Skeletal fluorosis

Skeletal fluorosis
Skeletal fluorosis
Classification and external resources
ICD-10 M85.1
ICD-9 733.9

Skeletal fluorosis is a bone disease caused by excessive consumption of fluoride. In advanced cases, skeletal fluorosis causes pain and damage to bones and joints.

Contents

Fluorine

Forms

Fluorine can be isolated in two different forms including the molecular, diatomic gas, F2, and the ionic form, F−. It is very difficult to isolate Fluorine in its atomic form due to its high reactivity and electronegativity.

Reactivity

Fluorine is the most reactive of the halogens. Fluorine is the most electronegative element currently known. This means the elemental form, F, will actively seek another electron to satisfy the octet rule (8 electrons in the outer s and p shells). This extra electron could come from anything. Because of this, Fluorine is the strongest known oxidizer. It is only found naturally on earth as 19F, its only stable isotope. Aqueous HF [Hydrofluoric acid], is weakly acidic. This acid will dissociate in water, but only to small extent. In its dissociated form, F−, it is a fairly strong base. Anhydrous HF (hydrogen fluoride) is a strong acid and its strength can be greatly increased through the addition of a lewis acid such as antimony pentafluoride.

Synthesis

Fluorine is not produced in a monatomic, uncharged form. It is generally always manufactured from the mineral Fluorite, which is the major source of Fluorine on earth. Fluorine can be produced in its ionic and diatomic gas forms. This is done by a method developed by Henri Moissan in 1886. The method begins by reacting Potassium Fluoride and Hydrogen Fluoride, KF and HF respectively, to form Potassium Bifluoride, KHF2. This compound is produced in an aqueous solution and is further electrolyzed to form gaseous Hydrogen, gaseous Fluorine, and ionic Fluorine in an aqueous solution, H2, F2, and F− respectively.

Reactions

Molecular Fluorine will act as an oxidant in most reactions. In electrochemistry, strong oxidizers have a high standard reduction potential. This value refers to the tendency of the compound or element in question to be reduced, or gain electrons. Fluorine has the highest standard reduction potential, +2.87V, making it the strongest oxidizer.[1] Fluorine is known to react violently with Hydrogen and alkali metals. It will react with alkali earth metals less violently and may form an insoluble salt. It is also know to form covalent bonds with transition metals, noble gases, and organic compounds. Due to its high reactivity, gaseous Fluorine must be kept under dry conditions. If it comes in contact with moisture it will decompose to form HF gas.

Available forms

Fluorine can be very dangerous in its gaseous form. However, it is still available for purchase from chemical suppliers around the world. It can also be obtained by the purchase of Fluorine containing compounds. It would have to be produced by one method or another of chemical conversion and isolation from these compounds.

Causes

Common causes of fluorosis include inhalation of fluoride dusts/fumes by workers in industry, use of coal as an indoor fuel source (a common practice in China), consumption of fluoride from drinking water (naturally occurring levels of fluoride in excess of the CDC recommended safe levels[2]), and consumption of fluoride from the drinking of tea, particularly brick tea.

In India, the most common cause of fluorosis is fluoride-laden water derived from deep bore wells. Over half of ground water sources in India have fluoride above recommended levels.[3]

Mechanism of Action

The best way to view the mechanism of action by which Fluorine breaks down bones and causes Skeletal Fluorosis is in a step-wise fashion.

  1. Fluorine enters the body by two paths: Ingestion or respiration. Both paths lead to corrosion of exposed tissue in high concentrations. Since the most likely form of Fluorine to enter the body is Hydrogen Fluoride gas, this is what starts the process. Exposed tissues will be utilized by HF in neutralization reactions.[4]
  2. This will leave F− free to pass further into the body.
  3. It reacts with the concentrated HCl in the stomach to form the weak acid, HF.
  4. This compound is then absorbed by the gastro-intestinal tract and passes into the liver via the portal vein. Since F is the strongest oxidizer known currently, it is immune to phase 1 metabolic reactions, which are generally oxidation reactions, in the liver. These reactions are the body’s first line of defense to biotransform harmful compounds into something more hydrophilic and more easily excreted.
  5. The HF is now free to pass into the blood stream and be distributed to all tissues including bones.
  6. Bones are largely composed of Ca compounds, particularly carbonated hydroxyapatite (Ca10(PO4)6(OH)2); the reaction of Ca and HF forms an insoluble salt, CaF2.
  7. This salt must be cleared by the body and as a result washes away some of the calcium that would be part of the bone matrix.
  8. This process results in increased density, but decreased strength in bones.[5]

Epidemiology

In some areas, skeletal fluorosis is endemic. While fluorosis is most severe and widespread in the two largest countries - India and China - UNICEF estimates that "fluorosis is endemic in at least 25 countries across the globe. The total number of people affected is not known, but a conservative estimate would number in the tens of millions."[6]

The World Health Organization recently estimated that 2.7 million people in China have the crippling form of skeletal fluorosis.[citation needed] In India, 20 states have been identified as endemic areas, with an estimated 60 million people at risk and 6 million people disabled; about 600,000 might develop a neurological disorder as a consequence.[3]

Although skeletal fluorosis has been studied intensely in other countries for more than 40 years, virtually no research has been done in the U.S. to determine how many people are afflicted with the earlier stages of the disease, particularly the preclinical stages. Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed. Even if a doctor is aware of the disease, the early stages are difficult to diagnose.[7] Given this, it may be beneficial for general physicians and neuromuscular specialists to familiarize themselves with this uncommon disease and monitor fluoride levels in patients diagnosed with arthritis over time.

Skeletal fluorosis phases

Osteosclerotic phase Ash concentration (mgF/kg) Symptoms and signs
Normal Bone 500 to 1,000 Normal
Preclinical Phase 3,500 to 5,500 Asymptomatic; slight radiographically-detectable increases in bone mass
Clinical Phase I 6,000 to 7,000 Sporadic pain; stiffness of joints; osteosclerosis of pelvis and vertebral spine
Clinical Phase II 7,500 to 9,000 Chronic joint pain; arthritic symptoms; slight calcification of ligaments' increased osteosclerosis and cancellous bones; with/without osteoporosis of long bones
Phase III: Crippling Fluorosis 8,400 Limitation of joint movement; calcification of ligaments of neck vertebral column; crippling deformities of the spine and major joints; muscle wasting; neurological defects/compression of spinal cord

Symptoms and side effects

Symptoms are mainly promoted in the bone structure. Due to a high Fluorine concentration in the body, the bone is hardened and thus less elastic, resulting in an increased frequency of fractures. Other symptoms include thickening of the bone structure and accumulation of bone tissue, which both contribute to impaired joint mobility. Most patients suffering from skeletal fluorosis show side effects from the high Fluorine dose such as ruptures of the stomach lining and nausea.[8] Fluorine can also damage the thyroid gland leading to hyperparatthyroidisme, the uncontrolled secretion of parathyroid hormones. These hormones regulate Calcium concentration in the body. An elevated parathyroid hormone concentration results in a depletion of Calcium in bone structures and thus a higher Calcium concentration in the blood. As a result, bone flexibility decreases making the bone more amenable to fractures.[9] Concluding, Fluorine also has the potential to exist as the ion, F−. This ion is very reactive as a base with organic molecules, resulting in possible reactions with any molecule in the body which can lead to damage at the tissue level.[10]

Effects on animals

The histological changes which are induced through Fluorine on rats resemble those of humans.[11] That has been observed in an experiment with young and old rats. NaF was dissolved in their drinking water. Young rats have shown to be more susceptible to skeletal Fluorosis, because their bones react faster with the Fluorine. Further aspects are major changes in teeth morphology, defects on dental enamel and abrasion of the incisors and porous compression of the upper and lower jaw.

Treatment

As of now, there are no established treatments for skeletal fluorosis patients.[12] However, it is reversible in some cases, depending on the progression of the disease. If Fluorine intake is stopped, the Fluorine existing in bone structures will deplete and be excreted via urine. However, it is a very slow process to eliminate the Fluorine from the body completely. Minimal results are seen in patients. Treatment of side effects is also very difficult. For example, a patient with a bone fracture cannot be treated according to standard procedures, because the bone is very brittle. In this case, recovery will take a very long time and a pristine healing is aleatory.[13]

References

  1. ^ Laird BB (2008). University Chemistry (1 ed.). McGraw-Hill Science Engineering. 
  2. ^ http://www.cdc.gov/fluoridation/safety/nrc_report.htm
  3. ^ a b Reddy DR (2009). "Neurology of endemic skeletal fluorosis". Neurol India 57 (1): 7–12. doi:10.4103/0028-3886.48793. PMID 19305069. http://neurologyindia.com/article.asp?issn=0028-3886;year=2009;volume=57;issue=1;spage=7;epage=12;aulast=Reddy. 
  4. ^ "Fluorine". http://web.princeton.edu/sites/ehs/labsafetymanual/cheminfo/flourine.htm. Retrieved 2011-03-18. 
  5. ^ Whitford GM (1994). "Intake and Metabolism of Fluoride". Advances in Dental Research 8 (1): 5–14. PMID 7993560. 
  6. ^ "UNICEF - Water, environment and sanitation - Common water and sanitation-related diseases". http://www.unicef.org/wes/index_wes_related.html. Retrieved 2007-09-17. 
  7. ^ http://www.slweb.org/hileman.html
  8. ^ Ott: Untersuchung eines Zusammenhanges von Fluoridkonzentrationen in privaten Trinkwasserversorgungsanlagen und Kariesentwicklung im Raum Ascheberg. In: DKHR. 2005
  9. ^ Teotia: Secondary Hyperparathyroidism in Patients with Endemic Skeletal Fluorosis In: British Medical Journal Nr. 1, 1973, S. 637-340.
  10. ^ Shivarajashankara: Oxidative stress in children with endemic skeletal fluorosis In: Fluoride Nr. 43, 2001, S. 103-107.
  11. ^ Franke, Runge, Fengler, Wanka: Int. Arch. Arbeitsmed., 1972, S. 31-48
  12. ^ Michael: Skeletal fluorosis and instant tea In: The American Journal of Medicine Nr. 118, 2005, S. 78-82.
  13. ^ Grandjean: Reversibility of Skeletal Fluorosis. In: British Journal of Industrial Medicine Nr. 40, 1983, S. 456-461.
v · d · eOsteochondropathy (M80–M94, 730–733)
Osteopathies
endocrine bone disease: Osteitis fibrosa cystica (Brown tumor)
Bone density
and structure
Continuity of bone
Other
Other
Chondropathies
Other
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