PATHOPHYSIOLOGY OF Fluorosis

Ingestion of fluoride causes decrease in ionised calcium. This hypocalcemia leads to changes in internal milieu of the body to maintain the calcium levels and leads to secondary hyperparathyroidism. The increased parathyroid hormone causes increased activity of Osteoclasts in bone by activating membrane bound 3'5' Cyclic AMP. This increased osteoclastic activity causes, increases in citric acid and lactic acid release from ruffled border of osteoclasts. This causes increase in hydrogen ion concentration, and hence lysis of lysosomes. Release of lysosomal enzymes viz. acid protease, collagenase, hyaluronic acid in bone and other tissues of the body which catalyzes the reactions favoring the depolymerization of the glycoprotein of bone and of cartilage. This causes breakdown of hydroxyproline, which is responsible for stabilization of collagen triple helix. As the protein polymer desegregates and dissolves, the mineral-binding capacity is also reduced and calcium is liberated, which helps in maintaining the serum calcium level. As a result the solubility of hydroxyappetite crystals also increases, causing its breakdown along with reduced laying down of collagen by reducing Hydroxylation of proline and lysine. This event simultaneously led to the elevation of the serum mucoprotein or polysaccharide levels. The net result of degradation of ground substance in, bones and other calcified tissues like teeth leads to symptoms of Fluorosis like, delayed eruption of teeth, dental Fluorosis, clinical Fluorosis, premature aging etc