Myofibroblasts in healing laser excision wounds
Background and Objective The lack of myofibroblasts, cells responsible for wound contraction, has been suggested to be the underlying factor to the clinically observed minimal contraction in CO2 laser wounds. However, the histologic background to this phenomenon in laser excisions has not been thoro...
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Veröffentlicht in: | Lasers in surgery and medicine 2001, Vol.28 (1), p.74-79 |
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Sprache: | eng |
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Zusammenfassung: | Background and Objective
The lack of myofibroblasts, cells responsible for wound contraction, has been suggested to be the underlying factor to the clinically observed minimal contraction in CO2 laser wounds. However, the histologic background to this phenomenon in laser excisions has not been thoroughly clarified. Therefore, we analyzed the expression of myofibroblasts in healing laser excisions and control excisions made by scalpel.
Study Design/Materials and Methods
CO2 laser (continuous wave, 5 W) or scalpel excision wounds were created in the dorsal tongue mucosa of 144 rats. Sixteen additional rats were kept as untreated controls. Specimens from the tongues were cut at 16 different healing time points and fixed in 10% formalin. Immunohistochemical stainings with monoclonal antibodies to vimentin and to α‐smooth muscle actin were done to determine microscopically the contractile type of myofibroblasts.
Results
The maximum amount of myofibroblasts was almost three times higher in scalpel than in laser excisions. The peak value was reached at 4 days in laser and at 3 days in scalpel wounds. The increase reverted to normal levels at 14 days in laser and at 6 days in scalpel wounds, respectively.
Conclusion
Myofibroblasts appeared and disappeared slower in laser wounds. There were clearly fewer myofibroblasts in CO2 laser than in corresponding scalpel excisions known to heal by contraction. The lack of contractile myofibroblasts, therefore, is suggested as the reason for the minimal degree of contraction in CO2 laser excision wounds. Lasers Surg. Med. 28:74–79, 2001. © 2001 Wiley‐Liss, Inc. |
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ISSN: | 0196-8092 1096-9101 |
DOI: | 10.1002/1096-9101(2001)28:1<74::AID-LSM1019>3.0.CO;2-B |