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Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.

Introduction Fluorosis has become a public health problem worldwide. Excessive fluoride intake can disrupt the processes of bone formation and resorption, which may lead to bone turnover disorders and further result in skeletal fluorosis (1). More than 16.1 million dental fluorosis patients and 1.8 million patients with skeletal fluorosis have been reported in the Chinese province of Guizhou. Patients with skeletal fluorosis experience persistent pain and bone and joint damage. They are physica

Role of renal function in the association of drinking water fluoride and plasma fluoride among adolescents in the United States: NHANES, 2013–2016.

Introduction Fluoride enrichment of drinking water is one of the major public health advances of the 21st century. While fluoride toxicity has been reported with acute intoxication (Gessner et al., 1994; Penman et al., 1997), emerging data suggests that even low levels of exposure may be associated with adverse effects in vulnerable populations (Wei et al., 2021a; Yasmin and Ranjan, 2015; Riddell et al., 2019; Green et al., 2019). While there are known determinants of fluoride toxicity, i

High Fluoride Ingestion Impairs Bone Fracture Healing by Attenuating M2 Macrophage Differentiation.

Introduction Long-term and excess fluoride consumption induces disturbed homeostasis of the bone and a series of chronic systemic diseases (Erdal and Buchanan, 2005). The World Health Organization has stated that the maximum safe limit of fluoride in drinking water is 1.5 ppm; however, more than 50 countries have high fluoride levels in drinking water (Rango et al., 2012; Perumal et al., 2013; Yu et al., 2018; Zhou et al., 2019). Fluorosis is endemic in at least 25 countries around the world, o

Necessity to Pay Attention to the Effects of Low Fluoride on Human Health: an Overview of Skeletal and Non-skeletal Damages in Epidemiologic Investigations and Laboratory Studies.

References Zhou G, Yang L, Luo C, Liu H, Li P, Cui Y, Liu L, Yu X, Zeng Q, Chen J, Zhao Q, Dong L, Niu Q, Zhang S, Wang A (2019) Low-to-moderate fluoride exposure, relative mitochondrial DNA levels, and dental fluorosis in Chinese children. Environ Int 127:70–77. https://doi.org/10.1016/j.envint.2019.03.033 CAS  Article  Google Scholar Sreemanta P, Depanwita S (2017) The genetic influence in fluorosis. Environ Toxicol Phar 56:157–162. https://doi.org/10.1016/j.etap.

Gestational exposure to fluoride impairs cognition in C57 BL/6 J male offspring mice via the p-Creb1-BDNF-TrkB signaling pathway.

References Adkins and Brunst, 2021 E.A. Adkins, K.J. Brunst Impacts of fluoride neurotoxicity and mitochondrial dysfunction on cognition and mental health: a literature review Int. J. Environ. Res. Public Health, 18 (24) (2021), p. 12884, 10.3390/ijerph182412884 View Record in ScopusGoogle Scholar Blaylock, 2004 R.L. Blaylock Excitotoxicity: A possible central mechanism in fluoride neurotoxicity Fluoride, 37 (4) (2004), pp. 301-314 View Record in

NHS general dental practitioner claims in the South West for provision of topical fluoride, fissure sealants, radiographs, fillings and extractions for children born in 2009: an analysis of a five-year period.

References Public Health England. National Dental Epidemiology Programme for England: oral health survey of 5-year-olds 2019. 2020. Available at https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/873492/NDEP_for_England_OH_Survey_5yr_2019_v1.0.pdf (accessed April 2022). Health and Social Care Information Centre. Children's Dental Health Survey 2013. Country specific report: England. 2015. Available at https://files.digital.nhs.uk