- A novel ultrasonic bone quality biomarker was tested in a population with low to high exposure to F.–
- Negative associations were found between F– exposure and bone quality
- Decreased bone quality reflects net bone loss, abnormal mineralization and altered collagen.
- The finding highlights that F– exposure has complex effects on bone quality that go beyond changes in bone density alone.
Background: Various studies, mostly with animals, have provided evidence of adverse impacts of fluoride (F–) on bone density, collagen and microstructure, yet its effects on overall bone quality (strength) has not been clearly or extensively characterized in human populations.
Objective: In this observational study, we assessed variation in an integrated measures of bone quality in a population exposed to wide-ranging F– levels (0.3 to 15.5 mg/L) in drinking water, using a novel application of non-ionizing ultrasonic method.
Method: We collected 871 speed of sound (SOS) measurements from 341 subjects residing in 25 communities, aged 10-70 years (188 males and 153 females). All subjects received scans of the cortical radius and tibia, and adults over the age of 19 received an additional scan of the phalanx. Associations between F– in drinking water and 24-h urine samples, and SOS as a measure of bone quality, were evaluated in bivariate and multivariable regressions adjusting for age, sex, BMI, smoking, and toothpaste use.
Results: We found negative associations between F– exposure and bone quality at all three bones. Adult tibial SOS showed the strongest inverse association with F– exposure, which accounted for 20% of the variance in SOS measures (r = 0.45; n = 199; p < 0.0001). In adjusted analysis, a 1 mg/L increase in F– in drinking water was related to a reduction of 15.8 m/s (95% CI: -21.3 to -10.3), whereas a 1 mg/L increase in 24-h urinary F– (range: 0.04-39.5 mg/L) was linked to a reduction of 8.4 m/s (95% CI: -12.7, -4.12) of adult tibial SOS. Among adolescents, in contrast, weaker and non-significant inverse associations between F– exposure and SOS were found, while age, gender, and BMI were more significant predictors than in adults.
Conclusions: These results are indicative of a fluoride-induced deterioration of bone quality in humans, likely reflecting a combination of factors related to SOS: net bone loss, abnormal mineralization and collagen formation, or altered microarchitecture. The portable and low-cost ultrasound technique appears potentially useful for assessment of bone quality, and should be tested in other locations and for other bone-related disorders, to assess the feasibility of its more extensive diagnostic use in hard-to-reach rural regions.
Acknowledgements and funding
This work was initiated through the NIH K99/R00 grant support that has a goal of understanding F– related mineralized tissue disorders and other potential health consequences in the Ethiopian Rift Valley population. We are immensely grateful for the NIEHS‘s career development grant (K99/R00 ES023472). We thank all the children and parents who participated in this study, and the local water bureaus for their help in recruiting them as well as guiding us during the field work. The content expressed in this paper is the responsibility of the authors and does not necessarily reflect the official views of the NIH.
*Original abstract online at https://www.sciencedirect.com/science/article/pii/S2352187219300415
Denser but Not Stronger? Fluoride-Induced Bone Growth and Increased Risk of Hip Fractures.
Abstract Since the mid-1940s, fluoride has been added to toothpaste and (in some countries) tap water, table salt, or milk to reduce dental cavities.1 Although low-level fluoride supplementation prevents cavities, higher levels cause white mottling of the teeth.2 What is more, some studies suggest fluoride in drinking water may increase the
Association between low-to-moderate fluoride exposure and bone mineral density in Chinese adults: Non-negligible role of RUNX2 promoter methylation.
Highlights RUNX2 promotor methylation is positively related to excessive fluoride (F) exposure. Bone mineral density (BMD) is negatively related to excessive F exposure in women. BMD is negatively associated with RUNX2 promotor methylation in women. RUNX2 methylation mediates the association of excessive F exposure and BMD in women. Bone mineral density
Fluoride exposure and CALCA methylation is associated with the bone mineral density of Chinese women.
Highlights Excessive fluoride exposure is positively related to CALCA methylation in women. CALCA methylation in Chinese women is negatively associated with BMD. Long-term excessive fluoride exposure is negatively related to BMD in women. BMD in women with CALCA hypermethylated is more susceptible to fluoride. The statistical associations are age-specific
[Osteofluorosis caused by excess use of toothpaste].
BACKGROUND: Osteofluorosis is caused by chronic fluoride intoxication. Fluoride is used in toothpaste for the prevention of dental caries, and dental fluorosis has often been reported among children and attributed to ingestion of fluoride toothpaste. We report a case of chronic fluoride intoxication caused by excess use of toothpaste in
Fluoride in Drinking Water, Diet, and Urine in Relation to Bone Mineral Density and Fracture Incidence in Postmenopausal Women.
Background: Although randomized controlled trials (RCTs) have demonstrated that high fluoride increases bone mineral density (BMD) and skeletal fragility, observational studies of low-dose chronic exposure through drinking water (<1.5mg/L, the maximum recommended by the World Health Organization) have been inconclusive. Objective: We assessed associations of fluoride in urine, and intake via
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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