Biomedical Engineering Reference
In-Depth Information
Table 5.3
(continued)
Animal
model (day
observed)
Reactant
C
a
S
a
R
a
References
G. Contracted collagen gel cultured with keratinocytes and fibroblasts (Living skin equivalent,
LSE)
Rat (Sprague-
Dawley; 720
days)
Contracted
collagen gel
cultured with
KC and FB
d
Contraction
inhibited
No rete ridges Dermis
formed
Bell et al.
1981a, b; Hull
et al. 1983b
Rat (Fischer) Contracted
collagen gel
cultured with
KC and FB
d
Contraction
inhibited
No rete ridges Dermis
formed
Bell et al.
1983; Hull
et al. 1983a
Rat (Lewis)
(30 days)
Contracted
collagen gel
cultured with
KC and FB
d
Contraction
inhibited
No rete ridges Dermis
formed
Hull et al.
1983b
Rat (Lewis;
14 days)
Contracted
collagen gel
cultured with
KC (FB
d
omitted)
No inhibition
of contraction
Scar formed
No dermis
formed
Hull et al.
1983b
Athymic
mouse (60
days)
Contracted
collagen gel
cultured with
KC and FB
d
Minimal
contraction
No rete ridges Dermis
formed
Hansbrough
et al. 1994
a
Numerical data entered whenever available; otherwise, investigators' comments were quoted.
Values in parentheses were estimated by the author of this volume, based on investigators' data
b
For abbreviations of growth factors used in table, see text (Chap. 5)
c
Data not available
d
Fibroblasts
table. Only data from studies with the dermis-free defect have been included. Quan-
titative data have been classified using the simple defect closure rule, discussed in
Chap. 4: The original defect area closes by fractional contributions from each of
three closure modes, i.e., contraction (
C
), scar synthesis (
S
), and regeneration®)
adding up to 100; or,
C
+
S
+
R
= 100.
The detailed data in Table
5.3
show that growth factors, including platelet-derived
growth factor (PDGF-BB), basic fibroblast growth factor (bFGF), and transforming
growth factor-b1 (TGF-b1), had no effect on the configuration of the control (un-
treated defect). Use of each of these growth factors typically led to a configuration
of the final state that was nearly identical to that of the untreated defect (i.e., repair).
Pharmacological agents, such as cortisone, prednisolone, aspirin, and prostaglandin
inhibitor (ETA), did not significantly modify the final state of repair (although the
kinetics of defect closure were affected occasionally). Neither did grafting with
keratinocyte sheets modify the final state of repair.
