|Classification and external resources|
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), and consumption of fluoride from the drinking of tea, particularly brick tea. Skeletal fluorosis can be caused by cryolite (Na3AlF6, sodium hexafluoroaluminate).
Fluorosis can also occur as a result of volcanic activity. The 1783 eruption of the Laki volcano in Iceland is estimated to have killed approximately 25% of the Icelandic population, and 50–80% of livestock, as a result of fluorosis and sulfur dioxide gases. The 1693 eruption of Hekla also led to fatalities of both people and livestock under similar conditions.
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.
- 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 (HF) gas, this is what starts the process. Exposed tissues will be utilized by HF in neutralization reactions.
- This will leave F− free to pass further into the body.
- It reacts with the concentrated HCl in the stomach to form the weak acid, HF.
- 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.
- The HF is now free to pass into the blood stream and be distributed to all tissues including bones.
- 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.
- 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.
- This process results in increased density, but decreased strength in bones.
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."
The World Health Organization recently estimated that 2.7 million people in China have the crippling form of skeletal fluorosis. 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.
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. Fluorine can also damage the thyroid gland leading to hyperparatthyroidism, 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.
Effects on animals 
The histological changes which are induced through fluorine on rats resemble those of humans. 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.
As of now, there are no established treatments for skeletal fluorosis patients. 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.
See also 
- Reddy DR (2009). "Neurology of endemic skeletal fluorosis". Neurol India 57 (1): 7–12. doi:10.4103/0028-3886.48793. PMID 19305069.
- "Fluorine". Retrieved 2011-03-18.
- Whitford GM (1994). "Intake and Metabolism of Fluoride". Advances in Dental Research 8 (1): 5–14. PMID 7993560.
- "UNICEF - Water, environment and sanitation - Common water and sanitation-related diseases". Retrieved 2007-09-17.
- Gönnewicht, Daniela (2005). "Untersuchung eines Zusammenhanges von Fluoridkonzentrationen in privaten Trinkwasserversorgungsanlagen und Kariesentwicklung im Raum Ascheberg (Südliches Münsterland/Westfalen)" (PDF). Dissertation. Universität Münster, Fachbereich Medizinische Fakultät.
- Teotia SP, Teotia M (March 1973). "Secondary hyperparathyroidism in patients with endemic skeletal fluorosis". Br Med J 1 (5854): 637–40. PMC 1588649. PMID 4692708.
- Franke J, Runge H, Fengler F, Wanka C (1972). "[Experimental bone fluorosis]". Int Arch Arbeitsmed (in German) 30 (1): 31–48. PMID 5084923.
- Whyte MP, Essmyer K, Gannon FH, Reinus WR (January 2005). "Skeletal fluorosis and instant tea". Am. J. Med. 118 (1): 78–82. doi:10.1016/j.amjmed.2004.07.046. PMID 15639213.
- Grandjean P, Thomsen G (November 1983). "Reversibility of skeletal fluorosis". Br J Ind Med 40 (4): 456–61. PMC 1009220. PMID 6626475.