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Epsilon Aminocaproic and Transexamic Acid Decrease Osteoblast Differentiation and Mineralization In Vitro: E‐Poster #53

Kara, Firas M. MD, PhD; Verma, Kushagra MS (NYU Hospital for Joint Diseases); Xavier, Shaun MD; PhD, Thorsten Kirsch; Errico, Thomas J. MD

Spine Journal Meeting Abstracts: September 2009 - Volume 10 - Issue - p 191
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Introduction: The two most common antifibrinoltyic treatments, tranexamic acid (TXA) and epsilon aminocaproic acid (EACA), have not been evaluated in vitro for their potential interaction with osteoblast cells. The purpose of this study was to evaluate the effect of TXA or EACA on osteoblastic differentiation and mineralization in vitro.

Methods: Murine osteoblastic cell line (MC3T3‐E1) was cultured for 17 or 21 days in alpha‐MEM media with 50µg/ml vitamin C and 10mmoles beta‐glycerolphosphate enrichment. EACA and TXA were added at concentrations of 10, 50, 100, 500 or 1000 μg/ml. To evaluate osteoblastic differentiation, alkaline phosphatase (ALP) activity was quantified on day 17. Alizarin red activity was measured on day 21 to assess osteoblastic mineralization.

Results: Osteoblastic differentiation and mineralization were decreased under the presence of EACA or TXA. With exposure to EACA, ALP activity decreased up to 62% on day 17 and alizarin red activity decreased up to 38% on day 21. With exposure to TXA, ALP activity decreased up to 63% on day 17 and alizarin red activity decreased up to 42% on day 21. The response to both medications was dose dependent.

Conclusion: With exposure to TXA or EACA, ALP and Alizarin red activity were both significantly decreased in a dose dependent manner. This reflects a disruption in osteoblastic differentiation and mineralization in vitro, which may have clinical implications.

Significance: We find that antifibrinolytic treatments interfere with osteoblastic cells, which are responsible for mediating spinal fusion after instrumentation. The use of these treatments may affect the rates of spinal fusion observed clinically.

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© 2009 Lippincott Williams & Wilkins, Inc.