Journal
JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART B-APPLIED BIOMATERIALS
Volume 74B, Issue 1, Pages 636-642Publisher
WILEY
DOI: 10.1002/jbm.b.30251
Keywords
blood-clot stabilization; bone healing; cell adhesion; fibrin scaffold; implant surface
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The aim of the present study was a quantitative evaluation of the in vitro fibrin clot extension on different implant surfaces. Forty-five disk-shaped commercially pure Grade 2 titanium samples with three different surface topographies (machined, DPS, and Plus) were used in the present study. For the quantitative evaluation of the fibrin clot, 30 specimens were used (10 per group); human whole blood was employed. Venous blood was drawn from three healthy adult volunteers, and 0.2 mL were immediately dropped onto the surface of each specimen. Contact time was 5 min at room temperature; then the samples were rinsed with saline solution and fixed in a buffered solution of glutaraldehyde and paraformaldehyde. Samples were washed again with buffer and dehydrated in an ascending alcohol series. Specimens belonging to all groups were observed under SEM at a magnification of 1000X. From each sample, 50 random micrographs were collected in .tif format with an N x M 1024 X 768 grid of pixels. Quantitative analysis of fibrin clot extension showed the following results: in machined samples fibrin clot extension was 345987.2 +/- 63747.7 pixels(2) (mean +/- SD), in DPS samples fibrin clot extension was 375930.9 +/- 54726.86 pixels(2) (mean +/- SD), and in Plus samples, fibrin clot extension was 612333.6 +/- 46268.42 pixels(2) (mean +/- SD). With ANOVA it was possible to find that there were significant differences among the groups. The Tukey test revealed that the extension of the fibrin clot of Plus samples was statistically higher compared to both machined and DPS samples. The results of this in vitro study indicate that there is a correlation between implant surface morphology and fibrin clot extension. Improvement in surface microtexture complexity seems to determine the formation of a more extensive and three dimensionally complex fibrin scaffold. Further investigations are necessary to explain in more detail the mechanisms that regulate the fibrin clot formation on different implant surfaces. (c) 2005 Wiley Periodicals, Inc.
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