ABSTRACT
The most consistent and the best characterized toxic response to uoride is its effect on the human skeleton, as 99% of the ingested uoride in the human body gets stored in bones. The highly vascularized soft tissues and blood store the remaining uoride. Once absorbed, the uoride gets readily accommodated in the active, growing, and cancellous areas than in compact regions. The concentration of uoride stored in various bones of the same skeleton differs with the type of bones. The pelvis accumulates higher uoride than the limb bones; young and cancellous bones are more receptive to uoride than old or cortical bones. Though factors such as sex, age, and type and specic part of the bone inuence the concentration of uoride in bones, uoride accumulation gets slower with age and reaches an “equilibrium” effect after about 50 years of age.1,2
The chemical composition and the physical structure of human bones get altered with ingested uoride. The resorption and accretion of bone tissue are altered by uoride intake, which in turn affects the homeostasis of bone mineral metabolism. A combination of osteomalacia, osteosclerosis, and osteoporosis of different degrees illustrates the bone lesions. Fluoride toxicity in bones imparts impaired bone collagen synthesis, increased metabolic turnover, and increased avidity for calcium. Fluoride toxicity is also reected in the structural changes of bones, namely, “increased bone mass and density, exostosis (bony outgrowth) at bone surfaces, increased osteoid seam and resorption surfaces, increased osteon diameter and mottling of osteons, increased trabecular bone volume, cortical porosity and development of cartilaginous lesions in the cancellous bones.”3,4 Fluoride can replace the hydroxyl and bicarbonate ions that are associated with hydroxyapatite
(mineral phase during formation of bone), forming hydroxyuorapatite and altering the mineral structure of bones. Thus, the uoride ions occupying the plane of the calcium ions form structurally compact and electrostatically stable structures that may shift the mineralization prole to higher levels of density and hardness. Thus, the remineralization process increases bone density, making denser and harder bones. However, high-dose administration of uoride over a long period reduces the mechanical strength of bones.5
