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ENDEMIC FLUOROSIS – Epidemiology, Pathophysiology, Clinical Features, Skeletal Fluorosis, Complications, Investigations, Treatment and Prevention

Endemic fluorosis is caused by chronic fluoride intoxication acquired by ingestion of water containing high concentration of fluorides. It is characterized by dental and skeletal changes.


The disease is present in many states in India where fluoride content of drinking water exceeds 2 ppm. Andhra Pradesh, Punjab and North Karnataka show high prevalence. Endemic areas have also been found in Tamil Nadu, Haryana, Rajasthan, Uttar Pradesh and Delhi and its surrounding areas. In Kerala three districts are affected. The disease is present in certain parts of China, Japan, South Africa, Saudi Arabia and USA. The disease is more prevalent in males who are engaged in hard manual work because of their higher consumption of water. Total hardness of drinking water (calcium and magnesium hardness) has a protective role. Presence of fluoride up to 0.5 to 0.8 ppm in drinking water is considered safe in India. With higher levels, fluoride accumulates in the skeletal system and teeth.


Ingestion of fluoride causes reduction of ionized calcium. This hypocalcemia leads on to secondary hyperparathyroidism and increased osteoclastic activity. Increased levels of lactic acid and citric acid are produced from the osteoclasts thereby increasing the hydrogen ion concentration and lysis of lysosomes. Lysosomal enzymes like protease, collagenase and hyaluronic acid produce disintegration of hydroxyproline and other ground substances of bone and other calcified tissues like teeth. This is responsible for the signs and symptoms of fluorosis like dental hypoplasia with areas of hypocalcification, hypomineralization and softening. The bones are heavier and irregular. There is excessive subperiosteal bone formation at the sites of muscular, fascial and tendinous attachments. Ligaments show various grades of calcification. The most advanced changes are seen in the spine. There is narrowing of the vertebral canal, which leads to compression of the spinal cord. Marked changes are seen in the ribs, pelvis, sternum, mandible, and skull. Over a period of 10-20 years, the subject develops crippling deformities.


Dental fluorosis Enamel and dentin of teeth have strong affinity for fluoride during the formation of teeth. Mottled enamel is an early, sensitive and easily distinguishable manifestation in children. This has been taken as an index of endemicity in epidemiological surveys. Dental fluorosis develops only if the child has lived in the endemic area during dentition. It can be graded depending on the severity.

Grade-I: White chalky opacities or patches on enamel without faint yellow lines.

Grade-II: Distinct brownish discoloration.

Grade-III: Besides pigmentation there is pitting of enamel surface, sometimes with chipping of edges

Premature loss of teeth is not rare. Both permanent and deciduous teeth may be affected.

Skeletal fluorosis

Skeletal fluorosis is not easily recognizable in the early stages. The initial symptoms are nonspecific such as pain in the neck and back associated with rigidity, joint pains, and paresthesia of the limbs.

These cases may be mistaken for rheumatoid arthritis, ankylosing spondylitis or osteoarthritis. The physical findings include kyphosis, limitation of movements of the spine and exostoses. Exostoses can easily be palpated along the anterior border of the tibia, over the olecranon, and along the medial border of the scapula. These are diagnostic. In advanced fluorosis, kyphosis, fixed flexion deformities of hips and knees and paraplegia, may develop.

Non-skeletal manifestations:

These include neurological manifestations like tingling sensation in fingers and toes, weakness and stiffness of skeletal muscles, nervousness and depression, gastrointestinal manifestations like non ulcer dyspepsia, abdominal pain, diarrhea and/or constipation. The red blood cell membrane becomes more pliable due to decreased calcium and forms into echinocytes. Early destruction of echinocytes results in anemia. Fluoride has inhibitory effect on iodine uptake and so may cause enlargement of thyroid.


About 8-10% of cases show compression of spinal cord and the roots by protruding osteophytes. The vertebral arteries may also be occluded. The clinical picture may resemble cervical myeloradiculopathy, cervical myelopathy or radiculopathy, dorsal myelopathy and peripheral neuropathy. Bladder involvement manifests as precipitancy of micturition or retention of urine.

Occasionally, peripheral neuropathy manifests as acroparesthesia, but with only minimal sensory or motor defects. Cranial nerve involvement is rare.


Radiologic and biochemical investigations should be carried out.


The classic features are osteosclerosis, irregular osteophyte formation, and calcification of ligaments, especially in the vertebral column. In advanced cases, the bones look chalky white. Irregular subperiosteal new bone formation may be observed along the muscular, fascial, and tendinous attachments. Interosseous membrane of the forearm shows calcification and this has been taken as a definite radiological index of skeletal fluorosis. Skull shows thickening and sclerosis of the vault.

CT and MRI

CT of the bones may show prominent cortical thickening and increased density with irregular contours. Bony excrescences are detected in both the pelvic bones and the lower extremities. The sacroiliac joints may be narrowed. MRI may show reduction in the intervertebral disc spaces and multiple disc prolapse. The medullary canal may be narrowed by bony excrescences and by the ossified posterior longitudinal ligament.


Fluoride content is increased in the blood, urine, and bone ash. Serum fluoride level varies from 0.05 to 0.8 mg/dL. Serum alkaline  phosphatase is moderately raised (15-30 KA units). Serum calcium, phosphorus and magnesium are normal.


Endemic fluorosis is a preventable disease, which can be eradicated by providing fluoride-free drinking water. Defluoridation of water may be affected by using bone meal and metasilicate of magnesium (serpentine) but this is not yet widely used. Vitamins and antioxidants have been tried in many cases. Changing the dietary habits by restricting use of fluoride rich food is also important. There is no effective treatment for the established case. Patients with skeletal fluorosis, when fed with fluoride-free drinking water, seem to improve over the years. Improvement in the dental changes is reported within weeks. Cases of spinal compression require laminectomy.

Prevention of Endemic Fluorosis

In endemic areas fluorosis can be prevented by reducing the fluoride content of water to less than 1 ppm. Two methods are available for defluoridation of water, the Nalgonda technology and the activated alumina technology. In Nalgonda technique alum and lime are used in various proportions depending on fluoride content of water. In activated alumina technology activated alumina is used in domestic filters. Encouraging the use of calcium, vitamin C and vitamin E may help to reduce the skeletal changes.

ENDEMIC FLUOROSIS – Epidemiology, Pathophysiology, Clinical Features, Skeletal Fluorosis, Complications, Investigations, Treatment and Prevention
ENDEMIC FLUOROSIS – Epidemiology, Pathophysiology, Clinical Features, Skeletal Fluorosis, Complications, Investigations, Treatment and Prevention
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