Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Tooth Discoloration Clinical Presentation

  • Author: Dharti N Patel, DMD, FDS, RCSEd, FICOI; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Sep 07, 2015
 

History

The patient's history of tooth discoloration provides useful information regarding the etiology.

  • Chief complaint and history of chief complaint
    • In most patients, the chief complaint is related to aesthetics. The complaint is a result of mild-to-severe discoloration of any or all portions of the teeth, typically the anterior teeth. Stains associated with foods (eg, blueberries), beverages (eg, tea, coffee), tobacco products, medications (eg, tetracycline), and other causes (eg, anemia) are almost universally painless. Alternatively, the patient may present with a chief complaint of a poor or unaesthetic smile and discolored teeth.
    • Some patients may present initially with pain. Pain and discoloration can be a result of dental caries, a dentoalveolar infection, deep dental restorations, severe developmental or acquired defects in the enamel or dentin, or trauma that leads to pulpal necrosis.[24]
    • Enamel and/or dentin defects increase the potential for pulpal penetration by bacteria, which can lead to irreversible pulpal disease.
    • Patients with early pulpal disease (ie, reversible pulpitis) have fleeting sharp pain that is elicited by a stimulus such as exposure to cold or something sweet.
    • Chronic and untreated pulpal disease progresses to irreversible pulpitis, a condition resulting in pulpal death. Irreversible pulpitis produces poorly localized, lingering pain that is described as boring or gnawing and is aggravated by eating, exposure to a cold stimulus, or lying down (eg, many patients wake from sleep because of pulpitis pain). Analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs) often relieve irreversible pulpitis pain.
    • The progression of pulpitis causes more pain, which is frequently severe in nature, aggravated by heat, and often relieved by application of cold. Occasionally, chronic pulpitis results in the spontaneous development of pain.
    • Pulpal death and necrosis can lead to an acute apical periodontitis and an acute apical abscess, both of which can cause severe throbbing pain localized to the involved tooth, as well as regional lymphadenopathy.
    • Ultimately, the abscess can progress to cellulitis and facial-space infection, which causes facial swelling, pain in the regional lymph nodes, fever, malaise, difficulty in eating or opening the mouth, and dysphagia. In extreme cases, the infection and associated inflammatory products can become life threatening if vital structures are involved (eg, cases of dyspnea due to compromised airway, infection of mediastinum, cavernous sinus).
  • Medical history: A history of maternal or childhood diseases or the use of medications (see Causes) may explain tooth discoloration because the conditions can adversely influence normal tooth development. Knowledge of the onset and duration of maternal or childhood disease and the dosing of medications also helps.
  • Family history: Several genetic diseases are associated with tooth-associated disorders the most common include AI, DI, and DD. Patients may be unaware of the diseases but often confirm that a family member had similar tooth discoloration.
  • Social history: The use of tobacco and similar products, such as the chewing of areca (betel) nuts, commonly leads to staining of the teeth. Determining the type of tobacco habit (eg, smoking vs chewing) is important because the distribution of the stain may vary.
  • Dental history: The dental history can reveal useful information regarding the last dental cleaning, previous dental treatments, amount and scheduling of fluoride intake, oral hygiene practices, use of mouthwash, and traumatic events involving dentition.
  • Diet history: A history of nutritional deficiencies or ingestion of foods that can stain teeth is important. Querying patients about the quality of their diet, including the amount and frequency of fresh fruits and vegetables consumed and the use of sugared beverages between meals, is always useful.
Next

Physical

Physical characteristics of extrinsic discoloration

Usually, discoloration colors include brown, black, gray, green, orange, and yellow; on occasion, a metallic sheen is present. The scratch test is usually used to distinguish between extrinsic and intrinsic discoloration.

In terms of distribution patterns, primary or secondary teeth (or both, as in a child in the mixed dentition stage) may be involved. The distribution is either generalized to all teeth or localized to certain teeth or tooth surfaces. Extrinsic staining of 1 tooth is unusual. Extrinsic stains often are found on surfaces with poorer toothbrush accessibility (eg, at the tooth-gingival interface [cervical regions] and between the teeth [interproximal regions]).

Regarding other physical findings, teeth with extrinsic tooth discoloration usually demonstrate no signs of pulpal disease.

Physical characteristics of intrinsic discoloration

Usually, discoloration colors include brown, black, gray, green, orange, and yellow; also, a metallic sheen may be observed. Unlike extrinsic discoloration, teeth with intrinsic discoloration may be red or pink. Under ultraviolet light, teeth with tetracycline staining and congenital porphyria may fluoresce yellow or red, respectively. Intrinsic discoloration cannot be removed by using the scratch test.

In terms of distribution patterns, primary and secondary teeth may be involved. The distribution is either generalized to all teeth or localized to certain teeth or tooth surfaces. An intrinsic etiology usually exists when a single tooth is discolored. When multiple teeth are involved, patterns of banding are indicative of intrinsic staining.

Regarding other physical findings, teeth with intrinsic discoloration may demonstrate signs of pulpal disease.

  • Inspection
    • Visual inspection requires the use of a handheld dental mirror and a good light source, which permit examination of the varying shades and patterns of tooth color and the integrity and surface texture of all enamel surfaces.
    • Transillumination is the simple process of directing a light source (eg, fiberoptic probe) through an anterior tooth from the buccal surface to the lingual surface. This process can facilitate inspection of tooth discoloration, particularly when associated with dental caries.
    • Ultraviolet light exposure is not a common diagnostic tool, but it may offer further clues about the etiology of intrinsic discoloration because the tooth may emit a characteristic fluorescence.
  • Scratch testing
    • Discolored tooth surfaces are scratched with care by using a dental explorer, scaler, or similar sharp instrument to assess surface texture.
    • Noncarious discolorations are hard and nonpenetrable.
    • Light scratching with a dental instrument removes weakly adherent plaque that causes extrinsic discoloration.
    • If the discoloration requires removal with a sharp dental scaler, the discoloration is considered to be tenacious.
  • Exploration
    • Use a sharp dental instrument to explore soft and penetrable discolorations that probably are dental caries and/or faulty restorations. Incipient caries can undergo remineralization, and defects left following overzealous exploration may be less amenable to remineralization, warranting judicious use of an explorer.
    • These dental disorders require definitive therapy.
  • Percussion and palpation
    • Percussion of a discolored tooth with the handle of a dental mirror and palpation of the tooth over the covered root surface may reveal additional information regarding pulpal disease.
    • Discolored teeth associated with infections (eg, acute pulpitis, apical periodontitis, apical abscess) are sensitive to percussion and palpation.
  • Pulp testing
    • Pulp testing techniques are used to diagnose the pulpal status of teeth discolored as a result of dental caries, deep dental restorations, severe developmental or acquired enamel/dentin defects, or trauma leading to pulpal necrosis.
    • Thermal testing of teeth is conducted by using the application of cold (ice or vapocoolant) or heat (thermoconductive material such as dental compound or gutta percha). Surrounding teeth should be covered with cotton rolls or similar material and the cold or heat source applied directly to the tooth in question.
    • Electric pulp testing is used to assess pulp vitality and degree of pulpal disease.
  • Extraoral and intraoral soft tissue examination: Swelling, tender lymphadenopathy, trismus, and other signs associated with facial-space infection of odontogenic origin may accompany the physical presentation of a discolored tooth.
  • Comprehensive head, neck, and oral examination
    • Neck lymphadenopathy and tenderness upon palpation to neck lymph nodes may be indicative of infection.
    • An asymmetric mandible may be a sign of previous trauma.
    • Ecchymoses may be suggestive of a bleeding disorder.
Previous
Next

Causes

The causes of extrinsic and intrinsic dental discoloration are as follows (see also Pathophysiology):

Extrinsic causes

  • Brown stain
    • Tobacco products
    • Dental plaque
    • Tea, coffee, wine, and other beverages
    • Certain foods
    • Metals
    • Iodine
    • Chlorhexidine rinse
    • Cetylpyridinium chloride rinse
    • Stannous fluoride
    • Khat leaf
    • Doxycycline
  • Black stain
    • Tobacco products
    • Betel nut
    • Dental plaque
    • Chromogenic bacteria
    • Tea, coffee, wine, and other beverages
    • Certain foods
    • Metals
  • Green stain
    • Chromogenic bacteria
    • Tea
    • Metals
  • Orange stain
    • Chromogenic bacteria
    • Metals
    • Doxycycline

Intrinsic causes - Localized color changes (in 1 or 2 adjacent teeth)

  • White (opaque) stain
    • Mild trauma to teeth during enamel formation (secondary teeth), eg, Turner tooth
    • Periapical infection of primary tooth
    • Traumatic injury to primary tooth or teeth
    • Incipient caries (primary or secondary teeth)
  • Yellow stain
    • Moderate trauma to teeth during enamel formation (secondary teeth), eg, Turner tooth
    • Periapical infection of primary tooth
    • Traumatic injury to primary tooth or teeth
    • Trauma without hemorrhage
    • Composites or glass ionomer or acrylic restoration
    • Caries (active)
    • Focal tooth abrasion
  • Brown stain
    • Severe trauma to teeth during enamel formation (secondary teeth), eg, Turner tooth
    • Periapical infection of primary tooth
    • Traumatic injury to primary tooth or teeth
    • Composite, glass ionomer, or acrylic restoration
    • Caries (active or remineralized)
    • Pulpal trauma with hemorrhage
  • Blue, gray, or black stain
    • Amalgam restoration
    • Glass ionomer or acrylic restoration
    • Metal crown margin associated with porcelain fused to metal crown
    • Pulpal trauma with hemorrhage

Intrinsic causes - Regional color changes

  • White (opaque) stain
    • Infection (maternal or childhood) during enamel formation
    • Trauma to multiple teeth during enamel formation
    • Mild fluorosis (short-term exposure)
    • Nutritional deficiency
  • Yellow stain
    • Infection (maternal or childhood) during enamel formation
    • Moderate fluorosis (short-term exposure)
    • Trauma to multiple teeth during enamel formation
    • Nutritional deficiency
    • Epidermolysis bullosa
    • Regional tooth abrasion or erosion
    • Diseases causing hyperbilirubinemia
  • Brown stain
    • Infection (maternal or childhood) during enamel formation
    • Severe fluorosis (short-term exposure)
    • Trauma to multiple teeth during enamel formation
  • Blue, gray, or black stain - Tetracycline therapy (short-term exposure)
  • Green stain - Diseases causing hyperbilirubinemia (eg, HDN, biliary atresia)

Intrinsic causes - Generalized changes (involving primary and/or permanent dentitions)

  • White (opaque) stain
    • Mild fluorosis
    • Amelogenesis imperfecta
  • Yellow stain
    • Moderate fluorosis
    • Amelogenesis imperfecta
    • Dentinogenesis imperfecta
    • Dentinal dysplasia
    • Epidermolysis bullosa
    • Diseases causing hyperbilirubinemia
    • Hemolytic diseases
    • Generalized tooth attrition, abrasion, or erosion
  • Brown stain
    • Porphyria
    • Tetracycline therapy (long-term exposure)
  • Blue, gray, or black stain
    • Tetracycline therapy (long-term exposure)
    • Minocycline therapy
  • Green stain - Diseases causing hyperbilirubinemia (eg, HDN, biliary atresia)
Previous
 
 
Contributor Information and Disclosures
Author

Dharti N Patel, DMD, FDS, RCSEd, FICOI Clinical Assistant Professor, Department of Oral and Maxillofacial Pathology, Radiology and Medicine, New York University College of Dentistry

Dharti N Patel, DMD, FDS, RCSEd, FICOI is a member of the following medical societies: American Academy of Oral Medicine, American Dental Association, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Coauthor(s)

A Ross Kerr, DDS Clinical Associate Professor, Department of Oral & Maxillofacial Pathology, Radiology and Medicine, New York University College of Dentistry

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Donald Belsito, MD Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center

Donald Belsito, MD is a member of the following medical societies: New York County Medical Society, Noah Worcester Dermatological Society, Phi Beta Kappa, American Contact Dermatitis Society, Dermatology Foundation, Dermatologic Society of Greater New York, Alpha Omega Alpha, American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, and previous author, Jonathan Ship, DMD , to the development and writing of this article.

References
  1. Vogel RI. Intrinsic and extrinsic discoloration of the dentition (a literature review). J Oral Med. 1975 Oct-Dec. 30(4):99-104. [Medline].

  2. Nathoo SA. The chemistry and mechanisms of extrinsic and intrinsic discoloration. J Am Dent Assoc. 1997 Apr. 128 Suppl:6S-10S. [Medline].

  3. Hattab FN, Qudeimat MA, al-Rimawi HS. Dental discoloration: an overview. J Esthet Dent. 1999. 11(6):291-310. [Medline].

  4. Norton SA. Betel: consumption and consequences. J Am Acad Dermatol. 1998 Jan. 38(1):81-8. [Medline].

  5. Reid JS, Beeley JA, MacDonald DG. Investigations into black extrinsic tooth stain. J Dent Res. 1977 Aug. 56(8):895-9. [Medline].

  6. Supranoto SC, Slot DE, Addy M, Van der Weijden GA. The effect of chlorhexidine dentifrice or gel versus chlorhexidine mouthwash on plaque, gingivitis, bleeding and tooth discoloration: a systematic review. Int J Dent Hyg. 2015 May. 13 (2):83-92. [Medline].

  7. Eriksen HM, Jemtland B, Finckenhagen HJ, Gjermo P. Evaluation of extrinsic tooth discoloration. Acta Odontol Scand. 1979. 37(6):371-5. [Medline].

  8. Ioannidis K, Mistakidis I, Beltes P, Karagiannis V. Spectrophotometric analysis of crown discoloration induced by MTA- and ZnOE-based sealers. J Appl Oral Sci. 2013. 21(2):[Medline].

  9. Kleter GA. Discoloration of dental carious lesions (a review). Arch Oral Biol. 1998 Aug. 43(8):629-32. [Medline].

  10. van der Bijl P, Pitigoi-Aron G. Tetracyclines and calcified tissues. Ann Dent. 1995 Summer-Fall. 54(1-2):69-72. [Medline].

  11. Patel K, Cheshire D, Vance A. Oral and systemic effects of prolonged minocycline therapy. Br Dent J. 1998 Dec 12-26. 185(11-12):560-2. [Medline].

  12. McKenna BE, Lamey PJ, Kennedy JG, Bateson J. Minocycline-induced staining of the adult permanent dentition: a review of the literature and report of a case. Dent Update. 1999 May. 26(4):160-2. [Medline].

  13. Ayaslioglu E, Erkek E, Oba AA, Cebecioglu E. Doxycycline-induced staining of permanent adult dentition. Aust Dent J. 2005 Dec. 50(4):273-5. [Medline].

  14. Nelson R, Parker SR. Doxycycline-induced staining of adult teeth: the first reported case. Arch Dermatol. 2006 Aug. 142(8):1081-2. [Medline].

  15. DenBesten PK. Biological mechanisms of dental fluorosis relevant to the use of fluoride supplements. Community Dent Oral Epidemiol. 1999 Feb. 27(1):41-7. [Medline].

  16. Pendrys DG. Risk of enamel fluorosis in nonfluoridated and optimally fluoridated populations: considerations for the dental professional. J Am Dent Assoc. 2000 Jun. 131(6):746-55. [Medline].

  17. Warren JJ, Kanellis MJ, Levy SM. Fluorosis of the primary dentition: what does it mean for permanent teeth?. J Am Dent Assoc. 1999 Mar. 130(3):347-56. [Medline].

  18. Rozier RG. Epidemiologic indices for measuring the clinical manifestations of dental fluorosis: overview and critique. Adv Dent Res. 1994 Jun. 8(1):39-55. [Medline].

  19. Kumar A, Kumar V, Singh J, Hooda A, Dutta S. Drug-Induced Discoloration of Teeth: An Updated Review. Clin Pediatr (Phila). 2011 Sep 13. [Medline].

  20. Morisaki I, Abe K, Tong LS, Kato K, Sobue S. Dental findings of children with biliary atresia: report of seven cases. ASDC J Dent Child. 1990 May-Jun. 57(3):220-3. [Medline].

  21. Cullen CL. Erythroblastosis fetalis produced by Kell immunization: dental findings. Pediatr Dent. 1990 Nov-Dec. 12(6):393-6. [Medline].

  22. Neville BW, Damm DD, Allen CM, Bouquot JE. Abnormalities of the teeth. Neville BW, Damm DD, Allen CM, Bouquot JE, eds. Oral & Maxillofacial Pathology. 1st ed. Philadelphia, Pa: WB Saunders; 1995.

  23. Trodahl JN, Schwartz S, Gorlin RJ. The pigmentation of dental tissues in erythropoietic (congenital) porphyria. J Oral Pathol. 1972. 1(4):159-71. [Medline].

  24. Cohen ES, Burns R. Pathways of the Pulp. 7th ed. Mosby: St. Louis, Mo; 1998.

  25. Azer SS, Hague AL, Johnston WM. Effect of bleaching on tooth discolouration from food colourant in vitro. J Dent. 2011 Sep 19. [Medline].

  26. Hosoya Y, Johnston JW. Evaluation of various cleaning and polishing methods on primary enamel. J Pedod. 1989 Spring. 13(3):253-69. [Medline].

  27. Weaks LM, Lescher NB, Barnes CM, Holroyd SV. Clinical evaluation of the Prophy-Jet as an instrument for routine removal of tooth stain and plaque. J Periodontol. 1984 Aug. 55(8):486-8. [Medline].

  28. Croll TP. Enamel microabrasion: observations after 10 years. J Am Dent Assoc. 1997 Apr. 128 Suppl:45S-50S. [Medline].

  29. Batista GR, Barcellos DC, Torres CR, Goto EH, Pucci CR, Borges AB. The influence of chemical activation on tooth bleaching using 10% carbamide peroxide. Oper Dent. 2011 Mar-Apr. 36(2):162-8. [Medline].

  30. Perdigão J, Baratieri LN, Arcari GM. Contemporary trends and techniques in tooth whitening: a review. Pract Proced Aesthet Dent. 2004 Apr. 16(3):185-92; quiz 194. [Medline].

  31. Kugel G, Ferreira S. The art and science of tooth whitening. J Mass Dent Soc. 2005 Winter. 53(4):34-7. [Medline].

  32. Goldstein RE, Garber DA. Complete Dental Bleaching. Quintessence Publishing: Chicago, Ill; 1995.

  33. Krastl G, Allgayer N, Lenherr P, Filippi A, Taneja P, Weiger R. Tooth discoloration induced by endodontic materials: a literature review. Dent Traumatol. 2013 Feb. 29(1):2-7. [Medline].

  34. Nathanson D. Vital tooth bleaching: sensitivity and pulpal considerations. J Am Dent Assoc. 1997 Apr. 128 Suppl:41S-44S. [Medline].

 
Previous
Next
 
Transverse section of a central incisor illustrates the different soft and hard tissue layers of the tooth and the supporting dental-alveolar apparatus.
Dental calculus accumulations on the mandibular anterior teeth.
Stained supragingival plaque and calculus deposits.
Severe tobacco staining.
Image demonstrates a red extrinsic stain at the gingival margins and interproximal and incisal regions of the teeth in a patient with a habit of chewing pan (a combination of betel nut of the areca palm, betel leaf, and lime).
Extrinsic dental staining caused by long-term topical use of 0.12% chlorhexidine mouthrinse.
Image demonstrates dental attrition in a 75-year-old patient due to loss of occlusal enamel structure that reveals the underlying dentin.
Severe dental abrasion and gingival recession due to long-term traumatic toothbrushing habit.
Root surface caries, severe periodontitis, and amalgam restorations.
Extensive dental caries.
Severe root surface and occlusal caries that necessitated tooth extraction.
Severe enamel hypoplasia (ie, Turner tooth) on a secondary (permanent) maxillary central incisor. The patient had an intrusion injury of the primary central incisor during childhood that interrupted the development of the secondary central incisor.
Intrinsic dental discoloration caused by blunt trauma to the mandibular incisors that led to pulpal necrosis.
Dental radiograph demonstrates external resorption and periapical bone loss in a patient with intrinsic dental discoloration caused by blunt trauma to the mandibular incisors that led to pulpal necrosis. Image was obtained in the same patient as in Image 15.
Enamel hypoplasia of the incisal half of the maxillary and mandibular secondary incisors caused by rubella infection when the patient was aged 4 months.
Tetracycline staining of mandibular teeth caused by the ingestion of tetracycline when the patient was aged 3 years.
Mild dental fluorosis causing mottled white intrinsic discoloration of the teeth.
Severe fluorosis of the teeth.
Amelogenesis imperfecta (hypoplastic type 1 form) and associated enamel pitting and extrinsic dental discoloration.
Amelogenesis imperfecta (hypomaturation type 2 form).
Porcelain laminate veneers for the treatment of tetracycline staining.
Table 1. Calcification and Eruption Sequence of Primary Dentition
  Primary Teeth Calcification Begins (Weeks In Utero) Enamel Completed (Months after Birth) Eruption (Months after Birth)
Maxilla      
Central incisor 13-16 1.5 8-12
Lateral incisor 14.5-16.5 2.5 8-13
Canine 15-18 9 16-22
First molar 14. 5-16.5 6 13-19
Second molar 16-23.5 11 25-33
Mandible      
Central incisor 13-16 2.5 6-10
Lateral incisor 14.5-16.5 3 10-16
Canine 16-18 9 17-23
First molar 14.5-17 5.5 14-18
Second molar 17-19.5 10 23-31
Table 2. Calcification and Eruption Sequence of Secondary Dentition
  Permanent Teeth Calcification Begins (Months) Eruption (Years)
Maxilla    
Central incisor 3-4 7-8
Lateral incisor 10-12 8-9
Canine 4-5 11-12
First premolar 8-21 10-11
Second premolar 24-27 10-12
First molar 0-1 5-6
Second molar 30-36 12-13
Mandible    
Central incisor 3-4 6-7
Lateral incisor 3-4 7-8
Canine 4-5 9-10
First premolar 21-24 10-12
Second premolar 27-30 11-12
First molar 0-1 5-6
Second molar 30-36 12-13
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.