Nonsteroidal anti-inflammatory drugs for wounds: pain relief or excessive scar formation?
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-beta (TGF-beta) and prostaglandin E2 (PGE2)--are lipid mediators of inflammation involving wound healing. Overproduction of TGF-beta 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-beta and PGE2.
Su
Wen-Hsiang
WH
Department of Obstetrics and Gynecology, Yee-Zen General Hospital, Tao-Yuan county 326, Taiwan.
Cheng
Ming-Huei
MH
Lee
Wen-Ling
WL
Tsou
Tsung-Shan
TS
Chang
Wen-Hsun
WH
Chen
Chien-Sheng
CS
Wang
Peng-Hui
PH
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use*; D002921:Cicatrix / Q000473:pathology / Q000503:physiopathology; D017439:Cicatrix, Hypertrophic / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D010146:Pain / Q000188:drug therapy* / Q000503:physiopathology; D012867:Skin / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D014945:Wound Healing / Q000187:drug effects*
D000894:Anti-Inflammatory Agents, Non-Steroidal