Abstract
Background
Hypertrophic scar (HS) is a refractory skin disease caused by major physical damage or other inflammation. Some reports found that botulinum toxin type A (BTXA) could be an alternative treatment of the HS. Therefore, the authors studied the effects of BTXA on the treatment of HS and the dose response of BTXA.
Methods
Hypertrophic scars were harvested from the ears of 18 young adult New Zealand big-eared rabbits and treated with BTXA or triamcinolone acetonide (TAC) in vivo experiment. The hypertrophic index (HI) was measured by histological examination. Collagen fibrils were checked by sirius red straining, and the cell nucleuses of fibroblasts were checked by Ki67.
Results
The HI of hypertrophic scars with BTXA treatment was lower than that with phosphate-buffered saline treatment (P < 0.05). Compared with the TAC treatment group, the efficacy of treatment with the middle dose of BTXA (1.0, 1.5 IU) had no significant difference, as shown by sirius red staining and immunohistochemistry Ki67.
Conclusion
These results demonstrated that BTXA effectively improved the appearance of hypertrophic scars and inhibited the formation of collagen fibrils and fibroblasts in vivo. Treatment with the middle dose of BTXA achieved similar efficacy as TAC treatment, indicating that BTXA might be useful for inhibiting hypertrophic scars and worth investigating further.
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The authors declared that they have no conflicts of interest to this work and that they do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.
Appendix
Appendix
Photographs of our model are shown here. The left picture shows the hypertrophic scars just after the surgical operation, and the right shows the hypertrophic scars after 60 days with BTXA treatment.
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Liu, Dq., Li, Xj. & Weng, Xj. Effect of BTXA on Inhibiting Hypertrophic Scar Formation in a Rabbit Ear Model. Aesth Plast Surg 41, 721–728 (2017). https://doi.org/10.1007/s00266-017-0803-5
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DOI: https://doi.org/10.1007/s00266-017-0803-5