Background: By this point in the 21st century, the treatment of tooth discoloration has evolved into an annual multibillion-dollar, highly sophisticated, scientific, and clinical discipline. However, the origins of the treatment date back thousands of years to ancient clinicians and beauticians who used rudimentary, yet innovative, natural materials to mask undesirable tooth discolorations. Function The oral cavity plays 3 important roles in the protection and preservation of systemic health; it is involved in nutritional intake, communication, and host defense. The teeth are involved in all 3 roles, and dental diseases can be a source of multiple problems, including oral and systemic infections and difficulty in chewing, swallowing, or phonation. Anatomy Cursory familiarity with basic dental anatomy and calcification and with the eruption sequence of teeth is helpful before physical examination. A tooth is composed of a crown (ie, the portion exposed to the oral cavity) and 1 or more roots (ie, the portion enveloped in bone and the periodontium)The crown of each tooth has 5 surfaces: buccal (facing the cheek or lip), lingual (facing the tongue), mesial (between the teeth), distal (between the teeth), and chewing (occlusal for molars and premolars, incisal for incisors and canines). In the transverse section, the tooth has 3 distinct layers. These include a surface enamel layer covering only the crown; an inner layer of dentin in both the crown and root; and the core area known as the pulp, which contains nerves, arteries, and veins Radiographically, the layers are easily identifiable because they have different radiopacities. Enamel is the most mineralized of the calcified tissues of the body, and it is the most radiopaque of the 3 tooth layers. Dentin is less radiopaque than enamel and has a radiopacity similar to that of bone. The pulp tissue is not mineralized and appears radiolucent. Primary (ie, deciduous) teeth number 20, and secondary (ie, adult) teeth number 32. A phase of mixed dentition exists, depending on the age of the patient (typically, 6-14 y). This phase is associated with simultaneous exfoliation or the eruption of primary and secondary teeth (see Tables 1-2).
Table 1. Calcification and Eruption Sequence of Primary Dentition
Table 2. Calcification and Eruption Sequence of Secondary Dentition
Tooth discoloration is caused by multiple local and systemic conditions (Vogel, 1975) Extrinsic dental stains are caused by predisposing factors and other factors such as dental plaque and calculus, foods and beverages, tobacco, chromogenic bacteria, and metallic compounds, and topical medications. Intrinsic dental stains are caused by dental materials (eg, tooth restorations), dental conditions and caries, trauma, infections, medications, nutritional deficiencies and other disorders (eg, complications of pregnancy, anemia and bleeding disorders, bile duct problems), and genetic defects and hereditary diseases (eg, those affecting enamel and dentin development or maturation).
Causes of extrinsic discoloration
Extrinsic stains are defined as stains located on the outer surface of the tooth structure and caused by topical or extrinsic agents. The Nathoo classification system of extrinsic dental stain describes 3 categories as follows (Nathoo, 1997):
Deposition of tannins found in tea, coffee, and other beverages cause brown stains on the outer (buccal, labial) and inner (lingual, palatal) surfaces of the teeth. Tobacco stains from cigarettes, cigars, pipes, and chewing tobacco cause tenacious dark brown and black stains that cover the cervical one third to one half of the tooth (midway on the tooth toward the gingival margin)
Pan (a combination of betel nut of the areca palm, betel leaf, and lime) is commonly chewed by more than 200 million persons in the western Pacific basin and South Asian region (Norton, 1998). It is used for its mild psychoactive and cholinergic effects, and it elicits a copious production of blood red saliva that results in a red-black stain on the teeth, gingiva, and oral mucosal surfaces.
Chromogenic bacteria cause stains, typically at the gingival margin of the tooth. The most common is a black stain caused by Actinomyces species. The stain is composed of ferric sulfide and is formed by the reaction between hydrogen sulfide produced by bacterial action and iron in the saliva and gingival exudates (Reid, 1977). Green stains are attributed to fluorescent bacteria and fungi such as Penicillium and Aspergillus species (Hattab, 1999). The organisms grow only in light and therefore cause staining on the maxillary surface of the anterior teeth. Orange stain is less common than green or brown stains and is caused by chromogenic bacteria such as Serratia marcescens and Flavobacterium lutescens.
Metallic compounds are also implicated in dental discolorations because of the interaction of the metals with dental plaque to produce surface stains (Hattab, 1999). Industrial exposure to iron, manganese, and silver may stain the teeth black. Mercury and lead dust can cause a blue-green stain; copper and nickel, green-to-blue-green stain; chromic acid fumes, deep orange stain; and iodine solution, brown stain. Topical medications cause staining. Chlorhexidine rinse (0.12%) causes brown staining after several weeks of use, particularly on acrylic and porcelain restorations. Cetylpyridinium chloride is an ingredient in several mouthwashes (eg, Cepacol, Scope) that can cause dental staining (Eriksen, 1979). Iron-containing oral solutions used for treatment of iron deficiency anemia cause black stains. Potassium permanganate mouthwash (violet-black stain), silver nitrate (black stain), and stannous fluoride (brown stain) also can induce dental discolorations (Hattab, 1999).
Causes of intrinsic discoloration
Areas of complete enamel loss are most commonly found on the incisal (chewing) surfaces of anterior teeth. This loss frequently occurs in older adults, whose teeth show a contrast in colors between enamel and dentin. Tooth abrasion manifests as yellow areas in which the enamel surface is lost (eg, buccal cervical regions) as a result of overzealous toothbrushing with a hard-bristled or medium-bristled toothbrush.
The erosion of enamel caused by frequent ingestion of acidic foods and beverages and from the regurgitation of acid from the stomach (eg, anorexia or bulimia nervosa) can lead to a yellow tooth discoloration. In patients with anorexia or bulimia, a yellow discoloration develops on lingual tooth surfaces where the acid reflux material makes contact with the teeth. Certain tooth surfaces are at greater risk for dental caries. These surfaces include the occlusal grooves and pits of posterior teeth (class I caries), the smooth surfaces between teeth (class II caries for posterior teeth, class III caries for anterior teeth), and the smooth surfaces at the enamel-cementum interface at the free gingival margin (cervical, root surface, or class V caries; Caries also may involve the incisal edge of anterior teeth (class IV or VI). The pathogenesis of dental caries begins with an incipient lesion confined to the enamel layer. Once the enamel layer is breached, caries tends to rapidly progress in the dentin, undermining the superficial enamel layer. Incipient carious lesions are associated with plaque accumulation and manifest as chalky white areas of discoloration secondary to hypocalcification. Patients with orthodontic brackets are at great risk for caries because of suboptimal plaque removal. As caries progresses into the dentin, the overlying translucent enamel reveals the color of the underlying caries and appears yellowish brown. Extensive caries that involve destruction of both enamel and dentin produce a color that ranges from light brown, to dark brown or almost black
The brown color is attributed to the formation of Maillard pigments (reaction between proteins and small aldehydes produced by cariogenic bacteria), melanins, lipofuscins, and uptake of various food colors and bacterial pigments (Kleter, 1998). In some patients, caries self-arrest, and remineralization may occur; however, the brown discolorations usually remain. Trauma Trauma to developing, yet unerupted, teeth can disturb enamel formation (amelogenesis) and may result in enamel hypoplasia, which is visualized as a localized opacity on the erupted tooth. Such teeth commonly are referred to as Turner teeth . Unerupted permanent incisors commonly are affected after intrusion injuries to primary incisors in young children who fall on their faces. Trauma that occurs to erupted teeth also causes discoloration This discoloration frequently occurs in teeth that have fully formed roots and have sustained irreversible pulpal injury caused by avulsions, intrusions, luxations and subluxations, or fractures involving the pulp chamber. Trauma can cause intrapulpal hemorrhage and iron sulfide deposition along the dentinal tubules, producing a bluish black cast. Some occlusal trauma occurs over a protracted period of time (eg, excessive orthodontic forces). Rarely, this trauma leads to pulpal hemorrhage; however, it can produce a subtle grayish brown cast. Infections Periapical odontogenic infections of the primary teeth can disrupt normal amelogenesis of the underlying secondary (permanent) successors and involve a potential for localized enamel hypoplasia. Crown formation begins in utero; therefore, the potential for extensive intrinsic discoloration of the primary dentition may be present throughout pregnancy. Although rare, maternal rubella or cytomegalovirus infection and toxemia of pregnancy can lead to tooth discoloration, which generally manifests as a focal opaque band of enamel hypoplasia that is confined to the primary teeth forming enamel at the time of maternal infection.
Crown formation of the secondary dentition occurs until the child is aged approximately 8 years. Systemic postnatal infections (eg, measles, chicken pox, streptococcal infections, scarlet fever) can also cause enamel hypoplasia. The bandlike discolorations on the tooth are visualized where the enamel layer has variable thickness and becomes extrinsically stained after tooth eruption. Medications Since the 1950s, drugs from the tetracycline family have been associated with intrinsic tooth discoloration. Once in the bloodstream, tetracycline can be incorporated into the calcification process of developing teeth, in which it affects either primary or secondary dentition after maternal or childhood ingestion, respectively. Tetracyclines diffuse through dentin to the enamel interface, chelating calcium ions and incorporating into hydroxyapatite as a stable orthophosphate complex. The amount of drug incorporation is ultimately determined by the distribution of tooth discoloration and is equivalent to serum blood levels and the duration of exposure. When the affected teeth first erupt, they have a bright-yellow bandlike appearance that fluoresces under ultraviolet light, although upon exposure to sunlight, the color gradually changes to gray or red-brown (van der Bijl P, 1995) . Tetracycline use does not lead to discoloration once tooth formation is complete. Minocycline is a second-generation derivative of tetracycline. The ingestion of minocycline can lead to a green-gray or blue-gray intrinsic staining of teeth. Unlike with other tetracyclines, staining occurs during and after the complete formation and eruption of teeth (Patel, 1998). Minocycline is a poor chelator of calcium ions, but it is believed to bind to iron ions. This binding causes the formation of insoluble salts that are either exuded from gingival crevicular fluid to extrinsically stain the enamel or intrinsically incorporated into the secondary dentin (McKenna, 1999). Minocycline is prescribed for long-term acne therapy in adolescents and adults, although it is being replaced by medications such as clindamycin and isotretinoin that do not cause tooth discoloration.
Dental fluorosis is characterized by enamel discoloration resulting from subsurface hypomineralization due to the excessive ingestion of fluoride during the early maturation stage of enamel formation (DenBesten, 1999). Fluorosis affects primary and secondary dentitions with a broad range of clinical findings. In its mildest form, fluorosis appears as faint white lines or streaks on the enamel. Moderate fluorosis has more obvious opaque regions referred to as enamel mottling, whereas severe fluorosis appears with extensive mottling that readily chips and stains and leads to pitting and brown discoloration. An increase in the prevalence of mild-to-moderate fluorosis has been observed in the United States over the last decade, even in areas with nonfluoridated public water supplies (Pendrys, 2000). The trend is explained by early overuse and ingestion of fluoridated toothpaste; the inappropriate use of fluoride supplements; and in fluoridated areas, the use of powdered infant formula mixed with local water. Clinicians can help in preventing fluorosis by teaching parents about fluoride use and good toothbrushing habits for children. Fluoride sources are numerous and include naturally or artificially fluoridated drinking water, commercially available beverages, foods prepared in fluoridated water, chewable vitamins, oral healthcare products (eg, toothpastes, mouthrinses, oral fluoride supplements), and professional fluoride products prescribed by dentists. The fluoride concentration of naturally fluoridated water varies depending on geographic location. For example, in some areas of Africa, the concentration may be as high as 10 parts per million (ppm), whereas many other regions have a concentration of 0 ppm. Artificially fluoridated water supplies usually have a fluoride concentration of 1 ppm (Warren, 1999). Similar to tetracycline exposure, the dose and duration of fluoride exposure in developing teeth is correlated with the extent and severity of the clinical findings. Several clinical indices have been developed to measure fluorosis (Rozier, 1994). Nutritional deficiencies and other disorders Regarding nutritional deficiencies, vitamins C and D, calcium, and phosphate are required for healthy tooth formation. Deficiencies can result in dose-related or exposure-related enamel hypoplasia. Diseases that can cause hyperbilirubinemia and intrinsic tooth discoloration include sickle cell anemia; thalassemia; hemolytic disease of the newborn (HDN) due to either Rhesus factor, ABO, or other erythrocyte antigen incompatibility; biliary atresia; and other rare pediatric diseases. These diseases have the potential to cause hyperbilirubinemia and the subsequent dose-dependent incorporation of biliverdin (a by-product pigment of bilirubin) into developing teeth, producing a jaundicelike yellow-green tint on the tooth surfaces (Cullen, 1990). Intrinsic tooth discoloration is reported in patients with blood dyscrasias such as sickle cell anemia, thalassemia, and HDN. These diseases have the potential to cause hemolysis and the subsequent dose-dependent incorporation of biliverdin (by-product pigment of bilirubin) into developing teeth, producing a jaundicelike yellow-green tint on the tooth surfaces (Cullen, 1990). Genetic defects and hereditary diseases Genetic defects in enamel or dentin formation include amelogenesis imperfecta (AI), dentinogenesis imperfecta (DI), and dentinal dysplasia (DD). These are hereditary diseases with a propensity for intrinsic tooth discoloration. AI affects both primary and secondary dentitions and demonstrates numerous clinical manifestations that are classified into 4 types (Neville, 1995). Type 1 AI involves hypoplastic dentition. Hypoplastic teeth with rough or pitted enamel surfaces are at a greater risk for extrinsic staining . The teeth typically have an abnormally thin enamel layer that reveals the yellow color of dentin beneath the enamel. Type 2 AI involves hypomaturation. Teeth with hypomaturation have soft enamel with a mottled opaque white, yellow, or brown discoloration. Type 3 AI involves hypocalcification. The enamel in the hypocalcified type is yellow to orange, soft, and lost soon after eruption. Therefore, hypocalcified teeth develop dark stains and are at high risk for dental caries. Type 4 AI involves hypomaturation or hypoplastic dentition with taurodontism. DI occurs in 2 types. One type is associated with osteogenesis imperfecta, and the other type affects the teeth alone. The primary and secondary teeth are affected, and they have a brown or blue appearance with a distinctive translucent quality. The enamel chips off easily, and the teeth are prone to occlusal wear and caries. DD occurs in 2 types. Teeth with type 2 DD have a blue, amber, or brown translucence. Teeth with type 1 DD have crowns with normal morphology and coloration. Other hereditary diseases include erythropoietic (congenital) porphyria and epidermolysis bullosa (EB). Erythropoietic porphyria is a rare disease of porphyrin metabolism. The abnormally high levels of reddish brown or burgundy-red porphyrin pigments have an affinity for calcium phosphate and are incorporated into teeth during dental formation. The entire primary and secondary dentitions are pink, although case reports also describe the color as reddish brown or purple (Trodahl, 1972). Teeth fluoresce red under ultraviolet light. Patients with EB may have enamel hypoplasia and pitting, which produce a yellowish tint. Patients are at risk for caries.
Race: No racial predilection exists for tooth discoloration. The fluoride concentration of naturally fluoridated water varies depending on geographic location. For example, in some areas of Africa, the concentration may be as high as 10 parts per million (ppm), whereas many other regions have a concentration of 0 ppm. Artificially fluoridated water supplies usually have a fluoride concentration of 1 ppm (Warren, 1999). Sex: No sex predilection exists for tooth discoloration. Age:
History: The patient's history of tooth discoloration provides useful information regarding the etiology.
Causes: The causes of extrinsic and intrinsic dental discoloration are as follows (see also Pathophysiology):
Medical Care: Dental treatment of tooth discoloration involves identifying the etiology and implementing therapy. Medical treatment also may be warranted, depending on the etiology of the tooth discoloration.
Further Outpatient Care: