P132. Epsilon Aminocaproic and Transexamic Acid Decrease Osteoblast Differentiation and Mineralization in Vitro: Could this Influence Spinal Fusion Rates Clinically?

Kara, Firas M.; Verma, Kushagra; Xavier, Shaun; Kamerlink, Jonathan; Kirsch, Thorsten

doi:10.1016/j.spinee.2009.08.392

Cited by 1 publication

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“…The increased rate of cell proliferation resulted in increased matrix mineralization and enhanced expression of key osteoblast markers following long-term TXA treatment. This is in contrast to previous studies reported in the abstract, which showed variable effects on osteoblasts due to protease inhibition or an inhibitory effect of TXA on osteoblast differentiation in vitro [ 19 , 24 ]. However, our results are in line with in vivo studies demonstrating enhanced bone formation and decreased bone resorption in mice lacking tissue-type plasminogen activator or urokinase-type plasminogen activator, which represent the molecular target of TXA [ 25 , 26 ].…”

Section: Discussioncontrasting

confidence: 99%

“…A potential negative or even toxic effect of systemically or locally applied TXA on bone cells could thus significantly delay regeneration and rehabilitation and may impair overall bone turnover in patients receiving TXA. While TXA was found not to affect lumbar spine fusion in mice [ 17 ], results reported in the abstract suggested that the related antifibrinolytic agent, caproic acid, inhibits osteoblast differentiation and matrix mineralization in vitro [ 18 , 19 ]. Together, currently available data are insufficient to allow definite conclusions regarding the effects of TXA on bone cells.…”

Section: Introductionmentioning

confidence: 99%

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Tranexamic Acid Promotes Murine Bone Marrow-Derived Osteoblast Proliferation and Inhibits Osteoclast Formation In Vitro

Baranowsky

Appelt

Tseneva

et al. 2021

IJMS

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Despite modern surgical trauma care, bleeding contributes to one-third of trauma-related death. A significant improvement was obtained through the introduction of tranexamic acid (TXA), which today is widely used in emergency and elective orthopedic surgery to control bleeding. However, concerns remain regarding potential adverse effects on bone turnover and regeneration. Therefore, we employed standardized cell culture systems including primary osteoblasts, osteoclasts, and macrophages to evaluate potential effects of TXA on murine bone cells. While osteoblasts derived from calvarial digestion were not affected, TXA increased cell proliferation and matrix mineralization in bone marrow-derived osteoblasts. Short-term TXA treatment (6 h) failed to alter the expression of osteoblast markers; however, long-term TXA stimulation (10 days) was associated with the increased expression of genes involved in osteoblast differentiation and extracellular matrix synthesis. Similarly, whereas short-term TXA treatment did not affect gene expression in terminally differentiated osteoclasts, long-term TXA stimulation resulted in the potent inhibition of osteoclastogenesis. Finally, in bone marrow-derived macrophages activated with LPS, simultaneous TXA treatment led to a reduced expression of inflammatory cytokines and chemokines. Collectively, our study demonstrates a differential action of TXA on bone cells including osteoanabolic, anti-resorptive, and anti-inflammatory effects in vitro which suggests novel treatment applications.

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