Abstract
We carried out a pilot project to examine the alterations in trabecular bone remodeling activity of spayed Beagle dams exposed to 0.7 mg/kg body wt/day of sodium fluoride (NaF) for a 6 month period. The results indicated that short-term NaF administration does activate trabecular bone remodeling activity by stimulating the formation of new Basic Multicellular Units (BMUs) of bone remodeling activity. However, interference with bone cell differentiation, with the functional efficiency and/or life-span of individual osteoclasts and osteoblasts followed. Cellular toxic effects appear early with NaF administration, and as such, suggest that the increases in bone mass seen early in the course of NaF treatment may be negated by prolonged administration of this substance. However, preservation of bone mass will probably result with long-term therapy, due to decreases in numbers of bone cells, in their functional efficiencies, and in their individual life-spans.
-
-
Is the severity of osteosclerosis of fluorosis proportional to the dose of fluoride intake?
Histomorphometric study was made on a series of sections of undecalcified epiphyseal femoral specimens from rats with experimental fluorosis. The results revealed osteosclerosis in Group A (5 ppm) being more severe than that in Group B (25 ppm). With the increase of fluoride dose, the parameters fell down instead of
-
Aberrant methylation-induced dysfunction of p16 is associated with osteoblast activation caused by fluoride.
Chronic exposure to fluoride continues to be a public health problem worldwide, affecting thousands of people. Fluoride can cause abnormal proliferation and activation of osteoblast and osteoclast, leading to skeletal fluorosis that can cause pain and harm to joints and bones and even lead to permanent disability. Nevertheless, there is
-
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
-
Efficacy and Safety of Postmenopausal Osteoporosis Treatments: A Systematic Review and Network Meta-Analysis of Randomized Controlled Trials.
Although a range of pharmacological interventions is available, it remains uncertain which treatment for osteoporosis is more effective. This network meta-analysis study aimed to compare different drug efficacy and safety in randomized controlled trials (RCTs) for the treatment of postmenopausal osteoporosis. PubMed, EMBASE, MEDLINE, Clinicaltrial.gov, Cochrane library, Google scholar were
-
Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.
Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts,
Related Studies :
-
-
-
Fluoride's Effect on Osteoblasts (Bone-Forming Cells)
As noted by the National Research Council, "[p]erhaps the single clearest effect of fluoride on the skeleton is its stimulation of osteoblast proliferation." (NRC 2006). Osteoblasts are bone-forming cells. "Stimulatory effects of fluoride on osteoblasts result in formation of osteoid, which subsequently undergoes mineralization." (Fisher RL, et al. 1989). If the new
-
"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 & Osteocytes
The osteocyte is a type of bone cell which is increasingly believed to play an important role in repairing defects that arise in bone, thereby maintaining the bone’s structural integrity. Because osteocytes are engulfed in fluoride-rich bone mineral and help resorb the bone as part of the remodeling process, they
-
Fluoride & Osteoclasts
It is well established that fluoride exposure can increase bone formation by increasing the proliferation of osteoblasts. Less clear is fluoride's impact on bone resorption and the cells (osteoclasts) that resorb bone. Many have assumed that fluoride's main effect on bone resorption and osteoclasts is an inhibitory one (i.e., less
Related FAN Content :
-