Signatures of stress: Pilot study of accentuated laminations in porcine enamel

Abstract

ObjectivesTo examine the correspondence between histology of defective enamel and documented developmental stressors using a pig proxy; with the ultimate goal of differentiating, within enamel, stressor types including birth, weaning, surgery, and social disruption.Materials and methodsLower first molars were removed from five female and four male domestic pigs, thin‐sectioned and examined with phase‐contrast microscopy for daily and accentuated laminations. Known stressor events include birth; processing (nonanesthetized clipping of needle teeth, tail docking, and castration) within 5 days of birth; weaning in nursery; penned vaccination 2–4 days later; transfer to grower barn; additional vaccination. Timing of accentuated laminations was derived from counts of daily laminations from birth and between accentuated laminations; or, more commonly, from measurements between accentuated laminations divided by average daily lamination width.ResultsAcknowledging our small sample, we confirm daily periodicity of laminations in pig enamel. Lamination width varies among sexes (males wider), cusps, crown decile, and enamel depth (wider toward surface). Accentuated laminations occurred at reconstructed median ages of 3.7 days after birth (cf. up to 5 days for “processing”), 19.7 days (cf. 18–25 days for weaning), 4.5 days (cf. 2–4 days for vaccination) and ~39.5 days (cf. 63 days for transfer).DiscussionEncouragingly, the timing of known stressors (birth, surgical processing, weaning, and vaccination) can be determined with high precision, in good thin sections, from accentuated laminations in pig enamel. Timing of transfer was poorly estimated, likely reflecting lesser severity and the occurrence of undocumented stress events in the nursery.

Assessment of physiological disturbances during pre‐ and early postnatal development based on microscopic analysis of human deciduous teeth from the Late Epipaleolithic site of Shubayqa 1 (Jordan)

“…Previous studies (e.g., Dirks et al, 2002Dirks et al, , 2010FitzGerald et al, 2006;FitzGerald & Saunders, 2005;Goodman & Rose, 1990;Lorentz et al, 2019;Schwartz et al, 2006;Skinner & Byra, 2019) employing microscopic analysis of microstructural alterations to assess disruptions of amelogenesis exclusively focused on the registration of ALs. In the present study we broadened this perspective and, in addition to ALs, also considered less marked although clearly discernible deviations from a regular enamel microstructure as Liversidge et al (1998).…”

“…What had caused the impairment of pre‐ and postnatal enamel formation in the Shubayqa 1 individuals cannot be inferred from the recorded enamel changes as these represent unspecific reactions of secretory ameloblasts that can be triggered by wide variety of factors (FitzGerald & Rose, 2000; FitzGerald & Saunders, 2005; Goodman & Rose, 1990; Hillson, 2014; Kierdorf et al, 2004; Kierdorf & Kierdorf, 1997; Schwartz et al, 2006; Skinner & Byra, 2019; Witzel et al, 2008).…”

“…This might also have been the case at Shubayqa 1, but our sample is too small for such an analysis. Age-at-death profiles provide an insight in a population's adaptive success, as infant deaths are influenced by the ability to provide biocultural means for offspring survival (Lewis & Gowland, 2007;Rousham & Humphrey, 2002 , 1990;Hillson, 2014;Kierdorf et al, 2004;Kierdorf & Kierdorf, 1997;Schwartz et al, 2006;Skinner & Byra, 2019;Witzel et al, 2008).…”

“…Deviations from the normal enamel microstructure (i.e., abnormal bending of the prism course, formation of aprismatic enamel, marked constrictions of prism diameters, and disruption of prism continuity) were used to identify periods of physiological disturbance impairing enamel matrix formation (FitzGerald et al, 2006;FitzGerald & Saunders, 2005;Hillson, 2014;Schwartz et al, 2006;Skinner & Byra, 2019). Identification of ALs in enamel was based on previously described criteria (FitzGerald & Rose, 2000;FitzGerald & Saunders, 2005;Goodman & Rose, 1990;Gustafson & Gustafson, 1967;Hillson, 2014 the EDJ to the OES.…”

“…Externally, periods of impaired enamel matrix secretion manifest as enamel hypoplasia, that is, as a deficiency in the amount of enamel formed, while internally they manifest as accentuated lines (ALs) or zones of prismless (aprismatic) enamel (Dirks et al, 2002, 2010; FitzGerald & Saunders, 2005; FitzGerald, Saunders, Bondioli, & Macchiarelli, 2006; Goodman & Rose, 1990; Gustafson & Gustafson, 1967; Hillson, 2014; Hillson & Bond, 1997; Kierdorf & Kierdorf, 1997; Kierdorf, Kierdorf, Richards, & Josephsen, 2004; Kierdorf, Kierdorf, Richards, & Sedlacek, 2000; Lorentz et al, 2019; McGrath et al, 2018; Skinner & Byra, 2019; Witzel et al, 2006, 2008). Different types of enamel hypoplasia (plane, furrow, and pit‐type) are distinguished that are considered to reflect varying intensity and duration of impairment of the synthetic/secretory activity of the ameloblasts (Hillson, 2014; Hillson & Bond, 1997; Witzel et al, 2008).…”