Osteoporosis as an Hereditary Disease

Ralston, Stuart H.

doi:10.1007/s12018-010-9073-3

Cited by 17 publications

(12 citation statements)

References 63 publications

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“…However, the results are somewhat disappointing and, as it also happens with other complex disorders, only a minor proportion of the disease risk is explained by the genetic loci so far identified. 22 Several anabolic and antiresorptive drugs are available to treat osteoporosis. Some of them have been shown to increase BMD and decrease the risk of vertebral fractures roughly by 50%, and the risk of peripheral fractures by 20-30%, approximately.…”

Section: Discussionmentioning

confidence: 99%

Common allelic variants of the farnesyl diphosphate synthase gene influence the response of osteoporotic women to bisphosphonates

et al. 2010

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Farnesyl diphosphate synthase (FDPS) is necessary for osteoclast survival and activity and is considered as a major molecular target of aminobisphosphonates. Our objective was to analyze the influence of FDPS polymorphisms on bone mineral density (BMD) and the response to antiresortive drugs. Three single-nucleotide polymorphisms of FDPS were analyzed in 1186 postmenopausal women. There was only a marginally significant association of baseline hip BMD with rs11264359 alleles (P=0.043). However, among 191 women receiving antiresortive therapy, there was a very significant association between rs2297480 or rs11264359 alleles and the BMD changes after aminobisphosphonate therapy for an average period of 2.5 years (P=0.001). The genotype explained 7.2% of the variance in the BMD response. On the other hand, there was no association between the BMD changes after raloxifene therapy and any of the polymorphisms studied. These results suggest that common polymorphisms of the FDPS gene influence the response to aminobisphosphonates.

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Section: Discussionmentioning

confidence: 99%

Common allelic variants of the farnesyl diphosphate synthase gene influence the response of osteoporotic women to bisphosphonates

et al. 2010

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“…In rare instances, osteoporosis can be inherited due to mutations in single genes. Mutations of two genes of type 1 collagen (COL1A1 and COL1A2) are responsible for the dominant osteoporotic disease called “osteogenesis imperfecta”, which is characterized by low bone mass and increased bone fragility [ 51 , 52 , 53 , 54 ]. Osteoporosis inheritance has also been linked with inactivating mutations in the aromatase (CYP19A1) and estrogen receptor alpha genes (ERα) [ 55 , 56 ].…”

Section: Postmenopausal Osteoporosis: a Silent Diseasementioning

confidence: 99%

Potential Role of Lycopene in the Prevention of Postmenopausal Bone Loss: Evidence from Molecular to Clinical Studies

Walallawita

Wolber

Ziv‐Gal

et al. 2020

IJMS

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Osteoporosis is a metabolic bone disease characterized by reduced bone mineral density, which affects the quality of life of the aging population. Furthermore, disruption of bone microarchitecture and the alteration of non-collagenous protein in bones lead to higher fracture risk. This is most common in postmenopausal women. Certain medications are being used for the treatment of osteoporosis; however, these may be accompanied by undesirable side effects. Phytochemicals from fruits and vegetables are a source of micronutrients for the maintenance of bone health. Among them, lycopene has recently been shown to have a potential protective effect against bone loss. Lycopene is a lipid-soluble carotenoid that exists in both all-trans and cis-configurations in nature. Tomato and tomato products are rich sources of lycopene. Several human epidemiological studies, supplemented by in vivo and in vitro studies, have shown decreased bone loss following the consumption of lycopene/tomato. However, there are still limited studies that have evaluated the effect of lycopene on the prevention of bone loss in postmenopausal women. Therefore, the aim of this review is to summarize the relevant literature on the potential impact of lycopene on postmenopausal bone loss with molecular and clinical evidence, including an overview of bone biology and the pathophysiology of osteoporosis.

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“…The genetic component in the pathogenesis of this disorder is clearly evidenced by its aggregation in families [2][3][4]. However, candidate gene and genome-wide association studies aiming to identify the loci involved have been somewhat disappointing, and the genes identified by those studies only explain a minor proportion of the genetic risk of the disease [5].…”

Section: Introductionmentioning

confidence: 99%

Analysis of the Bone MicroRNome in Osteoporotic Fractures

et al. 2014

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Osteoporosis causes important morbidity among elderly individuals. Fragility fractures, and especially hip fractures, have a particularly negative impact on the patients' quality of life. The role of epigenetic mechanisms in the pathogenesis of many disorders is increasingly recognized, yet little is known about their role in non-malignant bone disorders such as osteoporosis. The aim of this study was to explore the expression of miRNAs in patients with osteoporotic hip fractures. Trabecular bone samples were obtained from the femoral heads of patients undergoing replacement surgery for osteoporotic hip fractures and non-fracture controls with hip osteoarthritis. Levels of 760 miRNA were analyzed by real-time PCR. Thirteen miRNAs showed nominally significant (p < 0.05) differences between both groups. Six miRNAs (miR-187, miR-193a-3p, miR-214, miR518f, miR-636, and miR-210) were selected for the replication stage. These miRNAs were individually analyzed in a larger group of 38 bone samples. At this stage, we confirmed statistically significant differences across groups for mir-187 and miR-518f. The median relative expression levels of miR-187 were 5.3-fold higher in the non-fracture group (p = 0.002). On the contrary, miR-518f was preferentially expressed in bones from osteoporotic patients (8.6-fold higher in fractures; p = 0.046). In this first hypothesis-free study of the bone microRNome we found two miRNAs, miR-187, and miR-518f, differentially regulated in osteoporotic bone. Further studies are needed to elucidate the mechanisms involved in the association of these miRNAs with fractures.

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Osteoporosis as an Hereditary Disease

Cited by 17 publications

References 63 publications

Common allelic variants of the farnesyl diphosphate synthase gene influence the response of osteoporotic women to bisphosphonates

Common allelic variants of the farnesyl diphosphate synthase gene influence the response of osteoporotic women to bisphosphonates

Potential Role of Lycopene in the Prevention of Postmenopausal Bone Loss: Evidence from Molecular to Clinical Studies

Analysis of the Bone MicroRNome in Osteoporotic Fractures

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