Please use this identifier to cite or link to this item: https://repository.unej.ac.id/xmlui/handle/123456789/83337
Title: Molecular mechanisms of Homeobox (HOX) Genes in Developmental Tooth Disturbances
Authors: Rahayu, Yani Corvianindya
Joelijanto, Rudy
Keywords: homeobox genes
development teeth
anomalies
Issue Date: 23-Nov-2017
Abstract: Development of teeth is under strict genetic control, which ensures the formation and renewal of a certain number of teeth with specific shapes and position. Gene mutations can disturb normal dental development and affect tooth number, shape, eruption or formation of dental hard tissues. The process of odontogenesis is under the control of homeobox (HOX) genes; a number of different mesenchymal regulatory molecules and their receptors. This article to review the role of homeobox genes in the developmental tooth disturbances. There are different molecular signalling that regulate tooth development and it is possible to observe that the molecular signals are expressed in different stages of odontogenesis. HOX genes are classified as muscle segment (MSX1 and MSX2), distal-less (Dlx), orthodontical, goosecoid, paired box gene 9 (Pax9) and sonic hedgehog (Shh). Msx1 and Msx2 genes are responsible for the developmental position and further development of tooth buds. Dlx-1, Dlx-2 and Barx-1 genes are involved in development of molar teeth. Pax9 is a transcription factor required for tooth morphogenesis. Dental anomalies are often observed as isolated, that is, only dentition is affected, and especially failure to develop all teeth. The genetic causes of dental pathologies are multiple causing phenotypic changes and the severity of which is dependant on the affected gene, the type and location of mutations.
Description: Proceeding 2nd Regional Oral Biology Scientific Meeting 2017
URI: http://repository.unej.ac.id/handle/123456789/83337
Appears in Collections:LSP-Conference Proceeding

Files in This Item:
File Description SizeFormat 
F. KG_Prosiding_Yani C_Molecular Mechanisms.pdf970.43 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.