SLC24A4 encodes a calcium transporter that mediates calcium transport to developing enamel during tooth development. Less is known about the function of other genes implicated in amelogenesis imperfecta.Researchers expect that mutations in further genes are likely to be identified as causes of amelogenesis imperfecta. Types include:

Amelogenesis imperfecta can have different inheritance patterns depending on the gene that is altered. Mutations in the ENAM gene are the most frequent known cause and are most commonly inherited in an autosomal dominant pattern. This type of inheritance means one copy of the altered gene in each cell is sufficient to cause the disorder.Amelogenesis imperfecta is also inherited in an autosomal recessive pattern; this form of the disorder can result from mutations in the ENAM, MMP20, KLK4, FAM20A, C4orf26 or SLC24A4 genes. Autosomal recessive inheritance means two copies of the gene in each cell are altered.About 5% of amelogenesis imperfecta cases are caused by mutations in the AMELX gene and are inherited in an X-linked pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In most cases, males with an X-linked form of this condition experience more severe dental abnormalities than affected females. Recent genetic studies suggest that the cause of a significant proportion of amelogenesis imperfecta cases remains to be discovered. Diagnosis
AI can be classified according to their clinical appearances:
Type 1 - Hypoplastic
Enamel of abnormal thickness due to malfunction in enamel matrix formation.
Denileukin diftitox (trade name Ontak) was an antineoplastic agent, an engineered protein combining interleukin-2 and diphtheria toxin. Denileukin diftitox could bind to interleukin-2 receptors and introduce the diphtheria toxin into cells that express those receptors, killing the cells. In some leukemias and lymphomas, malignant cells express these receptors, so denileukin diftitox can target these. In 1999, Ontak was approved by the U.S. Food and Drug Administration (FDA) for treatment of Cutaneous T-cell lymphoma (CTCL).There is some evidence tying it to vision loss, and in 2006 the FDA added a black box warning to the drugs label.In 2014, marketing of Ontak was discontinued in the US. References
External links
FDA Safety Alert