- 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 (BMD) changes were reported to be associated with excessive fluoride exposure and abnormal expression of RUNX2. However, whether the alteration of methylation status, a most commonly used marker for the alteration of gene expression in epidemiological investigation, of RUNX2 is associated with low-to-moderate fluoride exposure and BMD changes has not been reported. Our study aims to explore the role of RUNX2 promoter methylation in BMD changes induced by low-to-moderate fluoride exposure. A total of 1124 adults (413 men and 711 women) were recruited from Kaifeng City in 2017. We measured BMD using ultrasound bone densitometer. Concentrations of urinary fluoride (UF) were measured using ion-selective electrode, and the participants were grouped into control group (CG) and excessive fluoride group (EFG) according to the concentration of UF. We extracted DNA from fasting peripheral blood samples and then detected the promoter methylation levels of RUNX2 using quantitative methylation-specific PCR. Relationships between UF concentration, RUNX2 promoter methylation and BMD changes were analyzed using generalized linear model and logistic regression. Results showed in EFG (UF concentration > 1.6 mg/L), BMD was negatively correlated with UF concentration B: -0.14; 95%CI: -0.26, -0.01) and RUNX2 promoter methylation (B: -0.13; 95%CI: -0.22, -0.03) in women. The methylation rate of RUNX2 promoter increased by 2.16% for each 1 mg/L increment in UF concentration of women in EFG (95%CI: 0.37, 3.96). No any significant associations between UF concentration, RUNX2 promoter methylation, and BMD were observed in the individuals in CG. Mediation analysis showed that RUNX2 promoter methylation mediated 18.2% (95% CI: 4.2%, 53.2%) of the association between UF concentration and BMD of women in EFG. In conclusion, excessive fluoride exposure (>1.6 mg/L) is associated with changes of BMD in women, and this association is mediated by RUNX2 promoter methylation.
*Original abstract online at https://www.sciencedirect.com/science/article/abs/pii/S0147651320308708
Bone quality in fluoride-exposed populations: A novel application of the ultrasonic method.
Highlights 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
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
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
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
A Case of Fluorosis: Fluoride-Induced Osteopetrosis.
There are multiple etiologies of increased bone density, including osteopetrosis and fluorosis. Osteopetrosis can either be a malignant autosomal recessive condition found in children or a benign autosomal dominant adult variant; both of which are characterized by decreased bone resorption. In contrast, fluorosis is characterized by increased bone formation secondary
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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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