Effects of short-term low-dose heparin administration on biochemical parameters of bone turnover

Wiel, H.E. van der; Lips, Paul; Huijgens, P.C.; Netelenbos, J. C.

doi:10.1016/s0169-6009(08)80078-5

Cited by 21 publications

(8 citation statements)

References 16 publications

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“…However, long-term heparin treatment is associated with systemic osteoporosis and imbalance of bone metabolism (4,5). Heparin contributes to bone loss by decreasing bone formation (6), and/or increasing bone resorption (7,8). Long-term heparin therapy reduces bone mineral density (BMD) (9).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effects of heparin and the direct factor Xa inhibitor, rivaroxaban, on bone microstructure and metabolism in adult rats

Xia

Zhang

Wang

et al. 2015

Connective Tissue Research

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Section: Introductionmentioning

confidence: 99%

Comparison of the effects of heparin and the direct factor Xa inhibitor, rivaroxaban, on bone microstructure and metabolism in adult rats

Xia

Zhang

Wang

et al. 2015

Connective Tissue Research

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“…Although we cannot rule that Mdk simply acts through modulating the well-known effects of heparin on bone cells, there are several in vitro studies demonstrating binding of Mdk and Ptn to specific membrane proteins, such as syndecans, integrins, low-density lipoprotein receptor-related proteins, the receptor tyrosine kinase ALK, or the receptor tyrosine phosphatase Rptpz. (4,(56)(57)(58)(59)(60)(61)(62)(63)(64)(65) Interestingly, we have observed previously that the expressions of both syndecan-3 and Rptpz increase in the course of osteoblast differentiation and that mice lacking Rptpz display a skeletal phenotype. (27,29) However, since the deficiency of Rptpz resulted in low bone mass, and since Rptpz-deficient calvarial osteoblasts, unlike Mdk-deficient cultures, displayed a marked increase in their proliferation rate, we would assume that Mdk regulates bone formation by other mechanisms.…”

Section: Discussionmentioning

confidence: 97%

Increased trabecular bone formation in mice lacking the growth factor midkine

Neunaber

Catalá-Lehnen

Beil

et al. 2010

Journal of Bone and Mineral Research

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Midkine (Mdk) and pleiotrophin (Ptn) comprise a family of heparin-binding growth factors known primarily for their effects on neuronal cells. Since transgenic mice overexpressing Ptn have been reported to display increased bone density, we have previously analyzed Ptndeficient mice but failed to detect any abnormality of skeletal development and remodeling. Together with the finding that Mdk expression increases in the course of primary osteoblast differentiation, we reasoned that Mdk, rather than Ptn, could play a physiologic role in bone formation. Here, we show that Mdk-deficient mice display an increased trabecular bone volume at 12 and 18 months of age, accompanied by cortical porosity. Histomorphometric quantification demonstrated an increased bone-formation rate compared with wild-type littermates, whereas bone resorption was differentially affected in trabecular and cortical bone of Mdk-deficient mice. To understand the effect of Mdk on bone formation at the molecular level, we performed a genome-wide expression analysis of primary osteoblasts and identified Ank and Enpp1 as Mdk-induced genes whose decreased expression in Mdk-deficient osteoblasts may explain, at least in part, the observed skeletal phenotype. Finally, we performed ovariectomy and observed bone loss only in wild-type but not in Mdk-deficient animals. Taken together, our data demonstrate that Mdk deficiency, at least in mice, results in an increased trabecular bone formation, thereby raising the possibility that Mdk-specific antagonists might prove beneficial in osteoporosis therapy. ß

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“…The findings of Matziolis et al [2002] do not contribute to explain to phenomenon of heparin induced osteoporosis, because inhibitory effects on bone in vivo have been predominantly observed in high dose and long term treatment (>10.000 I.E./day, several weeks of heparin therapy) but not in therapeutical doses used in their experiment. Short-term low-dose heparin administration does not change biochemical parameters of bone resorption [van der Wiel et al, 1993]. We suggest, that in future in vitro experiments on heparin osteoporosis, high doses should be chosen to reach a biological effect on osteoblasts.…”

Section: Heparin Effect On Osteoblast-like Cells In Vitromentioning

confidence: 85%