Abstract

• Related Studies :

  • 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,

  • Fluorosilicic acid induces DNA damage and oxidative stress in bone marrow mesenchymal stem cells.

    Highlights Fluorosilicic acid is the most used additive for water fluoridation. Dental fluorosis can be caused by fluorosilicic acid present in drinking water. DNA damage was caused by fluorosilicic acid in mesenchymal stem cells. Fluorosilicic acid altered bone mineralization in mesenchymal stem cells. DNA damage caused by fluorosilicic acid

  • Bone quality in fluoride-exposed populations: A novel application of the ultrasonic method.

    Highlights A novel ultrasonic bone quality biomarker was tested in a population with low to high exposure to F.- Negative associations were found between F- exposure and bone quality Decreased bone quality reflects net bone loss, abnormal mineralization and altered collagen. The finding highlights that F- exposure has complex

  • 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

  • Cellular and histochemical characteristics of osteoid formed in experimental fluoride poisoning

    The present study on the cellular and histochemical characteristics of osteoid formed in iliac crest bone during fluoride poisoning in rabbits was carried out as there is no information available to date either on its structural or biochemical characteristics. Osteoid formation in bone is prevalent both in fluorosis and 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.