Microsurgery and external fixation in orthoplastic reconstruction of tibial injuries

Background Orthoplastics is a relatively new approach to lower limb reconstruction, where an integration of both plastic and orthopedic expertise is required, together with the availability of well-equipped facilities. Acute shortening and long-term frames for lengthening are generally considered alternatives to length preservation and soft tissue microsurgical reconstruction, but an integration of external fixation and reconstructive microsurgery is gaining an increasing role with refinements of joint approaches. Material and methods Data on sixteen patients who underwent microsurgical lower limb reconstruction and external fixation with an orthoplastic approach, following acute or chronic tibial injury, were retrospectively reviewed. All patients presented a post traumatic soft tissue defect associated with a Gustilo III tibial fracture or a tibial septic pseudarthrosis. Data on type and timing of bone and soft tissue reconstruction, outcomes, complications and need for re-operation were extrapolated and compared to an historic group of patients treated with an orthopedic-based approach. Results In the orthoplastic group, soft tissues were reconstructed with an ALT flap in most cases; a muscle-sparing VL or ALT-VL chimeric flap was necessary in cases with a very extensive defect. In the orthopedic group, soft tissues were left to heal by second intention or patients were lately referred to plastic surgeons. Statistical comparison between the two groups has showed significant differences on the following data: Time for soft tissue healing, time to bone union, number of reinterventions, post-operative deep infection rate, time to return to work. Conclusion The orthoplastic approach to complex leg defects yields shorter treatment time and better functional results compared to the orthopedic-based approach. External fixation and microsurgical reconstruction are not necessarily alternative procedures but can integrate in an orthoplastic path to address at best both soft tissue and bone reconstruction

Notch signaling regulates tubular morphogenesis during repair from biliary damage in mice.

BACKGROUND & AIMS: Repair from biliary damages requires the biliary specification of hepatic progenitor cells and the remodeling of ductular reactive structures into branching biliary tubules. We hypothesized that the morphogenetic role of Notch signaling is maintained during the repair process and have addressed this hypothesis using pharmacologic and genetic models of defective Notch signaling. METHODS: Treatment with DDC (3,5-diethoxycarbonyl-1,4-dihydrocollidine) or ANIT (alpha-naphthyl-isothiocyanate) was used to induce biliary damage in wild type mice and in mice with a liver specific defect in the Notch-2 receptor (Notch-2-cKO) or in RPB-Jk. Hepatic progenitor cells, ductular reaction, and mature ductules were quantified using K19 and SOX-9. RESULTS: In DDC treated wild type mice, pharmacologic Notch inhibition with dibenzazepine decreased the number of both ductular reaction and hepatic progenitor cells. Notch-2-cKO mice treated with DDC or ANIT accumulated hepatic progenitor cells that failed to progress into mature ducts. In RBP-Jk-cKO mice, mature ducts and hepatic progenitor cells were both significantly reduced with respect to similarly treated wild type mice. The mouse progenitor cell line BMOL cultured on matrigel, formed a tubular network allowing the study of tubule formation in vitro; \u3b3-secretase inhibitor treatment and siRNAs silencing of Notch-1, Notch-2 or Jagged-1 significantly reduced both the length and number of tubular branches. CONCLUSIONS: These data demonstrate that Notch signaling plays an essential role in biliary repair. Lack of Notch-2 prevents biliary tubule formation, both in vivo and in vitro. Lack of RBP-Jk inhibits the generation of biliary-committed precursors and tubule formation