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Updated: May 20, 2026

Murine Flexor Tendon Injury and Repair Surgery
07:32

Murine Flexor Tendon Injury and Repair Surgery

Published on: September 19, 2016

Bone marrow-derived matrix metalloproteinase-9 is associated with fibrous adhesion formation after murine flexor

Alayna E Loiselle1, Benjamin J Frisch, Matthew Wolenski

  • 1Center for Musculoskeletal Research, University of Rochester, Rochester, New York, United States of America.

Plos One
|July 14, 2012
PubMed

Insights

Matrix metalloproteinase-9 (Mmp9) contributes to tendon adhesions after injury. Reducing Mmp9 in mice lessened adhesions without compromising tendon strength, identifying Mmp9 as a therapeutic target.

Area of Science:

  • Biomedical Engineering
  • Musculoskeletal Research
  • Wound Healing

Background:

  • Adhesion formation after tendon repair is a significant clinical problem.
  • The role of matrix metalloproteinases (MMPs), particularly MMP9, in adhesion pathogenesis is not fully understood.
  • Previous work linked increased MMP9 expression to adhesions in a murine flexor digitorum (FDL) tendon repair model.

Purpose of the Study:

  • To investigate the specific role of MMP9 in tendon healing and adhesion formation.
  • To elucidate the cellular source and mechanism by which MMP9 influences adhesions.
  • To evaluate MMP9 as a potential therapeutic target for reducing adhesions.

Main Methods:

  • Utilized a murine FDL tendon repair model in wild-type (WT) and Mmp9 knockout (Mmp9(-/-)) mice.
  • Assessed cellular, molecular, and biomechanical properties of tendon healing.
  • Employed bone marrow transplantation studies using GFP-labeled WT cells in myeloablated Mmp9(-/-) mice.

Main Results:

  • Mmp9(-/-) mice exhibited significantly reduced adhesions by 21 days post-repair compared to WT mice, with no loss of tendon strength.
  • MMP9 deletion altered the expression timing of key tendon healing genes, including Gdf5, Smad8, collagen I, and collagen III.
  • WT bone marrow cells migrated to the repair site, and their presence in Mmp9(-/-) mice increased adhesion formation.

Conclusions:

  • MMP9, primarily sourced from bone marrow-derived cells migrating to the injury site, plays a critical role in mediating adhesion formation following tendon repair.
  • Targeting MMP9 presents a promising strategy to mitigate adhesion development and improve outcomes in tendon healing.

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