Abstract
Long-term excessive fluoride intake is linked to skeletal disease. Skeletal health is influenced by the balance between bone formation and resorption of which osteoblast function is critical. The objectives of this study were to determine the effect of fluoride treatment on osteoblast proliferation, apoptosis and caspase-3 and caspase-9 mRNA expression in vitro. Neonatal rat osteoblasts were cultured in the presence of varying concentrations (0.5-30 mg/l) of sodium fluoride and effects of treatments were determined. Treatment with sodium fluoride inhibited osteoblast proliferation in a dose-dependent fashion and effects were maximal after 120 h incubation. A significant increase in osteoblast apoptosis was observed (after 24 and 72-h treatment) in response to the lowest dose of sodium fluoride (0.5 mg/l) and osteoblast apoptosis was further increased in response to higher doses. Increased-osteoblast caspase-3 and caspase-9 mRNA was also observed in response to sodium fluoride treatment (5 mg/l) for 72 h. Results indicate that negative effects of excess fluoride on skeletal health may be mediated in part by inhibition of osteoblast survival.
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Neuroligin-3 activates Akt-dependent Nrf2 cascade to protect osteoblasts from oxidative stress.
Excessive oxidative stress will cause significant injury to osteoblasts, serving as one major pathological mechanism of osteoporosis. Neuroligin-3 (NLGN3) is a postsynaptic cell adhesion protein and is expressed in the bone. We here explored its potential activity against hydrogen peroxide (H2O2)-induced oxidative injury in cultured osteoblasts. In primary murine and
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Expression of autophagy-related factors LC3A and Beclin 1 and apoptosis-related factors Bcl-2 and BAX in osteoblasts treated with Sodium Fluoride.
Objective: This study aims to analyze the expressions of autophagy-related factors light chain 3 alpha (LC3A) and Beclin 1 and apoptosis-related factors B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (BAX) in primary osteoblasts treated with sodium fluoride (NaF). Methods: Osteoblasts were extracted from Sprague-Dawley rats and treated with 0, 2.5, 5,
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Fluorosis induces endoplasmic reticulum stress and apoptosis in osteoblasts in vivo
The present study investigated the effects of fluoride on endoplasmic reticulum (ER) stress (ERS) and osteoblast apoptosis in vivo. Forty-eight Wistar rats were randomly divided into four groups (12/group) and exposed to 0, 50, 100, and 150 mg/L of fluoride in drinking water for 8 weeks, respectively. Peripheral blood samples and bilateral
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Sodium fluoride suppress proliferation and induce apoptosis through decreased insulin-like growth factor-I expression and oxidative stress in primary cultured mouse osteoblasts
It has been reported that sodium fluoride suppressed proliferation and induced apoptosis in osteoblasts. However, the details about the mechanism at work in bone metabolism are limited. In this study, we further investigated the mechanisms of NaF on proliferation and apoptosis in the primary cultured mouse osteoblasts, which were exposed
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Simultaneous administration of fluoride and selenite regulates proliferation and apoptosis in murine osteoblast-like MC3T3-E1 cells by altering osteoprotegerin.
The receptor activator nuclear factor kappa-B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), are important for maintaining the balance between bone formation and resorption. However, the regulation of microelements on these factors remains unclear. In this study, we used murine osteoblast-like MC3T3-E1 cells to examine the impact of sodium
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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
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"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.
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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
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Fluoride Increases Osteoid Content of Bone
Fluoride's ability to increase the osteoid content of bone is now undisputed. Osteoid is an unmineralized tissue in bone that, in the normal bone remodeling process, ultimately becomes calcified. As some observers have noted, "[t]he main histological change induced by fluoride is the increase of osteoid volume." (Arnala 1985). One way fluoride
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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
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