Abstract

Fluoride as a supplement can affect the structural integrity of bone. Fluoride that is incorporated in the mineral, substitutes for the hydroxyl group producing hydroxyfluorapatite crystals and presumed to increase bone strength by preventing resorption. Because of this, fluoride therapy has been carried out in clinical trials for the treatment of osteoporosis. Although fluoride renders the mineralized tissues resistant to resorption, the effects of fluoride on bone strength and cortical bone mass specially that of the developing bone has not yet been characterized. The purpose of the study was to analyze the effect of fluoride on developing teeth and bone in young rats through histomorphometry. Sixteen wistar rats were used and divided into two groups; non-fluoride supplemented (control) and fluoride-supplemented groups. Four weeks after, the rats were sacrificed and the mandible and femur were subjected to histological and histomorphometric analyses. No clinical difference was observed between the two groups. The amount of mineralized cartilage was higher in fluoride-supplemented group compared to the control group. However, the amount of new bone was lesser in fluoride-supplemented group compared to the control group. This histomorphometric analysis showed that during endochondral ossification, 10 ppm fluoride administration caused some changes in calcified cartilage and bone mineralization in young rats.

• Related Studies :

  • Periarticular calcifications containing giant pseudo-crystals of francolite in skeletal fluorosis from 1,1-difluoroethane 'huffing".

    Highlights Diagnosing inhalant use disorder can be lifesaving. Chronic inhalation of F--containing vapors can cause skeletal fluorosis (SF). SF can elevate bone density and cause periostitis and ectopic calcification. Francolite is a carbonate-rich fluorapatite. Periarticular calcification in SF can comprise giant pseudo-crystals of francolite. Inhalant use disorder is a psychiatric

  • Fluoride increases the susceptibility of developmental dysplasia of the hip via increasing capsular laxity triggered by cell apoptosis and oxidative stress in vivo and in vitro.

    Highlights Fluoride does not cause DDH directly but increases its susceptibility by increasing hip capsular laxity. Hip laxity results from apoptosis occurring in capsular fibroblast after fluoride exposure. Fluoride-induced fibroblast apoptosis was triggered by oxidative stress via mitochondrial pathway. The etiology of developmental dysplasia of the hip (DDH) is multifactorial,

  • Rachitomimetic effects of fluoride feeding on the skeletal tissues of growing pigs

    Young pigs, fed for 30, 6o and 90 days on a diet containing 1,000 parts per million of sodium fluoride, have shown defective growth and mineralization of bones, costochondral beading, softened and deformed epiphyseal plates, and enlarged and malformed bone trabeculae. Histochemical studies of demineralized sections have revealed a decrease in

  • Effects of fluoride on cortical bone remodeling in the growing domestic pig

    The purpose of the experiment was to assess the effects of fluoride (F-) on the remodeling process of cortical bone. Sixteen pigs, eight experimental animals receiving a supplement of 2 mg F-/kg b.w. and eight controls, were studied in individual sites from age 8 to 14 months. At slaughter samples

  • Effects of fluoride on bone in Finland. Histomorphometry of cadaver bone from low and high fluoride areas

    In three different areas of Finland, fluoride in bone and its effect on the histomorphometry of trabecular bone was studied. Bone samples were taken from cadavers from a low-fluoride area (fluoride concentration under 0.3 ppm), an area with fluoridated drinking water (1.0-1.2 ppm) and a high-fluoride area (over 1.5 ppm).

• 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.

  • 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 & 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.