- 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.
BMI, Body Mass Index; Bone biomarker; Bone quality; Ethiopian Rift Valley; F-, qFluoride; Fluoride exposure; IRB, Institutional Review Board; ISE, Ion Selective Electrode; MER, Main Ethiopian Rift; NOAEL, No-Observed-Adverse-Effects-Level; Quantitative ultrasound; SOS, Speed of Sound; Speed of sound; TISAB, Total Ionic Strength Adjuster Buffer; U.S. EPA, U.S. Environmental Protection Agency; U.S. NRC, U.S. National Research Institute; WHO, World Health Organization; bw, body weight; mg/L, milligram per liter; mg/kg bw/day, milligram per kilogram body weight per day
Effect of ultrastructural changes on the toughness of bone.
The ultrastructure of bone can be considered as a conjunction between the biology and the biomechanics of the tissue. It is the result of cellular and molecular activities of bone formation, and its organization dominates the mechanical behavior of bone. Following this perspective, the objective of this review is to
Cellular and histochemical characteristics of osteoid formed in experimental fluoride poisoning
The present study on the cellular and histochemical characteristics of osteoid formed in iliac crest bone during fluoride poisoning in rabbits was carried out as there is no information available to date either on its structural or biochemical characteristics. Osteoid formation in bone is prevalent both in fluorosis and in
Anabolic effects of fluoride on bone
Fluoride exerts a biphasic action at the level of osteoblasts, on bone mineral, on bone structure and function, and in the treatment of osteoporosis. At low circulating concentrations, skeletal uptake of fluoride is limited and the effects are beneficial. At higher concentrations and greater skeletal uptake, fluoride may cause the
Fluorosis increases the risk of postmenopausal osteoporosis by stimulating interferon y
Estrogen deficiency in postmenopausal women frequently activates osteoclasts (OC), accelerates bone resorption, and leads to osteoporosis (OP). Previous studies have demonstrated that interferon y (IFNy) could increase bone resorption and may be involved in postmenopausal OP. Fluorosis also increased the risk of fractures and dental fluorosis, and fluoride may enhance osteoclast formation and
Circulating levels of sialic acid and glycosaminoglycans: a diagnostic test for ankylosing spondylitis
The circulating levels of sialic acid (N-acetylneuraminic acid) and glycosaminoglycans (GAGs) were measured in 69 patients with spinal disorders of orthopaedic interest (ankylosing spondylitis 17, osteofluorosis 6, idiopathic backache 10, osteoarthrosis 16, osteoporosis 20). The serum GAG levels showed no statistically significant change from control values in the five disorders
Related Studies :
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.
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.
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.
Related FAN Content :