The antioxidant effect of estrogen and Selective Estrogen Receptor Modulators in the inhibition of osteocyte apoptosis in vitro

Mann, V.; Huber, C.; Kogianni, Giolanta; Collins, Frances; Noble, Brendon

doi:10.1016/j.bone.2006.10.014

Cited by 102 publications

(69 citation statements)

References 42 publications

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“…Healthy bone is tightly regulated and maintained in order to prevent significant alterations in bone mass or mechanical strength after each remodeling cycle (29). Indeed, oxidative stress alters bone remodeling process causing an unbalance between osteoclast and osteoblast activity, this can lead to metabolic bone diseases and contribute to the pathogenesis of skeletal system disorders including osteoporosis characterized by low bone mineral density and decrease in bone mass, which makes the bone weak and more prone to fracture (18,(33)(34)(35)(36). Recent evidences in a limited number of clinical studies have shown that ROS and/or antioxidant systems can be involved in the pathogenesis of bone loss (36)(37)(38)(39).…”

Section: Oxidative Stress In Bone Remodelingmentioning

confidence: 99%

Oxidative stress in bone remodeling: role of antioxidants

Domazetovic

Marcucci

Iantomasi

et al. 2017

ccmbm

511

524

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SummaryROS are highly reactive molecules which consist of a number of diverse chemical species, including radical and non-radical oxygen species. Oxidative stress occurs as a result of an overproduction of ROS not balanced by an adequate level of antioxidants. The natural antioxidants are: thiol compounds among which GSH is the most representative, and non-thiol compounds such as polyphenols, vitamins and also various enzymes. Many diseases have been linked to oxidative stress including bone diseases among which one of the most important is the osteoporosis. The redox state changes are also related to the bone remodeling process which allows the continuous bone regeneration through the coordinated action of bone cells: osteoclasts, osteoblasts and osteocytes. Changes in ROS and/or antioxidant systems seem to be involved in the pathogenesis of bone loss. ROS induce the apoptosis of osteoblasts and osteocytes, and this favours osteoclastogenesis and inhibits the mineralization and osteogenesis. Excessive osteocyte apoptosis correlates with oxidative stress causing an imbalance in favor of osteoclastogenesis which leads to increased turnover of bone remodeling and bone loss. Antioxidants either directly or by counteracting the action of oxidants contribute to activate the differentiation of osteoblasts, mineralization process and the reduction of osteoclast activity. In fact, a marked decrease in plasma antioxidants was found in aged or osteoporotic women. Some evidence shows a link among nutrients, antioxidant intake and bone health. Recent data demonstrate the antioxidant properties of various nutrients and their influence on bone metabolism. Polyphenols and anthocyanins are the most abundant antioxidants in the diet, and nutritional approaches to antioxidant strategies, in animals or selected groups of patients with osteoporosis or inflammatory bone diseases, suggest the antioxidant use in anti-resorptive therapies for the treatment and prevention of bone loss.

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Section: Oxidative Stress In Bone Remodelingmentioning

confidence: 99%

Oxidative stress in bone remodeling: role of antioxidants

Domazetovic

Marcucci

Iantomasi

et al. 2017

ccmbm

511

524

View full text Add to dashboard Cite

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“…Additionally, as described above, it is assumed that a significant increase in AGEs cross-link formation in the Met/OVX group may be attributed to elevated oxidation reactions induced by hyperhomocysteinemia [50]. Interestingly, Mann et al [59] showed that RLX decreased circulating Hcys levels and also oxidative stress resulting in the inhibition of osteocyte apoptosis via reduction in oxygen species. Therefore, we suggest that RLX may ameliorate excessive accumulation of AGEs regardless of estrogen and circulating Hcys status.…”

Section: Raloxifene and Cross-linksmentioning

confidence: 99%

Raloxifene ameliorates detrimental enzymatic and nonenzymatic collagen cross-links and bone strength in rabbits with hyperhomocysteinemia

et al. 2009

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“…(40) The mechanism by which raloxifene exerts its beneficial effect at the material level is not well understood; however, it has been hypothesized that raloxifene may alter the organic matrix, (38) and in particular, collagen, which is known to contribute to the biomechanical (41) and intrinsic properties of bone. (42) It should also be noted that SERMs are known to have a protective effect on osteocytes in vitro (43) ; however, no convincing evidence of this has been observed in vivo in humans. (44) PTH induced the highest increase in maximal load of all treatments tested; in fact, maximal load was increased by almost 50% compared with OVX and significantly higher than in sham.…”

mentioning

confidence: 99%

Selective Modification of Bone Quality by PTH, Pamidronate, or Raloxifene

Brennan

Rizzoli

Ammann

2009

Journal of Bone and Mineral Research

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Bone strength, a determinant of resistance to fracture, depends on BMD, geometry, microarchitecture, bone turnover rates, and properties of the bone at the material level. Despite comparable antifracture efficacy, anti-catabolics and bone anabolic agents are likely to modify the various determinants of bone strength in very different ways. Eight weeks after ovariectomy (OVX), 8-mo-old osteoporotic rats received pamidronate (APD; 0.6 mg/kg, 5 days/mo, SC), raloxifene (3 mg/kg, 5/7 days, tube feeding), PTH(1-34) (10 mg/kg, 5/7 days, SC), or vehicle for 16 wk, and we measured vertebral BMD, maximal load, stiffness and energy, microarchitecture, and material properties by nanoindentation, which allows the calculation of the elastic modulus, tissue hardness, and working energy. Markers of bone turnover, plasma osteocalcin, and urinary deoxypyridinoline (Dpd) were also determined. PTH induced greater maximal load than APD or raloxifene, as well as greater absorbed energy, BMD, and increased bone turnover markers. PTH markedly increased trabecular bone volume and connectivity to values higher than sham. Animals treated with APD had BV/TV values significantly higher than OVX but lower than sham, whereas raloxifene had no effect. Tissue hardness was identical in PTH-treated and OVX untreated controls. In contrast, APD reversed the decline in strength to levels not significantly different to sham, reduced bone turnover, and increased hardness. Raloxifene markedly increased material level cortical hardness and elastic modulus. These results show the different mechanisms by which anti-catabolics and bone anabolics reduce fracture risk. PTH influences microarchitecture, whereas bisphosphonates alter material-level bone properties, with probable opposite effects on remodeling space. Raloxifene primarily improved the material stiffness at the cortical level.

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The antioxidant effect of estrogen and Selective Estrogen Receptor Modulators in the inhibition of osteocyte apoptosis in vitro

Cited by 102 publications

References 42 publications

Oxidative stress in bone remodeling: role of antioxidants

Oxidative stress in bone remodeling: role of antioxidants

Raloxifene ameliorates detrimental enzymatic and nonenzymatic collagen cross-links and bone strength in rabbits with hyperhomocysteinemia

Selective Modification of Bone Quality by PTH, Pamidronate, or Raloxifene

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