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Treatment of injuries of the flexor digitorum profundus (FDP) tendon insertion site has changed little during the past 50 years. in part because there are no reports describing flexor tendon insertion site healing. Our objective was to assess the effects of repair technique and post-operative time on tendon-bone healing using a canine model of injury and repair. We transected 48 FDP tendons from 24 dogs at their insertions and repaired them using either a four-or eight-strand suture technique. We assessed the mechanical properties of the repaired tendon-bone construct, tendon collagen biochemistry, and distal phalanx bone tnineral density (BMD) at 0, 10, 21 and 42 days. Suture metliod had no significant eKect on any outcome ( j~ > 0.05). In particular, use of an eight-strand double modified Kessler technique did not result in increased stiffness or strength compared to a four-strand technique. With time, the repair site became stiffer, as demonstrated by a 230% increase in rigidity and a 50% decrease in strain from 0 to 42 days. However, from 0 to 42 days the ultiinate force of the inset-tion site did not increase. This lack of increase in ultimate force was consistent with decreases in collagen content, non-reducible crossli~iks and distal phalanx BMD. Taken together, our results indicate that the canine FDP tendon heals slowly after it is injured at its insertion site and sutured onto the distal phalanx. While these findings may be limited to the particular repair method we used, they demonstrate a need for devising new treatment strategies to improve healing of flexor tendon insertion site injuries.

Neither technique reproduced the biomechanical profile of the native ulnar collateral ligament; the findings of this study suggest that the docking construct may offer initial biomechanical advantage over the Jobe construct.

The current data strongly indicate that in vivo chondrocyte apoptosis can be stimulated by the application of a single, rapid impact load and that the extent of chondrocyte apoptosis is related to the amount of load applied. The contribution chondrocyte apoptosis makes to the development of posttraumatic arthritis following joint injury or intra-articular fracture still remains to be determined.