DOI: 10.1097/PRS.0b013e3181d51419
,
Issn Print: 0032-1052
Publication Date: 2010/05/01
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Excerpt
I carefully read the letter entitled “Reduce Scar Formation after Lip Repair by Injecting Botulinum Toxin” with great interest and am pleased to reply here. The main content of this letter was to reduce hypertrophic scar after operation to repair cleft lip by using botulinum toxin type A. Because the cause of hypertrophic scar formation is not fully understood, the clinical management of hypertrophic scar remains problematic. Although numerous treatments are currently available, including surgical excision, steroid injection, radiation therapy, laser, and pressure therapy, few can achieve excellent therapeutic results. Thus, I firmly believe that it is necessary to find a better alternative method for treating hypertrophic scar.
On the basis of the above background, some scholars, including Professor Shu-juan Zou, the corresponding author of this letter, are paying more attention to the application of botulinum toxin type A in treating hypertrophic scar. In fact, some clinical observations about improving the eventual appearance of hypertrophic scar by using botulinum toxin type A had been reported several years previously.1,2 Compared with the articles published previously, the purpose of this letter is to give the reader some explanation regarding the reasons for using botulinum toxin type A in treating hypertrophic scar, and their explanation is reasonable and logical. I think that the greatest obstacle to the wide application of botulinum toxin type A in controlling hypertrophic scar is the lack of good understanding of the molecular mechanism of action of botulinum toxin type A on hypertrophic scar. In other words, the molecular mechanism has not been clearly elucidated, with botulinum toxin type A never having been used widely in treating hypertrophic scar. Therefore, it is very important to explain the molecular mechanism of action of botulinum toxin type A on hypertrophic scar. Apart from Professor Shu-juan Zou's viewpoint that botulinum toxin type A improves hypertrophic scar by decreasing tensile force during the course of hypertrophic scar formation, I raised three new points regarding this problem. First, I reviewed some articles published previously. Some scholars have reported that botulinum toxin type A could promote the atrophy of benign prostatic hyperplasia by inducing apoptosis of prostatic epithelium and inhibiting the growth of prostate cancer by inducing apoptotic cancer cells.3,4 Botulinum toxin type A could also induce the temporary apoptosis of nasal glandular cells.5 These articles led me to consider the relationship between botulinum toxin type A and cellular dynamics of fibroblasts derived from hypertrophic scar. My colleagues and I have carried out some experimental research. We found that botulinum toxin type A could influence the cell cycle of fibroblasts derived from hypertrophic scar, and botulinum toxin type A can inhibit the proliferation and promote apoptosis of fibroblasts derived from hypertrophic scar.6,7 Second, botulinum toxin type A could be closely associated with transforming growth factor (TGF)-β1. As is known, TGF-β1 plays an important role in the formation of hypertrophic scar. The high expression of TGF-β1 has obviously promoted the formation and growth of hypertrophic scar. Recent reports have shown that botulinum toxin type A can reduce the expression of TGF-β1 protein in fibroblasts derived from an in vitro experiment.8 The latest advancement I mentioned may partly explain the molecular mechanism of action of botulinum toxin type A on hypertrophic scar. Of course, I have believed that the limitations of the above finding cannot be ignored. The findings were obtained only in fibroblasts cultured in vitro. The in vitro environment may cause some experimental error. Thus, the in vivo experiment should be performed to strengthen the finding.
