Amelogenesis

Abstract: Dental enamel hypoplasias are deficiencies in enamel thickness resulting from physiological perturbations (stress) during the secretory phase of amelogenesis. The results of a wide variety of experimental, clinical, and epidemiological studies strongly suggest that these defects and their associated histological abnormalities (such as accentuated stria of Retzius and Wilson bands) are relatively sensitive and nonspecific indicators of stress. Because of the inability of enamel to remodel, and the regular and ring-like nature of their development, these defects can provide an indelible, chronological record of stress during tooth crown formation. For these reasons, along with the ease with which they are studied, enamel hypoplasias have been increasingly employed as indicators of nutritional and disease status in paleopathology, and their study has begun to extend into other subdisciplines of physical anthropology. In order to provide the reader with a better understanding of the current issues in this field, we first review normal enamel development, historical advances in the study of enamel developmental abnormalities, and provide a threshold model to help conceptualize the etiology of enamel developmental defects. Specific attention is then centered on extant, fundamental issues in the use of enamel hypoplasias and histological structures as epidemiological indicators of nonspecific stress. Most enamel hypoplasias are associated with abnormal histological changes (accentuated stria of Retzius or “Wilson” and “Cluster” bands). However, the lack of association of some mild surface irregularities, characteristically seen as thin, perikymata-like surface depressions, with abnormal prism morphology suggests that these surface features may not be evidence of physiological perturbation. Methods now exist to reliably identify both histological and enamel surface defects. However, further research is needed on methods for determining the size of defects and the epidemiological significance of defect widths and depths. Similarly, the general relationship between the location of enamel hypoplasias and associated histological structures on the one hand, and an individual's age at the time of their development on the other hand, is also well understood. However, better estimates of intra- and inter-population variation in the timing of enamel matrix formation are needed before these defects can reach their full potential as chronometric measures of stresses. Lack of understanding patterns of differential susceptibility of enamekl to developmental disruption has likely hindered interpretations of the results of a number of past experiments. The seemingly strong pattern of differential suscetibility of enamel to disruption-within teeth and across tooth classes, dentitions, and taxa-may yield a number of significant clues to understanding basic issues in enamel development. Populations that are exposed to a high degree of undernutrition and disease, from prehistoric to contemporary times, share high rates of linear enamel hypoplasias. While these defects seem to relate to bouts of undernutrition and infection, their specific etiology is still unknown. In the next decade we expect to develop more precise information on the specificity and sensitivity of secretory ameloblaste to disruption. A variety of research directions are suggested for further anthropological study.

Abstract: This review focuses on the process of enamel maturation, a series of events associated with slow, progressive growth in the width and thickness of apatitic crystals. This developmental step causes gradual physical hardening and transformation of soft, newly formed enamel into one of the most durable mineralized tissues produced biologically. Enamel is the secretory product of specialized epithelial cells, the ameloblasts, which make this covering on the crowns of teeth in two steps. First, they roughly "map out" the location and limits (overall thickness) of the entire extracellular layer as a protein-rich, acellular, and avascular matrix filled with thin, ribbon-like crystals of carbonated hydroxyapatite. These initial crystals are organized spatially into rod and interrod territories as they form, and rod crystals are lengthened by Tomes' processes in tandem with appositional movement of ameloblasts away from the dentin surface. Once the full thickness of enamel has been formed, ameloblasts initiate a series of repetitive morphological changes at the enamel surface in which tight junctions and deep membrane infoldings periodically appear (ruffle-ended), then disappear for short intervals (smooth-ended), from the apical ends of the cells. As this happens, the enamel covered by these cells changes rhythmically in net pH from mildly acidic (ruffle-ended) to near-physiologic (smooth-ended) as mineral crystals slowly expand into the "spaces" (volume) formerly occupied by matrix proteins and water. Matrix proteins are processed and degraded by proteinases throughout amelogenesis, but they undergo more rapid destruction once ameloblast modulation begins. Ruffle-ended ameloblasts appear to function primarily as a regulatory and transport epithelium for controlling the movement of calcium and other ions such as bicarbonate into enamel to maintain buffering capacity and driving forces optimized for surface crystal growth. The reason ruffle-ended ameloblasts become smooth-ended periodically is unknown, although this event seems to be crucial for sustaining long-term crystal growth.

Abstract: Teeth develop from composite organ rudiments that are formed through the interaction of oral epithelium and mesenchyme of the first branchial arch; cells of the former differentiate into enamel-secreting ameloblasts whereas those of the latter differentiate into dentine-secreting odontoblasts. Experimental analysis of odontogenic tissue interactions in mammalian embryos has focused on the late developmental stages of morphogenesis and cytodifferentiation; little is known about initial pattern-forming events, during which presumptive tooth-forming cells are specified and the sites of tooth initiation become established. It requires to be shown, for example, whether the mesenchymal cells of mammalian teeth are derived, like those of amphibians, from the cranial neural crest, and if so, whether these form a specified subpopulation in the neural folds. Alternatively, are they specified after migration into the mandibular arch, possibly by interaction with the oral epithelium? The developmental potentials of mouse embryo premigratory cranial neural crest cells (CNC - explanted from the caudal mesencephalic and rostral metencephalic neural folds) have been studied in intraocular homograft recombinations with various regions of embryonic surface ectoderm. Cartilage, bone and neural tissue developed in all combinations of CNC and epithelium. Teeth formed in combinations of CNC with mandibular arch epithelium but not in combinations of CNC with limb bud epithelium. Teeth also formed in combinations of mandibular arch epithelium with neural crest explanted from the trunk level. These results indicate that mammalian neural crest has an odontogenic potential but that this is not restricted to the crest of presumptive tooth-forming levels. Normal migration appears not to be a prerequisite for expression of odontogenic potential but this does require an interaction with region-specific epithelium. It is reasonable to infer that during normal development the neural crest that enters the mandibular arch is odontogenically unspecified before or during migration and that the oral epithelium is the earliest known site of tooth pattern.