Dupuytren’s disease cords are weakened ex vivo by injection of recombinant collagenase G – A proof-of-concept study
- 1Orthopedic Department, Emek Medical Center, Afula, Israel
- 2Faculty of Medicine, Technion, Haifa, Israel
- 3Department of Oral Biology, Goldschleger School of Dental Medicine, Gray Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel
Abstract
Objectives: Dupuytren’s disease is a fibroproliferative disorder that is characterized by collagen-rich cords that cause progressive flexion contractures. Collagenase from Clostridium histolyticum is an established nonsurgical therapy. Herein, we evaluated whether a recombinant form of collagenase G (ColG), expressed in Escherichia coli, weakens Dupuytren’s cords ex vivo. Methods: Cords from Dupuytren’s disease patients were excised during surgery. Using a 30G needle, 0.5 mL of 4 mg/ml ColG or phosphate buffer Saline (PBS) was injected into the cord center. Samples were incubated in saline at 37 °C and mounted via size-1 Prolene Krackow sutures on an Instron tensile testing system. Force vs. displacement curves were recorded. Results: Six cords from five patients were tested (ColG n = 4; PBS n = 2). Representative force–displacement curves showed a reduced slope and lower peak force prior to rupture in ColG-treated samples compared with vehicle. The mean maximum rupture force was lower with ColG than with PBS (0.047 kN vs 0.069 kN), corresponding to ~32% reduction in the force required to tear the cord in this series. Conclusions: Recombinant ColG weakens the tensile strength of Dupuytren’s cords ex vivo, consistent with potent collagenolytic activity. These proof-of-concept pilot data support further studies to define dose–response, optimize formulation and exposure time, and evaluate safety and clinical performance relative to current collagenase-based treatments.
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BibTeX
@article{rubin2026dupuytrens,
title = {{Dupuytren’s disease cords are weakened ex vivo by injection of recombinant collagenase G – A proof-of-concept study}},
author = {Guy Rubin and David Rothem and Ran Tohar and Maayan Gal},
journal = {PLOS One},
year = {2026},
month = sep,
doi = {10.1371/journal.pone.0359330},
url = {https://doi.org/10.1371/journal.pone.0359330},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Dupuytren’s disease cords are weakened ex vivo by injection of recombinant collagenase G – A proof-of-concept study
AU - Guy Rubin
AU - David Rothem
AU - Ran Tohar
AU - Maayan Gal
PY - 2026
DA - 2026/09/24
JO - PLOS One
DO - 10.1371/journal.pone.0359330
UR - https://doi.org/10.1371/journal.pone.0359330
AB - Objectives: Dupuytren’s disease is a fibroproliferative disorder that is characterized by collagen-rich cords that cause progressive flexion contractures. Collagenase from Clostridium histolyticum is an established nonsurgical therapy. Herein, we evaluated whether a recombinant form of collagenase G (ColG), expressed in Escherichia coli, weakens Dupuytren’s cords ex vivo. Methods: Cords from Dupuytren’s disease patients were excised during surgery. Using a 30G needle, 0.5 mL of 4 mg/ml ColG or phosphate buffer Saline (PBS) was injected into the cord center. Samples were incubated in saline at 37 °C and mounted via size-1 Prolene Krackow sutures on an Instron tensile testing system. Force vs. displacement curves were recorded. Results: Six cords from five patients were tested (ColG n = 4; PBS n = 2). Representative force–displacement curves showed a reduced slope and lower peak force prior to rupture in ColG-treated samples compared with vehicle. The mean maximum rupture force was lower with ColG than with PBS (0.047 kN vs 0.069 kN), corresponding to ~32% reduction in the force required to tear the cord in this series. Conclusions: Recombinant ColG weakens the tensile strength of Dupuytren’s cords ex vivo, consistent with potent collagenolytic activity. These proof-of-concept pilot data support further studies to define dose–response, optimize formulation and exposure time, and evaluate safety and clinical performance relative to current collagenase-based treatments.
SN - 1932-6203
ER -