Abstract
The present study was conducted on 42 postmenopausal women subjects in Vailapally village, Nalgonda district, Andhra Pradesh, India, an endemic fluorotic area (water fluoride >4 ppm) and 34 postmenopausal women of nonfluorotic villages (water fluoride <0.4 ppm) of the Nalgonda area. The age group of the recruited subjects was 48–58 years and their years since menopause (YSM) was <10 years. Serum levels of fluoride (F), total alkaline phosphatase (ALP), tartarate resistant acid phosphatase-5b (TRAP-5b), catalase (CAT), glutathione-S-transferase (GST) and malondialdehyde (MDA) were estimated for bone mineral antioxidant and lipid peroxidation status. Significantly increased bone turnover markers ALP, TRAP-5b (p<0.01), and oxidative stress were observed with decreased levels of CAT and GST (p<0.01) activity in postmenopausal women residing in the fluorotic village. Significantly elevated levels of MDA (p<0.01) in these women compared to those in the nonfluorotic village indicated an increase in lipid peroxidation under fluoride stress.
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The toxic effect of fluoride on MG-63 osteoblast cells is also dependent on the production of nitric oxide
Some soda-lime-phospho-silicate glasses, such as Hench's Bioglass(®) 45S5, form bone-like apatite on their surface when bound to living bone. To improve their osteointegration for clinical purposes, the fluoride insertion in their structure has been proposed, but we recently showed that fluoride causes oxidative damage in human MG-63 osteoblasts, via inhibition
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Fluoride-induced oxidative stress of osteoblasts and protective effects of baicalein against fluoride toxicity
The key role of osteoblasts in skeletal fluorosis makes the exploration of the possible mechanisms of the fluoride-induced oxidative stress of osteoblasts of great importance. In this article, the in vitro effects of fluoride on the oxidative stress of osteoblasts are presented. To study the inhibitory effect of baicalein on
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Fluoride increases the susceptibility of developmental dysplasia of the hip via increasing capsular laxity triggered by cell apoptosis and oxidative stress in vivo and in vitro.
Highlights Fluoride does not cause DDH directly but increases its susceptibility by increasing hip capsular laxity. Hip laxity results from apoptosis occurring in capsular fibroblast after fluoride exposure. Fluoride-induced fibroblast apoptosis was triggered by oxidative stress via mitochondrial pathway. The etiology of developmental dysplasia of the hip (DDH) is multifactorial,
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Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.
Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts,
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WITHDRAWN: Co-exposure effects of arsenic and fluoride on intelligence and oxidative stress in school-aged children: a cohort study.
This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. as of November 6, 2020 Highlights Pioneer biomonitoring study on rural children to address As and F- co-exposure. High dental Fluorosis found in relation to urinary As and F- levels in
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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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"Pre-Skeletal" Fluorosis
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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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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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.
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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.
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