Introduction

Chronic fluoride intoxication, also known as fluorosis, was first described as an occupational hazard in 1932.¹ Subsequent cases have been reported as a result of both occupational and endemic exposure.^2-5 Endemic fluorosis is acquired through drinking water. Ground water sources with high fluoride content occur worldwide. According to the latest estimates from UNICEF, “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 fluorosis problem is most severe in the two largest countries of the world, China and India.
 

In China, the World Health Organization recently estimated that 2.7 million people have the crippling form of skeletal fluorosis. In India, 15 of its 32 states have been identified as “endemic”, with more than 6 million people seriously afflicted. Fluoride has become a major public health problem in both of these countries.
 

Drinking water accounts for an estimated 70% to 90% of total fluoride intake, with food accounting for the remaining 10% to 30%. To prevent dental caries, current recommendations for the optimal fluoride level in drinking water range from 0.7 ppm in warm climates to 1.2 ppm in cooler climates.³ Existing data suggest that clinical effect of fluorosis does not generally develop at fluoride levels less than 3 ppm in drinking water (Table 1).⁶

Table 1. Effect of fluoride levels in drinking water

Predisposing Factors

High levels of fluoride in drinking water are a particularly important factor in tropical areas with endemic fluorosis (Table 2). The increased volume of water consumption in hot, arid climate is thought to contribute significantly to a higher incidence of clinical fluorosis.^2,7,8 Additional predisposing factors are calcium deficiency, poor nutrition, syndromes associated with polydypsia, and excessive water consumption.⁹ Rare cases of fluorosis include geophagia, anaesthetic abuse, intentional ingestion of fluoride, and treatment of osteoporosis.
 

Table 2. Predisposing Factors

Mechanism of Action

The exact mechanism of action on bone remains controversial. Fluoride is deposited in the apatite mineral lattice of bone by ionic substitution with the hydroxyl group. Stimulatory effects of fluoride on osteoblasts results in formation of osteoid, which subsequently undergoes mineralization.¹⁰ The fluoroapatite structure is more resistant to parathyroid hormone than normal bone resulting in depressed resorption of fluoride containing bone with compensatory increased resorption of normal bone. This results in increased architecturally abnormal bone.

Generally, sustained ingestion of excess fluoride over a 10- to 20-year period is required before symptoms develop (Table 3). Severity of symptoms directly correlates with duration of exposure. Fluoride’s effects are cumulative. For this reason, any skeletal changes it causes progress through a number of stages with the less serious occurring early in the natural course of the disease. Whatever may be the type of fluorine exposure, the clinical picture in chronic poisoning occurs in the following phased manner:

• Preclinical phase: Asymptomatic; slight radiographically detectable increases in bone mass
• Phase I: Musculoskeletal – sporadic pain; stiffness of joints; osteosclerosis of pelvis and spine
• Phase II: Degenerative and destructive – chronic joint pain; arthritic symptoms; slight calcification of ligaments; increased osteosclerosis/cancellous bones; with or without osteoporosis of long bones
• Phase III: Crippling fluorosis – limitation of joint movement; calcification of ligaments/neck, spinal column; crippling deformities/spine and major joints; muscle wasting; neurological defects/compression of spinal cord

Table 3. Clinical presentation of endemic fluorosis^2-5

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Radiographic Manifestations

Radiographic features of skeletal fluorosis provide the only means of diagnosis in its asymptomatic phase. Diffuse osteosclerosis, a chalky bone appearance, interosseous or ligamentous calcification, and osteophyte formation are characteristic (Slide 2, Slide 3, Slide 4, Slide 5, Slide 6, Slide 7). Axial skeleton involvement is prominent. Cervical vertebrae and pelvis display the earliest and most severe radiographic changes.

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Table 4. Differential diagnosis

Sparing of skull from osteosclerosis distinguishes skeletal fluorosis from Paget’s disease. Interosseous membrane calcification remains the most characteristic radiographic finding of fluorosis(Table 4).

Laboratory Diagnosis

Urinary fluoride measurement (normal 0.2 mg/L to 1.0 mg/L) remains the most accurate screening method available.⁴ Definitive confirmation of fluorosis is made through quantitative measurement of dry ashed bone fluoride(normal 0 µg/g to 140 µg/g). Measuring plasma fluoride levels is an unreliable method due to high protein binding and rapid renal excretion of fluoride.⁷

Treatment

Therapeutic options in skeletal fluorosis are limited. The initial step is to identify and remove the source of fluoride. The urinary fluoride level can then be monitored until returning to a normal value.⁸ Specific pharmacological intervention has not been proven clinically beneficial. If the fluoride exposure can be removed, then the prognosis is usually good. Neurological deficits once present are frequently irreversible. Laminectomy with cord decompression can be performed with guarded prognosis.

References

1. Moller PF, Gondjonsson SV. Massive fluorosis of bones and ligaments. Acta Radiol. 1932; 13:269-293.
2. Singh A, Jolly SS, Bansal BC, et al. Endemic fluorosis. Medicine. 1963; 42:229-246.
3. Teotia M, Teotia SPD, Kunwar KB. Endemic skeletal fluorosis. Arch Dis Child. 1971; 46:686-691.
4. Grandjean P. Occupational fluorosis through 50 years: Clinical and epidemiological experiences. Am J Int Med. 1982; 3:227-236.
5. Hodge HC, Smith FA. Occupational fluoride exposure. J Occup Med. 1977; 19:12-39.
6. National Academy of Sciences. Drinking Water and Health. Washington DC: National Academy Press;1980:vol 3.
7. Fluorine and Fluorides. Environmental Health Criteria 36. WHO, Geneva. 1984.
8. Bell ME, Largent EJ, Ludwig TG, et al. The supply of fluorine to man. WHO Monograph Series. 1970; 59:17-74.
9. Sauerbrum BJL, Hyan CM, Shaw JF. Chronic fluoride intoxication with fluoride radiculomyelopathy. Ann Intern Med. 1965; 63:1074-1078.
10. Arnala I, Alhava EM, Kauranen P. Effects of fluorides on bone in Finland. Acta Orthop Scand. 1985; 56:161-166.
11. Evans RA, Hughes WG, Dunstan CR, et al. Adult osteosclerosis. Metab Bone Dis Rel Res. 1983; 5:111-117.