Abstract

Effects of fluoride (as NaF) on cell cycle, DNA content, and apoptosis of mouse fetal long bone cultures were examined and analyzed by flow cytometry (FCM). The results showed that NaF at 2.5–5.0 µg/mL (2.5–5.0 ppm) had only slight effects on the DNA content and cell cycle distributions. At 10.0 µg/mL, however, NaF increased the number of cells in S phase but did not change the frequency of the G0/G1 and G2/M phase. At 20.0 µg /mL NaF not only increased the number of cells in S phase but also decreased the frequency of the G2/M phase. Cell proliferation was also influenced. At 2.5–10.0 µg/mL NaF did not induce increased apoptosis, but the number of apoptotic cells was significantly increased at 20.0 µg NaF/mL. Therefore F damage to bone may involve promoting apoptosis and disordering cell cycle distributions. Although the differences in DNA content, cell cycle distributions, and apoptosis between controls and the two lower NaF concentrations were not statistically significant, there was evidence of hormesis (paradoxical stimulatory) effects. The results indicate that F exerts a dual influence on osteocytes.

• Related Studies :

  • 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

  • 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

  • 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

  • TGF-ß1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells.

    Highlights NaF exposure significantly decreased the proliferation rate of mouse osteoblast cells in a dose dependent manner. NaF exposure induced autophagy in the osteoblast cells with an increase in TGF-ß1 expression. Overexpression of TGF-ß1 enhanced NaF-induced autophagy. Silencing of TGF-ß1 reduced NaF-induced autophagy. Abstract It is well known that excess fluoride intake

  • 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

• Related FAN Content :

  • 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

  • "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.

  • 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'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 & 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.