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Uptake of nickel from 316L stainless steel into contacting osteoblastic cells and metal ion interference with BMP‐2‐induced alkaline phosphatase
Author(s) -
Mölders Martina,
Felix Joachim,
Bingmann Dieter,
Hirner Alfred,
Wiemann Martin
Publication year - 2007
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.31244
Subject(s) - alkaline phosphatase , bone morphogenetic protein 2 , stromal cell , materials science , nickel , metal , bone morphogenetic protein , chelation , bone cell , cell culture , biophysics , biochemistry , nuclear chemistry , metallurgy , microbiology and biotechnology , medicine , enzyme , chemistry , in vitro , biology , genetics , gene
Bone cells contacting nickel (Ni)‐containing implant materials may be affected by Ni species via disturbed signaling pathways involved in bone cell development. Here we analyze effects of the Ni‐containing steel 316L and major metal constituents thereof on bone morphogenetic protein‐2 (BMP‐2)‐induced alkaline phosphatase (ALP) of MC3T3‐E1 cells. While cells grew normally on 316L, cellular Ni content increased 10‐fold vs. control within 4 days. With respect to the major components of 316L, Ni 2+ (3–50 μM) was most inhibitory to BMP‐2‐induced ALP, whereas even 50 μM Fe 3+ , Cr 3+ , Mo 5+ , or Mn 2+ had no such effect. In line with this, BMP‐2‐induced ALP was significantly reduced in cells on 316L. This effect was not prevented by the metal ion chelator diethylenetriaminepentaacetic acid (DTPA). Instead, DTPA abolished the stimulatory effect of BMP‐2 on ALP, pointing to chelatable metal ions involved. Zn 2+ , as one possible candidate, antagonized the Ni 2+ inhibition of BMP‐2‐induced ALP in both MC3T3‐E1 and human bone marrow stromal cells. Results show that cells contacting 316L steel are exposed to increased concentrations of Ni which suffice to impair BMP‐2‐induced ALP activity. Zn 2+ , as a competitor of this inhibition, may help to restore normal osteoblastic function and bone development under these conditions. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res 2007