Biomedical Engineering Reference
In-Depth Information
xyapatite) [133−135], polymers (such as poly lactic-glycolic acid, and
polyurethane) [58], carbon nanoibers/nanotubes and composites
[58, 105].
Another study suggested higher adsorption of ibronectin on
hydrophilic self-assembled monolayers (SAMs) surfaces with greater
focal adhesion formation (integrin binding) evident in the osteoblast
cells adhered to the hydrophilic SAM treated surfaces [113].
Both cell speciicity and extent of cell adhesion are altered, too.
Depending on the nano-architecture cell, spreading may be increased
or decreased. Lim and coworkers [80] more directly related protein
adsorption, cell adhesion and the active process of attachment by
measurement of increased focal adhesion kinase (FAK) activity.
Surface roughness at the nanoscale is an important determinant of
protein interactions that ultimately direct cell activity in control of
tissue formation at implant surfaces [101].
Nanofeatures of a surface affect both cell adhesion and cell
motility. Andersson and coworkers [11] compared cell morphology
and cytokine production on titanium substrates with 15 mm wide
and 185 nm-deep grooves versus Ti substrates with 100 nm high,
168 nm diameter hemispherical nanopillars. The cells appeared
partially aligned to the grooves and had a cytokine release similar to
that found from cells on lat surfaces. Osteoprogenitor cell adhesion
was enhanced on poly-L-lactide (PLLA) and polystyrene (PS) surface
with nanoscale and micron-scale roughness compared to smooth
surfaces. OCT-1 osteoblast-like cells grew along the surface with two
different nanoscale surfaces (PLLA) and grew inside micron-scale
pits of PS [127]. Similar conclusions were made when comparing
nano- and micron-scale grain boundary effects on osteoblast cell
adhesion and proliferation [142].
Cell proliferation appears to be enhanced by nanoscale
topography, too. Webster and coworkers [135] observed increased
osteoblast proliferation on the nanoscale materials tested. The
mechanism(s) affecting this process is not deined. However, it can
be speculated that many of the events associated with adhesion can
affect signaling pathways that control proliferation.
Several investigators have demonstrated the relative diminution
of ibroblast adhesion compared to osteoblast adhesion when
nano- and micron-structured surfaces were evaluated [83, 104].
For example, on nano-sized materials, the afinity ratio between
osteoblasts and ibroblasts was 3 to 1. In the conventional materials,
the ratio was 1 to 1 [136]. Bacterial adhesion and proliferation is
