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Amelogenesis imperfecta
Amelogenesis imperfecta is a tooth development disorder. It causes the tooth enamel to be thin and abnormally formed. Enamel is the outer layer of teeth.
Causes
Amelogenesis imperfecta is passed down through families as a dominant trait . That means you only need to get the abnormal gene from one parent in order to get the disease.
Dominant trait
Autosomal dominant is one of several ways that a trait or disorder can be passed down (inherited) through families. In an autosomal dominant disease,...
Symptoms
The enamel of the tooth is soft and thin. The teeth appear yellow and are easily damaged. Both baby teeth and permanent teeth are affected.
Teeth appear yellow
Abnormal tooth color is any color other than white to yellowish-white.
Exams and Tests
A dentist can identify and diagnose this condition.
Treatment
The treatment depends on how severe the problem is. Full crowns will improve the appearance of the teeth and protect them from damage. Eating a diet that is low in sugar and practicing very good oral hygiene can reduce the chance of developing cavities.
Outlook (Prognosis)
Treatment is often successful in protecting the teeth.
Possible Complications
The enamel is easily damaged, which affects the appearance of the teeth, especially if left untreated.
When to Contact a Medical Professional
Call your dentist if you have symptoms of this condition.
References
Neville BW, Damm DD, Allen CM, Chi AC. Abnormalities of teeth. In: Neville BW, Damm DD, Allen CM, Chi AC, eds. Oral and Maxillofacial Pathology . 4th ed. St. Louis, MO: Elsevier Saunders; 2016:chap 2.
Tinanoff N. Development and developmental anomalies of the teeth. In: Kliegman RM, Stanton BF, St Geme JW, Schor NF, eds. Nelson Textbook of Pediatrics . 20th ed. Philadelphia, PA: Elsevier; 2016:chap 307.
Review Date: 2/22/2016
Reviewed By: Michael Kapner, DDS, general and aesthetic dentistry, Norwalk Medical Center, Norwalk, CT. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team.
