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Journal of the Anatomical Society of India

Vol. 51, No. 1 (2002-01 - 2002-06)

Editorial

"Fluorisis" a wound inflicted by one of the edges of the "double edged weapon", Fluoride is due of its excess, of the deficiency causing caries. None of the medical or dental professionals or the later at least can afford to be ignorant about the etiology symptomatology, & management of the disease due to its wide prevelance all over the world particularly in India. The magnitude of the problem can be gauged from the fact that around 30-35 researches have been done on its different aspects at G.M.C. Patiala to be in the recent past & still many more are going on.

The primary source of fluorides, apart from foods, & soil etc is considered to be drinking water, the optimal & safe range being 0.5-0.8 ppm, excess & deficiency both being offenders. Khosla et al(1965) studying the role of water constituents in fluorosis endemic areas pointed out that statistically significant less Ca, Mg & total hardness and high Na+ K+, -HCO3 SO4- -, & Cl- are seen in the water in these regions. Bansal & Jolly (1978) found that apart from fluoride, solids & alkanity of water is also high in fluorosis endemic areas while Zn content is low & Ca is equal when compared with non endemic areas However the last is found to more in cereals in endemic areas. Singhal et al (1979) studied the role of Ca in Fluoride toxicity in rabbits & concluded that with same amount of fluoride (subtethal) low amount of Ca++, facilitates dental fluorosis but high Ca++ doesn"t delay it. Fluoride causes increase in bone content of Ca++ & Mg++, decreae in bone content of Cu with no change in Bone Zn++, However though in the presence of high Ca++, bone fluoride, decreases low Ca++ doesn"t increase bone fluoride. chances of fluorosis are more in winter as compared with summers Bhatnagar & Jolly (1978) explain it as though intake of water is very large in summers but still balance is not high. It could be due to protective role of sweating which might excrete more of fluorides.

Goyal et al (1963) found that 70% of patients of skeletal fluorosis have dental manifestations as well. The commonest complaints of sketetal fluorosis are vague pains & stiffness of body with deformity of spine & limbs, with or without ms wasting & neurological complications due to compression of spinal cord & spinal nerves in advanced cases.

Chander et al (1972), in a study on rabbits found that fluoride content of bones increases proportional to the amount of fluoride taken & its duration. Further with increases in fluoride, Ca++ content of bones increases while that of Mg, P remaining unaltered. Histologically, there occurs bone resoprtion, defective & decreased mineralisation & disturbed lamellar pattern. Effect of Al++ has been studied on the bones by Sood et al (1984). They found that Al+++ enhances thickening & bowing of bones, calcification of interosseous memberane exostosis. Wt. gain/length of bone is more when Al is combined with fluoride. Radiological evidence of osteosclerosis is evident as fluoride causes new bone formen under periosteum while Al coauses new bone formation under endosteum. In combination, new bone is formed at both places.

Bansal et al (1990) showed that in male rabbits, fluorides cause osteoporsis in early stages & osteosclerosis in late stages & since Mg causes osteosklerosis in all stages so prevents osteoporsis induced by fluorides in early stages while in later stages in enchances osteosclerosis. However in females since osteoslerosis in seen right from begining with no osteoporosis, so Mg is having no helping hand even in early stages of fluorosis.

Similarly Khokhar et al (1986) showed that Cu++ in a dose of05 mg/kg prevents osteoporosis in early stages so may be advantageous while in late stages since it produces osteosclerosis it may be harmful. Kumar et al (1989) points out that increasing dose of Zn alone causes increase in wt. However when given in fluorotic patients it leads to decrease in dental menifestation wt & deformity thus nullifying the effect of Fon bone. This is attributed to its preventive effect on osteosclerosis & distortion of haversian system. The authors have recommended its use as subcutaneous as orally it interferes with Fe & Cu absorption.

Gupta et al (1976) found that 4-6 Months of administration of fluoride in albiuno rats leads to histopathological changes in liver in the form of hepatic cell necrosis, round cell infiltration sinusoidal delatation, balloning degeneration & increase in total fluoride content. However no changes were seen in heart, skeletal muscles thyorid & parathyroid. In the same year Kaur et al (1976) studied effects of fluoride on kidneys of rats in the form of cloudy swelling of PCT & DCT & interstitial nephritis leading to albuminuria & some impairment of glomerular function.

Sharma & Singh (1967) studied the fluoride content of urinary tract calculi in patients from fluorosis endemic areas & found it to be significantly higher as compared with non endemic areas. urinary hydroxy Proline is also found to be increased (39.71 ± 15.01 mg/24 hrs urine) by Singh et al. (1980) indicating increased collagen turnover in fluorosis, Garge Jolly (1975) found that S. alk PO4 ase is significantly increased while S. acid PO4 ase, choline esterase, LDH, SG0T, SGPT dont show any significant change Earlier Goyal et al (1963) had attributed increase in S.alk Pb4 ase to the increased osteoblastic activity. They also found increased Blood fluoride level (0.08-0.67 mg%), increase being proportional to disease clinical severity of & a partial black & increase proteins in csf. Singh et al (1980) found that all proven patients of skeletal fluorosis show evidence of ossification of interosseous memberane while evidence of hyperparathyroidism was seein in 79.16% of cases.

Batish et al (1980) studied finger ball dermatoglyphics of fluorotic patients & found an association between AL, & arches in 3rd digit in right hand of male & fluorosis while W.S.S & Whorls are resistant.

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