Estimation of age at onset of linear enamel hypoplasia. New calculation tool, description and comparison of current methods

Abstract

Enamel Hypoplasia (EH) is known to be a useful indicator for wide range of detrimental factors in early childhood in past populations, such as nutritional disturbances, mechanical trauma, disease, metabolic, and/or genetic disorders. EH may be divided into three categories: pits, grooves, and lines, where the last two are referred to as “Linear Enamel Hypoplasia” (LEH). The regularity of enamel formation allows retrospective determination of the age of LEH formation. The current article reviews and compares the best‐known methods used to estimate age at LEH formation and provides a new computational tool. Growth curves for canines and incisors were developed based on tooth growth tables by previous authors. Optimal models were selected using the Akaike Information Criterion. A Microsoft Excel spreadsheet was created to calculate age at LEH formation using the most common methods. All method results were compared with an archaeological sample (44 teeth of 18 individuals from an early modern cemetery from Wrocław, Poland) and a theoretical model. The results of the methods were compared pairwise with Bland‐Altman plots. The current article provides a quick and easy‐to‐use tool for analyzing LEH chronology and comparing the results of different methods. As shown by the Bland‐Altman plots, most methods provide approximately consistent results for LEHs formed at around 2–3 years of age. However, LEHs formed particularly early or late are more prone to discrepancies between different methods. Comparison of the age at LEH formation obtained by different methods should be done carefully ‐ and the new LEH calculation tool with optimized equations provided in this publication can facilitate this process.

Life and death in the Roman period Pula – A bioanthropological analysis of human skeletal remains from the Ozad Arene site

“…Linear enamel hypoplasia (LEH) is a good indicator of metabolic stress in childhood (Littleton & Townsend, 2005;Novak et al, 2009;Dąbrowski et al, 2021). In the Pula sample, LEH is present in almost all examined incisors and canines, representing a very high prevalence of enamel defects in this population.…”

“…This high frequency is probably not related to the small sample size, as the defects were consistently present in every individual. High rates of LEH were linked to the increased physiological stress in the population because of disease, nutritional deficiencies (Littleton & Townsend, 2005;Dąbrowski et al, 2021), lifestyle based on agriculture, increase in population (Cohen & Armelagos, 1984) and population aggregation (Ham et al, 2020). This stress could result from weaning when children transition from consuming breast milk to other foods that contain microorganisms that can cause digestive distress, reduce appetite, and cause nutritional deficiencies.…”

Urban Beings

“…It was scored as present in cases where at least one tooth manifested a reduction in the normal thickness of enamel, usually in the form of horizontal grooves (Riga et al, 2014;Ritzman et al, 2008). In bioarchaeology, linear enamel hypoplasia is considered indicative of metabolic stress during childhood, as the physiological disruptions that cause it only affect the portion of the crown that is in the process of forming (Dąbrowski et al, 2021;Guatelli-Steinberg, 2004;Ritzman et al, 2008). Although the precise etiology of linear enamel hypoplasia is not well understood yet, it is most commonly associated with protein and vitamin deficiencies, childhood disease and injuries (Armelagos et al, 2009;Nunn, 2001;King et al, 2002;Tomczyk et al, 2012).…”

Nostalgia for the old country—A histological exploration of early childhood physiological stress experiences in colonial Otago, New Zealand

“…The most frequently observed surface hypoplastic defect in bioarcheological studies is linear enamel hypoplasia (LEH), transverse lines, or pits on the lateral enamel surface (Hillson, 2005). However, LEH-based studies often provide only a crude chronology of physiological stress experiences in comparison to observations of internal incremental enamel structures (Armelagos et al, 2009;Blakey, 1998;Boldsen, 2007;Dąbrowski et al, 2021;Goodman & Rose, 1990;Miszkiewicz, 2015). There has been some discussion as to whether ameloblasts are more or less sensitive to stressors at different periods of their secretory lifespan, and it has been suggested that this may influence the severity or intensity of ameloblast dysfunction (Aris & Street, 2021;Dean et al, 2020;FitzGerald et al, 2006;FitzGerald & Saunders, 2005;Kierdorf et al, 2021;Witzel et al, 2008).…”