In this study, we established a delayed healing chronic type wound model in
order to investigate the etiology of chronic wound healing, including woun
d contraction. Establishment of the model was important for clarification o
f the mechanism(s) of chronic wound healing and wound contraction and for u
se in evaluating therapeutic efficacy. A pedicled skin flap was raised bene
ath the panniculus carnosus membrane on the backs of mice, and after the lo
ose connective tissue at the base of the flap was completely removed surgic
ally, the flap was replaced and sutured. Seven days after surgery, a full-t
hickness defect measuring 1.5 x 1.5 cm was made in the center of the skin f
lap. At that time, a defect of the same size, including the panniculus carn
osus membrane, was made in another group of mice as controls, and changes w
ith time in wound area were compared between the two groups. The exudate re
tained on the wound surface was collected, and various cytokines contained
in the exudate were measured. In the control group, the wound rapidly contr
acted and almost completely epithelialized and closed 27 days after surgery
. On the other hand, the wound area was significantly larger in the delayed
model than in the control animals during the observation period, revealing
a delay in wound contraction. Transforming growth factor-beta, interleukin
-1 beta, and tumor necrosis factor-alpha in the exudates from the wound of
the model were significantly higher than in those of the control group, whe
reas interleukin-6 was low in the model. From these results, it was conclud
ed that this model could be a useful experimental system for studies on wou
nd contraction as well as clarifying the mechanism of so called chronic typ
e wounds.