title: Disturbed enamel mineralization in a rat incisor model.
abstract: Possession of full-thickness hard enamel appears to be one of the indispensable life-saving characteristics of rats. Previous studies by Suga and his colleagues and by others demonstrated that various types of malformation are evoked in continuously erupting rat incisors. In the current report, we directed our effort to oversee various types of enamel malformation caused experimentally in rat incisors. We surveyed the specimens collected by Suga and his colleagues, as well as specimens we obtained. From the results, it is conceivable that perturbation of the programmed sequential events during enamel development is a major factor in the establishment of enamel malformation. Animal studies with either 1-hydroxyethylidene-1,1-bisphosphonate (HEBP) or a multidentate phosphonic acid (EDTPO) confirmed that dentin mineralization provides a certain inductive effect on the secretion of enamel matrix and subsequent enamel crystallization. Our recent studies using anti-microtubular agents led to the conclusion that the acceleration of mineralization in outer enamel is a type of enamel malformation, most likely due to disruption of the cellular regulation of calcium transport under severe toxic regimens. In future work, experimental approaches combining measurements of kinetic factors with static observation of enamel lesions are required before we can gain a comprehensive understanding of the pathogenesis of disturbed enamel mineralization. The kinetic factors to be considered include the rates of tissue apposition and tooth eruption which determine the total volume of tooth substance formed, and the rate of mineral accretion. Furthermore, information as to the composition, crystallinity, solubility, and mechanical properties of enamel defects is needed before we can assess the susceptibility of teeth having those lesions to caries and other physico-chemical attacks in the oral environment.
authors.affiliation: Nippon Dental University, Department of Pathology, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Hattori
authors.forename: T
authors.initials: T
authors.lastname: Aoba
mesh_terms: D000565:Ameloblasts / Q000378:metabolism; D000566:Amelogenesis / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000172:deficiency / Q000378:metabolism; D003743:Dental Enamel / Q000378:metabolism*; D003744:Dental Enamel Hypoplasia / Q000378:metabolism*; D003810:Dentinogenesis / Q000502:physiology; D005260:Female; D007180:Incisor / Q000254:growth & development*; D051381:Rats; D017208:Rats, Wistar; D014074:Tooth Calcification / Q000502:physiology*; D014078:Tooth Eruption / Q000502:physiology*
chemical_list: D002118:Calcium