Intrinsic Discolorations Created During Odontogenesis

Alkaptonuria. Alkaptonuria is also known as phenylketonuria and ochronosis. It is a recessive genetic deficiency resulting in incomplete oxidation of tyrosine and phenylalanine, causing an increased level of homogentisic acid. This condition sometimes causes a dark brown pigmentation of Lhe permanent teeth.6

Treatment: Tooth whitening can lessen or even eliminate the discolorations. In. severe cases the teeth may need additional esthetic procedures to achieve perfection.

Amelogenesis Imperfecta. Generally considered a genetic dcfect, this condition affects both the primary and permanent dentitions.7 The most common modes of inheritance are either autosomal recessive or autosomal dominant. The .category of amelogenesis imperfecta can be further subdivided into three groups: hypomaturation, hypocalcifie, and hypoplastic. There is great variety of appearance displayed by these groups, both between the groups and even within each group.

Hypomaturation. The enamel has chipped away from the underlying dentin. In Lhe hypomaturation type, the enamel shows an autosomal dominant mode of inheritance. (From Ishikawa's Color Atlas of Oral Pathology. Ishikawa G , Waldron C. St. Louis: Ishiyaku Euro-America, 1987.)

Teeth Erythroblastosis Fetalis
Fig. 3-2

Hypocalcific. The enamel found in this group exhibits normal thickness, but it is soft. Often the enamel is completely abraded away soon after eruption. This results in a tooth with a crown that ranges in appearance from a dull opaque white to a dark brown. In addition, these teeth are usually rough and pitted.

Erythroblastosis Fetalis Teeth

Hypoplastic. Enamel found in this group is usually quite thin, often to the point of eliminating interproximal contacts. They usually have a smooth, hard, yellow appearance, although some pitting is found on occasion. (From Ishikawa's Color Atlas of Oral Pathology. Ishikawa G , Waldron C. St. Louis: Ishiyaku Euro-America, 1987.)

Hypocalcified Amelogenesis Imperfecta
Fig. 3-4

Treatment: If the amelogenesis imperfecta is of a variety which exhibits sufficient enamel thickness, the teeth should be aggressively treated with topical fluoride. Following this treatment, the enamel may be found to be suitable for bonding. The more common, as well as predictable, treatment is to provide full prosthetic coverage for the affected teeth. Those teeth which exhibit either insufficient, weak, or abraded enamel must be treated by full prosthetic coverage. Any vital bleaching technique is contra indicated.

Dentinogenesis Imperfecta. This inherited trait is the most prevalent hereditary dystrophy affecting the structure of teeth. It usually affects the primary dentition more seriously than the permanent dentition.7 The clinical crowns appear reddish-brown to gray opalescent. Often the enamel is friable, and breaks off soon after eruption. The exposed softened dentin then rapidly abrades away.

Treatment: Due to the thin or even non-existent enamel, there are no other options than to treat this condition with full prosthetic coverage. Vital bleaching is contraindicated.

Endemic Fluorosis. This condition is an enamel alteration caused by the excessive intake of fluoride during odontogenesis. The appearance of fluorosed teeth ranges from slight wisps and flecks of opaque white to mottled or pitted darkened sections next to normal looking areas.8 It was noticed and described as early as 1916, although the causative agent was not discovered until 1931. Black thought that the stain was caused by the replacement of the normal cementing substance between enamel rods by "brownin". We now understand that dental fluorosis is a form of enamel hypoplasia.9 Currently, it is believed that the hypoplasia is caused by metabolic alteration of the ameloblast during enamel formation.

Dental fluorosis is often found in communities in which the fluoride content of the drinking water exceeds one part per million.10 The degree of severity of the staining is directly proportional to the amount of fluoride absorbed, and the teeth can be affected from the second trimester in utero through age nine.11

Corroded Teeth

On the left are maxillary incisors with very mild mottled enamel. On the right are teeth displaying corroded and stained surfaces, (From Ishikawa's Color Atlas of Oral Pathology. Ishikawa G Waldron C. St. Louis: Ishiyaku Euro-America, 1987.)

Treatment: Areas of the tooth darkened by endemic fluorosis respond to vital tooth whitening. If the stains are set deep into the tooth and are very opaque, however, only limited success should be expected. In these cases, the proper technique is to perform tooth whitening procedures followed by bonded porcelain or composite. Those teeth which exhibit white areas obviously cannot be darkened by tooth whitening procedures. If the areas are superficial, they can be treated by enamel abrasion. If the tooth exhibits both dark and opaque white areas, the treatment of choice is to abrade those areas where the stain appears superficial, and then to institute tooth whitening procedures. Finally, if the improvement is not sufficient, conservative bonding procedures can be used.

Erythroblastosis Fetalis. This is a blood disorder of the neonate due to Rh incompatibility of the fetal and maternal blood supplies. It is characterized by agglutination and hemolysis of the erythrocytes, resulting in free blood pigments. These pigments sometimes discolor all the teeth which are in formation at the time. The affected teeth can range in color from brown to greenish-blue.12 This condition is usually self treating, and the staining resolves as the child matures.

Discolored deciduous teeth in a six-year-old child with a history of erythroblastosis fetalis. (From Ishikawa's Color Atlas of Oral Pathology. Ishikawa G, Waldron C. St, Louis: Ishiyaku Euro-America, 1987.)

Alkaptonuria Teeth
Fig. 3-6

Treatment: Usually none is necessary.

Porphyria. This is a disorder of porphyrin metabolism which results in increased formation and excretion of porphyrins. It is a rare condition which is usually genetically transmitted, although it may develop later in life. The disease exhibits neurological, psychological, and gastrointestinal symptoms. In addition, the hematoporphyrin pigment creates a characteristic reddish-brown discoloration of the teeth sometimes known as "erythrodontia".1314 The dental effects are more commonly seen in the primary dentition than the permanent dentition. The coloration is dispersed throughout the enamel, dentin, and ccmentum, and fluoresces red under ultraviolet light.

Treatment: Tooth whitening, sometimes in conjunction with bonding.

Sickle Cell Anemia and Thalassemia. These arc both inherited blood dyscrasias which on occasion result in tooth discolorations similar to those of erythroblastosis fetalis. Unfortunately, unlike erythroblastosis fetalis, the discoloraLions from these two dyscrasias are more severe and do not improve with time.

Treatment: Tooth whitening, with the addition of bonding procedures for the more intractable cases.

Tetracycline Staining. The potential for tetracycline to cause discoloration of the dentition has been well documented and explored since First reported by Schwashman and

Schuster in 1956.15 Since tetracycline can cross the placental barrier, tetracycline affects both the deciduous and permanent dentitions, making the teeth vulnerable throughout odontogenesis. Even as short an exposure as three days can cause discoloration of the teeth any time from four months in utero through age nine.16

Much study has gone into the mechanism of staining caused by tetracyclines, and it now seems clear that tetracycline binds to the calcium in the tooth, forming a tctracycline-calcium-phosphate complex. It is found throughout the tooth, but by far the greatest concentration is in the dentin near the dentino-enamel junction. Both the quality and the severity of the discoloration are directly related to the specific tetracycline ingested as w7ell as the dose.

Some of the early investigations revealed that the teeth affectcd by tetracycline first exhibit a yellow color and display a bright yellow fluorescence far different from the blue fluorescence of normal (healthy) teeth.17 The yellow fluorescence and yellow color are visible in both the dentin and the enamel of the affected teeth, although the greatest concentration is found in the dentin near the dentino-enamel margin.

Tetracycline-induced discoloration can be seen on the incisal edges of the permanent anterior teeth of this 14-year-old. Massive doses of tetracycline were administered when this individual was an infant. (From Ishikawa's Color Atlas of Oral Pathology. Ishikawa G , Waldron C. St. Louis: Ishiyaku EuroAmerica, 1987.)

Fig. 3-7

Interestingly, the color of the affected teeth gradually changes over a period of time ranging from months to years. This color change is most pronounced in Lhose teeth which are most exposed to light, the facial surfaces of the anterior teeth.18

Wallman and Hilton clearly demonstrated the role of light in this process in 1962, by splitting a tetr ac y dine - st am ed tooth lengthwise and exposing only one half to light. The half which was exposed to light underwent a color change, becoming brown, while the half which was unexposed to the light remained yellow.19 It is for this reason that many researchers feel that the use of heat and light bleaching systems in the treatment of tetracycline stained teeth may be contraindicated.

In 1983, Davies, et al., produced a study which gave strong support to the belief that the tetracycline was transformed into 4a,12 a-anhydro-4-oxo-4-dedimethylaminotetracycline (AODTC).20

The clinical appearance of tetracycline-stained teeth ranges from light yellow to dark gray bands. Usually the darker shades are confined to the gingival one-third of the teeth, but the lighter, hay-colored shades will often be located exclusively in the incisal one-third.

Treatment: Standard tooth whitening usually results in an improvement, although it is often an incomplete solution to the problem. The differentiation between the light and dark areas of the tooth is usually diminished after tooth whitening. On some teeth, selective etching of the enamel of the darker areas prior to whitening may be a further help. Bonding is usually necessary in the darker cases for perfection, although the degree of improvement from vital tooth whitening alone can be profound. Since the differentiation between the darker and lighter areas becomes less distinct, many patients are content to defer any bonding. Those cases exhibiting a yellow or brown discoloration generally whiten more completely than those with a gray or blue hue.

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    When will be the right to do the dental treatment due to odontogenesis?
    7 years ago
  • brigitte
    What it is the relationship between tooth discoloration and alkaptonuria?
    3 years ago

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