Examination of the Process Underlying Healing of Epithelial Defects by Using Different Wound Dressings

Toshiro Kibe PhD, Oral and Maxillofacial Surgery, Kagoshima University, Graduate School of Medicine and Dental Sciences, Kagoshima, Japan
Kentaro Oyama , Oral and Maxillofacial Surgery, Kagoshima University, Graduate School of Medicine and Dental Sciences, Kagoshima, Japan
Takao Fuchigami , Oral and Maxillofacial Surgery, Kagoshima University, Graduate School of Medicine and Dental Sciences, Kagoshima, Japan
Takuya Yoshimura , Oral and Maxillofacial Surgery, Kagoshima University, Graduate School of Medicine and Dental Sciences, Kagoshima, Japan
Kazuhide Matsunaga PhD, Oral and Maxillofacial Surgery, Kagoshima University, Graduate School of Medicine and Dental Sciences, Kagoshima, Japan
Kazuhide Nishihara , Department of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
Tetsushi Taguchi Ph.D., Biomaterials Unit, National Institute for Materials Science, Tsukuba, Japan
Norifumi Nakamura PhD, Department of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
Introduction: Scar contracture occurring during recovery of epithelial defects after the oral and maxillofacial surgery including palatoplasty is known to cause various functional disorders, such as facial deformities, disturbance of maxillary development, speech disorders, and dysphasia. Various types of wound-healing dressings have been used to assist recovery of epithelial defects. However, conventional dressings result in scar contracture around the epithelial defect after the oral and maxillofacial surgery. Therefore, we suggest that it is important to develop a new wound dressing that can suppress scar contracture after oral and maxillofacial surgery and can improve the quality of life of patients. Scar contracture is thought to be caused by α-smooth muscle actin (α-SMA) expressed in myofibroblasts; however, the mechanism underlying scar contracture is not well understood. Therefore, before developing a new dressing, it is important to understand this mechanism. To this end, we analyzed the wound-healing process using existing wound dressings.  

Material: Full-thickness defects (8 mm in diameter) were created busing a biopsy punch on the backs of 7-week-old rats, and the wound areas were marked. Then, the wounded areas were covered with NEOVEIL® or TERUDERMIS® and fixed using a rat jacket. In the control rats, the wounded areas were not covered with any dressing. The rats were killed on day 4 or 7 after injury, and the wound area, neo-epithelium length, and α-SMA expression were evaluated and compared between the control, NEOVEIL®, and TERUDERMIS® groups. We measured distance and the area between markings and observed the contracture of the wound. For histopathological investigation, we measured the neo-epithelium length by hematoxylin and eosin staining and determined α-SMA expression in the wound area tissue.

Result: The epithelial defect areas in the control group on day 4 or 7 were significantly smaller than those in the NEOVEIL® and TERUDERMIS® groups.　There was no significant difference in the neo-epithelium length among the control, NEOVEIL®, and TERUDERMIS® groups. The expression of α-SMA in granulation tissue on day 4 peaked in all groups. The expression of α-SMA in the control groups on day 4 or 7 after injury was greater than that in the NEOVEIL® and TERUDERMIS® groups.　However, there was no significant difference between the expression of α-SMA between the NEOVEIL® and TERUDERMIS® groups.

Conclusion: In this study, the NEOVEIL® and TERUDERMIS® groups showed a suppression in contracture and lower expression of α-SMA in the wound areas. However, there was no significant difference in the neo-epithelium length among the control, NEOVEIL®, and TERUDERMIS® groups. These results suggest that the difference in the closure speed of the epithelial defect area is caused by contracture instead of the neo-epithelium length. On the basis of these results, we intend to develop a new wound-healing dressing.

References

1. P. H. Liem, N. Morimoto, R. Ito, K. Kawai, S. Suzuki. Treating a collagen scaffold with a low concentration of nicotine promoted angiogenesis and wound healing. J SURG RES. 2012;E1-E9

2. U. Mirastschijski, R. Schnabel, J. Claes, W. Schneider, M. S. Ågren, C. Haaksma, J.J. Tomasek. Matrix metalloproteinase inhibition delays wound healing and blocks the latent transforming growth factor-β1-promoted myofibroblast formation and function. WOUND REPAIR and REGENERATION 2010;(18) 223-234

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