Relation of folates, vitamin B12 and homocysteine to vertebral bone mineral density change in postmenopausal women. A five-year longitudinal evaluation

Cagnacci, Angelo; Bagni, B; Zini, Annalisa; Cannoletta, Marianna; Generali, Matteo; Volpe, Annibale

doi:10.1016/j.bone.2007.10.022

Cited by 69 publications

(36 citation statements)

References 36 publications

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“…Evidence to support an effect of folate on bone While folate has been linked to BMD and a reduced fracture risk (54,70) , there is limited evidence to support a direct mechanistic effect of folate on bone, although one study reported a reduced trabecular thickness of bone in individuals with low folate status v. those with higher status (71) . Folate could have an indirect role on bone remodelling cells via its metabolic link (as a methyl source) to the methylation of DNA, proteins and other molecules and there is evidence, albeit somewhat inconsistent, to support a reduced methylation capacity as a pathomechanism responsible for poor bone health (57,(72)(73)(74) .…”

Section: Evidence To Support An Effect Of Homocysteine On Bonementioning

confidence: 99%

B-vitamins and bone in health and disease: the current evidence

et al. 2014

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Osteoporosis, a metabolic skeletal disease characterised by decreased bone mass and increased fracture risk, is a growing public health problem. Among the various risk factors for osteoporosis, calcium and vitamin D have well-established protective roles, but it is likely that other nutritional factors are also implicated. This review will explore the emerging evidence supporting a role for certain B-vitamins, homocysteine and the 677C→T polymorphism in the gene encoding the folate-metabolising enzyme methylenetetrahydrofolate reductase, in bone health and disease. The evidence, however, is not entirely consistent and as yet no clear mechanism has been defined to explain the potential link between B-vitamins and bone health. Coeliac disease, a common condition of malabsorption, induced by gluten ingestion in genetically susceptible individuals, is associated with an increased risk both of osteoporosis and inadequate B-vitamin status. Given the growing body of evidence linking low bone mineral density and/or increased fracture risk with low B-vitamin status and elevated homocysteine, optimal B-vitamin status may play an important protective role against osteoporosis in coeliac disease; to date, no trial has addressed this possible link.

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Section: Evidence To Support An Effect Of Homocysteine On Bonementioning

confidence: 99%

B-vitamins and bone in health and disease: the current evidence

et al. 2014

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“…Several studies have reported that low plasma B 12 levels are associated with reduced bone quality [5,8,9,13,14], but this relation has not been observed by others [15][16][17]. More consistently, however, are the observations that increased Hcy may be a predictive factor for fracture risk [13][14][15][18][19][20][21].…”

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confidence: 99%

Vitamin B12 Deficiency Stimulates Osteoclastogenesis via Increased Homocysteine and Methylmalonic Acid

et al. 2009

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The risk of nutrient deficiencies increases with age in our modern Western society, and vitamin B 12 deficiency is especially prevalent in the elderly and causes increased homocysteine (Hcy) and methylmalonic acid (MMA) levels. These three factors have been recognized as risk factors for reduced bone mineral density and increased fracture risk, though mechanistic evidence is still lacking. In the present study, we investigated the influence of B 12 , Hcy, and MMA on differentiation and activity of bone cells. B 12 deficiency did not affect the onset of osteoblast differentiation, maturation, matrix mineralization, or adipocyte differentiation from human mesenchymal stem cells (hMSCs). B 12 deficiency caused an increase in the secretion of Hcy and MMA into the culture medium by osteoblasts, but Hcy and MMA appeared to have no effect on hMSC osteoblast differentiation. We further studied the effect of B 12 , Hcy, and MMA on the formation of multinucleated tartrate-resistant acid phosphatase-positive osteoclasts from mouse bone marrow. We observed that B 12 did not show an effect on osteoclastogenesis. However, Hcy as well as MMA were found to induce osteoclastogenesis in a dose-dependent manner. On the basis of these results, we conclude that B 12 deficiency may lead to decreased bone mass by increased osteoclast formation due to increased MMA and Hcy levels.Osteoporosis is a complex multifactorial disease with a strong genetic component, but lifestyle factors are also important for maintenance of bone mass. Nutrition is one of the factors that contributes to bone health. During the first decades of life, adequate intake of calcium and vitamin D is essential to establish peak bone mass (see [1,2] and references therein). It has also been observed that nutritional deficiencies can cause impaired growth and skeletal abnormalities during childhood [3], while in adults inadequate intake of nutrients such as proteins, vitamins, and minerals has been associated with loss of bone quality [2,4]. Nutritional deficiency is very common in the elderly, emphasizing that adequate nutrient intake may slow down the age-related loss of bone mass.A challenge in nutrition research is to identify food components that contribute to the maintenance of bone health. During the last years, vitamin B 12 has gained particular attention since a number of epidemiological studies have reported a correlation between B 12 status and bone quality and fracture risk [5][6][7][8][9]. The micronutrient B 12 is involved as a cofactor in two enzymatic reactions [10]. The enzyme methionine synthase requires B 12 for the remethylation of homocysteine (Hcy) into methionine. The other enzyme dependent on B 12 is methylmalonyl-CoA mutase, which catalyzes the conversion of methylmalonyl-CoA into succinyl-CoA. As a consequence of B 12 deficiency, these

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“…Indeed, there were more cases than controls in the quartile with the highest Hcy levels, however, the difference was not statistically significant. The mechanisms which have been suggested to explain the effect of Hcy include impaired bone collagen formation by Hcy and increased osteoclast activity (Cagnacci et al, 2008). Several studies have reported that levels of Hcy, particularly those in the upper quartile, represent an independent risk factor for osteoporotic fractures (van Meurs et al, 2004;McLean et al, 2004;Sato et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Recent data suggest that homocysteine (Hcy) and folate affects bone metabolism, bone quality, and fracture risk in humans. Because circulating Hcy depends on folate, vitamin B6, and vitamin B12, Hcy may be suitable as a risk indicator for micronutrient deficiency-related osteoporotic fractures (Herrmann et al, 2005;Cagnacci et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Association of vascular endothelial growth factor gene polymorphisms with osteoporotic vertebral compression fractures in postmenopausal women

et al. 2010

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Vascular endothelial growth factor (VEGF) is involved in bone formation through its role in angiogenesis. VEGF is also known to promote the healing of fractures. Thus, we determined whether or not VEGF -2578C>A, -1154G>A, -634G>C, and 936C>T polymorphisms and haplotypes are associated with osteoporotic vertebral compression fractures (OVCF) in postmenopausal Korean women. The study subjects consisted of 82 patients with osteoporotic vertebral compression fractures and 117 control postmenopausal Korean women. PCR-RFLP and real-time PCR were used to analyze the VEGF polymorphisms. Homocysteine levels were also measured to determine whether or not polymorphisms of the VEGFgene affect homocysteine/folate metabolism. The AA genotype of the -2578C>A polymorphism was significantly

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Relation of folates, vitamin B12 and homocysteine to vertebral bone mineral density change in postmenopausal women. A five-year longitudinal evaluation

Cited by 69 publications

References 36 publications

B-vitamins and bone in health and disease: the current evidence

B-vitamins and bone in health and disease: the current evidence

Vitamin B12 Deficiency Stimulates Osteoclastogenesis via Increased Homocysteine and Methylmalonic Acid

Association of vascular endothelial growth factor gene polymorphisms with osteoporotic vertebral compression fractures in postmenopausal women

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