Author: Buzalaf MA, Whitford GM.
Source: Monogr Oral Sci.
Year: 2011
Comment:
The researchers conclude, “It is clear that the beneficial as well as the adverse effects of fluoride can be attributed to the magnitude and duration of the concentration of the ion at specific tissue or cellular sites. In addition to the level of prior fluoride exposure, these concentrations are determined by the characteristics of the general metabolism of fluoride within the individual."
Abstract / Excerpt:
“Knowledge of all aspects of fluoride metabolism is essential for comprehending the biological effects of this ion in humans as well as to drive the prevention (and treatment) of fluoride toxicity. Several aspects of fluoride metabolism – including gastric absorption, distribution and renal excretion – are pH-dependent because the coefficient of permeability of lipid bilayer membranes to hydrogen fluoride (HF) is 1 million times higher than that of F(-). This means that fluoride readily crosses cell membranes as HF, in response to a pH gradient between adjacent body fluid compartments. After ingestion, plasma fluoride levels increase rapidly due to the rapid absorption from the stomach, an event that is pH-dependent and distinguishes fluoride from other halogens and most other substances. The majority of fluoride not absorbed from the stomach will be absorbed from the small intestine. In this case, absorption is not pH-dependent. Fluoride not absorbed will be excreted in feces. Peak plasma fluoride concentrations are reached within 20-60 min following ingestion. The levels start declining thereafter due to two main reasons: uptake in calcified tissues and excretion in urine. Plasma fluoride levels are not homeostatically regulated and vary according to the levels of intake, deposition in hard tissues and excretion of fluoride. Many factors can modify the metabolism and effects of fluoride in the organism, such as chronic and acute acid-base disturbances, hematocrit, altitude, physical activity, circadian rhythm and hormones, nutritional status, diet, and genetic predisposition. These will be discussed in detail in this review.”
Citation:
Buzalaf MA, Whitford GM. Fluoride metabolism. Monogr Oral Sci. 2011;22:20-36.