Long-term hypothesis is that enamel crystal's nucleation, growth, orientation, and arrangement (into prisms) is dependent on a unique relationship of the crystal to the organic matrix and the ameloblast. Overall objective is to clarify the ultrastructural arrangement and disarrangement of enamel tissue components in normal and pathological states. The research approach acknowledges that the ultrastructure of enamel tissue and its malformation is best resolved in the transmission electron microscope (TEM). When TEM results are directly correlated wit other techniques new understanding can be gained regarding the structure, function,a and ultrastucural histopathology of enamel. Crystal alterations - first aim is to study posteruptive and pathological changes in crystal morphology with a focus on demineralization/remineralization (demin/remin). Hypothesis is that remin may involve a different mechanism within the enamel prisms compared to the prism periphery. Demin/remin of human enamel and synthetic apatite will be monitored by constant composition methods correlated with TEM with the objective of remin of crystal core defects. Results will be compared with human white spot enamel and distinguished from any posteruptive changes. Organic matrix distribution - second aim is to determine the distribution of organic matrix in developing and mature enamel. Hypothesis is that protein is restricted in mature enamel so that most crystals have little or no protein coat. Rat, human, and synthetic apatite will be examined untreated and treated wit organic solvents to determine if stain artefacts occur in deorganified enamel. Protein distribution in human enamel will be compared to rate enamel, and developing rate enamel will be examined for ameloblast remnants. Finally, to determine the role maturation ameloblasts play in matrix removal, ameloblasts will be stripped away and the maturing enamel examined in TEM to detect changes that may occur in vitro. Histopathology - third aim is to determine how results of first two studies are modified by fluoride (F), diphosphonates, and genetic disturbances. Topical F effects of demin/remin and systemic F effects on matrix removal will be studied via TEM. Diphosphonates will continue to be studied via TEM, particularly for their effects on rat incisor enamel nucleation, growth, and recovery. Finally, genetically defective human enamel will be compared with controls for crystal and matrix alterations. Results will have relevance in developing the optimal environment for enamel caries resistance without fluorosis.
| Johnsen, D C; Weissman, B M; Murray, G S et al. (1990) Enamel defects: a developmental marker for hemifacial microsomia. Am J Med Genet 36:444-8 |
| Simmelink, J W (1987) Ultrastructural effects of diphosphonates on dental enamel. Adv Dent Res 1:356-65 |
| Simmelink, J W; Lange, A (1986) Ultrastructure of altered rat enamel beneath fluoride-induced cysts. J Oral Pathol 15:155-61 |
| Nordlund, A L; Simmelink, J W; Henell, F et al. (1986) Ultrastructure of fluoride-induced cysts in the rat molar enamel organ. Scand J Dent Res 94:327-37 |
