Low-Dose and Short-Duration Matrix Metalloproteinase 9 Inhibition Does Not Affect Adhesion Formation during Murine Flexor Tendon Healing. Issue 3 (March 2016)

• Record Type: Journal Article
• Authors: Orner, Caitlin A.; Geary, Michael B.; Hammert, Warren C.; O'Keefe, Regis J.; Loiselle, Alayna E.
• Is Part Of: Plastic and reconstructive surgery. Volume 137:Issue 3(2016:Mar.)
• Publication Date: 2016-03
• Subjects: Surgery, Plastic -- Periodicals; 617.95205
• DOI: 10.1097/01.prs.0000475823.01907.53
• Languages: English
• ISSNs: 0032-1052

Abstract

Abstract : Background: After flexor tendon injury and repair, adhesion formation is a substantial concern, as it can result in loss of motion and functional disability. Matrix metalloproteinase 9 (Mmp9) is a gelatinase that contributes to degradation of extracellular matrix and is expressed during flexor tendon healing. Mmp9 -/- mice have accelerated remodeling of adhesions during flexor tendon healing, relative to wild-type mice. The purpose of this study was to investigate whether Ro 32-3555, an Mmp9 inhibitor, can improve flexor tendon healing by limiting adhesion formation or enhancing remodeling of scar tissue during murine flexor tendon healing. Methods: Flexor digitorum longus laceration and repair was performed in female C57BL/6J mice. Mice were treated with vehicle or the Mmp9 inhibitor Ro 32-3555 for 8 days. Analysis was performed for digit range of motion and gliding function, biomechanics, gene expression, and Mmp9 activity. Results: An Mmp9 activity assay and zymography confirmed suppression of Mmp9 activity in mice treated with Ro 32-3555. There was no significant difference in tendon gliding or range of motion between vehicle and Ro 32-3555–treated mice. There was also no difference in tendon biomechanical properties between the two groups. Conclusion: Local inhibition of Mmp9 gelatinolytic activity at the flexor tendon repair site is insufficient to alter adhesion formation, remodeling of adhesions, or mechanical properties of healing murine flexor tendons. Abstract : Supplemental Digital Content is available in the text.