Highlights
Fluoride damaged intestinal epithelial cells.
Fluoride inhibited intestinal epithelial cells proliferation.
Fluoride disrupted expression of junctional complexes proteins.
Fluoride reduced glycoproteins secretion.
Estrogen deficiency exacerbated fluoride-induced enterotoxicity.
*Original full-text article online at: https://www.sciencedirect.com/science/article/pii/S0147651322010211?via%3Dihub
Highlights
Fluoride exacerbates obesity in HFD fed mice, while shows limited effect in ND mice.
Fluoride induced obesity is mediated by gut microbiota and intestinal barrier.
Fluoride exacerbates the obesity in HFD mice through a TLR4-dependent mechanism.
Erysipelatoclostridium ramosum was identified as a crucial mediator of fluoride induced obesity.
*Original full-text article online at: https://www.sciencedirect.com/science/article/pii/S2090123222002399
Background
Fluoride is a highly electronegative anion which, when present in saliva or other topical dental products, enhances the precipitation of calcium phosphates on the tooth enamel surface [1]. The observation that naturally fluoridated water was associated with reduced dental decay [2] lead the U.S. Public Health Service (PHS) to recommend that 1 ppm fluoride be added to the drinking water as a public health measure to prevent dental caries. In 2015, these recommendations were r
1. Introduction
Dental caries is the quintessential disease of civilization, a disease which became prevalent with the start of cereal agriculture and rampant with the start of industrial sugar production [1]. A body of evidence supports the hypothesis that a diet leading to dental caries also leads to chronic non-communicable diseases [2].
Most authoritative organizations aimed to protect public health ignore this evidence and take the view that dental caries is the only adverse side-effect
