I. Pathological basis and X-ray signs of fluorine-associated arthropathy
Long-term uptake of excessive fluorine may cause pathological changes of bone structure and bone periphery; furthermore, animal experiments and epidemiological investigations demonstrate that fluorosis may cause necrosis, degeneration and ulceration of articular cartilage, and also cause necrosis of subchondral bones, leading to hypertrophy of synovium and joint capsule and a series of reparative changes which will resul
The most severe consequence of intensive exposure to fluorides is skeletal injury with initial injury of spongy bones (pelvis and spine) and calcification of the ligaments, followed by involvement of the long bones in the disease. These radiological-morphological abnormalities are the diagnostic criteria and have been made the basis for classification of skeletal fluorosis [5, 6]. A number of studies demonstrated similar events with occupational exposure to fluorides and with endemic fluorosis.
Diagnosis of professional fluorosis (PF) and its classification have been poorly studied. After development of PF classification by D. M. Zislin and E. Ya. Girskaya [3], new study methods have been introduced in clinical practice which have allowed some indications of the disease to be revealed [2, 5, 6, 8]. However, this classification does not take etiology into account. There are no parameters for fluorine in the human biological environment. Both domestic and foreign authors have confirmed t
Deforming osteoarthrosis (DOA) has the highest prevalence rate among joint diseases [1, 3-9]. There is little information about the development of DOA in subjects in contact with fluoride compounds [2].
We have studied the characteristics of the diagnosis and treatment of DOA with patients who had previous contact with fluoride compounds in comparison to primary DOA. 484 patients have been examined, of them 106 had primary DOA, and 378 were workers in the main professions of electrolysis depa
