Assessment of systemic physiological perturbations from dental enamel hypoplasias and associated histological structures

Abstract

KEY WORDSEnamel hypoplasia, dental histology, stress 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 a n 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 epidemiclogical 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 a n 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 0 1990 Wiley-Liss, Inc.

Skeletal and dental indicators of health in the late mediaeval (12–15th century) population from Nin, southern Croatia

“…Caries size was classified into four categories according to Metress and Conway (1975): 1) pit or slight fissural start of lesion, 2) lesion covering less than 50% of the tooth's surface, 3) lesion covering over 50% of the tooth's surface, and 4) lesion that has completely destroyed the crown with only the root remaining. The presence of dental enamel hypoplasia was analyzed on the permanent maxillary central incisors and on the permanent maxillary and mandibular canines for the following reasons: 1) central incisors and canines are more susceptible to hypoplastic defects than other teeth (Goodman and Rose, 1990); 2) canines develop and grow for a relatively long time -from the fourth month to the sixth year of life; 3) incisors and canines have the lowest amount of mineralized dental deposits which sometimes may cover the crown of the teeth and prevent determination of the presence of hypoplasia. All skulls with preserved both orbital roofs were macroscopically examined under powerful illumination for the possible presence of cribra orbitalia.…”

Limiting the impact of destructive analytical techniques through sequential microspatial sampling of the enamel from single teeth

“…To be counted as accentuated striae of Retzius, bands of dense enamel had to be visible from the enamel surface to the dentine-enamel junction (see Rose and Goodman 1990;Fitzgerald and Saunders 2005). The frequency and timing of periods of physiological disruption were documented for each individual in the sample.…”

Vida y muerte en el Perú colonial: inicios de la bioarqueología en Lambayeque histórico (1536-1750 d.C.)

“…4, superior). Estos defectos se asocian a las formas agudas de estrés a partir de infección, nutrición inadecuada y diarrea al momento del destete (Goodman y Rose 1990). Las HLE son observables macroscópicamente y bajo una lupa de mano de diez aumentos, lo que ayuda a definir las variaciones normales de los perikymata y la hipoplasia del esmalte.…”