REVIEW ARTICLE

https://doi.org/10.5005/jp-journals-10062-0187
Journal of Oral Health and Community Dentistry
Volume 18 | Issue 2 | Year 2024

Tooth Discoloration: Causes and Clinical Presentation—Part I

Faiez N Hattab

Department of Cariology and Pediatric Dentistry, Munich, Germany

How to cite this article: Faiez N Hattab, Department of Cariology and Pediatric Dentistry, Munich, Germany, Phone: +49 17665006632, e-mail: f_hattab@hotmail.com

How to cite this article: Hattab FN. Tooth Discoloration: Causes and Clinical Presentation—Part I. J Oral Health Comm Dent 2024;18(2):63–74.

Source of support: Nil

Conflict of interest: None

Received on: 02 March 2024; Accepted on: 12 July 2024; Published on: 19 November 2024

ABSTRACT

Background: The first evidence of variation from normal in human dentition is usually a noticeable difference in tooth color. Tooth discoloration, a change in natural tooth color, is a common dental finding that is esthetically unpleasant, psychologically traumatic, and socially unacceptable, causing people to seek treatment. This condition affects both children and adults and worsens with age.

Aim: The aim of this extensive review is to provide up-to-date information on the types, causes, and clinical features of tooth discoloration that are essential for managing the discoloration.

Results: The cause of tooth discolorations is multifactorial and varies in appearance, composition, location, adhesion to tooth surfaces, severity, and treatment. Depending on the cause, tooth discoloration is mainly classified into extrinsic and intrinsic, a combination of both, and intercategory types. Extrinsic stains are deposited on the surface of the outer teeth surfaces. Most chromogenic (color-producing) substances are organic in nature and are found in foods, beverages, tobacco, betel nuts, and chromogenic bacteria. Intrinsic discoloration occurs during tooth development or after tooth eruption and is associated with chemical and structural hard tissue changes.

Conclusion: Tooth discoloration presents two challenges for the dentists. The first is to find out the cause of the stain. The second is its management. Tooth discoloration appear in yellow, green, orange, brown, or black, etc., and each color may represent a different origin and the mechanism of staining. Pitting, cracks, and irregularities in tooth enamel can exacerbate discoloration.

Clinical significance: This article reviews the etiology and clinical presentation of tooth discoloration. Understanding the cause of discoloration and the physiochemical interaction of chromogens with the tooth surfaces enable dentists to make a correct diagnosis and appropriate treatment. It can also explain to e-patients the nature of the condition and how to prevent it.

Keywords: Appearance, Etiology, Prevalence, Tooth stains, Types.

INTRODUCTION

Dental discoloration is an alteration of the natural tooth color. It is a common clinical and esthetic problem that has a significant impact on psychological status, social interaction, and wellbeing. The demand for conservative cosmetic dentistry has grown dramatically over the past three decades due to the growing public interest in having whiter, brighter teeth. For dentists, the management of tooth discoloration presents two challenges. First, they should find out the cause of the stain; second, they should treat it. Tooth discoloration varies in etiology, appearance, composition, location, severity, and treatment. Hattab et al.1 provide the only comprehensive review of publications on these topics since the 1940s. According to the cause, tooth discoloration is mainly classified into extrinsic and intrinsic, combination of both and intercategory type.1–3 Chromogens (colored substances) are commonly found in foods, beverages, fruits, life habits and bacterial causing yellow, green, brown, and black stains. Enamel defects increase the intensity of stains. Intrinsic tooth discoloration occurs within the hard tooth structure during tooth formation; is caused by metabolic disorders, systemic diseases, medications, and chemicals. It may also occur in erupted teeth, with discoloration affecting a few teeth or the entire dentition. Intrinsic discoloration is associate with structural changes in the enamel (e.g., fluorosis, amelogenesis imperfecta, enamel hypoplasia) or changes in the dentin (e.g., tetracycline, dentinogenesis imperfecta, dentin dysplasia). Intrinsic stains are more difficult to remove than extrinsic stains. Tooth discolorations can be found in various color spectrums, including yellow, blue, green, orange, pink, red, gray, brown, and black, with each color representing a different origin. Occupational exposure to iron, manganese, and silver may cause brown to black tooth staining. Teeth become discolored with age due to enamel wear revealing darkened dentin, and stains accumulate. The aim of this comprehensive review is to provide up-to-date information on the types, causes, effects, and clinical manifestations of tooth discoloration that are critical to the control and management of discoloration.

Extrinsic Tooth Discoloration

This type of staining is caused by external organic and inorganic stains that deposit on the dental plaque (biofilm)/acquired pellicle/enamel surface. Most tooth discoloration is extrinsic in nature and is caused by chromogen deposits on the outer tooth surface, which are exacerbated by pitting, irregularities, cracks in the enamel and insufficient salivary protection. Acidic foods and beverages are more likely to stain than those with a higher pH. In addition, acidic compounds can erode and increase enamel roughness, making it more susceptible to chromogenic deposition.1,4 The affinity of chromogenic to enamel and dentin plays a crucial role in stain intensity and management. Whether stains absorb, adsorb, or chemically interact with dental surfaces is based on their physio chemical properties. There is considerable individual variation in the degree of staining, depending on the type and frequency of colored items consumed, exposure to chemicals and drugs, as well as oral hygiene. The tooth color is difficult to quantify and highly subjective. Various indices and photometric are used for the evaluation of tooth discoloration. The most popular method of clinical assessment of tooth color is visual comparison with a dental shade guide, although this does not cover the entire tooth color range. Color notation is based on hue, value, and chroma. Hue is the color that enables the clinician to distinguish between different colors. Value indicates the lightness of a color and ranges from zero for black to 10 for white. Chroma indicates the degree of color saturation (hue intensity).5 Extrinsic stains are classified according to their source, i.e., non-metallic stains or metallic stains.1,2 Possible factors causing non-metallic stains are certain foods and beverages, tobacco, and others. Metallic stains occur due to occupational exposure to metallic salts or vapors, certain mouthwashes, dental therapeutic agents, certain medicines, etc.

Non-metallic Stains

There are several causes of extrinsic stains, including chromogenic foods (grapes, berries, strawberries, beets, tomatoes, radish), beverages (coffee, tea, cola, or red wine), life habits (smoking, chewing tobacco, khat, and betel nuts). The FDA has approved 36 food dyes, of which nine are artificial color additives used in foods and beverages. Carotenoids, chlorophyll, and flavonoids give food color. Most brown soft drinks are tannin-based. There are three basic categories of colorings in soft drinks: natural colors, artificial colors, and caramels. Natural pigments are extracted from plants, fruits, and vegetables and include yellow-to-orange carotenoids and red-to-purple anthocyanins. The most common artificial dye found in food and beverages is yellow to black caramel. Black tea is the most consumed tea globally, followed by green tea. In addition to chromogenic tannin content, tea also contains a variety of elements that contribute to stain adhesion. Tea has about twice as much tannin as coffee and is more likely to stain teeth than coffee. Tar in cigarettes is a sticky, dark brown to black substance that stains smokers’ teeth and fingers yellow-brown. It is a viscous liquid of hydrocarbons, produced in cigarettes by the incomplete combustion of organic matter in the absence of oxygen.

Metallic Stains

These occur due to exposure to metal-containing drugs, topical agents, occupational, and others. Metals interact with plaque/acquired pellicle/enamel surfaces to produce surface stains, or penetrate the tooth substance to cause a permanent staining, such as in enamel fluorosis and developmental hypoplasia or hypo calcification. Oral iron solution for treatment of iron-deficiency anemia is causing tooth dark staining. Oral iodine solution given to make thyroid hormones can cause brown tooth staining. Topical stannous fluoride (SnF2) produces a golden-brown discoloration. Metallic mouthwashes (chlorhexidine digluconate, phenolic Listerine®, quaternary ammonium salt, and others) can stain the teeth. Potassium permanganate (KMnO4) mouthwash can cause a violet-black discoloration. The polyvalent metals in the mouthwashes can precipitate dietary chromogenes.6 Tooth discoloration occurs in industrial workers exposed to iron (red-brown), manganese (brown-black), silver (gray-black), lead, mercury, and nickel (blue-green), copper (green), chromic acid (orange), cadmium (yellow-brown).1,7 Silver diamine fluoride (F) solutions used to control caries and tooth sensitivity can cause dark teeth.

Types and Causes of Extrinsic Staining

Extrinsic stain, as the name implies, is caused by the interaction of external discoloring substances with the tooth surface complex. They can be identified by color, distribution, adhesion, age, sex, home care, and other factors.1 Extrinsic stains can be present in green, orange, brown, yellow, or black. Green and orange stains are typically found in patients with the presence of chromogenic bacteria and poor hygiene. The most common teeth stains are yellowish-brown caused by drinking tea and coffee. Factors that modify the occurrence of extrinsic stains include, enamel defects, salivary glands dysfunction, and poor oral hygiene.

Black Stain

This stain appears as a thin black line, band, or dark dots on the facial and lingual tooth surfaces near the gingival margin, but may extend to the proximal surface (Fig. 1). A black stain is firmly attached to the tooth surface, difficult to remove with a brush, and tends to recur after removal. They may occur in children with good oral hygiene and a low incidence of caries. Black stain is caused by chromogenic bacteria, such as Actinomyces and Bacteroides melaninogenicus, where hydrogen sulfide (H2S) produced by bacteria in dental plaque reacts with iron in saliva, producing a grayish black iron sulfide (Fe2S3) stain.1 The prevalence varies between different populations, ranging between 2 and 20% with no gender predilection.

Fig. 1: Black stains on the gingival margins of the lower anterior teeth

Green Stain

It manifests as a tenacious, thick deposit band on the labial surface of the maxillary anterior teeth at the gingival third (Fig. 2). This stain is common in children, with boys being more likely to be affected than girls. Green stain can be caused by fluorescent bacteria and fungi such as Penicillium and Aspergillus.1 It grows when exposed to light, so there will be more stains on the upper front teeth, and they tend to recur after removal.

Fig. 2: Green stains on the upper anterior teeth

Orange Stain

This stain occurs on the labial surface of upper and lower teeth at the cervical margin or gingival third (Fig. 3). Chromogenic bacteria, such as Serratia marcescens and Flavobacterium lutescens are the likely cause.1 It is easier to remove than green stains, especially in cases of poor oral hygiene.

Fig. 3: Orange stains on the upper and lower teeth

Chlorhexidine Stain

Chlorhexidine gluconate (CHX) is a broad-spectrum antimicrobial agent that works against gram-positive and gram-negative bacteria, yeasts, and viruses. It is one of the most commonly used antiseptics in the treatment of skin and mucous membrane injuries. In dental practice, control dental plaque and gingivitis. It is available as a mouth rinse (0.12 or 0.2%), spray (0.2%), gel or toothpaste (1%), root canal irrigates (2%), varnish, and periodontal chip. The CHX molecule is positively charged and reacts and destroys the negatively charged microbial cell membrane, as well as being attracted to negatively charged tooth surfaces and dentin. The long-lasting antiseptic effect of CHX is due to its strong ability to adhere to soft and hard tissues and maintain a sustained release “substantivity.” There is evidence that CHX remains effective up to 24 hours after application, have only a local effect, and does not penetrate the oral epithelium.8 The mechanism of CHX staining is not fully understood, but it is thought that CHX denatures proteins, leading to the formation of metal sulfides and damaging the cell membrane.9 The binding of CHX to the chromogens in food, tea, coffee, tobacco, etc. causes brown-black tooth staining (Fig. 4). Dentin acquires more CHX staining than enamel. The co-administration of CHX and F maximizes their diffusion in human enamel more than either alone.10

Fig. 4: Chlorhexidine stains

Tea and Coffee Stains

These beverages contain the chromogenic organic tannin, which has an affinity to adsorb to dental plaque and interact with the tooth surface, forming brown-black stains (Fig. 5). Tannins are found in plants, tree barks, and fruits that have an astringent acidic polyphenolic compound and are orange-brown in color. Tannin combines with colored foods and beverages, proteins, sugars, and minerals, forming unsolvable and stable complexes. Acidic tannins give coffee a pH of approximately 5.2, thus, exacerbating its coloring effect. Black and green tea are less acidic than coffee, but iced tea has a pH of about 3.5. Tea is a complex, homogenous solution composed of organic and inorganic compounds. The average element concentration (mg/L) in the Chinese and Indian tea infusions is as follows: F–1.48, P–12.7, Mg–9.3, Ca–5.6, Al–3.9, Mn–3.4, Zn–0.17.11,12 The cationic tea minerals can bind the negatively charged tannin, forming a more cohesive stain on the tooth surface that is resistant to brushing. The addition of milk to tea and coffee modifies the stain and reduces its adhesion to the tooth surface, as well as reducing F availability.13,14

Fig. 5: Generalized tea and coffee stains

Tobacco Stain

The two substances in tobacco that cause tooth staining are nicotine and tar. Nicotine is colorless, but when combined with oxygen, it turns yellow, causing tooth discoloration. Tar is a dark brown or black viscous liquid composed of hydrocarbons and free carbon, obtained from a variety of organic materials. It contains a variety of organic and inorganic compounds. Cigarettes, the most commonly used form of tobacco, contain 8–43 mg tar and 0.3–2.6 mg nicotine per cigarette. The mainstream smoke emission per cigarette is 6.8–21.6 mg tar, 0.5–1.6 mg nicotine, and 5.9–17.4 mg CO.15 Tar can be seen as a residual black substance in cigarette filters when smoking. Nicotine and tar are deposited in plaque and diffuse through enamel pores/defects to the exposed dentin. Smokeless chewing tobacco (snuff) is made from ground or crushed tobacco leaves and has a higher nicotine content than cigarettes. During chewing, brown tobacco leaves mix with saliva, and pigments deposit on the tooth surface. Smoking and chewing tobacco cause teeth to discolor from yellow-brown to brown-black (Fig. 6). The electronic cigarette (e-cigarette) for “vaping” simulates tobacco smoking but produces an aerosol containing nicotine. Unlike cigarettes, e-cigarettes do not contain tar, but over time, the oxidized nicotine aerosol turns brown and discolors teeth. Nicotine is absorbed into the body when smoked and delivered through the skin, lungs, and mucous membranes. There are 82 million e-cigarette users worldwide. According to the World Health Organization (WHO) around 80% of the world’s 1.3 billion tobacco users live in low- and middle-income countries.

Fig. 6: Tobacco stain

Khat Chewing Stain

Khat or Qat (Catha edulis) is an evergreen plant that grows in the Horn of Africa, and Southern Arabian Peninsula. Chewing Khat leaves is very common in Yemen, and Ethiopia, Somalia, and Saudi Arabia among many Muslims as an alternative to alcohol. Mature leaves have a bitter taste, and fragrant with tannin contents, while young leaves are slightly sweet. A literature review of secondary and university students in these countries showed that khat chewing ranged from 14 to 37%, with approximately six times as many males as females and up to 60% of chewers smoking. Khat contains various compounds, including alkaloids, flavonoids, glycosides, tannins, amino acids, vitamins, minerals, and traces of F.16 The active ingredients of khat are cathine and cathinone (nor-pseudoephedrine), whose structure and psychoactivity are closely related to amphetamines in affecting the central and peripheral nervous systems. Chewing khat releases these substances into saliva, where they are quickly absorbed and eliminated. Cathinone is the main psychoactive component in khat, inducing stimulant and euphoric effects last about one hour after chewing.17 The khat bolus is chewed gradually and continuously for 2–10 hours. Only fresh leaves of greenish-brown in color are used, as cathinone in dried khat degrades and loses its effect. Habitual chewing of khat can turn the teeth dark brown (Fig. 7), and causing whitish or hyper pigmented mucous membranes, gingivitis, periodontal pocket, gingival recession, tooth attrition, mouth dryness, temporomandibular joint problems, mucosal keratosis.

Fig. 7: Khat chewing stain

Betel-nut Chewing Stain

The betel nut (Areca nut) is a seed of the fruit of the areca palm tree, mainly used in Southeast Asia. People chewing betel nuts can produce a sense of wellbeing, euphoria, increase alertness, improve work ability and suppress appetite. Common effects are increased heart rate, high blood pressure, and gastritis. Betel nuts contain a variety of chemicals, including alkaloids, tannins, steroids, volatile oils, and gums. Alkaloid arecoline is the main psychoactive ingredient, absorbed by the body during a nut’s chewing and affecting the central and autonomic nervous systems.18 It is also found in the saliva, blood, urine, and breast milk of the chewers. Chewing nuts can cause teeth and gingiva to discolor reddish-brown (Fig. 8), mouth ulcers, and mucous fibrosis. Tannins in nut juices react with proteins and minerals in saliva to form staining complexes. The hard texture of nuts leads to dental abrasion, and tooth sensitivity. The habit of chewing nuts can be addictive. The WHO has classified betel nuts as a carcinogen to the oral cavity and esophagus.

Fig. 8: Betel nut chewing stain

Iron Supplements

Iron is essential for all living tissues, and its deficiency is one of the most common nutritional deficiencies worldwide, causing serious behavioral, functional, and cognitive problems in children. Although the American Academy of Pediatrics (AAP) strongly supports breastfeeding, globally, only 38% of infants are exclusively breastfed. In the United States, only 75% of infants begin breastfeeding from birth, and by the age of three months, 67% of them are dependent on infant formula. The AAP advocates the use of iron-fortified infant formula to reduce the incidence of anemia in the first year of life.19 Health professionals often prescribe iron supplements in the form of drops, syrups, multivitamins, and iron-fortified formulas. Iron in the oral solution may react with H2S produced by chromogenic bacterial metabolites in gingival crevicular fluid, dental plaque fluid, and saliva to form ferric sulfide (Fe2S3), resulting in reddish-brown tooth staining that is difficult to remove by brushing (Fig. 9). This extrinsic staining is particularly common in enamel defects but does not cause any changes to its surface. Studies have reported that more than half of children who received iron supplements developed stained teeth. Parents may mistake iron staining for dental caries.

Fig. 9: Iron stain from syrup intake

Ageing

Are physiological changes that occur at varying rates over time and are related to lifestyle, environment, and genetics. Teeth discolor with age due to enamel wear from chewing, grinding, and acidic drinks. The thin enamel may reveal darkened dentin underneath, associated with the gradual deposition of extrinsic stains. Exposed dentin allows more chromogens to enter the body of the tooth. Plaque deposits increase the permeability of tooth enamel to minerals and chromogens. Aging teeth appear yellow to dark. Some medications that older adults take, such as antihistamines and high blood pressure, may worsen tooth discoloration. Reduced saliva flow during aging is conducive to the accumulation of stains. Cracks, chipping, fracture lines, and irregularities in the enamel exacerbate stain deposits.

Occupational Tooth Discoloration

Workers in various industries may be exposed to hazardous conditions with varying degrees of oral and general adverse effects. Workers in acid industrials are at risk for dental erosion and tooth discoloration.1,7 Sulfuric acid (H2SO4) is the most commonly used acid in the industry. In battery factories, lead plates are immersed in 35% sulfuric acid, creating dense lead sulfate (PbSO4) vapor (mist and fume) during the open process. Exposure to this vapor results in bluish-green staining on eroded tooth surfaces, primarily confined to the labial surfaces of the anterior teeth, and occlusal wear of the posterior teeth (Fig. 10). Studies showed that more than two-thirds of long-term workers in battery industry have significantly higher scores of tooth erosion, gingivitis, and poor oral hygiene.7,20 The phosphate fertilizer industry is another source of occupational hazards. During the treatment of phosphate rock with sulfuric acid, hydrofluoric acid (HF) and metals are released and dispersed into the open working site. The emitted vapor cause tooth erosion and discoloration, as well as affecting the growth and differentiation of mucosal and periodontal cells.

Figs 10A and B: Occupational dental hazards for battery workers: (A) The maxillary anterior teeth show tenacious bluish-green stains deposited on carious lesions and accumulated debris; (B) Distinctive labial erosion of the maxillary anterior teeth with debris

Intrinsic Tooth Discoloration

Types and Causes

Unlike extrinsic discoloration, which occurs on the tooth surface, intrinsic discoloration is caused by chromogenic substances that are incorporated into the enamel and dentin either during tooth development or after tooth eruption, resulting changes in the structure and composition of the discolored tissue. Several metabolic, systemic, and genetic disorders can affect the development of the dentition and cause tooth discoloration in yellow, orange, gray, or brownish black. Examples of pre-eruptive tooth discoloration are enamel fluorosis, tetracycline, and developmental defects, with enamel fluorosis being the most common tooth discoloration. Certain infections and drugs in pregnant mothers can cause discoloration of the infant’s teeth. Genetic and metabolic disorders affecting tooth development can alter tooth appearance and structure, including amelogenesis imperfecta, dentinogenesis imperfecta, dentin dysplasia, hyperbilirubinemia, erythropoietic porphyria, thalassemia, and sickle cell anemia.1,2,21,22 The intrinsic post-eruptive tooth discoloration can occur as a result of intrapulpal hemorrhage, pulpal necrosis, endodontic treatment, restorative materials, and aging. Discoloration of non-vital permanent incisors due to trauma and endodontics may have an esthetic and social impact on children and adolescents.

Genetic/Congenital Diseases

Amelogenesis imperfecta (AI) is a genetically and clinically heterogeneous group of conditions that affect the enamel, and are often associated with other dental and oral tissues abnormalities. The condition is inherited as autosomal dominant or recessive, and is more evident in families with consanguinity. Amelogenesis imperfecta affects nearly all teeth in the primary and permanent dentition. It can occur alone or as a part of a syndrome. Based on the phenotypes, AI is classified into hypo plastic, hypo calcification, hypo maturation, and pigmented (Fig. 11), with enamel being discolored, pitted, or grooved, prone to rapid wear and breakage. The teeth are yellow or brown, and stains build up more readily on the defective enamel structure. Prevalence ranges from 1:700 to 1:4000, depending on the population studied. In treating AI, improving tooth appearance and restoration of occlusion are of prime importance. Treatment planning should consider the patient’s age, degree of enamel damage, and general oral status. Treatment should begin as early as possible to avoid further tooth damage, and negative social and functional consequences. Hypo plastic enamel with a reasonably well-mineralized structure is suitable for composite resin restoration. In poorly mineralized enamel, composite restorations have retention problems due to weak adhesion. For severely affected teeth, full crown coverage is required. For the primary dentition, there are esthetic crowns for the anterior dentition and stainless-steel crowns for the molars. For permanent teeth, veneers, ceramics, porcelain, or porcelain fused to metal crowns.

Figs 11A and B: Amelogenesis imperfecta (AI). (A) Hypoplastic pitted type; (B) Hypomaturation type. Note the occurrence of gingivitis

Dentinogenesis imperfecta (DI) is an autosomal dominant inherited disorder; therefore, a 50% of children born to an affected parent are at risk of having the condition. Dentinogenesis imperfecta is characterized by dentin malformation in both primary and permanent dentitions. It occurs during the histo-differentiation stage of tooth development. The prevalence of DI is 1 in 6,000 to 8,000. There are three types of DI based on their clinical presentations. Type I: occurs in people with osteogenesis imperfecta, type II: Occurs in people without systemic disease. Type III is characterized by rapid wear of the crowns, and is limited to certain geographic areas. Types I and II show obliteration of the pulp cavity and root canals by dentin, while type III shows an enlarged pulp cavity. After a tooth erupts, the enamel wears, chips, or peels off, and the exposed soft dentin may wear down to the level of the gums. A variety of tooth discolorations may occur, including blue, reddish-brown, yellow-brown, or opalescent (Figs 12A and B). Radiographically, DI is characterized by bulbous crowns, cervical constriction, pulp chamber obliteration, narrow roots, and root canal loss (Fig. 12C). Timely diagnosis and treatment are required to prevent further loss of tooth structure. Treatments vary depending on the patient’s age, severity of the problem, and chief complaint.

Figs 12A to C: Dentinogenesis imperfecta (DI). (A) Teeth exhibit bluish-gray discoloration; (B) Opalescent tooth discoloration; (C) Note the bulbous crowns, missing pulp chamber and root canals

Thalassemia and sickle cell anemia. They are common genetic disorders that pose major public health and social challenges in high-prevalence areas. Approximately 5% of the world’s population are carriers of thalassemia or sickle-cell anemia gene. Traits for thalassemia are more common in people from Mediterranean countries. Sickle cell disease is more common in people of sub-Saharan Africa, Indian, and Mediterranean ancestry. Both disorders are autosomal recessive and affect the structure and function of hemoglobin. Red blood cells (RBCs) become deformed and break down prematurely, leading to lifelong hemolytic anemia and requiring blood transfusions in severe cases. Signs and symptoms of thalassemia and sickle cell disease usually begin in early childhood. The rapid breakdown of red blood cells may cause the yellowing of the eyes and skin, which are signs of jaundice. Thalassemia is clinically divided into transfusion-dependent and non-transfusion-dependent, or genetically divided into mild, intermedia, and major. The severe type of thalassemia major (TM) is characterized by excessive destruction of RBCs, chronic anemia, ineffective erythropoiesis, and iron overload.22,23 Hemoglobin in the RBC is composed of a protein (“globin”) and iron (“heme”). The breakdown of heme produces green biliverdin, which is rapidly reduced to bilirubin, an orange-yellow pigment. During tooth formation, the incorporation of bilirubin pigment into the dentinal tubules causes a yellow discoloration that may turn brown with ferrous ion deposition. The gum may color brown to black due to iron deposits, and the mucous membrane may appear pallorous due to anemia (Fig. 13).

Fig. 13: Pallor oral mucosa and yellowish dental discoloration in TM22

Hyperbilirubinemia, or jaundice (icterus) is not a disease in itself. It may be physiologic or pathologic, depending on its cause and severity. Physiological jaundice is the most common type. Up to 60% of full-term newborns develop physiological jaundice. Most symptoms are mild and disappear on their own without treatment. Pathological jaundice is common in some areas and may lead to hepatocellular dysfunction and biliary obstruction. Deposition of bilirubin happens only when there is an excess of bilirubin and impaired excretion. Most bilirubin is produced by the breakdown of red blood cells, causing yellow discoloration of the sclera, skin, and mucous membranes. When the condition goes into remission, bilirubin disappears from the soft tissues. Hyperbilirubinemia causes yellowish-green tooth discoloration due to the incorporation of bilirubin during tooth formation (Fig. 14).

Fig. 14: Jaundice teeth discoloration

Congenital erythropoietic porphyria (Gunther’s disease) is the rarest type of porphyria and is commonly seen in infancy. This is an inherited metabolic disorder in which excess porphyrins accumulate in bones, plasma, RBCs, urine, and teeth. The major symptom of this disorder is the hypersensitivity of the skin to sunlight and some types of artificial light, such as fluorescent lights. Upon exposure to light, the photo-activated porphyrins in the skin cause fluid-filled blisters to tend to rupture, infected, scarring, and bone deformities. The hands, arms, and face are the most commonly affected areas. Deposition of porphyrin during tooth and bone development results in a reddish-brown discoloration (Fig. 15).

Figs 15A and B: Erythropoietic porphyria. (A) In infant; (B) In 5-year-old with dark reddish-brown discoloration

Chemicals and Drugs

Certain chemicals and drugs, such as fluoride (F) and tetracyclines can cause generalized intrinsic discoloration during tooth development. The severity of discoloration is related to the dose, frequency, timing, and stage of tooth formation. Certain antihistamines, antihypertensives, and antipsychotic drugs may also cause tooth discoloration. The silver in amalgam restoration and bismuth oxide in mineral trioxide aggregate (MTA) cement can cause gray-black tooth staining. Crown discoloration has been reported in 40% of teeth treated with triple antibiotic pastes.

Enamel Fluorosis

This is the most common type of intrinsic tooth discoloration, affecting people who live in areas where drinking water contains F above the optimal level of 0.7–1.2 ppm, and those exposed to other F sources.24–26 India has the highest rate of endemic dental fluorosis, with almost all the children living in the area with 4 ppm F in drinking water affected. Dental fluorosis is a caused by excessive F intake during enamel formation, which inhibits the enzymatic function of ameloblasts. This leads to enamel deficient matrix formation, subsurface hypo mineralization, pitting, porosity, and enamel surface breakdown. After enamel is fully formed, dental fluorosis will not occur even if much F is taken, but it can lead to osteofluorosis in the elderly. In primary teeth, enamel formation is completed at 10–12 months after birth, and in permanent teeth at the age of 7–8 years. Enamel fluorosis is characterized by bilateral symmetrical changes in the appearance and texture of enamel, manifested as fine white streaks, white paper-like areas, brown spots or brown-black surfaces, as well as enamel demineralizing, roughening, pitting or grooved (Fig. 16). In the primary dentition, fluorosis is less severe than in permanent dentition, due to the shorter duration of enamel formation. Fluorosis in the primary dentition is a strong indicator of fluorosis in the permanent dentition. Although fluorosis is not a disease, it is cosmetically unpleasant, psychologically distressing, and requires treatment and prevention.

Fig. 16: Grades of enamel fluorosis according to Dean’s index criteria (Hattab FN, original). Normal: The enamel is smooth, glossy, pale milky white transparent surface; Questionable: Aberrations from the translucency of normal enamel, with few white flecks or spots; Very mild: Opaque, small paper-white areas involving less than 25% of the enamel surface; Mild: White areas covering less than 50% of the enamel surface; Moderately severe: Enamel surface show pitting and marked brown stains, often disfiguring; Severe: The enamel is hypo plastic with discrete or confluent pitting, severely disfiguring brown-black stains showing a corrosion-like appearance

Tetracycline Staining

Tetracycline is an antibiotic introduced in the 1940s and used to treat a variety of infectious diseases. In 1963, the U.S. Food and Drug Administration (FDA) issued a warning prohibiting the use of tetracyclines by pregnant women, young children, and breastfeeding women because tetracyclines can cross the placenta and be excreted in breast milk. Currently, the incidence of tetracycline discoloration is 1–6%.27 Earlier study indicated that over one-fifth of the American Indian children had discoloration of the dentition due to the ingestion of tetracycline during the years of tooth formation.28 Teeth are strongly susceptible to tetracycline discoloration during the formation period. Tetracycline particles are incorporated along the incremental growth lines of enamel and dentin. They combine with calcium in hydroxyapatite crystals to form a tetracycline-calcium orthophosphate complex, which may lead to enamel hypoplasia. Dentin absorbs a greater amount of tetracycline pigments because it has a greater surface area than enamel. Tetracycline chromogens are permanently bound to the hard tooth structure, whereas in bone they are released by bone remodeling. The released tetracycline molecules enter the circulation and become incorporated into calcifying hard tissue. The severity of stains depends on the time and duration of tetracycline administration, dosage, and types (Aureomycin, Terramycin, Minocycline, and Ledermycin). The location of staining on the tooth surface is related to the developmental stage of the tooth at the time of exposure to tetracycline.27,29 Reports showed that minocycline intake for 1 week can induce intense tooth discoloration.29 Categories of tetracycline staining: Mild: Slight and evenly distributed pale discoloration ranging from yellow, brown, or gray staining, limited to the incisal part of the crown. Moderate: The discoloration is slightly darker and more even, with no band stains. Severe: Pronounced blue-gray or brown-black band stain on the tooth surface. Very severe: An intense dark band stain across the tooth surface (Fig. 17).

Fig. 17: Tetracycline discolorations

Intercategory Tooth Discoloration

Teeth with vital or non-vital pulps, as well as endodontically treated teeth, can be discolored. Vital teeth may be discolored at the time the crowns are forming. The staining may be located in enamel or dentin and may be localized or generalized. In addition to the extrinsic and intrinsic tooth discoloration, some discolorations have a specific cause and characteristics that do not fall completely into the two main classifications, referred to as inter category tooth discoloration. These include hypo mineralized or hypo plastic enamel, pulpal hemorrhage, endodontic treatment, tooth wear, caries, and restorative materials. Endodontically treated teeth often lead to tooth crown discoloration due to intrapulpal blood degradation, necrotic pulpal tissue, and the endodontic materials. Tooth enamel wear may expose the yellow dentin, and the roughened enamel surface may promote chromogens deposition. Some filling materials, cements, and medicaments can darken dentin, such as amalgam, eugenol, MTA, formocresol, iodoform, antibiotic pastes, and others:

  • Enamel developmental defects: Hypo mineralized lesions are often visible due to their translucency, which differs from sound enamel. They can be well-demarcated or diffusely distributed on the labial surface of the permanent anterior teeth, and can be opaque, milky white, or yellowish brown (Fig. 18A). Enamel hypoplasia occurs when the growth of the organic matrix that is subsequently mineralized to form enamel is disturbed, resulting in a reduction in the amount of enamel that manifests as irregular tooth surfaces, lines, pits, or grooves. Hypo plastic lesions can be yellow or brown in color. Both hypo plastic and hypo calcified lesions are susceptible to stain deposition.

  • Intrapulpal hemorrhage: Trauma is the major cause of tooth discoloration. A severe blow can cause blood vessels within the pulp to rupture, allowing RBCs to extravasate into the dentinal tubules. Hemolysis of RBCs releases hemoglobin (Hb), and the degraded Hb releases bilirubin and ferric ions (Fe3+) where Fe3+ reacts with H2S to form dark ferric sulfide (Fe2S3). With age, bilirubin oxidizes into the green biliverdin pigment, causing the yellow crown to turn bluish-dark (Fig. 18B). Pulp necrosis can be caused by bacterial, mechanical, or chemical irritation, where the teeth may become yellowish-brown (Fig. 18C). These teeth require endodontic treatment.

  • Physical trauma: Tooth discoloration may occur after dental trauma, depending on the intensity of the trauma. Chewing hard foods and putting pressure on the teeth can cause hair-like enamel cracks that can appear gray, yellow, or brown in the teeth of people who smoke, drink coffee, tea, etc. In severe trauma, the crown may become discolored immediately or may gradually darken over time. Immediate tooth discoloration is reversible, but progressive discoloration may require root canal treatment and bleaching.

  • Dental caries: The various stages of the caries process can be identified by color changes. Bjørndal et al.,30 classified caries into three categories based on their color: Actively progressing caries are light yellow, slowly progressing caries are light brown, and slowly progressing/arrested caries are dark brown. White spot lesions are an early characteristic of active carious lesions, while inactive carious lesions appear dark brown or black.

Figs 18A to C: Post-eruption tooth discoloration. (A) Enamel opacity on the lower right central incisor; (B) Discolored incisor due to pulp hemorrhage; (C) Discolored incisor due to pulp necrosis1

Amalgam

This material is suitable for large cavity restorations, and situations where moisture control is difficult. Micro-leakage may occur around new amalgam restorations due to the amalgam’s lack of adhesion to tooth structure. Aging amalgam restorations may produce corrosion products, mainly tin (stannous, Sn), that discolor the tooth structure to gray or black by the reaction of the amalgam corrosion elements with salivary and bacterial sulfides at the amalgam-tooth interface (Fig. 19). Laboratory studies have shown that amalgam produces significant amounts of corrosion products after 3 months of storage in a 0.19% F (as NaF) solution.31

Figs 19A and B: Amalgam tooth discoloration. (A) Internal discolored crown of old amalgam restorations; (B) Scanning electron microscopic (SEM) image showing amalgam corrosion products

CONCLUSION

Tooth discoloration is esthetically displeasing, psychologically traumatizing, and socially unacceptable. The cause of discoloration is multifactorial and manifests as a complex physiochemical interaction between chromogens and dental plaque/acquired pellicle/hard tooth structures. Tooth discoloration is classified mainly into extrinsic and intrinsic discoloration, a combination of the two and inter category type. Most tooth staining is extrinsic; it originates from pigments in foods, beverages, habits, mouth rinses, and occupation that deposited or reacted with the tooth surface microenvironment. Chromogens (chromophores) are non-metallic or metallic in nature. There is considerable individual variation in the appearance, severity, and treatment of tooth discoloration, depending on the type of tooth discoloration, frequency of exposure, age, and home care. Intrinsic tooth discoloration is caused by the incorporation of chromogens during tooth development due to metabolic, systemic, and genetic disorders, or drugs and tooth discoloration after tooth eruption is caused by drugs, chemicals, and pulpal sources. Dentists should have a good understanding of the types and mechanisms of stain formation so that appropriate treatment can be performed, as well as explaining to the patient the nature of the staining and prevention.

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