Fluoride Reduces Bone Strength in Older Rats

Turner, Charles H.; Hasegawa, Koutaro; Zhang, W.; Wilson, Marie; Li, Y.; Dunipace, Ann J.

doi:10.1177/00220345950740080701

Cited by 47 publications

(16 citation statements)

References 23 publications

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“…Fluoride treatment can cause secondary hyperparathyroidism [9] and, therefore, affect levels of some calciumregulating hormones. It has yet to be determined whether fluoride's anabolic effects on bone are mediated by changes in calcium-regulating hormones or mitogenic growth factors.Besides increasing bone mass, fluoride treatment has resulted in decreased bone tissue strength in many animal studies [10][11][12][13][14][15], whereas other animal studies showed no effect of fluoride on bone strength [for example, 16]. Reduced bone strength may be caused by mineralization defects in the bone that can result from high serum fluoride levels [17][18][19][20][21].…”

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confidence: 99%

Fluoride Treatment Increased Serum IGF-1, Bone Turnover, and Bone Mass, but Not Bone Strength, in Rabbits

et al. 1997

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We hypothesized that fluoride partly acts by changing the levels of circulating calcium-regulating hormones and skeletal growth factors. The effects of oral fluoride on 24 female, Dutch-Belted, young adult rabbits were studied. The rabbits were divided into two study groups, one control and the other receiving about 16 mg fluoride/rabbit/day in their drinking water. After 6 months of fluoride dosing, all rabbits were euthanized and bone and blood samples were taken for analyses. Fluoride treatment increased serum and bone fluoride levels by over an order of magnitude (P < 0.001), but did not affect body weight or the following serum biochemical variables: urea, creatinine, phosphorus, total protein, albumin, bilirubin, SGOT, or total alkaline phosphatase. No skeletal fluorosis or osteomalacia was observed histologically, nor did fluoride affect serum PTH or Vitamin D metabolites (P > 0.4). BAP was increased 37% (P < 0.05) by fluoride; serum TRAP was increased 42% (P < 0.05); serum IGF-1 was increased 40% (P < 0.05). Fluoride increased the vertebral BV/TV by 35% (P < 0.05) and tibial ash weight by 10% (P < 0.05). However, the increases in bone mass and bone formation were not reflected in improved bone strength. Fluoride decreased bone strength by about 19% in the L5 vertebra (P < 0.01) and 25% in the femoral neck (P < 0. 05). X-ray diffraction showed altered mineral crystal thickness in fluoride-treated bones (P < 0.001), and there was a negative association between crystal width and fracture stress of the femur (P < 0.02). In conclusion, fluoride's effects on bone mass and bone turnover were not mediated by PTH. IGF-1 was increased by fluoride and was associated with increased bone turnover, but was not correlated with bone formation markers. High-dose fluoride treatment did not improve, but decreased, bone strength in rabbits, even in the absence of impaired mineralization.

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Fluoride Treatment Increased Serum IGF-1, Bone Turnover, and Bone Mass, but Not Bone Strength, in Rabbits

et al. 1997

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“…It is this lack of trabecular connectivity that reduces bone quality despite the increase in bone mass. These observations in humans have been extended in rodents (Søgaard et al, 1995;Turner et al, 1995). At low local concentrations such as those that occur following fluoride modification of dental implants, there is enhanced osteoblastic differentiation and interfacial bone formation concomitant with increased expression of osteogenic markers at the implant site (Cooper et al, 2006;Monjo et al, 2008).…”

Section: Actions On Bone and Bone Cellsmentioning

confidence: 93%

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

2010

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Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride's actions on bone cells predominate as anabolic effects both in vitro and in vivo. More recently, fluoride has been shown to induce osteoclastogenesis in mice. Fluorides appear to mediate their actions through the MAPK signaling pathway and can lead to changes in gene expression, cell stress, and cell death. Different strains of inbred mice demonstrate differential physiological responses to ingested fluoride. Genetic studies in mice are capable of identifying and characterizing fluoride-responsive genetic variations. Ultimately, this can lead to the identification of at-risk human populations who are susceptible to the unwanted or potentially adverse effects of fluoride action and to the elucidation of fundamental mechanisms by which fluoride affects biomineralization.

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“…A good example is fluoride treatment. While fluoride can improve bone mass [4,5], fluoride incorporation into bone mineral reduces intrinsic biomechanical properties [6]. Simply soaking bone samples in fluoride solution can reduce bone strength by as much as 62% [7] (Fig.…”

Section: Figmentioning

confidence: 99%

Biomechanics of Bone: Determinants of Skeletal Fragility and Bone Quality

Turner

2002

Osteoporosis International

457

290

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Bone fragility can be defined by biomechanical parameters, including ultimate force (a measure of strength), ultimate displacement (reciprocal of brittleness) and work to failure (energy absorption). Bone fragility is influenced by bone size, shape, architecture and tissue 'quality'. Many osteoporosis treatments build bone mass but also change tissue quality. Antiresorptive therapies, such as bisphosphonates, substantially reduce bone turnover, impairing microdamage repair and causing increased bone mineralization, which can increase the brittleness of bone. Anabolic therapies, such as parathyroid hormone (PTH-(1-84)) or teriparatide (PTH-( 1-34)), increase bone turnover and porosity, which offset some of the positive effects on bone strength. Osteoporosis therapies may also affect bone architecture by causing the redistribution of bone structure. Restructuring of bone during treatment may change bone fragility, even in the absence of drug effects on bone mineral density (BMD). This effect may explain why some drugs can affect fracture incidence disproportionately to changes in BMD. For instance, in a recent clinical trial, PTH-(1-34) therapy caused a dose-related increase in spinal BMD without any dose-dependent effect on the observed decrease in spinal fracture incidence. This apparent disassociation between spinal BMD and bone fragility is probably due to effects of PTH-(1-34) on bone architecture within vertebral bodies. While it has been shown that BMD is highly heritable, bone mineral distribution and architecture are also under strong genetic influence. Recent findings suggest that different genes regulate trabecular and cortical structures within lumbar vertebrae, producing a wide range of bone architectural designs. These findings suggest that there is no single optimal bone architecture; instead many different architectural solutions produce adequate bone strength.

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Fluoride Reduces Bone Strength in Older Rats

Cited by 47 publications

References 23 publications

Fluoride Treatment Increased Serum IGF-1, Bone Turnover, and Bone Mass, but Not Bone Strength, in Rabbits

Fluoride Treatment Increased Serum IGF-1, Bone Turnover, and Bone Mass, but Not Bone Strength, in Rabbits

Fluoride’s Effects on the Formation of Teeth and Bones, and the Influence of Genetics

Biomechanics of Bone: Determinants of Skeletal Fragility and Bone Quality

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