Human Biology Open Access Pre-Prints

Document Type

Article

Anticipated Volume

95

Anticipated Issue

1

Abstract

Existing research supports both embodiment of stress through epigenetics and epigenetic impacts on dental development. Two models for embodiment of stress in dental development are proposed. Stress-delay proposes that increased stress during development will produce delays in dental development. Inflammation-acceleration proposes that increased stress will produce faster dental development through inflammatory pathways. These models were tested on dental development scores from the New Mexico Decedent Image Database by using non-accidental manner of death (homicide, suicide, and natural) as a proxy for elevated stress exposure during life and cadaver BMI percentile as a proxy for living BMI. Sex was treated as a positive control because females typically show more rapid dental development than males. Non-accidental manner of death and male sex were both associated with slower dental development; however, manner of death was only significant for 7/32 teeth. Mean BMI percentile was highest for natural manner of death and lowest for homicide. These findings support the stress-delay model while also according with existing studies that found limited evidence for embodied effects on dental development being sufficiently large to affect estimates of age.

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