The effect of suture coated with mesenchymal stem cells and bioactive substrate on tendon repair strength in a rat model.
OBJECTIVE
Exogenously administered mesenchymal stem cells and bioactive molecules are known to enhance tendon healing. Biomolecules have been successfully delivered using sutures that elute growth factors over time. We sought to evaluate the histologic and biomechanical effect of delivering both cells and bioactive substrates on a suture delivery vehicle in comparison with sutures coated with bioactive substrates alone.


METHODS
Bone marrow-derived stem cells were harvested from Sprague-Dawley rat femurs. Experimental cell and substrate-coated, coated suture (CS) group sutures were precoated with intercellular cell adhesion molecule 1 and poly-L-lysine and seeded with labeled bone marrow-derived stem cells. Control (substrate-only [SO] coated) group sutures were coated with intercellular cell adhesion molecule 1 and poly-L-lysine only. Using a matched-paired design, bilateral Sprague-Dawley rat Achilles tendons (n = 105 rats) were transected and randomized to CS or SO repairs. Tendons were harvested at 4, 7, 10, 14, and 28 days and subjected to histologic and mechanical assessment.


RESULTS
Labeled cells were present at repair sites at all time points. The CS suture repairs displayed statistically greater strength compared to SO repairs at 7 days (12.6 ± 5.0 N vs 8.6 ± 3.7 N, respectively) and 10 days (21.2 ± 4.9 N vs 16.4 ± 4.8 N, respectively). There was no significant difference between the strength of CS suture repairs compared with SO repairs at 4 days (8.1 ± 5.1 N vs 6.6 ± 2.3 N, respectively), 14 days (22.8 ± 7.3 N vs 25.1 ± 9.7 N, respectively), and 28 days (40.9 ± 12.4 N vs 34.6 ± 15.0 N, respectively).


CONCLUSIONS
Bioactive CS sutures enhanced repair strength at 7 to 10 days. There was no significant effect at later stages.


CONCLUSIONS
The strength nadir of a tendon repair occurs in the first 2 weeks after surgery. Bioactive suture repair might provide a clinical advantage by jump-starting the repair process during this strength nadir. Improved early strength might, in turn allow earlier unprotected mobilization.
Department of Orthopaedic Surgery, Stanford University Medical Center, Palo Alto, CA, USA. jyao@stanford.edu
Jeffrey
J
Yao
Colin Yi-Loong
CY
Woon
Anthony
A
Behn
Tatiana
T
Korotkova
Don-Young
DY
Park
Varun
V
Gajendran
R Lane
RL
Smith
D000818:Animals; D016009:Chi-Square Distribution; D020099:Coated Materials, Biocompatible; D004195:Disease Models, Animal; D018799:Intercellular Adhesion Molecule-1 / Q000494:pharmacology*; D008297:Male; D059630:Mesenchymal Stem Cells; D011092:Polyethylene Glycols / Q000494:pharmacology*; D011107:Polylysine / Q000031:analogs & derivatives* / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013537:Sutures; D013710:Tendons / Q000601:surgery*; D014945:Wound Healing / Q000502:physiology*
D020099:Coated Materials, Biocompatible; C443714:polylysine-graft-(poly(ethylene glycol)); D018799:Intercellular Adhesion Molecule-1; D011107:Polylysine; D011092:Polyethylene Glycols