Biomedical Engineering Reference
In-Depth Information
In contrast, standard TAN does not negatively influence osteoblast attachment
and proliferation in this manner (Fig. 1 ), even in its standard microrough form
[ 60 ].
The effect of altering surface microtopography has also been shown to be
beneficial for selective cell adhesion [ 61 , 62 ]. Differences in surface microto-
pography have also been implicated in controlling proliferation, with several
studies indicating that microrough surfaces have reduced proliferative capacity
compared with smooth surfaces [ 63 - 66 ]. However, with this reduced proliferative
capacity emerges as a more differentiated osteoblast phenotype on the microrough
surfaces as indicated by alkaline phosphatase activity [ 63 , 65 , 66 ]. Moreover, it is
suggested that the process of matrix mineralization is dependent on surface
microroughness [ 65 ]. This roughness-dependent response is also seen for ECM
components with surfaces of varying roughness displaying varied synthesis of
collagen type I, vitronectin and fibronectin [ 40 , 66 ].
Both cytokine and growth factors involved in modulating fracture healing
response have been shown to be differentially influenced by surface microto-
pography. Boyan et al. [ 67 ] have extensively shown that local factors such as
TGFb 1 and prostaglandin E 2 display a surface-roughness-dependent response.
Kieswetter et al. [ 68 ] also identified the relationship between surface micror-
oughness and TGFb 1 levels, reporting a 3-5 times higher activity on coarse
sandblasted and titanium-plasma-sprayed surfaces, respectively, compared with
tissue culture plastic. In a similar trend to prostaglandin E 2 production, TGFb 1 is
also found at low levels on smooth surfaces, whereas a marked increase is
reported for microrough substrates. This growth factor has been shown to be
pivotal to bone formation for many reasons, some of which include its ability to
stimulate
MSC
proliferation,
matrix
production
and
the
downregulation
of
osteoclast activity.
Osseointegration at the bone-implant interface requires key regulatory
pathways which influence osteoblastogenesis, promotion of osteoblastic differ-
entiation and maturation. Some studies claim to identify 'roughness response
genes' via microarrays and although some of the data may be valuable, given the
differences between relatively similar studies, it is often difficult to consolidate
the findings [ 69 , 70 ]. Other studies prefer to focus on specific genes or tran-
scription factors known to be fundamental for osteoblast differentiation. Most of
the time, this includes real-time PCR, which is a powerful and sensitive method
for detecting changes at an mRNA level. It should be noted, however, that
confirmation at the protein level is also an important consideration as it is
known, for instance, that changes in mRNA levels may not be efficiently
translated to similar changes in protein level. Many of these studies have
highlighted specific bone-related markers involved in osteoblast differentiation
and mineralization that are regulated in a substrate-dependent manner [ 71 - 74 ].
Furthermore, osteospecific MSC fate determination also appears to be substrate-
dependent [ 75 , 76 ].
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