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慢性氟中毒时,人和动物骨骼系统的病理表现不同,有四种情况:(1)骨质硬化(人);(2)骨质软化(人和反刍动物);(3)继发性副甲亢(人和羊);(4)骨质疏松(大鼠)。这些矛盾的病理所见,是由于氟直接作用于成骨细胞,破骨细胞,改进骨盐结晶的稳定性及继发性引起副甲亢的结果。 氟化物通过刺激酶的活性直接刺激成骨细胞,这就解释了氟化物的强成骨效应,氟沉积骨表面、血管附近及新生骨结晶中,提高局部氟浓度,使其在低剂量时就能激活某些酶。每天剂量为40～60毫克NaF时,就能刺激成骨细胞形成新骨,尤其在骨膜(先形成纤维状骨后变为板状骨),骨内及原来的骨小粱处。剂量增加则能抑制某些酶。剂量再高,便形成不规则基质,甚至抑制骨基质形成。
Chronic fluorosis, the pathological manifestations of human and animal skeletal systems are different, there are four situations: (1) bone sclerosis (human); (2) osteomalacia (human and ruminant); (3) secondary Hyperthyroidism (human and sheep); (4) Osteoporosis (rat). These contradictory pathology is due to the direct effect of fluorine on osteoblasts, osteoclasts, the stability of the bone salt crystals and secondary hyperparathyroidism. Fluoride stimulates osteoblasts directly by stimulating the activity of enzymes, which explains the strong osteogenic effect of fluoride on the surface of the fluoride-deposited bone, near the blood vessels and in the nascent bone crystals, increasing the local fluoride concentration at low doses Can activate certain enzymes. At daily doses of 40 to 60 milligrams of NaF, osteoblasts can be stimulated to form new bone, especially at the periosteum (the first form of fibroid bone into plate-like bone), the bone and the original bone sorghum. Increased dose can inhibit certain enzymes. The higher dose, they formed an irregular matrix, and even inhibit the formation of bone matrix.