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Mediators of Inflammation
Volume 2010, Article ID 413238, 8 pages
Review Article

Nonsteroidal Anti-Inflammatory Drugs for Wounds: Pain Relief or Excessive Scar Formation?

1Department of Obstetrics and Gynecology, Yee-Zen General Hospital, Tao-Yuan county 326, Taiwan
2Graduate Institute of Systems Biology and Bioinformatics, National Central University, Jhongli city, Tao-Yuan county 320, Taiwan
3Institute of Statistics, National Central University, Jhongli city, Tao-Yuan county 320, Taiwan
4Department of Obstetrics and Gynecology and Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei 112, Taiwan
5Department of Life Science, National Central University, Jhongli city, Tao-Yuan county 320, Taiwan
6Department of Medicine, Cheng-Hsin General Hospital, Taipei 112, Taiwan
7Department of Nursing, Taipei Veterans General Hospital, Taipei 112, Taiwan
8Department of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei 112, and National Yang-Ming University Hospital, Ilan 260, Taiwan

Received 3 May 2010; Accepted 2 June 2010

Academic Editor: Philip W. Wertz

Copyright © 2010 Wen-Hsiang Su et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The inflammatory process has direct effects on normal and abnormal wound healing. Hypertrophic scar formation is an aberrant form of wound healing and is an indication of an exaggerated function of fibroblasts and excess accumulation of extracellular matrix during wound healing. Two cytokines—transforming growth factor- (TGF- ) and prostaglandin E2 (PGE2)—are lipid mediators of inflammation involving wound healing. Overproduction of TGF- and suppression of PGE2 are found in excessive wound scarring compared with normal wound healing. Nonsteroidal anti-inflammatory drugs (NSAIDs) or their selective cyclooxygenase-2 (COX-2) inhibitors are frequently used as a pain-killer. However, both NSAIDs and COX-2 inhibitors inhibit PGE2 production, which might exacerbate excessive scar formation, especially when used during the later proliferative phase. Therefore, a balance between cytokines and medication in the pathogenesis of wound healing is needed. This report is a literature review pertaining to wound healing and is focused on TGF- and PGE2.