The association between fluoride concentrations and spontaneous humeral fracture in first-lactation dairy cows: results from two New Zealand studies.

Aim: To assess whether the fluoride concentration in the humeri of first-lactation, 2-year-old dairy cows with a spontaneous humeral fracture is significantly different from that of first-lactation, 2-year-old dairy cows without a humeral fracture.
Methods: Two studies were conducted, the first with nine bone samples from 2-year-old, first-calving dairy cows with a humeral fracture (all from the Waikato region) age-matched with seven control bone samples from the Waikato, Bay of Plenty and Manawatū-Whanganui regions. The second study used 26 bone samples from 2-year-old, first-lactation dairy cows with a humeral fracture (from the Otago, Canterbury, Southland, West Coast, Waikato and Manawatū-Whanganui regions) age-matched with 14 control bone samples (all from the Manawatū-Whanganui region or unknown). Control bone samples were from first-lactation, 2-year-old dairy cows that did not have humeral fractures. Bone fluoride concentration was quantified for all samples.
Results: The median fluoride concentration of humeri from first-lactation, 2-year-old dairy cows with a humeral fracture was significantly higher than humeri from unaffected control cows in both studies. In Study 1, the median bone fluoride concentration was 599 (IQR 562.7-763.5) mg/kg from case cows and 296.6 (IQR: 191.2-391.7) mg/kg from control cows (p < 0.001), and in Study 2 the median bone fluoride concentration from case and control cows was 415 (IQR: 312.5-515) mg/kg and 290 (IQR: 262.5-410) mg/kg (p = 0.04) respectively.
Conclusions and Clinical Relevance: Although there are limitations to this study due to the unbalanced regional distribution of cases and controls, the results indicate that sub-clinical fluoride toxicosis may be linked to spontaneous humeral fractures in first-lactation dairy cows in New Zealand. Further research is required to determine if bone fluoride concentrations play a role in the pathogenesis of these fractures.