Strength enhancement of the interlocking mechanism in cross-stitch peripheral sutures for flexor tendon repair: biomechanical comparisons by cyclic loading.

The fatigue strength of three peripheral suture techniques for flexor tendon repair was compared by cyclic loading of repairs in a cotton dental roll tendon model. Thirty pairs of dental roll were sutured using only peripheral sutures with 6-0 polypropylene. An initial cyclic load of 5 N for 500 cycles was applied and increased by 5 N for an additional 500 cycles at each new load until rupture. The fatigue strength of an interlocking cross-stitch suture was 113% greater than a running suture and 36% greater than a standard cross-stitch suture. Interlocking the cross-stitch prevented shortening of the transverse portions under load and appears to be a useful technique for increasing the strength of the peripheral suture.

The mechanical properties of locking and grasping suture loop configurations in four-strand core suture techniques.

We have compared the effect of locking and grasping suture loop configurations in four-strand core suture techniques for tendon repair. Forty canine flexor digitorum profundus tendons were repaired with one of four suture techniques (the grasping cruciate, the double-modified grasping Kessler, the locking cruciate and the double-modified locking Kessler) and tested to failure in a tensile testing machine. The mode of failure in all the locking suture specimens was breakage of the sutures in the locking loops or at suture knots. The sutures did not pull out of the tendon, as was seen in the grasping suture specimens. The greatest tensile strength was found with the double-modified locking Kessler technique which incorporated eight rectangular locking loop configurations.

Differences between locking loops and grasping loops: effects on 2-strand core suture.

The differences between locking and grasping configurations used to suture lacerated flexor tendons were evaluated using a 2-strand core model in human cadaver tendon. Locking suture configurations tighten around bundles of tendon fibers with tension, while grasping loops do not tighten around but pull through tendon fibers and distract with tension. The greatest tensile strength was found in 1-locking, 2-locking, and 2-grasping suture loop configurations per suture strand. The 2-grasping loops per suture strand, however, had the greatest distraction (gapping) as the suture material pulled through the tendon. A single locking configuration per strand yielded the maximum tensile strength with reduced distraction (gapping) at the repair site.

In vivo gene transfer and overexpression of focal adhesion kinase (pp125 FAK) mediated by recombinant adenovirus-induced tendon adhesion formation and epitenon cell change.

Adhesion formation is a frequent complication of tendon injury repair: however, little is known about its mechanisms. The intracellular focal adhesion kinase (FAK)-related signaling pathway may be one of the mechanisms involved in the induction of tendon adhesions. The replication deficient adenovirus containing the FAK gene (pp125 FAK) was constructed and named Adv-Fak. By in vitro transductions with the recombinant virus, overexpression of the FAK protein was documented in transduced cultured primary tendon cells. By in vivo direct injection of Adv-FAK into the space between the tendon and tendon sheath of White Leghorn chickens, FAK gene transfer with overexpression of the FAK protein was detected by immunohistological staining. The morphology of these stained cells changed from the normal flat shape to cuboid. The group with overexpressed adenovirus-mediated FAK had significant adhesion formation, as seen by increased work of flexion (118.197 +/- 29.616), compared with the group with overexpressed adenovirus-mediated beta-galactosidase (67.507 +/- 36.066) (p < 0.0393) and the group with adenovirus-mediated FAK antisense gene transfer (60.357 +/- 48.562) (p < 0.0211). Histological examination of the samples from tendons with Adv-FAK showed fibers between the tendon and tendon sheath; there were no fibers in the cavities of samples of injured tendons infected with Adv-beta gal. Moreover, at the application site of the former tendons, a thick fiber layer without epitenon cells was built up on the outer surface, whereas a thin fiber layer with clear epitenon cells was observed in the tendons to which Adv-beta gal was applied. Our results show that overexpression of FAK can induce tendon adhesion formation in vivo. This indicates that FAK and the FAK-related signaling pathway may be involved in the process of tendon adhesion formation. Understanding the details of this process may help to prevent tendon adhesion and improve healing.