Heparin effect on osteoblast‐like cells in vitro

Handschin, Alexander E.; Wanner, Guido A.; Trentz, O.

doi:10.1002/jcb.20176

Cited by 2 publications

(2 citation statements)

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“…However, the findings of in vivo animal studies of the effect of LMWHs on fracture healing remain contentious and no conclusive findings can be drawn from these studies [6,8,9]. Nevertheless, in vitro studies on bone cells [10][11][12] and in vitro studies on bone metabolism [6,[13][14][15][16][17] demonstrate that LMWHs decrease bone formation and, therefore, could potentially delay fracture healing. Evidence exists that LMWHs reduce cancellous bone volume [15,17,19] in a dose-dependent manner [15] and reduce the biomechanical strength of bone [14,15].…”

Section: Discussionmentioning

confidence: 99%

“…In vitro studies have shown that the differentiation of osteoblasts from mesenchymal stem cells is inhibited by heparin and LMWHs, albeit to different extents [11]. Moreover, there is evidence that heparin and LMWH down-regulate genes that are necessary for the maturation of the osteoblasts [11,12]. But not only bone formation can be affected by LMWHs, also fracture haematoma and angiogenesis can be influenced by these substances [8,[18][19][20][21].…”

Section: Discussionmentioning

confidence: 99%

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The influence of low molecular weight heparin on the expression of osteogenic growth factors in human fracture healing

Sarahrudi

Kaiser

Thomas

et al. 2011

International Orthopaedics (SICOT)

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Purpose Anticoagulant therapy with low molecular weight heparins (LMWH) and mechanical compression is considered the gold standard for the prevention of thrombosis. However, evidence exists that LMWHs impair bone metabolism. The aim of this study was therefore to analyse alterations in the expression of M-CSF, VEGF and TGF-ß1 after treatment with enoxaparin in patients with long bone fracture to investigate the effect of LMWH on human fracture healing. Methods A total of 81 patients with long bone fractures were included in the study and divided into two groups. One group comprised patients who received enoxaparin and the other group, patients who did not receive enoxaparin postoperatively. Growth factor levels were analysed in patients' serum and different groups were retrospectively compared. Results M-CSF serum concentrations were found to be significantly higher only at 48 weeks after surgery in enoxaparin. Mean overall VEGF serum concentration was higher in patients with enoxaparin. TGF-β1 serum concentrations were higher at 48 weeks after surgery in patients with enoxaparin. Conclusion This is the first comparative systemic measurement of M-CSF, VEGF and TGF-ß1 serum levels in patients with and without enoxaparin after long bone fracture. Significant differences of the expression of the growth factors after enoxaparin therapy were only observed at week 48 after surgery for M-CSF and TGF-ß1.

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