Enamel Hypoplasia, Fluoride Toxicosis and Bison

An appreciation for the palaeoecology of prey species is a recognised necessity for modelling prehistoric human subsistence behaviours, such as the interaction between humans and bison on the North American Great Plains from the late Pleistocene into the Holocene. Previous investigations have emphasised the prominence of dental enamel hypoplasia (DEH) in such studies, where it has been valued both as a palaeoclimate proxy and an indicator of seasonally-variable stress. However, DEH is a common response to multiple pathological agents, making the isolation of specific aetiologies difficult. It is hypothesised, however, that DEH was related to common seasonal variables (birthing, weaning, and forage quality) and thus exacerbated by external stimuli such as human hunting pressure, drought and winter conditions. In this paper, fluoride toxicosis was examined as a potential contributor to this DEH formation.

Dental enamel hypoplasia

DEH is a deficency in enamel thickness stemming from the temporary cessation of amelogenesis. Among prehistoric bison, hypothesised causes include: foetal nutritional strain related to departure from umbilical input, juvenile nutritional upset caused by weaning, dietary stress stemming from seasonal changes and vitamin deficiencies reflecting photoperiodicity.

Fluoride toxicosis

Fluorides are beneficial in moderation, but overdose is hazardous. In the absence of industrial output and agricultural contamination, animals are typically introduced to excess fluoride via long-term ingestion of geothermal waters and by foraging in areas of volcanic soils. Prehistoric bison regularly utilising such environments may have invited toxicosis. With intoxication, new-forming hard tissues readily absorb excess fluoride, causing chronic diarrhoea, low milk yield, anaemia, cachexia, and marrow atrophy. As bones absorb fluorine, hydroxyls are replaced on the apatite lattice, resulting in a weakened structure prompting compensatory growth that can engender lameness-inducing hyperostosis, osteosclerosis, osteomalacia, and osteoporosis in long bones.

Enamel fluorosis is characterised by mottling and hypomineralisation of incisive and cheek dentition, and hypoplasia if toxicosis occurs during enamel formation. Enamel softened by fluorosis is prone to aberrant wear, which can result in reduced feed intake, premature senescence, diminished body condition and retarded milk production.


The characteristic mottling and/or enamel chalkiness were absent on the teeth studied. No significant inter-site difference in cusp attrition were apparent. Pedal elements are likewise devoid of osteofluorosis and bear no pathologies beyond limited articular surface exostosis, common in larger and older-aged individuals. A single metacarpal displayed a small ossified haematoma on the anteromedial aspect of the proximal metaphysis, but lameness is not implied.

DEH was significantly abundant at one site (Frasca), but only generally more so at Lamb Spring when compared to Hudson-Meng and Jones-Miller. DEH was significantly more prevalent on the second molars and less so on the third molars. Seasonal estimates suggest fairly consistent timing among modern and archaeological populations, coinciding with late summer/early autumn of the first year and spring of the first and second years, assuming May calving.


  • The over-abundance of molars with DEH and the significantly worn M1 occlusal surfaces at Frasca may indicate fluoride toxicosis. However, the lack of aberrant wear, combined with a dearth of supporting evidence, speaks against a chronic condition.
  • The relative consistency of DEH frequencies across all examined sites supports the idea of common agents.


Byerly, R.M. 2007. Palaeopathology in late Pleistocene and early Holocene Central Plains bison: dental enamel hypoplasia, fluoride toxicosis and the archaeological record. Journal of Archaeological Science 34: 1847-1858


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