Congenital Missing Teeth
- Jessica Anggono, Elza Ibrahim Auerkari
- Corresponding Author
- Jessica Anggono
Available Online May 2018.
- https://doi.org/10.2991/idsm-17.2018.12How to use a DOI?
- Congenital missing teeth, Genetics, Gene mutations
- Oral health plays a major role in an individual’s well-being, affecting all aspects of quality of life: esthetics, function, and speech. Abnormalities in oral health may disrupt any or all of these aspects. One of the challenging and most common dental anomalies found in daily practice is congenital missing teeth (CMT). CMT affects more than 20% of the human population and can negatively affect mouth esthetics, dental function, and even a person’s speech. CMT essentially re-sult from a defect in tooth development, which is a complex process. Environ-mental and genetic factors, combined with epigenetics, have been credited with disrupting tooth development, causing CMT. Most cases of CMT are found in a familial pattern, and among all factors, genetics plays a fundamental part; there-fore, heredity has a crucial role in determining an individual’s phenotype of CMT. There are more than 300 genes that contribute to odontogenesis, and their muta-tions may be manifest as hypodontia with varying degrees of penetrance and ex-pressivity. A major cause of autosomal dominant non-syndromic hypodontia is mutation in the MSX1 and PAX9 genes in humans. In the present paper, we will discuss in brief the definition, prevalence, etiology, and roles of genetics and epi-genetics in CMT, as well as the types of gene mutation, with emphasis on muta-tion in the MSX1 and PAX9 genes related to CMT.
- Open Access
- This is an open access article distributed under the CC BY-NC license.
Cite this article
TY - CONF AU - Jessica Anggono AU - Elza Ibrahim Auerkari PY - 2018/05 DA - 2018/05 TI - Congenital Missing Teeth BT - 11th International Dentistry Scientific Meeting (IDSM 2017) PB - Atlantis Press SN - 2468-5739 UR - https://doi.org/10.2991/idsm-17.2018.12 DO - https://doi.org/10.2991/idsm-17.2018.12 ID - Anggono2018/05 ER -