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Bone mineral structure after six years fluoride treatment investigated by backscattered electron imaging (BSEI) and small angle X-ray scattering (SAXS): A case report
Abstract
NaF, a bone formation stimulating agent, is used for the treatment of
osteoporosis. Controversy exists concerning the quality of the newly
formed bone and the antifracture effectiveness(I). We report about a 70
years old woman, who had received 50 mg NaF/d for about 6 years.
Calcium or Vit D supplements had not been prescribed. She presented a
history of pain in her legs with recurrent character. Spontaneous fractures
of the metatarsal bones II and III of the left foot had occurred 6 month
before the first clinical visit in our institution. Besides mild anemia and
leukocytosis the routine laboratory tests were normal. Ionized Ca was
decreased, 25-OH-Vit D3 was slightly elevated. Radiographs of the
skeleton and bone scintigraphy showed degenerative osteoathritis. DXA
revealed: L2-L4 1.12; neck 0.65; Ward's triangle 0.51; trochanteric region
0.53 g/cm 2 (all within 1 S.D. of normal range). Due to clinical suspicion of
skeletal fluorosis with lower leg syndrome, a transiliacal bone biopsy was
taken. Histomorphometry revealed a bulky trabecular architecture, high
osteoblastic activity and an increased amount of osteoid The Goldner- and
calcium salt-stainings displayed abnormal patchy areas. Undecalcified
plastic embedded 100 µm thick ground sections were examined by BSEI
and SAXS(1). BSEI of trabecular and compact bone showed irregularly
shaped and pathologically mineralized bone areas, known as mottled
bone. SAXS in these areas revealed abnormally large mineral crystals (in all
dimensions larger than 50 nm), which from their size can only be
extrafibrillarly located. These findings correspond well to observations in
fluorosis(1). The severe deterioration of the collagen/mineral compound
and the nearly complete lack of normal "old" bone suggest biomechanical
incompetence and explain the pathological fractures.
In this patient after 6 years treatment with 50 m 9 NaF/d skeletal
fluorosis caused pain, disturbed gait and atraumatic fractures. Interestingly,
laboratory findings, skeletal radiographs and bone densitometry, gave no
indication for abnormalities of bone metabolism or mineralization. Without
bone biopsy we would have failed the correct diagnosis. Careful clinical
follow up , therefore, is undispensible whenever NaF is used for the
treatment of osteoporosis. Invasive investigation of the skeleton (bone
biopsy, histomorphometry, BSEI plus SAXS) is the only diagnostic tool,
when skeletal fluorosis is suspected.
(1) P Fratzl et al., J. Bone Miner. Res (1994) 9: 1541-1549.
... These symptoms are very similar to osteoarthritis (OA), making diagnosis more di cult. As Roschger's team concluded in 1995, SF can be a very sneaky disease highlighting the di culty of its diagnostic [14]. Many observations made in the endemic areas suggested that uoride can damage articular cartilage and even worsen OA's symptoms, and the most recent and of particular importance was done in Turkey 2001 [15][16]. ...
Background: Fluoride is an environmental chemical that has adverse effects on health, probably increasing osteoarthritis (OA) risk. However, whether fluoride is a serious risk factor for OA is still inconsistent among current evidence. The aim of this study was to determine the relationships between chronic fluoride exposure and OA risk among the residents living in Tongyu County, China 2019.
Method: 186 cases and 186 controls aged 26 to 86 years were recruited after x-ray examination with Kellgren and Lawrence criteria by two independent evaluators. Urinary fluoride (UF) in a spot sample was measured by fluoride ion-selective electrode, and water fluoride data were used as community level of exposure. Associations between fluoride exposure and OA risk were examined by the unconditional logistic regression. Covariates included age, gender, body mass index, duration of living, daily water drunk, income, sport and filter use with stratified analysis.
Results: Mean UF concentration 2.54 ± 1.22 mg/L was higher than the mean of community water fluoride concentration 1.49 ± 0.32 mg/L. The mean UF concentration 2.73 ± 1.18 mg/L was significantly higher in cases compared to 2.35 ± 1.24 mg/L in controls group (p < 0.02). In full sample analysis, a 1mg/L increase in UF level was associated with a 27% higher risk of OA (95% CI: 1.06 - 1.52, p = 0.008), and 4th quartile participants were associated with higher risk when compared to 1st quartile (OR: 2.46, 95% CI: 1.34 – 4.57, p = 0.003). In stratified analysis, compared to 1st quartile, 4th quartile participants were 4 times more likely to have OA (95% CI: 1.86 – 8.82, p = 0.000) in the non-obese group, 7.7 times more likely to have OA (95% CI: 2.58 – 25.05, p = 0.000) among adults ≤ 60-year and 12 times more likely to have OA (95% CI: 2.15 – 99.65, p = 0.008) in non-obese adult women ≤ 60-year group.
Conclusion: Water fluoride exposure may increase OA risk and could have more impact on a specific group such as non-obese and adult ≤ 60-year population.
... As Krishnamachari (1986) described, a combination of osteosclerosis, osteomalacia, and osteoporosis of varying degrees as well as exostosis formation characterizes the progression of skeletal fluorosis [223]. While F therapy has previously been used extensively in the treatment of osteoporosis, it can result in pathological changes to mineralized bone, biomechanical incompetence, and skeletal fluorosis [224,225]. While F has been found to increase bone mineral density [226], the increase in bone mass does not necessarily result in an increase in bone strength as the bone is poorly mineralized and exhibits inflammatory foci [227]. ...
In countries with fluoridation of public water, it is imperative to determine other dietary sources of fluoride intake to reduce the public health risk of chronic exposure. New Zealand has one of the highest per capita consumption rates of black tea internationally and is one of the few countries to artificially fluoridate public water; yet no information is available to consumers on the fluoride levels in tea products. In this study, we determined the contribution of black tea as a source of dietary fluoride intake by measuring the fluoride content in 18 brands of commercially available products in New Zealand. Fluoride concentrations were measured by potentiometric method with a fluoride ion-selective electrode and the contribution of black tea to Adequate Intake (AI) and Tolerable Upper Intake Level (UL) was calculated for a range of consumption scenarios. We examined factors that influence the fluoride content in manufactured tea and tea infusions, as well as temporal changes in fluoride exposure from black tea. We review the international evidence regarding chronic fluoride intake and its association with chronic pain, arthritic disease, and musculoskeletal disorders and provide insights into possible association between fluoride intake and the high prevalence of these disorders in New Zealand.
... While not everyone with pre-crippling clinical fluorosis will experience arthritic pain (Franke 1975), the evidence is clear that some people will (Singh 1963;Singh & Jolly 1970;Vischer 1970;Cook 1971;Schlegel 1974;Franke 1975;Teotia 1976;Czerwinski 1977;Boillat 1980;Carnow 1981;Czerwinski 1988;PHS 1991;Roschger 1995;Savas 2001;Eichmiller 2005). ...
Fluoride is an environmental chemical that has adverse effects on articular cartilage, probably increasing osteoarthritis (OA) risk. However, this association still needs more epidemiological evidence to clarify. The aim of this study was to determine the relationships between chronic fluoride exposure and OA risk among the residents living in Tongyu County, China, 2019, with a frequency-matched case–control study (186 OA patients and 186 healthy participants). The results showed that urinary fluoride (UF) (2.73 ± 1.18 mg/L) was significantly higher in OA patients compared to the controls (2.35 ± 1.24 mg/L) (p < 0.002). After adjustment, the odds ratios (ORs) with 95% confidence intervals (95% CIs) between the OA risk and fluoride were calculated by the unconditional logistic regression. In full sample analysis, a 1 mg/L increase in UF level was associated with a 27% higher risk of OA (1.06–1.52, p = 0.008), and 4th quarter’s participants were associated with higher risk when compared to 1st quarter (OR: 2.46, 95% CI: 1.34–4.57, p = 0.003). In stratified analysis, compared to 1st quarter, 4th quarter’s participants were 4 times more likely to have OA (1.86–8.82, p < 0.001) in the non-obese group and 7.7 times more likely to have OA (2.58–25.05, p < 0.001) among adults ≤ 60 years. In conclusion, excessive exposure of water fluoride may increase OA risk, and could have more impact on the specific population such as non-obese, and adult aged ≤ 60 years.
DNA methylation is an epigenetic modification of genome that is involved in many human diseases. Recent studies revealed DNA methylation may be associated with fluorosis. This study was aimed to evaluate the dose-response effect of fluoride on DNA methylation in human and rat blood. A commercial ELISA kit was employed to evaluate 5-methylcytosine (5-mC) level of genome in human and rat blood. A total of 281 subjects were enrolled in this study and divided into four equal-size groups by the quartile of fluoride in drinking water. The difference of 5-mC among the four groups was significant. The U-shaped relationship was found between fluoride and 5-mC in the population. The U-shaped curve was also observed in the rats with three months of fluoride treatments. Taken together, these results clue the disruption of DNA methylation in mammals may has a certain association with fluoride in natural exposures.
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