[The experimental search of immunological criteria for identifying stages of development of chronic fluoride intoxication].

The experiment has shown the staging of the development of immune response to the chronic fluoride intoxication. Diagnostic criteria of the initial compensation stage are: leukocytosis against the background of reduced number of lymphocytes and increased one of monocytes; high levels of ceruloplasmin in blood plasma, a progressive increase in TNFalpha and cytokine IL-10. At the decompensation stage there are: leukocytosis with increased number of neutrophils; low levels of ceruloplasmin and the cytokines IL-1beta, IL-4 and the high level of TNFalpha, IL-6, IL-10. At the stage of exhaustion there are: leukopenia against the background of lymphocytosis, a high level of Hp, the low values of the level of IgM, IgG.

[The interrelationship of the thyroid and immune statuses of workers with long-term fluorine exposure]. / Vzaimosviaz' tireoidnogo i immunnogo statusov u rabochikh pri dlitel'nom vozdeistvii ftora.

Thyroid and immune statuses were studied in workers continuously exposed to fluorine. The examinees with euthyroid condition had immune disorders with an allergic tendency (increased number of B-lymphocytes, immunoglobulins A). In workers with subclinical hypothyrosis (tri-iodothyronine reduced in 51%), the immune alterations were more evident, T-lymphocytes count rose, but their functional activity declined, indicating impaired cooperation of immunocytes as a result of imperfect control under low concentrations of tri-iodothyronine.

Immunoglobulin G in cystic lesions of rat enamel organ following fluoride intoxication.

Fluoride given as a high single dose to young rats with developing molars has earlier been shown to cause subameloblastic cysts with disorganized ameloblasts in the cystic wall and an irregular mineralization pattern of the underlying enamel. In the present study immunohistochemistry has been employed to determine if an increased permeability of the enamel organ occurred at the areas of cell disturbances. For this purpose 5-day-old rats were injected with 60 mg sodium fluoride per kg body weight. They were decapitated after 24 h, the maxilla prepared histologically and paraffin sections incubated for the demonstration of IgG according to the avidin-biotin-peroxidase complex method. Staining for IgG was present in the cystic lumina and in areas of disorganized ameloblasts. No reaction was observed in areas of unaffected ameloblasts. It was suggested that the fluoride-induced cell injury increased the permeability of the ameloblastic cell layer. Diffusion of IgG and most likely other substances as well, through the ameloblastic layer may have contributed to cyst formation and to the irregular mineral deposits that have been found in the ameloblastic layer and at the enamel surface.