Download tooth staining

tooth staining
Staining on the teeth is very common, and seems to affect men more commonly than
women. Some people naturally have slightly yellow or grey teeth, but this does not
necessarily mean that they are not healthy. The color of normal teeth varies and depends on
the shade, translucency and thickness of the enamel.
Discoloration is slightly different from staining, but occurs, for example, when a filling
bleeds within the tooth, changing its color; or if the nerve from the tooth dies and bleeds into
the root canal. Erosion or wear of the tooth can also cause discoloration.
There are two main types of tooth stain: extrinsic staining on the surface of the teeth, and
intrinsic staining within the structure of the tooth.
Extrinsic stains occur from surface accumulation of an exogenous pigment and typically can
be removed with a surface treatment and may be caused by:
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Poor oral hygiene - plaque stuck on the teeth can turn yellow
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Bacterial stains
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Foods and drinks
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Tobacco
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Medication
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Gingival haemorrage
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Restorative material
Intrinsic stains arise from an endogenous material that is incorporated into the enamel or
dentin and can not be removed by prophylaxis with toothpaste or pumice and may be caused
by:
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Amelogenssis imperfaca
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Dentinogenesis imperfacta
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Dental fluoride
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Erthropletic porphyria
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Hyperbilirubinemia
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Ochronosis
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Trauma
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Localized red blood cell breakdown
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Medication:
Combination stains:
Smoking can cause a combination of surface and, over the long term, intrinsic staining
of the tooth structure. Tooth decay can cause both intrinsic and extrinsic staining
CLINICAL FEATURES
EXTRINSIC STAINS
Bacterial stains: are a common cause of surface staining of exposed enamel, dentin, and
cementum. Chromogenic bacteria can produce colorations that vary from green or blackbrown to orange. The discoloration occurs most frequently in children and is usually seen
initially on the labial surface of the maxillary anterior teeth in the gingival one third. In
contrast to most plaque-related discolorations, the black-brown stains most likely are not
primarily of bacterial origin but are secondary to the formation of ferric sulfide from an
interaction between bacterial hydrogen sulfide and iron in the saliva or gingival crevicular
fluid.
Tobacco: Extensive use of tobacco products, tea, or coffee often results in significant brown
discoloration of the surface enamel. The tar within the tobacco dissolves in the saliva and
easily penetrates the pits and fissures of the enamel. Smokers (of tobacco or marijuana) most
frequently exhibit involvement of the lingual surface of the mandibular incisors; users of
smokeless tobacco often demonstrate involvement of the enamel in the area of tobacco
placement.
Foods and drinks: Stains from beverages also often involve the lingual surface of the
anterior teeth, but the stains are usually more widespread and less intense. In addition, foods
that contain abundant chlorophyll can produce a green discoloration of the enamel surface.
The green discoloration associated with chromogenic bacteria or the frequent consumption
of chlorophyll containing foods can resemble the pattern of green staining seen secondary to
gingival hemorrhage. As would be expected, this pattern of discoloration occurs most
frequently in patients with poor oral hygiene and erythematous, hemorrhagic, and enlarged
gingiva. The color results from the breakdown of hemoglobin into green biliverdin.
A large number of medications may result in surface staining of the teeth. In the past, use
of products containing high amounts of iron or iodine was associated with significant black
pigmentation of the teeth. Exposure to sulfides, silver nitrate, or manganese can cause stains
that vary from gray to yellow to brown to black, Copper or nickel may produce a green stain;
cadmium, essential oils, and co-amoxiclav may be associated yellow to brown discoloration.
Multiple recent reports have documented a yellow-brown staining of teet associated with
doxycycline, which can be removed by professional abrasive cleaning; the cause of this
discoloration is unclear.
More recently, the most frequently reported culprits :include stannous fluoride and
chlorhexidine. Fluoride staining may be associated with the use of 8% stannous fluoride and
is thought to be secondary to the of the stannous (tin) ion with bacterial black stain occurs
predominantly in people with oral hygiene in areas of a tooth previously affectec by early
carious involvement. The labial surface of affected of anterior teeth and the occlusal surfaces
of posterior teeth are the most frequently affected. Chlohexidine is associated with a yellowbrown stain that predominantly involves the interproximal surfaces near the gingival
margins. The degree of staining varies with the concentration of the medication and the
patient's susceptibility. Although an increased frequency has been associated with the use of
tannin-containing beverages, such as tea and wine, effective brushing and flossing or
frequent gum chewing can minimize staining. Chlorhexidine is not alone in its association
with tooth staining; many oral antiseptics, such as Listerine and sanguinarine, also may
produce similar changes.
INTRINSIC STAINS
Congenital erythropoietic porphyria (Giinther disease) is an autosomal recessive disorder of
porphyrin metabolism that results in the increased synthesis and excretion of porphyrins and
their related precursors. Significant diffuse discoloration of the dentition is noted as a result
of the deposition of porphyrin in the teeth (Fig. 2-31). Affected teeth demonstrate a marked
red-brown coloration that exhibits a red fluorescence when exposed to a Wood's ultraviolet
(UV) light. The deciduous teeth demonstrate a more intense coloration because porphyrin is
present in the enamel and the dentin; in the permanent teeth, only the dentin is affected.
Excess porphyrins also are present in the urine, which may reveal a similar fluorescence
when exposed to a Wood's light.
Another autosomal recessive metabolic disorder, alkaptonuria, is associated with a blueblack discoloration termed ochronosis that occurs in connective tissue, tendons, and
cartilage. On rare occasions, a blue discoloration of the dentition may be seen in patients
who also are affected with Parkinson's disease.
Bilirubin is a breakdown product of red blood cells, and excess levels can be released into
the blood in a number of conditions. The increased amount of bilirubin can accumulate in
the interstitial fluid, mucosa, serosa, and skin, resulting in a yellow-green discoloration
known as jaundice (see page 821). During periods of hyperbilirubinemia, developing teeth
also may accumulate the pigment and become stained intrinsically. In most cases the
deciduous teeth are affected as a result of hyperbilirubinemia during the neonatal period. The
two most common causes are erythroblastosis fetalis and biliary atresia. Other diseases that
less frequently display intrinsic staining of this type include the following:
• Premature birth
• ABO incompatibility
• Neonatal respiratory distress
• Significant internal hemorrhage
• Congenital hypothyroidism
• Biliary hypoplasia
• Metabolic diseases (tyrosinemia, al-antitrypsin deficiency)
• Neonatal hepatitis
Erythroblastosis fetalis is a hemolytic anemia of newborns secondary to a blood
incompatibility (usually Rh factor) between the mother and the fetus. Currently, this disorder
is relatively uncommon because of the use of antiantigen gamma globulin at delivery in
mothers with Rh-negative blood.
Biliary atresia is a sclerosing process of the biliary tree and is the leading cause of death
from hepatic failure in children in North America. However, many affected children live
after successful liver transplantation.
The extent of the dental changes correlates with the period of hyperbilirubinemia, and most
patients exhibit involvement limited to the primary dentition. Occasionally, the cusps of the
permanent first molars may be affected. In addition to enamel hypoplasia, the affected teeth
frequently demonstrate a green discoloration (chlorodontia). The color is the result of the
deposition of biliverdin (the breakdown product of bilirubin that causes jaundice) and may
vary from yellow to deep shades of green. The color of tooth structure formed after the
resolution of the hyperbilirubinemia appears normal. The teeth often demonstrate a sharp
dividing line, separating green portions (formed during hyperbilirubinemia) from normalcolored portions (formed after normal levels of bilirubin were restored).
Coronal discoloration is a frequent finding after trauma, especially in the deciduous
dentition. Post-traumatic injuries may create pink, yellow, or dark-gray discoloration.
Temporary pink discoloration that arises 1 to 3 weeks after trauma may represent localized
vascular damage and often returns to normal in 1 to 3 weeks. In these instances, periapical
radiographs are warranted to rule out internal resorption that may produce a similar clinical
presentation. A yellow discoloration is indicative of pulpal obliteration, termed calcific
metamorphosis. The dark-gray discoloration is long-term and occurs in teeth with significant
pulpal pathosis in which blood degradation products have diffused into the dentinal tubules.
Endodontic therapy initiated before or shortly after the total death of the pulp often prevents
the discoloration. The pulpal necrosis may be aseptic and not associated with significant
tenderness to percussion, mobility, or associated periapical inflammatory disease. A related
process secondary to localized red blood cell destruction also can result in discoloration of
the teeth. Occasionally, during a postmortem examination, a pink discoloration of teeth is
found. The crowns and necks of the teeth are affected most frequently, and the process is
thought to arise from hemoglobin breakdown within the necrotic pulp tissue in patients in
whom blood has accumulated in the head.
A similar pink or red discoloration of the maxillary incisors has been reported in living
patients with le-promatous leprosy (see page 198). Although controversial, some
investigators believe these teeth are involved selectively because of the decreased temperature preferred by the causative organism. This process is thought to be secondary to
infection-related necrosis and the rupture of numerous small blood vessels within the pulp,
with a secondary release of hemoglobin into the adjacent dentinal tubules.
Dental restorative materials, especially amalgam, can result in black-gray discolorations of
teeth. This most frequently arises in younger patients who presumably have more open
dentinal tubules. Large Class II proximal restorations of posterior teeth can produce
discoloration of the overlying facial surface. In assition deep lingua] metallic restorations on
anterior incisors can significantly stain underlying dentin and produce visible grayish
discoloration on the labial surface. To help reduce the possibility of discoloration, the
clinician should not restore endodontically treated anterior teeth with amalgam.
Several different medications can become incorporporated into the developing tooth and
result in clinically evident discoloration. The severity of the alterations is dependent on the
time of administration, the dose, and the duration of the druge's. use. The most infamous is
tetracycline, with the affected teeth varying from a bright yellow to dark brown and, in UV
light, showing .bright yellow fluorescence. After chronic exposure to ambient light, the
fluorescent yellow discoloration fades over months to years into a nonfluorescent brown
discloration. Often facial surfaces of the anterior teeth will darken while the posterior
dentition and lingual surfaces remain a fluorescent yellow. The drug and its homologues can
cross the placenta! barrier; therefore, administration should, if possible, be avoided during
pregnancy and in children up to 8 years of age. All homologues of tetracycline are associated
with discoloration and include chlortetracy-cline (gray-brown discoloration) and
demethylchlortet-racycline and oxytetracycline (yellow).
One semisynthetic derivative of tetracycline, rnino-cycline hydrochloride, has been shown to
produce significant discoloration of the dentition and also may affect teeth that are fully
developed. Minocycline is a widely used medication for the treatment of acne and also is
occasionally prescribed to treat rheumatoid arthritis. Its prevalence of use is increasing (and,
presumably, so will the number of patients affected with discolored teeth and bone).
Although the mechanism is unknown, minocycline appears to bind preferentially to certain
types of col-lagenous tissues (e.g., dental pulp, dentin, bone, dermis). Once in these tissues,
oxidation occurs and may produce the distinctive discoloration. Some investigators believe
supplementation with ascorbic acid (an antioxidanf) can block formation of the
discoloration. No matter the cause, once the pulp tissues are stained, the coloration can be
seen through the overlying translucent dentin and enamel. The staining is not universal; only
3% to 6% of long-term users become affected. In those affected, the period of time before
discoloration becomes evident can range from just 1 month to several years.
In susceptible individuals, minocycline creates discoloration in the skin, oral mucosa (see
page 318), nails, sclera, conjunctiva, thyroid, bone, and teeth. Coloration of the bone
occasionally results in a distinctive blue-gray appearance of the palate, mandibular tori, or
anterior alveolar mucosa, which represents the black bone showing through the thin,
translucent oral mucosa (see page 317). Several patterns of staining are noted in the
dentition. Fully erupted teeth typically reveal a blue-gray discoloration of the incisal three
fourths, with the middle one third being maximally involved. The exposed roots of erupted
teeth demonstrate a dark-green discoloration, although the roots of developing teeth are
stained dark black.
Another antibiotic, ciprofioxacin, is given intravenously to infants for Klebsiella spp.
infections. Although less notable than tetracycline, this medication also has been associated
with intrinsic tooth staining, usually a greenish discoloration.
TREATMENT AND PROGNOSIS
Careful polishing with fine pumice can remove most extrinsic stains on the teeth; typically,
normal prophylaxis paste is insufficient. Stubborn stains often are resolved by mixing 3%
hydrogen peroxide with the pumice or by using bicarbonated spray solutions. The use of jet
prophylactic devices with a mild abrasive is the most effective. Recurrence of the stains is
not uncommon unless the cause is reduced or eliminated. Improving the level of oral
hygiene often minimizes the chance of recurrence.
Intrinsic discoloration is much more difficult to resolve because of the frequent extensive
involvement of the dentin. Suggested aesthetic remedies include external bleaching of vital
teeth, internal bleaching of nonvital teeth, bonded restorations, composite buildups, laminate
veneer crowns, and full crowns. The treatment must be individualized to fulfill the unique
needs of each patient and his or her specific pattern of discoloration.