Research report Fluoride 40(3)190–197 July-September 2007 Dual energy X-ray absorptiometry study of endemic skeletal fluorosis in Andhra Pradesh, India Khandare, Rao, Balakrishna 190 190 DUAL ENERGY X-RAY ABSORPTIOMETRY (DXA) STUDY OF ENDEMIC SKELETAL FLUOROSIS IN A VILLAGE OF NALGONDA DISTRICT, ANDHRA PRADESH, INDIA Arjun L Khandare, a Rao GS, b N Balakrishna c Hyderabad, India. SUMMARY: A comparative study of bone mineral density (BMD) and bone fracture was conducted in a fluorotic and a nonfluorotic area of the Nalgonda District, Andhra Pradesh, India. BMD measured by dual X-ray absorptiometry (DXA) of L2–L4 vertebrae, femoral neck, hip, and whole body was significantly higher by 112%, 43%, 57%, and 50%, respectively, in 12 fluorotic subjects than in 14 nonfluorotic subjects (p<0.01). However, there was an 11% decrease, although not statistically significant, in forearm BMD in the fluorotic subjects compared to the nonfluorotic subjects. Serum levels of total and bone specific alkaline phosphatase in the fluorotic subjects were significantly elevated by 219 and 313%, respectively (p<0.01), whereas serum Ca, protein, and phosphorus were 10, 12, and 32% lower, respectively (p<0.01). On the other hand, serum creatinine, urea, and zinc levels in the two groups of subjects were not significantly different. In the fluorotic village, with a 34% lower average consumption unit intake of calcium, the overall bone fracture rate of 6.3% was significantly higher than the 2.1% rate in the nonfluorotic village (p<0.05). Keywords: Bone fracture; Bone mineral density; Dietary calcium; Dual energy X-ray absorptiometry; Endemic fluoride area; Skeletal fluorosis. INTRODUCTION Fluoride (F) is toxic to osteoblasts (bone forming cells) and resorbing osteocytes. 1 A first response to cell injury is to initiate repair, and when that fails the cell dies. In F intoxication the repair mechanism fails, and the result is an initial increase in both bone formation and resorption. This response to cell injury by F leads to pathological bone formation, and such increased formation or decreased resorption of bone results in increased bone mass. 2 When injured osteoclasts die, new osteoclasts are formed from monocytes. Thus secondary injury of osteoclasts does not result in a paucity of osteoclasts on the surface of fluorotic bone. 3 F injures cells involved in bone formation, and a poorer quality bone accumulates in patients with increased intake of F. 4 However, the newly formed bone is inferior, and the matrix is irregular. 3,5-7 Its collagen structure also differs from that associated with normal bone, 6 and its mineralization is enhanced. 3,5-10 Although F increases bone mass or bone mineral density (BMD), the newly formed bone may have reduced strength, since F increases widening of osteoid seams and creates cytological and matrix abnormalities. Increased brittleness and fragility due to increase in osteocyte resorption leads to an increase in the number of micro fractures in bone. 11-13 This has been proved in a field study 14 showing that higher F intake increases bone fracture incidence, and it did not benefit vertebral fracture risk. a For Correspondence: Arjun L Khandare, Assistant Director, Food and Drug Toxicology Research Center, National Institute of Nutrition (NIN), Indian Council of Medical Research (ICMR), Jamai-Osmania, Hyderabad-500007, Andhra Pradesh, India. E-mail: alkhandare@yahoo.com; b,c National Institute of Nutrition, Jamai-Osmania, Hyderabad, India.