Insights from the inside: Histological analysis of abnormal enamel microstructure associated with hypoplastic enamel defects in human teeth (original) (raw)
Related papers
Journal of Anatomy, 2006
We studied the relationship between the macroscopic appearance of hypoplastic defects in the dental enamel of wild boar and domestic pigs, and microstructural enamel changes, at both the light and the scanning electron microscopic levels. Deviations from normal enamel microstructure were used to reconstruct the functional and related morphological changes of the secretory ameloblasts caused by the action of stress factors during amelogenesis. The deduced reaction pattern of the secretory ameloblasts can be grouped in a sequence of increasingly severe impairments of cell function. The reactions ranged from a slight enhancement of the periodicity of enamel matrix secretion, over a temporary reduction in the amount of secreted enamel matrix, with reduction of the distal portion of the Tomes’ process, to either a temporary or a definite cessation of matrix formation. The results demonstrate that analysis of structural changes in dental enamel allows a detailed reconstruction of the reaction of secretory ameloblasts to stress events, enabling an assessment of duration and intensity of these events. Analysing the deviations from normal enamel microstructure provides a deeper insight into the cellular changes underlying the formation of hypoplastic enamel defects than can be achieved by mere inspection of tooth surface characteristics alone.
Enamel mineralization in the absence of maturation stage ameloblasts
Archives of Oral Biology, 2009
The role of maturation stage ameloblasts is not clear yet. The aim of this study was to verify to which extent enamel mineralizes in the absence of these cells. Maturation stage ameloblasts and adjacent dental follicle cells from rat lower incisors were surgically removed and the limits of this removal were marked by notches made in the enamel. Histological analysis confirmed that the ameloblasts had been removed within the limits of the notches. The teeth erupted and when the notches appeared in the mouth, the enamel in the experimental teeth was hard but whitish compared to the yellowish colour of the contralateral incisors used as control. SEM images revealed similar enamel rod arrangement in both groups. Decreased mineral content was observed in some specimens by polarized light microscopy, and microhardness values were much lower in the experimental teeth. FTIR analysis showed that higher amounts of protein were found in most experimental teeth, compared with the control teeth. Enamel proteins could not be resolved on 15% SDS-PAGE gels, suggesting that most of them were below 5 kDa. These results suggest that the enamel matured in the absence of ameloblasts has increased protein content and a much lower mineral content, suggesting that maturation stage ameloblasts are essential for proper enamel mineralization.
Enamel maturation: a brief background with implications for some enamel dysplasias
Frontiers in physiology, 2014
The maturation stage of enamel development begins once the final tissue thickness has been laid down. Maturation includes an initial transitional pre-stage during which morphology and function of the enamel organ cells change. When this is complete, maturation proper begins. Fully functional maturation stage cells are concerned with final proteolytic degradation and removal of secretory matrix components which are replaced by tissue fluid. Crystals, initiated during the secretory stage, then grow replacing the tissue fluid. Crystals grow in both width and thickness until crystals abut each other occupying most of the tissue volume i.e. full maturation. If this is not complete at eruption, a further post eruptive maturation can occur via mineral ions from the saliva. During maturation calcium and phosphate enter the tissue to facilitate crystal growth. Whether transport is entirely active or not is unclear. Ion transport is also not unidirectional and phosphate, for example, can diff...
The Anatomical record, 1977
During renewal of the enamel organ in the rat incisor cohorts of epithelial cells are transported sequentially through presecretory, secretory and maturation zones to the gingival margin where the life cycles of these cells terminate. This process was examined kinetically by determining the absolute flux of cells within each of these zones of amelogenesis. It was found that the efflux of ameloblasts, stratum intermedium and papillary layer cells from the presecretory zone was about equal to the efflux plus expected growth within the secretory zone. However, between the secretory and maturation zones about 50% more ameloblasts entered the maturation zone than were required to account for the egress at the gingival margin and the expected growth. Since there was no similar imbalance between these zones for papillary layer cells, it was concluded that this discrepancy must represent a 50% reduction in the size of the ameloblast population during the maturation stage of amelogenesis. It...
Enamel hypoplasia in an early medieval population of Prząsław ( 11-12 th century )
2014
The aim of the study was to determine the frequency of enamel hypoplasia, and to estimate the developmental age at formation of the earliest hypoplastic defect in the permanent teeth of individuals buried at the early medieval cemetery in Prząsław. Analysis included teeth from 41 adult individuals (22 male and 19 female). In total, assessment was performed for 795 permanent teeth. Bone and tooth preservation quality was estimated as satisfactory. Enamel hypoplasia in permanent teeth was found in 34% of adult individuals, which is slightly lower than the frequency rate found in other studies on historic bone materials. The higher frequency of teeth with hypoplastic defects in women compared with men may be explained by the higher ecosensitivity of the male sex, but also by economic, social and cultural preference factors and parental investments. The retrospective analysis of stress episodes in early childhood revealed the increased frequency of factors disturbing ameloblast metaboli...
Endocytosis and Enamel Formation
Enamel formation requires consecutive stages of development to achieve its characteristic extreme mineral hardness. Mineralization depends on the initial presence then removal of degraded enamel proteins from the matrix via endocytosis. The ameloblast membrane resides at the interface between matrix and cell. Enamel formation is controlled by ameloblasts that produce enamel in stages to build the enamel layer (secretory stage) and to reach final mineralization (maturation stage). Each stage has specific functional requirements for the ameloblasts. Ameloblasts adopt different cell morphologies during each stage. Protein trafficking including the secretion and endocytosis of enamel proteins is a fundamental task in ameloblasts. The sites of internalization of enamel proteins on the ameloblast membrane are specific for every stage. In this review, an overview of endocytosis and trafficking of vesicles in ameloblasts is presented. The pathways for internalization and routing of vesicles are described. Endocytosis is proposed as a mechanism to remove debris of degraded enamel protein and to obtain feedback from the matrix on the status of the maturing enamel. Enamel formation is a unique process that coordinates the movement of proteins and ions between ameloblasts and the developing extracellular matrix (Smith and Nanci, 1996; Lacruz et al., 2013b). The extracellular matrix represents a sealed compartment between ameloblasts and the mineralized dentin without direct access to the vascular system or the connective tissue compartment (Bronckers, 2016). The transport of proteins and ions between ameloblasts and matrix for crystal mineralization is controlled by ameloblasts. As the enamel organ develops, the inner epithelial cells differentiate into polarized ameloblasts. The two key protein transport functions of ameloblasts are the secretion and the resorption of enamel proteins. Ameloblasts secrete enamel proteins at the surface of forming enamel that assemble into a scaffold to initiate and lengthen the growing mineral crystals (Smith et al., 2016). As enamel proteins are selectively cleaved by proteinases, fragments and perhaps some almost intact proteins are removed from the matrix via endocytosis by ameloblasts, a process that speeds up over time as enamel formation continues (Reith and Cotty, 1967; Smith, 1979; Kallenbach, 1980a,b). The freed up space is then utilized to widen the individual enamel ribbons. The final product contains <5% of proteins and water (Schmitz et al., 2014). The failure of efficient removal of enamel proteins and deposition of mineral results in hypomineralized or hypomature enamel. The enamel proteins constitute the protein backbone of the enamel matrix and include amelogenin, ameloblastin, and enamelin. All of them are part of the cluster called secreted calcium-binding phosphoproteins