Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone diease and deformities in India: Year 2000

Teotia, M; Teotia, S. P. S.; Singh, Kartar

doi:10.1007/bf02761130

Cited by 82 publications

(51 citation statements)

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“…In India, there is evidence that when calcium intake is marginal, fluoride in drinking water induces rickets which is cured by calcium supplementation. 12 There is also a report that strontium in the soil can have a similar effect. 36 In contrast to an earlier report from Tanzania, 37 Thacher and colleagues 32 found no differences in the source of water between patients and controls living around Jos, but they did not report fluoride concentrations.…”

Section: Discussionmentioning

confidence: 96%

“…[6][7][8][9] More recently there have been reports of rickets apparently caused by calcium deficiency in Bangladesh 10 and also Colombia, 11 whereas the rickets associated with dietary calcium deficiency in India appears to be linked to fluoride toxicity. 12 Some evidence of healing of rickets with calcium has been reported from South Africa [13][14][15] and in Nigerian infants, 4 but this has remained controversial. Recently, following our preliminary report 16 in which we described clinical and radiological improvement in seven patients with calcium supplementation alone, our results have been confirmed by Thacher and colleagues.…”

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confidence: 99%

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Radiological and biochemical resolution of nutritional rickets with calcium * COMMENTARY

Oginni

Sharp²,

Badru³

et al. 2003

Archives of Disease in Childhood

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Aims: To determine the response to oral calcium in Nigerian children with rickets. Methods: In a teaching hospital in Western Nigeria, 26 children (13 boys, 13 girls, aged 2-5 years) with confirmed rickets received calcium lactate (2.7 g/day). Results: Within one month of treatment leg pain was relieved and the children were more active. The mean x ray score improved from 3.3 at baseline to 1.7 at three months and 0.9 at six months (arbitrary scoring system, 0-6). Twelve cases were healed radiologically after six months, 11 others improved considerably, two showed no significant improvement, and a non-compliant patient was worse. There was progressive reversal of biochemical features. Median plasma alkaline phosphatase fell from 519 (range 178-1078) to 283 (209-443) IU/l (p = 0.04) in four months, while mean 1,25-dihydroxyvitamin D fell from 473 (251-1057) to 281 (155-481) pmol/l (p = 0.04), and mean plasma calcium increased from 2.26 (1.63-2.54) to 2.37 (2.06-2.54) mmol/l (p = 0.13). Parathyroid hormone fell from 5.3 (0.4-21.5) to 1.7 (0.45-7.4) pmol/l. Type I collagen carboxy terminal cross linked telopeptide was very high at baseline (20 (7.2-103) to 14 (11-24) µg/l) (p = 0.03) and fell promptly to normal. Conclusion: Calcium supplementation alone effected healing of rickets in most of these Nigerian children and may provide sufficient treatment in this environment.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Radiological and biochemical resolution of nutritional rickets with calcium * COMMENTARY

Oginni

Sharp²,

Badru³

et al. 2003

Archives of Disease in Childhood

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“…In patients with voriconazole-related periostitis, elevations in serum fluoride and bone alkaline phosphatase (ALP) levels have been observed (13,(16)(17)(18). These findings are similar to those for individuals with skeletal fluorosis, a pathological condition characterized by disturbances of bone homeostasis resulting from chronic fluoride intake, typically through endogenous water sources (19,20), and they suggest a role for free fluoride in the underlying pathology.Although the exact mechanisms vary, the pathogenesis of a number of human disorders characterized by abnormal bone formation, including heterotopic ossification (HO), hypertrophic osteoarthropathy (HOA), and fluorosis, is attributed to enhanced activity of osteoblast precursor cells (19,(21)(22)(23). Osteoblasts facilitate new bone formation by differentiating into mature osteocytes capable of producing and depositing large amounts of bone extracellular matrix (24).…”

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confidence: 61%

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confidence: 61%

Voriconazole Enhances the Osteogenic Activity of Human Osteoblasts In Vitro through a Fluoride-Independent Mechanism

Allen

Sánchez

Niece

et al. 2015

Antimicrob Agents Chemother

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b Periostitis, which is characterized by bony pain and diffuse periosteal ossification, has been increasingly reported with prolonged clinical use of voriconazole. While resolution of clinical symptoms following discontinuation of therapy suggests a causative role for voriconazole, the biological mechanisms contributing to voriconazole-induced periostitis are unknown. To elucidate potential mechanisms, we exposed human osteoblasts in vitro to voriconazole or fluconazole at 15 or 200 g/ml (reflecting systemic or local administration, respectively), under nonosteogenic or osteogenic conditions, for 1, 3, or 7 days and evaluated the effects on cell proliferation (reflected by total cellular DNA) and osteogenic differentiation (reflected by alkaline phosphatase activity, calcium accumulation, and expression of genes involved in osteogenic differentiation). Release of free fluoride, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) was also measured in cell supernatants of osteoblasts exposed to triazoles, with an ion-selective electrode (for free fluoride) and enzyme-linked immunosorbent assays (ELISAs) (for VEGF and PDGF). Voriconazole but not fluconazole significantly enhanced the proliferation and differentiation of osteoblasts. In contrast to clinical observations, no increases in free fluoride levels were detected following exposure to either voriconazole or fluconazole; however, significant increases in the expression of VEGF and PDGF by osteoblasts were observed following exposure to voriconazole. Our results demonstrate that voriconazole can induce osteoblast proliferation and enhance osteogenic activity in vitro. Importantly, and in contrast to the previously proposed mechanism of fluoride-stimulated osteogenesis, our findings suggest that voriconazole-induced periostitis may also occur through fluoride-independent mechanisms that enhance the expression of cytokines that can augment osteoblastic activity. Invasive fungal infections (IFIs) rarely occur in immunocompetent individuals but are potentially devastating in certain patient populations, including patients undergoing intensive chemotherapy or receiving autologous or allogeneic hematopoietic stem cell transplants for the treatment of hematological malignancies (1, 2). In recent years, there have been reports of cutaneous IFIs among immunocompetent individuals, with traumatic injuries, including motor vehicle accidents, natural disasters, and combat-related trauma, being cited as significant risk factors for infection with environmental molds, of which Aspergillus spp. are among the most commonly isolated (3-5). The recommended therapy for treatment of cutaneous IFIs involves extensive surgical debridement combined with empirical systemic antifungal therapy, for which fluorinated triazoles, including voriconazole, are important options for susceptible fungi. As the incidence rates of IFIs have been reported to be as high as 12% among immunocompromised patients (6) and up to 3.5% among U.S. military personnel admitted ...

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“…(Teotia 1998 Evidence of effectiveness for the prevention of dental caries: The draft report appears to privileged the fact that ingestion of fluoride has a systemic benefit on the prevention of dental caries. The York Review which is still the best assessment of the evidence highlights the poor quality of studies on the effectiveness of water fluoridation (McDonagh et al 2000).…”

Section: Intakementioning

confidence: 99%

Outcome of a public consultation on the Draft Scientific Opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) on Dietary Reference Values for fluoride

2013

EFSA Supporting Publications

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Panel wish to thank all stakeholders for their contributions. The current report summarises the outcome of the public consultation, and includes a brief summary of the comments received and how the comments were addressed. The NDA Panel prepared an updated version of the Scientific Opinion on Dietary Reference Values for fluoride taking into account the questions/comments received. This Opinion was discussed and adopted at the NDA Plenary meeting on 11 July 2013, and is published in the EFSA Journal. ) (see Appendix A). The NDA Panel prepared an updated version of the Scientific Opinion, taking into account the comments received. The updated Scientific Opinion was discussed and adopted at the NDA Plenary meeting on 11 July 2013, and is published in the EFSA Journal (EFSA NDA Panel). EFSA is committed to publishing the comments received during the public consultation, as well as a short report on the outcome of the consultation. KEY WORDS 2.Screening and evaluation of comments received Comments receivedEFSA received 68 comments from six interested parties. Three were from (non-profit) NonGovernmental Organisations dedicated to promoting natural approaches to healthcare or to campaigns for non-fluoridated water and for increasing awareness about the toxicity of fluoride compounds, and three were submitted by individuals in a personal capacity. A summary of the comments is given below, and all written comments received are listed in Appendix B. The numerous comments related to policy or risk management aspects were considered to be outside the scope of the consultation, and are not covered in this report. Nature of specific commentsThe main issues raised in the comments received are summarised below. The NDA Panel has reviewed all comments carefully and has updated the Scientific Opinion on Dietary Reference Values for fluoride accordingly. The updated Scientific Opinion is published in the EFSA Journal 4 . Functions and health consequences of fluorideComments received -The inverse relationship between fluoride intake and dental caries and the beneficial effect of fluoride on dental health was questioned. Publication bias was suggested as one reason that led to the establishment of this association.-It was hypothesised and repeatedly mentioned that the caries-preventive effect may be due to vitamin D and not to fluoride, and that scientific studies evaluating the effect of fluoridation measures have usually not accounted for UV-B exposure.-It was stated that the lower prevalence of caries is due to a delay in tooth eruption caused by fluoride (in water), and consequently to a lower exposure time to a cariogenic environment rather than to fluoride per se; it was also stated that this confounder has mostly not been taken into account in scientific studies. 4 The foreseen closure date of the public consultation was 13 June 2013. However, on 13 June 2013 it was impossible to submit comments between noon and 5:30 pm due to technical problems. Therefore, the time for submitting comments was extended until 14 June 2014,...

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Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone diease and deformities in India: Year 2000

Cited by 82 publications

References 4 publications

Radiological and biochemical resolution of nutritional rickets with calcium * COMMENTARY

Radiological and biochemical resolution of nutritional rickets with calcium * COMMENTARY

Voriconazole Enhances the Osteogenic Activity of Human Osteoblasts In Vitro through a Fluoride-Independent Mechanism

Outcome of a public consultation on the Draft Scientific Opinion of the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) on Dietary Reference Values for fluoride

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