Non union of long bone remains a dreadful complication.

The introduction of new strategies for orthopaedic surgeons to control and modulate bone healing using growth factors such as bone morphogenetic proteins (BMP) have been shown to induce bone formation and union in long bone defects and non unions.

A recombinant form of BMP (BMP-2) is FDA approved to promote fracture healing in tibial non unions.

The study aim was the assessment of the safety and efficacy of a single dose of recombinant human bone morphogenetic protein-2 (INDUCTOS^®) combined with bank bone on the rate of bone formation and union in long bone defects and non unions.

Since October 2005, 44 patients (28 men, 16 women) with a median age of 41.81 (range: 14–78) received a single dose of BMP-2 (INDUCTOS^®) in an extensive segmental long bone defects (mean score: 31.7 cc +/− 63.2; range: 5–261) in combination with bone bank graft (chips or cancellous bone blocs), without any adjunct of autologous bone or bone marrow. The series included 12 femur, 24 tibia, 5 radius/ulna, 3 humerus. All fractures were stabilised using external or internal fixation (mostly Ilizarov). All cases are available for complete follow-up.

Assessment of fusion was performed using digital radiographs at postoperative time, at 10 to 15 days and 1, 2, 3 month and every month till healing. Outcomes of the defects were evaluated using the Imagika^® software.

Clinical stabilisation of the diaphyseal non unions, restoration of the limb length and axis, solid bone fusion were observed in all but two patients within a median time of 6.1 +/− 3.0 months (range: 2.5–15.0).

We observed that BMP-2 induced bone formation across the defect; radiographs showed rapid ossification, with bone graft densification and margin’s shadings.

With no need for donor sites, BMP restored the continuity and stability of critical-size defects faster than what we had observed in our former practice using large amounts of autograft combined with bank bone when necessary. We believe that this procedure provide faster healing, give more comfort and less sequel to patients.

Introduction: Abnormalities of mesenchymal stem cells and osteoblastic cells (Obs) might play a role in producing bone collapse due to insufficient repair of the necrotic area in osteonecrosis of the femoral head (ON). Osteoblast and osteocyte apoptosis should be increased at the osteonecrotic site.

Materials and Methods: We compared the TRAIL (TNF-related apoptosis-inducing ligand) cytotoxicity in primary Obs isolated from femoral heads from patients with ON or osteoarthritis (OA) and on two human osteosarcoma cell lines, MG-63 and SaOS₂.

Results and Discussion: We showed that ON but also OA Obs were sensitive to TRAIL. We also observed TRAIL cytotoxicity on MG-63 but not SaOS₂ cells. Moreover, we saw that TRAIL negatively regulated Akt and ERK survival pathways in MG-63 cells. We also investigated the IL-6 influences on apoptotic response of Obs to TRAIL. Even though decreased IL-6 and sIL-6R levels were observed at peripheral sites of the ON in regard to the levels produced in the iliac crest, IL-6 had no protective effects on TRAIL-induced apoptosis in ON Obs and only a weak protective effect in MG-63 cells. However, TRAIL stimulated IL-6 production in MG-63 cells and, cells and OA Obs, suggesting to a lesser extend, in SaOS₂ other roles of TRAIL in the bone environment.