Abstract

• Related Studies :

  • Involvement of Bmal1 and circadian clock signaling in chondrogenic differentiation of ATDC5 cells by fluoride.

    Highlights Fluoride inhibited chondrocyte viability and delayed chondrocyte differentiation. Fluoride disrupted the circadian clock signaling pathway in ATDC5 cells. Overexpression of Bmal1 reversed the delayed chondrogenic differentiation induced by fluoride. Skeletal fluorosis causes growth plate impairment and growth retardation during bone development. However, the mechanism of how fluoride impairs chondrocyte

  • Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis.

    Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in

  • Expression of core-binding factor a1 and osteocalcin in fluoride-treated fibroblasts and osteoblasts

    To study the effects and importance of fluoride on FBs in the development of extraperiosteal calcification and the ossification of skeletal fluorosis, the presence of the osteogenic phenotype, which is indicated by the expression of core-binding factor a1 (Cbfa1) and osteocalcin (OCN), in an FB cell line (L929) and in

  • Long-term exposure to the fluoride blocks the development of chondrocytes in the ducks: The molecular mechanism of fluoride regulating autophagy and apoptosis.

    Highlights Long-term fluoride exposure blocks the development of chondrocytes. Excessive fluoride could induce chondrocytes apoptosis. Long-term excessive fluoride triggered autophagy. Fluoride-induced chondrocytes apoptosis is associated with CytC/Bcl-2/P53 pathways. Long-term exposure to excessive fluoride causes chronic damage in the body tissues and could lead to skeletal and dental fluorosis. Cartilage damage

  • miR-486-3p regulates CyclinD1 and promotes fluoride-induced osteoblast proliferation and activation.

    Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis. The mechanisms underlying fluoride-induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified. As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism. On the basis

• Related FAN Content :

  • 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.

  • "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 & Osteopetrosis

    One of the most common radiological findings in skeletal fluorosis is osteosclerosis - a hardening of bones with a blurring of the trabecular structure. In advanced cases, the osteosclerotic form of fluorosis may closely resemble the appearance of osteopetrosis, a "marble bone" disease in which the bones are dense, but fragile and prone to fracture.

  • 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.