Differential evaluation of excisional non-occluded wound healing in db/db mice.
The full-thickness wound in the genetically diabetic (db/db) mouse is a commonly used model of impaired wound healing. We investigated delayed healing of non-occluded, excisional, full-thickness, dermal wounds in db/db mice in comparison to their normal littermate controls and refined methods for monitoring skin wound re-epithelialization, contraction, granulation tissue formation, and inflammation. We have confirmed with a computer-assisted planimetry method the results of previous studies showing that healing of non-occluded full excision wounds in db/db mice does not occur by contraction as much as in healthy mice. In addition, we have developed separate histological methods for the assessment of re-epithelialization, contraction, granulation tissue (mature, immature, fibrosis), and inflammation (lipogranulomas, secondary, nonspecific). Using a new approach to histological assessment, we have shown that wound closure in db/db mice is delayed owing to: (1) delayed granulation tissue maturation; (2) ''laced,'' widely distributed granulation tissue around fat lobules; and (3) obstruction by lipogranulomas, whereas the rate of re-epithelialization seems to be the same as in C57Bl/6 mice. This methodology should permit a more precise differentiation of effects of novel therapeutic agents on the wound healing process in db/db mice.
Tkalcević
Vanesa Ivetić
VI
GSK Research Centre Zagreb Ltd., Prilaz baruna Filipovića 29, Zagreb, Croatia. vanesa.i.ivetic-tkalcevic@gsk.com
Cuzić
Snjezana
S
Parnham
Michael J
MJ
Pasalić
Ivanka
I
Brajsa
Karmen
K
D000818:Animals; D003920:Diabetes Mellitus / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D005355:Fibrosis / Q000473:pathology; D006097:Granulation Tissue / Q000473:pathology; D007249:Inflammation / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D012867:Skin / Q000293:injuries* / Q000473:pathology; D014945:Wound Healing / Q000502:physiology*; D014950:Wounds, Penetrating / Q000209:etiology / Q000473:pathology*