Scarless healing of oral mucosa is characterized by faster resolution of inflammation and control of myofibroblast action compared to skin wounds in the red Duroc pig model
Received 8 April 2009; received in revised form 21 July 2009; accepted 11 September 2009. published online 12 July 2010. Corrected Proof
Abstract
Background
Scar formation following skin trauma can have devastating consequences causing physiological and psychosocial concerns. Currently, there are no accepted predictable treatments to prevent scarring which emphasizes a need for a better understanding of the wound healing and scar formation process.
Objectives
Previously it was shown that healing of small experimental wounds in the oral mucosa of red Duroc pigs results in significantly reduced scar formation as compared with equivalent full-thickness skin wounds. In the present study, scar formation was assessed in 17 times larger experimental wounds in both oral mucosa and skin of the red Duroc pigs.
Methods
Equivalent experimental wounds were created in the oral mucosa and dorsal skin of red Duroc pigs, and scar formation, localization and abundance of key wound healing cells, transforming growth factor-β (TGF-β) and phosphorylated Smad3 (pSmad3) were assessed.
Results
Oral mucosal wounds displayed significantly less clinical and histological scar formation than did the corresponding skin wounds. The number of macrophages, mast cells, TGF-β and pSmad3 immunopositive cells was significantly reduced in the oral mucosal wounds as compared with skin wounds during the maturation stage of the healing process. Although the number of myofibroblasts was significantly elevated, the oral mucosal wounds showed significantly less contraction than did the skin wounds over time.
Conclusions
Earlier resolution of the inflammatory reaction and reduced wound contraction may promote scarless oral mucosal wound healing. In addition, scar formation likely depends not only on the number of myofibroblasts but also on the extracellular environment which regulates their function.
aFaculty of Dentistry, University of British Columbia, Vancouver, BC, Canada
bSchulich School of Dentistry, University of Western Ontario, London, ON, Canada
cDepartment of Surgery, McCaig Institute of Bone and Joint Health, University of Calgary, Calgary, AB, Canada
dDepartment of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
Corresponding author at: Faculty of Dentistry, University of British Columbia, Department of Oral Biological and Medical Sciences, Laboratory of Periodontal Biology, 2199 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. Tel.: +1 604 822 0096; fax: +1 604 822 3562.
ABSTRACT