Abstract
Damage to collagen protein and its gene expression caused by excessive fluoride (F) ingestion plays an important role in the etiology of skeletal fluorosis. Recently we found that industrial F pollution significantly increased the expression level of type II collagen gene (COL2A1) in rib cartilage of Inner Mongolia cashmere goats. With the same goats and methods, we have now quantified another important collagen gene, the rib COL1A2 gene, which encodes an ?2(I) polypeptide chain assembled into collagen molecules. The results showed that the expression level of COL1A2 and COL1A2/?-actin increased by 88% and 81%, respectively.
-
-
The dose-time effects of fluoride on the expression and DNA methylation level of the promoter region of BMP-2 and BMP-7 in rats.
Highlights Fluoride has a dose-time effect on Bone Morphogenetic Protein-2 expression. Fluoride increases the expression of Bone Morphogenetic Protein-2 and 7. DNA methylation may be involved in fluoride regulation of target protein expression. Skeletal fluorosis is a chronic metabolic bone disease caused by excessive exposed to fluoride. Recent studies have
-
Suppression of Sclerostin and Dickkopf-1 levels in patients with fluorine bone injury
Evidence has been accumulating for the role of Sclerostin and Dickkopf-1 as the antagonists of Wnt/B-Catenin signaling pathway, which suppresses bone formation through inhibiting osteoblastic function. To get deep-inside information about the expression of the antagonists in patients with fluorine bone injury, a case-control study was conducted in two counties
-
Fluoride regulates the expression of extracellular matrix HSPG and related signaling pathways FGFR3 and Ihh/PTHrP feedback loop during endochondral ossification.
Highlights Fluoride promotes the expression of HSPG in growth plate of rats during endochondral ossification. Fluoride activates FGFR3 signaling pathway during endochondral ossification. Fluoride inhibits Ihh/PTHrP feedback loop during endochondral ossification. Abstract Fluoride promotes the expression of HSPG in growth plate of rats during endochondral ossification. Fluoride activates FGFR3 signaling pathway
-
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
-
Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.
Background: Oxidative stress plays an important role in the pathogenesis of endemic fluorosis. We analyzed associations between oxidative stress-related gene polymorphisms (PON1 rs662, CAT rs769217, rs2300182, and SOD2 rs11968525) and skeletal fluorosis, and examined potential gene–environment interactions with dietary vitamin C, vitamin E, zinc, and selenium intake. Methods: A cross-sectional study
Related Studies :
-
-
-
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.
-
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.
-
Skeletal Fluorosis in India & China
In India and China, scientists have repeatedly found that skeletal fluorosis occurs in populations drinking water with just 0.7 to 1.5 ppm fluoride. Although nutritional deficiencies and hot climates make populations in India and China more susceptible to fluoride toxicity than is generally the case in western countries, this fact does not remove the relevance of the Indian and Chinese experience to the situation in fluoridating countries. This is because (a) nutritional deficiencies also exist in the western world, particularly in low-income communities, and (b) some individuals, including those with kidney disease, can be just as -- if not more -- susceptible to fluoride toxicity.
-
X-Ray Diagnosis of Skeletal Fluorosis
In 1937, Kaj Roholm published his seminal study Fluorine Intoxication in which he described three phases of bone changes that occur in skeletal fluorosis. (See below). These three phases, which are detectable by x-ray, have been widely used as a diagnostic guide for detecting the disease. They describe an osteosclerotic bone disease that develops first in the axial skeleton (the spine, pelvis, and ribs), and ultimately results in extensive calcification of ligaments and cartilage, as well as bony outgrowths such as osteophytes and exostoses. Subsequent research has found, however, that x-rays provide a very crude measure for diagnosing fluorosis since the disease can cause symptoms and effects (e.g., osteoarthritis) before, and in the absence of, radiologicaly detectable osteosclerosis in the spine.
Related FAN Content :
-