 1.30]) • Iron supplements (Figures 1.34) |
|
Intrinsic stains |
|
Pre-eruptive |
|
Disease • Hematologic diseases (Figure 1.15) • Liver diseases • Diseases of enamel and dentin (Figure 1.5) |
|
Medication • Tetracycline stains (Figures 1.8–1.10) • Other antibiotics • Fluorosis stains (Figure 1.7) |
|
Posteruptive • Trauma (Figure 1.4), intrapulpal hemorrhage (Figure 1.14A), pulp necrosis (Figure 1.15B) • Primary and secondary caries (Figure 1.27) and erosion, buccal (Figure 1.36) and palatal (Figures 1.22–1.24, 1.38) • Dental restorative materials (Figures 1.17 and 1.18), endodontic materials (Figure 1.4, lower right incisor tooth) • Aging (Figure 1.25) • Smoking (Figures 1.33 and 1.35) • Chemicals • Some foodstuffs (long-term use causes deeper intrinsic staining) • Minocycline (Figure 1.12) • Tetracycline (Figure 1.37) • Functional and parafunctional changes (Figure 1.25) |
Stannous fluoride treatment causes discoloration by reactions of the tooth with the tin ion (Shannon 1978). No intraoral discolorations occur from topical use of fluoride at low concentrations. The severity and degree of staining are directly related to the amount of fluoride ingested during odontogenesis.
Tetracycline
Tetracycline is a broad-spectrum bacteriostatic antibiotic (van der Bijl and Ptitgoi-Aron 1995) that is used to treat a variety of infections. The tetracycline antibiotics are a group of related compounds that are effective against gram-negative and gram-positive bacteria. It is well known that the administration of tetracycline during odontogenesis causes unsightly discoloration of both primary and secondary dentitions (Thomas and Denny 2014). The discoloration varies according to the type of tetracycline used (Table 1.2). The staining effects are a result of chelation of the tetracycline molecule with calcium ions in hydroxyapatite crystals, primarily in the dentin (Swift 1988). The tetracycline is incorporated into the enamel and dentin. The chelated molecule arrives at the mineralizing predentin–dentin junction via the terminal capillaries of the dental pulp (Patel et al. 1998). The brown discoloration is a result of photooxidation, which occurs on exposure of the tooth to light.
|
Drug |
Color stain on teeth |
|
Chlortetracycline (Aureomycin) |
Gray-brown |
|
Demethylchlortetracycline (Ledermycin) |
Yellow |
|
Oxytetracycline (Terramycin) |
Yellow—lowest amount |
|
Tetracycline (Achromycin) Yellow |
Doxycycline (Vibramycin) No reported changes |
|
Minocycline |
Black |
Adapted from Hayes et al. 1986.
The staining can be classified according to the developmental stage, banding, and color (Jordan and Boksman 1984):
• First-degree (mild) tetracycline staining is yellow to gray, which is uniformly spread through the tooth. There is no banding (see Figure 1.8).
• Second-degree (moderate) staining (Figure 1.9) is yellow-brown to dark gray.
• Third-degree (severe) staining is blue-gray or black and is accompanied by significant banding across the tooth (see Figure 1.10).
• Fourth-degree (intractable) staining has been suggested by Feinman et al. (1987), designated for those stains that are so dark that whitening is ineffective (see Figures 1.11 and 1.12).
All degrees of stain become more intense on chronic exposure to artificial light and sunlight. The severity of pigmentation depends on three factors: time and duration of administration, the type of tetracycline administered, and the dosage (Dayan et al. 1983, Shearer 1991).
First- or second-degree staining is normally amenable to whitening treatments (Haywood 1997). Prolonged home whitening has been reported in the literature to be successful for tetracycline staining. This may take 3–6 months or longer (see Figure 1.13). The whitening material penetrates into the dentin structure of the tooth and causes a permanent color change in the dentin (McCaslin et al. 1999).
Illness and trauma during tooth formation
The effects of illness, trauma, and medication (e.g., porphyria, infant jaundice, vitamin deficiency, phenylketonuria, hematologic anemia) are cumulative, creating stains and defects that cannot be altered by whitening. Staining may result from hematologic disorders such as erythroblastosis fetalis (Atasu et al. 1998), porphyria, phenylketonuria, hemolytic anemia, sickle cell anemia, and thalassemia. Because the coagulation system is affected, discoloration occurs as a result of the presence of blood within the dentinal tubules (Nathoo 1997). Bilirubinemia in patients with liver dysfunction can cause bilirubin pigmentation in deciduous teeth (Watanabe et al. 1999). These disorders can result in molar incisor hypoplasia, which reflects as white spots and white marks on the central incisors and the first permanent molars.
STAINS AFTER ODONTOGENESIS (POSTERUPTIVE)
Minocycline
Minocycline is a semisynthetic second-generation tetracycline derivative (Goldstein 1998) that is often used for acne treatment. It is a broad-spectrum antibiotic that is highly plasma bound and lipophilic (McKenna et al. 1999). It is bacteriostatic and produces greater antimicrobial activity than tetracycline or its analogues (Salman et al. 1985). The drug is used to treat acne and various infections. Its lipophilicity facilitates penetration into body fluids, and after oral administration the minocycline concentration in saliva is 30–60% of the serum concentration (McKenna et al. 1999). In addition, minocycline hydrochloride has been shown to cause pigmentation of a variety of tissues including skin, thyroid, nails, sclera, teeth, conjunctiva, and bone. Adult-onset tooth discoloration after long-term ingestion of tetracycline and minocycline has also been reported (Sánchez et al. 2004). The remarkable side effect of minocycline on the oral cavity is the singular occurrence of “black bones,” “black or green roots,” and a blue-gray to gray darkening of the crowns of permanent teeth. The prevalence of tetracycline and minocycline staining is 3–6% (Sánchez et al. 2004).
Minocycline is absorbed from the gastrointestinal tract and combines poorly with calcium. See Table 1.3.
Adolescents and adults who take the drug are at risk for developing intrinsic staining on their teeth, gingivae, oral mucosa, and bones (Bowles and Bokmeyer 1997). It causes tooth discoloration by chelating with iron to form insoluble complexes. It is also thought that the discoloration may be a result of its forming a complex with secondary dentin (Salman et al. 1985). The discoloration does not resolve after discontinuation of therapy. The resultant staining is normally milder than that from tetracycline and may be amenable to whitening and lightening, although this is case specific. In a study examining 17 discolored third molars under fluorescent microscopy, Antonini and Luder (2011) found that when acne was treated between 15 and 22 years of age, only the roots of the third molars displayed annular discolorations, which seemed to result from the incorporation of tetracyclines into dentin, whereas fine fluorescent incremental lines in root cementum were too thin to be apparent clinically. Three accidentally removed interradicular bony septa revealed that tetracyclines incorporated into alveolar bone remained there for about 2 years, but thereafter disappeared as a result of physiologic remodeling.
Pulpal changes
Pulp necrosis
Pulp necrosis can be the result of bacterial, mechanical, or chemical irritation to the pulp. Substances can enter the dentinal tubules and cause the teeth to discolor. These teeth will require endodontic treatment before whitening, the latter using the intracoronal method (see Chapter 8) or the outside-inside technique (see Chapter 15). See Table 1.4.
Table 1.3 Tooth discoloration: causes and colors
|
Cause |
Color |
|
Extrinsic discoloration |
|
|
Cigarettes, pipes, cigars, chewing tobacco |
Yellow-brown to black (Figure 1.39) |
|
Marijuana |
Dark-brown to black rings |
|
Coffee, tea, foods |
Brown to black |
|
Poor oral hygiene |
Yellow or brown shades |
|
Chromogenic bacteria and plaque |
Green |
|
Extrinsic and intrinsic discoloration |
|
|
Fluorosis |
White, yellow, brown, orange, gray, or black |
|
Aging |
Yellow to orange |
|
Intrinsic discoloration |
|
|
Genetic conditions (e.g., amelogenesis imperfecta) |
Brown, black |
|
Systemic conditions—for example: |
|
|
Jaundice |
Blue-green or brown |
|
Porphyria |
Purple-brown |
|
Medications during tooth development (e.g., tetracycline, fluoride) |
Brown, gray, or black |
|
Body byproducts—for example: |
|
|
Bilirubin |
Blue-green, brown |
|
Hemoglobin |
Gray, black (Figure 1.15) |
|
Pulp changes |
|
|
Trauma |
Yellow, orange, purple, gray |
|
Intrapulpal hemorrhage (Figure 1.14B) |
Gray, brown |
|
Pulp canal obliteration |
Yellow |
|
Pulp necrosis (Figure 1.15B) |
Yellow, brown, black |
|
With hemorrhage |
Gray, black |
|
Without hemorrhage |
Yellow, gray-brown |
|
Iatrogenic causes |
|
|
Trauma during pulp extirpation |
Gray, black |
|
Tissue remnants in pulp chamber |
Brown, gray, black |
|
Inappropriate design of access cavity (traps pulp chromophore materials inside the pulp chamber) |
Yellow, gray (Plotino et al. 2008) |
|
Products of tissue decomposition |
Yellow, brown, gray |
|
Restorative dental materials |
Brown, gray amalgam (Figures 1.17, 1.18, and 1.19), black |
|
Endodontic materials (cement and gutta percha) |
Gray, black |
Adapted from Abbott 1997, with permission.
Intrapulpal hemorrhage caused by trauma
Accidental injury to the tooth can cause pulpal and dentinal degenerative changes that alter the color of the teeth (see Figure 1.14). Pulpal hemorrhage may occur, giving the tooth a gray, nonvital appearance (Nathanson and Parra 1987). The discoloration is a result of the hemorrhage, which causes lysis of red blood cells. Blood disintegration products such as iron sulfides enter the dentin tubules and discolor the surrounding dentin, which causes discoloration of the tooth (Baratieri et al. 1995). Sometimes the tooth can recover from such an episode (Marin et al. 1997) and the discoloration can reverse naturally without whitening. These discolored teeth should be vitality tested, because those that are still vital (see Chapter 4) can be successfully whitened using the home whitening technique (see Chapter 5).
Table 1.4 Mechanisms that cause nonvital teeth to discolor
|
• Tissue degradation during the necrotic process (Baratieri et al. 1995). • Trauma causing rupture of blood vessels. This results in hemolysis of red blood cells, which release hemoglobin and hematin derivatives. Iron in red blood cells may be aspirated into dentinal tubules. This may also occur if there is uncontrolled hemorrhage during endodontic treatment. • Intracanal medications such as phenolics and iodoform-based medications can cause gradual discoloration. The dentin is penetrated, causing oxidation. • Silver points may corrode inside the root canal. • Coronally placed leaking restorative materials. • Endodontic cement. • Inadequate coronal access leaves pulp remnants and necrotic tissue in the pulp chamber. • Contamination of the pulp cavity during endodontics. • Insufficient irrigation and debridement. |
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