Fluorosis

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A fluorosis is caused by excessive fluoride supply. A distinction is made between acute and chronic ( skeletal fluorosis and dental or dental fluorosis ) forms, although some authors use the term fluorosis in a limited way to chronic forms and consider acute fluoride poisoning in isolation.

Cause of fluorosis

Acute poisoning by fluorine compounds manifests itself with different symptoms depending on the type of compound, the route and the dose in which they entered the body. A gastrointestinal resulting acute poisoning with fluoride leads to mucosal burns, nausea, initially mucous, later bloody vomiting, unquenchable thirst, severe abdominal pain and bloody diarrhea. Some of those affected die. If hydrogen fluoride and dust-like fluorides are absorbed with the breath, tears, sneezing, coughing, dyspnoea, pulmonary edema and even death with convulsions follow . If the skin is poisoned with hydrogen fluoride (also in acidic solutions of fluoride), it leads to profound necrosis and poorly healing ulcers .

As a weakly dissociated molecule, hydrogen fluoride is easily absorbed through the skin. It leads to painful inflammation, later to stubborn, poorly healing ulcers. In addition, HF forms strong hydrogen bonds and is thus able to change the tertiary structure of proteins. Fluoride forms fluoridoaluminate complexes with aluminum ions, which have a phosphate-like structure and thus contribute to the deregulation of G proteins . The result is an intervention in the receptor-coupled signal transmission and - via signal-dependent phosphorylation / dephosphorylation - in the activity of many enzymes. The best known example of an enzyme inhibition by fluoride is enolase , an enzyme in the glycolysis chain.

The highly toxic fluoroacetates and fluoroacetamide are metabolized to fluorocitrate after absorption . This connection leads to the blockage of the enzyme aconitase, which is important for the citric acid cycle . This causes an accumulation of citrate in the blood, which in turn cuts off the body cells from the energy supply. Perfluorinated alkanes , which are being tested as blood substitutes , and the commercially available fluorocarbons such as PTFE (Teflon) , PVDF or PFA are considered non-toxic.

The sparingly soluble calcium fluoride , which is formed when it reacts with calcium - for example in the bones - was previously thought to be inert and therefore harmless. At least the dusts of calcium fluoride have proven to be toxic both in animal experiments and in humans. Whether poorly soluble calcium fluoride is actually formed in vivo in acute fluoride poisoning, as is so often assumed, could not be proven in the context of specific investigations.

Forms of fluorosis

Acute fluorosis

Symptoms of acute fluoride poisoning include nausea, vomiting, diarrhea, abdominal pain, and paresthesia .

As probably toxic dose ( Probably Toxic Dose ; PTD) a value of 5 mg of fluoride per kilogram of body weight is given. For an adult who weighs 70 kg, this corresponds to 350 mg of fluoride (in around 3–4 tubes of toothpaste or a tube of dental gel such as elmex gelée). The safely toxic dose ( Certainly Toxic Dose ; CTD) is 32–64 mg fluoride per kilogram of body weight.

Acute fluoride poisoning (occasionally with fatal outcome) has also been observed in children, especially after the unsupervised ingestion of fluoride tablets or by swallowing (instead of rinsing and spitting out) highly concentrated fluoride gels applied in the dental practice.

Chronic fluorosis

Excessive exposure to fluoride over a longer period of time can lead to chronic fluorosis, which is associated with various symptoms of the skin and gastrointestinal tract, possibly also other organs (e.g. kidneys ). While these symptoms are not specific to a chronic fluoride poisoning are (ie not only in fluoride poisoning occur), there is for skeletal fluorosis and dental fluorosis typical diagnostic criteria. Sources of chronic fluoride poisoning are not only dental-relevant products, but also, of course, foods and drinks that are higher in fluoride (black tea, some mineral waters, tap water in some regions) and fluoride exposure at the workplace.

Bone fluorosis (skeletal fluorosis)

Classification according to ICD-10
M85.1 Skeletal fluorosis
ICD-10 online (WHO version 2019)

If more than 10 mg fluoride per day is chronically ingested over a long period of time (approx. 10 years), the bones react with the formation of hardened and compacted spongiosa and partial thickening of the cortex (outer bone layer). As a result of this bone growth, elasticity is lost and the bone becomes less resilient and more fragile. Under certain circumstances, the joints stiffen due to the increase in bone. The spine can also ankylosing (stiffening). This clinical picture was observed first in cattle that ate green fodder with dust deposits from chimneys of fluoride-processing factories, then (1932) also in workers in cryolite processing (e.g. in aluminum production ). It was not until the fifth ordinance on the extension of accident insurance to include occupational diseases as of July 16, 1952, under item 31, diseases of the bones, joints and ligaments caused by fluorine compounds (fluorosis) in the series of occupational diseases subject to compensation. In a later system, Bk no. 13 08 summarized damage caused by fluorine and its compounds, which are "acute local burns of the skin as well as irritation of the airways and possible affections of the gastrointestinal tract". Chronic occupational effects on the bone system (osteosclerosis, osteoporosis) are still in the foreground.

Since the late 1930s, skeletal fluorosis has also been described in India and Bahrain , in places whose drinking water contains 1 mg of fluoride per liter (and more). The phenomenon occurs here because of the higher water consumption (due to climate) at relatively low fluoride concentrations in the water.

Skeletal diseases caused by fluorosis are difficult to differentiate from age-related wear and tear diseases. This is especially true for the variable expressions fluoride-induced damage to the spine, which primarily in endemic were recorded regions and adjacent to non-specific sclerosis and ligamentous lesions by Osteo - or spondylophyte and spondylarthrosis , kyphosis , of the intervertebral spaces and degenerative disc disease ( protrusion , prolapse ), foraminal stenosis , spinal Stenosis as well as radiculopathy and myelopathy are characterized.

Nevertheless, only severe bone fluoroses have a disease value; They arise from systemic and long-term intake of high doses of fluoride (20–80 mg daily for 10–20 years). This manifests itself in a bony narrowing of the spinal canal and a (partial) loss of the sense of touch.

Dental fluorosis

Mild form of dental fluorosis

Dental fluorosis, also known as dental fluorosis, is the only visible symptom that results from excessive fluoride intake during tooth development .

History of fluorosis research

Frederick Sumner McKay researched for 30 years to find out the cause of dental fluorosis (dental fluorosis).

Individual evidence

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  12. ↑ Acute poisoning with fluoride tablets
  13. ↑ Acute poisoning with fluoride gel
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  31. ↑ Ancient and recent evidence of endemic fluorosis in the Naples area . In: Journal of Geochemical Exploration . tape 131 , August 1, 2013, ISSN  0375-6742 , p. 14–27 , doi : 10.1016 / j.gexplo.2012.11.012 ( sciencedirect.com [accessed June 23, 2018]).
  32. ↑ Kenneth Izuora, Jennifer G. Twombly, Gary M. Whitford, Jennifer Demertzis, Roberto Pacifici: Skeletal Fluorosis from Brewed Tea . In: The Journal of Clinical Endocrinology & Metabolism . tape 96 , no. 8 , August 2011, ISSN  0021-972X , p. 2318–2324 , doi : 10.1210 / jc.2010-2891 ( oup.com [accessed June 23, 2018]).
  33. ↑ Javed Ahsan Quadri, Mohd Meraj Alam, Saba Sarwar, Ashraf Ghanai, A. Shariff: Multiple Myeloma-Like Spinal MRI Findings in Skeletal Fluorosis: An Unusual Presentation of Fluoride Toxicity in Human . In: Frontiers in Oncology . tape 6 , 2016, ISSN  2234-943X , doi : 10.3389 / fonc.2016.00245 ( frontiersin.org [accessed June 23, 2018]).
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  35. ↑ Yingpeng Xia, Jun Wan, Bin Yu, Xueli Zhang, Rong Tian: [Treatment of fluorosis cervical canal stenosis by open-door cervical expansive laminoplasty using anchor fixation] . In: Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi = Zhongguo Xiufu Chongjian Waike Zazhi = Chinese Journal of Reparative and Reconstructive Surgery . tape 23 , no. October 10 , 2009, ISSN  1002-1892 , p. 1204-1208 , PMID 19957840 .
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