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Syndromes of bone disease and deformities consequent to disorders of nutrition, bone and mineral metabolism constitute a serious national health problem. The studies on this subject are scanty. Data on nutritional bone disease are described and discussed. We had surveyed 337.68 million population residing in 0.39 million villages in 22 States of India during the period 1963 to 2005. Of the 4,11,744 patients identified with the disorders of bone and mineral metabolism, 2,13,760 (52%) had nutritional bone disease, 1,77,200 (43%) had endemic skeletal fluorosis and 20,784 (5%) had metabolic bone disease and in 41 patients (0.19%) the bone disease was rare, mixed or unidentified. Vitamin D deficiency osteomalacia and rickets caused by inadequate exposure to sunlight (290-315 nm), dietary calcium deficiency (<300 mg/day) and fluoride interaction syndromes, calcium deficiency induced osteoporosis and calcium and vitamin D deficiency induced osteoporosis in the elderly, were the commonest disorders responsible for bone disease and deformities, besides caused by endemic skeletal fluorosis as a single entity in endemic fluorosis villages. Calcium deficiency per se dose not cause rickets, as revealed in our long-term follow up study on 47,500 calcium deficient children. Only mothers with severely depleted bone mineral and vitamin D stores gave birth to their babies with congenital rickets. Vitamin D deficiency rickets in children and osteomalacia in the mothers are the commonest disorders prevalent in the rural population of India. These disorders and the syndromes of calcium deficiency and fluoride interactions are largely responsible for the morbidity and mortality in the young and promising individuals, with economic consequences.

Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extracellular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.

Syndromes of bone disease and deformities consequent to disorders of nutrition, bone and mineral metabolism constitute a serious national health problem. The studies on this subject are scanty. Data on nutritional bone disease are described and discussed. We had surveyed 337.68 million population residing in 0.39 million villages in 22 States of India during the period 1963 to 2005. Of the 4,11,744 patients identified with the disorders of bone and mineral metabolism, 2,13,760 (52%) had nutritional bone disease, 1,77,200 (43%) had endemic skeletal fluorosis and 20,784 (5%) had metabolic bone disease and in 41 patients (0.19%) the bone disease was rare, mixed or unidentified. Vitamin D deficiency osteomalacia and rickets caused by inadequate exposure to sunlight (290-315 nm), dietary calcium deficiency (<300 mg/day) and fluoride interaction syndromes, calcium deficiency induced osteoporosis and calcium and vitamin D deficiency induced osteoporosis in the elderly, were the commonest disorders responsible for bone disease and deformities, besides caused by endemic skeletal fluorosis as a single entity in endemic fluorosis villages. Calcium deficiency per se dose not cause rickets, as revealed in our long-term follow up study on 47,500 calcium deficient children. Only mothers with severely depleted bone mineral and vitamin D stores gave birth to their babies with congenital rickets. Vitamin D deficiency rickets in children and osteomalacia in the mothers are the commonest disorders prevalent in the rural population of India. These disorders and the syndromes of calcium deficiency and fluoride interactions are largely responsible for the morbidity and mortality in the young and promising individuals, with economic consequences. [ABSTRACT FROM AUTHOR]

Epidemiological studies during 1963–1997 were conducted in 45,725 children exposed to high intake of endemic fluoride in the drinking water since their birth. Children with adequate (dietary calcium >800 mg/d) and inadequate (dietary calcium <300 mg/d) calcium nutrition and with comparable intakes of fluoride (mean 9.5±1.9 mg/d) were compared. The toxic effects of fluoride were severe and more complex and the incidence of metabolic bone disease (rickets, osteoporosis. PTH bone disease) and bony leg deformities (genu valgum, genu varum, bowing, rotational and wind-swept) was greater (>90%) in children with calcium deficiency as compared to <25% in children with adequate calcium who largely had osteosclerotic form of skeletal fluorosis with minimal secondary hyperparathyroidism. The syndrome of skeletal fluorosis and associated metabolic bone disease and deformity is a unique clinical entity classified as a variant of osteosclerotic form of skeletal fluorosis. This syndrome chiefly results from the biological impact of excess fluoride, low calcium, high PTH and 1,25 (OH)2D3 separately and through their interactions on bone structure and metabolism as studied by radiology, bone scanning, bone histomorphometry and relevant metabolic and endocrine laboratory investigations. Metabolically active and vascular bones of children accumulate fluoride at faster and greater rate than adults (at the sites of active growth). In calcium deficient children the toxic effects of fluoride manifest even at marginally high (> 2.5 mg/d) exposures to fluoride. Fluoride toxicity also exaggerates the metabolic effects of calcium deficiency on bone. The findings strongly suggest that children with calcium deficiency rickets reported in the literature should be re-investigated for possible fluoride interactions. Deep bore drinking water supply with fluoride <0.5 ppm and improvement of calcium nutrition provide 100% protection against the toxic effects of fluoride and are recommended as the cost effective and practical public health measures for the prevention and control of endemic fluorosis. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Nutritional Bone Disease in Indian Population," by S. P. S. Teotia and M. Teotia in the March 2008 issue.