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.
-
-
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
-
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
-
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
-
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
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.
-
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.
-
"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.
-
Symposium on the non-skeletal phase of chronic fluorosis: The Joints
Of 300 patients with endemic skeletal fluorosis 187 (110 children and 77 adults) showed evidence of arthritis. The spine, especially its cervical portion, appeared to be mainly involved; elbow, hip and knee joints followed next in order.
-
Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
Related FAN Content :
-