Abstract

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 fluoride (NaF) and/or sodium selenite (Na2SeO3) on the OPG/RANKL system. MC3T3-E1 cells were treated with OPG or RANKL siRNA (or left untreated), and subsequently divided into a control group and five experimental groups, which were exposed to different concentrations of NaF and/or Na2SeO3, and subsequently analysed at 24 h. In particular, we examined cell viability, OPG and RANKL mRNA and protein expression, caspase-3 activity, and the cell cycle of the various cell groups. In summary, our findings suggest that the administration of NaF and/or Na2SeO3 affects the expression of OPG in osteoblast-like MC3T3-E1 cells, thereby contributing to the proliferation and apoptosis induced by the OPG.

• Related Studies :

  • 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

  • Sodium fluoride modulates caprine osteoblast proliferation and differentiation

    The cellular and molecular pathways of fluoride toxicity in osteoblasts are not very well understood. Therefore, the objective of the present study was to evaluate the effects of sodium fluoride (NaF) on caprine osteoblasts cultured in vitro. Caprine osteoblasts at 2.0 x 10(-4) cells/ml were incubated in vitro with NaF

  • 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

  • Effect of fluoride on expression of pura gene and CaM gene in newborn rat osteoblasts.

    To explore the effect of fluoride (F) on the expression of purine-rich element-binding protein (PURA) gene and calmodulin (CaM) gene in osteoblasts of newborn rats, parietal calvaria bone osteoblast cultures of 48-hr-old rats were treated for 48 hr with sodium fluoride (NaF) at concentrations of 0 (control), 0.5, 2, and

  • Different Effects of Fluoride Exposure on the Three Major Bone Cell Types.

    Fluoride accumulates and is toxic to bones. Clinical bone lesions occur in a phased manner, being less severe early in the natural course of skeletal fluorosis. Previous research rarely focused on osteocyte, osteoclast, and osteoblast at the same time, although these three types of cells are involved in the process

• Related FAN Content :

  • 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

  • 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

  • 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

  • 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.