Abstract

Little is known about the localized changes in bone mass that occur following tendon or ligament injury. Interruption of normal load transfer at the insertion site will presumably lead to a localized loss of bone, although few data exist to support this claim. To test this hypothesis, we transected the canine flexor digitorum profundus (FDP) tendon from its insertion, and either repaired it using a trans-osseous suture technique or left it unrepaired (laceration only). Post-operatively, forelimbs in the repair group were cast immobilized except for 10 min of daily passive mobilization rehabilitation, whereas in the laceration only group dogs were allowed full weight bearing. At 5–42 days post-injury, we assessed bone mineral density (BMD) using pQCT and osteoclast surface by histomorphometry. We measured significant bone loss in the distal phalanx after combined FDP tendon laceration, repair, and post-operative passive mobilization, with BMD decreases of 20%, 40%, and 41% at 10, 21, and 42 days ( p<0.01). Moreover, we observed that passive mobilization and tendon laceration each contributed independently to the observed bone loss. At 42 days, BMD was reduced by 21% in bones that were not injured but were subjected to the post-operative passive mobilization protocol, while BMD was reduced by 28% in bones subjected to tendon laceration and full weight bearing ( p<0.01). In both the passive mobilization and laceration specimens, we counted significantly increased osteoclasts after only 7–10 days, and these increases persisted through 42 days ( p<0.05). We conclude that rapid and sustained bone resorption leads to significant bone loss in the 6-week period following flexor tendon injury and repair. This bone loss may impact healing by impeding the restoration of a strong tendon–bone interface.

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