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  To understand how molecular biologists are attacking the problem of inherited disorders of enamel, a brief review of dental embryology is needed, The early stages of tooth development are characterized by a budding off of epithelium from the oral epithelium itself into the area of the future alveolar bone. This tooth precursor will give rise to both primary and permanent dentitions in the area (incisor, premolar, etc.). Only the inner layer of the double layer of cells (the inner enamel epithelium) has a functional tooth fate-it gives rise to the enamel. The sequence in which this occurs is now well documented and provides an excellent example of how embryonic tissues differentiate under the influence of adjacent but developmentally different cells. In this case, neural crest cells migrating into the dental lamina area from around the developing neural tube came to lie in an intimate but not touching relationship next to the inner enamel epithelium. The two developmentally different cell layers (inner enamel epithelium [enamel] and the neural crest [dentin]) are separated by an extracellular matrix, the ECM. The sequence of molecular events leading to enamel formation may be summarized as follows:
     l. Neural crest cells secrete an enamel-inducing substance that migrates across the intervening matrix (ECM) as a matrix vesicle and makes contact with the inner enamel epithelium (IEE).
     2. This enamel-inducing substance penetrates the IEE cell and activates that cell to begin producing its organic enamel matrix.
     3. The future enamel cell (preamloblast) in turn sends a different organic molecule (message) back across the matrix to the neural crest cells (preodontoblasts) where it signals these cells to initiate the full scale production of dentin.
     4. The matrices of both cell types (ameloblast and odontoblast) consist of specific proteins that will ultimately calcify into enamel, which is much harder than dentin. Molecular biologists working in this area recognize two proteins in enamel (amelogenin and enamelin) and a phosphoprotein in dentin.
     To be consistent with current genetic concepts, we presume that all the inherited defects of enamel can be traced to DNA alterations (mutations) that will result in errors in either one or both of these proteins. The most intriguing dental research today is l) the attempt to localize the genes for these proteins to a given chromosome and 2) the biochemical identification of specific defect in the protein that prevents it form functioning normally. The following is a discussion of genetic principles best exemplified by the heritable disorders of enamel.
     Based upon the clinical appearance, radiographic characteristics and microscopic features, oral pathologists have recognized three major types of inherited enamel defects: hypoplasia, hypocalcification and hypomaturation. These terms also provide us with the general description of the disease phenotypes. For example, in type l, enamel hypoplasia, the enamel is hard, well calcified but defective in amount. Two types of deficient enamel phenotypes are seen: generalized     (all the enamel) and localized (pits and grooves in specific areas). Type 2, hypocalcification. Disorders are those in which the enamel matrix is so drastically altered, that normal calcificatio本论文由英语论文网提供整理，提供论文代写，英语论文代写，代写论文，代写英语论文，代写留学生论文，代写英文论文，留学生论文代写相关核心关键词搜索。