Dental Stress Indicators from Micro‐ to Macroscopic

Guatelli‐Steinberg, Debbie

doi:10.1002/9781118845486.ch27

Cited by 18 publications

(19 citation statements)

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“…The secretory phase of amelogenesis can be disrupted in such a way as to lead to reductions in enamel thickness, for example, linear enamel hypoplasias (LEH) (Hubbard, Guatelli‐Steinberg, & Sciulli, ; Guatelli‐Steinberg, ). Across animals and humans, the function of ameloblasts, cells which secrete a protein matrix into which mineral is embedded, is often reduced or impaired during periods of physiological stress, and, notably, malnutrition (Goodman & Rose, ; Hillson, ; May et al, ).…”

Section: Measuring Stressmentioning

confidence: 99%

In sickness and in death: Assessing frailty in human skeletal remains

Marklein

Leahy

Crews

2016

American J Phys Anthropol

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Stress plays an important role in the etiology of multiple morbid and mortal outcomes among the living. Drawing on health paradigms constructed among the living augments our evolving knowledge of relationships between stress and health. Therefore, elucidating relationships between stress and both chronic and acute skeletal lesions may help clarify our understanding of long-term health trends in the past. In this study, we propose an index of "skeletal frailty," based on models of frailty used to evaluate the life-long effects of stress on health among living populations. Here, we assess the possible applicability of frailty to archaeological populations. The skeletal frailty index (SFI) is proposed as a methodological liaison between advances made by biological anthropologists studying relationships between stress and health among the living and bioarchaeologists studying stress and health among the dead. In a case study examining skeletal stress in Medieval London, the SFI is applied to nonmonastic (N = 60) and monastic (N = 74) samples. We used analysis of variance/analysis of covariance to compare SFI values between nonmonastic-monastic groups, sexes, and age cohorts. Results indicate higher lifetime morbidity among monastic groups. These results complement previous bioarchaeological findings on the same London populations, wherein lower risks of mortality and longer lifespans were observed for monastic populations. SFI data reflect the morbidity-mortality paradox observed in modern populations and accompany recent findings in bioarchaeology of variation in Medieval monastic and nonmonastic "health." Ultimately, this study demonstrates the SFI's utility in bioarchaeology, through its application of commonly assessed skeletal biomarkers, its ease of applicability, and its potential usefulness for assessing changes in skeletal health over time and across specific geographies.

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Section: Measuring Stressmentioning

confidence: 99%

In sickness and in death: Assessing frailty in human skeletal remains

Marklein

Leahy

Crews

2016

American J Phys Anthropol

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“…Enamel hypoplasia occurs during the secretory stage of formation, whereas other enamel defects form during the maturation stage, e.g., hypocalcification and dental fluorosis (Ten Cate, 1994;Guatelli-Steinberg, 2015;Xing et al, 2015). Defects take a variety of forms, most of which have been found in fossil hominins (e.g., Tobias, 1967;Goodman et al, 1987;Moggi-Cecchi, 2000;Lukacs et al, 2001;Guatelli-Steinberg et al, 2004;Xing et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

A probable genetic origin for pitting enamel hypoplasia on the molars of Paranthropus robustus

Towle

2019

Journal of Human Evolution

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We report the frequencies of linear enamel hypoplasia (LEH) and, specifically, pitting enamel hypoplasia (PEH) defects in the teeth of Paranthropus robustus, for comparison with four other South African hominin species and three extant nonhuman primate species. Unlike LEH, the lesser known PEH is characterized by multiple circular depression defects across a tooth crown and is often difficult to interpret in terms of developmental timing and etiology. Teeth in all samples were examined macroscopically with type, position and number of defects recorded. Frequencies of teeth with LEH vary among hominin species, but the differences in PEH are considerable. That is, P. robustus has much higher rates of pitting defects, with 47% of deciduous teeth and 14% of permanent teeth affected, relative to 6.7% and 4.3%, respectively, for all other hominin teeth combined; none of the extant primate samples evidence comparable rates. The defects on P. robustus molars are unlike those in other species, with entire crowns often covered in small circular depressions. The PEH is most consistent with modern human examples of amelogenesis imperfecta. Additionally, the defects are: 1) not found on anterior teeth, 2) uniform in shape and size, and 3) similar in appearance/severity on all molars. A possible reason for this form of PEH is as a side effect of selection on another phenotype that shares the same coding gene(s), i.e., a genetic origin. Recent research on the ENAM gene provides one such possibility. Paranthropus likely underwent rapid evolution in the ENAM loci, with changes in this gene contributing to larger posterior teeth and thicker enamel. This same gene is associated with amelogenesis imperfecta; therefore, pleiotropy effects, relating to high selection on this gene during Paranthropus evolution, could have yielded this unique condition.

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“…The uniform pattern on anterior teeth, and lack of same on the molars, strongly suggests the defects are not related to physiological stress during development. 2,22,23 Further, the defects do not resemble those caused by congenital viruses, vitamin deficiencies, malnutrition, fluorosis or other mineral contaminants in humans. [24][25][26] A congenitally missing tooth may further support an AI diagnosis because these conditions often co-occur.…”

Section: Discussionmentioning

confidence: 99%