Abstract

The prevalence of dental and skeletal fluorosis was determined among children of Kheru Nayak Thanda of Gulbarga district, where the fluoride concentration in drinking water ranges from 0.6 to 13.4 ppm and the water has low levels of copper and zinc. These children were investigated clinically, radiologically and biochemically. The study revealed that 89% of the children had dental fluorosis and 39% exhibited skeletal fluorosis. Serum samples of these children showed elevated levels of alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), and decreased levels of total protein, albumin, and potassium. Radiographic changes suggestive of osteoporosis, osteosclerosis, and genu valgum were observed.

• Related Studies :

  • Experimental fluorosis in rats: NaF induced changes of bone and bone marrow

    The results of our experiments suggest that increased doses of NaF cause more extensive osteosclerosis due to the decrease in number and/or activity of osteoclasts. Therefore oateosclerosis is caused primarily, not by increased bone formation but, by the inhibition of bone resorption. This view is supported by the fact that

  • Distribution of Fluoride in Plasma, Brain, and Bones and Associated Oxidative Damage After Induced Chronic Fluorosis in Wistar Rats.

    The study was aimed to determine fluoride levels in plasma, brain, and bones of Wistar rats following chronic administration of fluoride at different dose levels and the consequent oxidative damage inflicted in these tissues. Brain histomorphology and bone radiographs were also evaluated to assess the extent of damage in these

  • Bovine calves as ideal bio-indicators for fluoridated drinking water and endemic osteo-dental fluorosis

    Relative susceptibility to fluoride (F) toxicosis in the form of osteo-dental fluorosis was observed in an observational survey of 2,747 mature and 887 immature domestic animals of diverse species living in areas with naturally fluoridated (>1.5 ppm F) drinking water. These animals included buffaloes (Bubalus bubalis), cattle (Bos taurus), camels (Camelus dromedarius),

  • [Clinical analysis and follow-up observation of nine cases of occupational chronic fluorosis in an aluminum factory]

    Objective: To observe the clinical characteristics of occupational chronic fluorosis cases and follow up patients?condition changes after they have been transferred from fluoride work. Methods: In January 2020, the clinical data of occupational chronic fluorosis cases diagnosed in our hospital and their corresponding two-year follow-up data were collected and analyzed. These

  • Effect of sodium fluoride on collagen cross-link precursors.

    Rabbits of similar age and body weight received sodium fluoride (NaF) (50 mg/kg body weight/day) intragastrically for up to 136 days. The acid-soluble collagen of bone, tendon, trachea and skin was extracted and purified. Aldehyde associated with the collagen was determined spectrophotometrically. Bone collagen, which had maximum aldehyde content in

• Related FAN Content :

  • "Pre-Skeletal" Fluorosis

    As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.

  • Fluoride & Osteoarthritis

    While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.

  • Skeletal Fluorosis: The Misdiagnosis Problem

    It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.

  • Fluoride & Spinal Stenosis

    Spinal stenosis is a narrowing of the spaces in the spine that results in pressure being placed on the spinal cord and/or nerve roots. Although stenosis can develop without symptoms, it may produce numbness, tingling, pain and difficulty in walking, as well as a heavy/tired feeling in the legs. It is estimated that 250,000 to 500,000 Americans currently have symptoms of spinal stenosis. Skeletal fluorosis is one cause of stenosis.

  • Factors which increase the risk for skeletal fluorosis

    The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.