Biomedical Engineering Reference
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5.3 Results of Implantation of Amidated Gels
There was little-observed cell infiltration of the gels implanted
intramuscularly in the rat after one week due to the high vis-
coelasticity of the gel, but cells were apparent after four weeks.
Cells had infiltrated throughout the gel and into the center of the
gel mass where the cells were actively producing an extracellular
matrix.Therewasnoappearanceofgeldegradationbefore8weeks,
and this was still only minimal after 12 weeks. The presence of
neovessels was observed in all samples beyond the two-week time
period.
Immunohistochemical analysis of the implants demonstrated
very low overall levels of inflammation before eight weeks that
reachedapeakateightweeksandthendeclinedthereafter.Thiswas
particularly so for the staining of the presence of immature and dif-
ferentiating macrophages and the expression of MHC-I antigen.
The positively stained cells were within both the gel and at the
host-gel interface. After 12 weeks, the positive staining was con-
fined to the interface only, with a reduction in the inflammatory
response within the gel samples. Overall, MHC-II expression was
low for all implantation periods. There was discrete TGF- β expres-
sion, possibly associated with the vasculature, but this was at a low
level.
Mature adipocytes were present within all 12-week implants
(Fig. 5.6), the variable size indicating progression of fat droplet
accumulationandthereforeadipocytedevelopmentandmaturation.
Althoughthepresenceofacertainnumberofmatureadipocytescan
be put down to infiltration from the indigenous subdermal fat layer,
many examples of gel without association with this layer containing
adipocytes were observed, strongly suggesting de novo adipogene-
sis. Tissue integration with the host was excellent, with no fibrous
layer evident at the interface between the gel and the indigenous
tissue (Fig 5.7).
Neovessels were observed from early time periods, demonstrat-
ing an angiogenic response due to the presence of the gel. We
propose that the inflammatory cell infiltration with low levels of
activation-related expression (e.g., MHC-II) linked with increased
angiogenesiswas responsible for in vivo adipogenesis.
 
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