There is evidence that fracture healing is impaired in patients with chronic immune disorders the reasons remaining unclear so far. To further elucidate the role of the immune system in bone healing, this study investigated the hypothesis that fracture healing would be considerably disturbed in a mouse model with severe defects of the innate as well as adaptive immune system.

Immune deficient Nod-scidIL2Rγ^null and immune competent BALBcByJ mice were used (12 weeks, male, each n=24). The mice received a femur osteotomy stabilized by an external fixator and were sacrificed at d 21, 28, and 35. The calli were evaluated by three-point-bending testing, μCT and histomorphometry.

The flexural rigidity of the callus did not significantly differ between both genotypes after 21 and 28 days but was significantly lower in Nod-scidIL2Rγ^null mice after 35 days (31%). The maximum moment of inertia was significantly increased after 21 days (by 34%), and the callus cross section area after 21, 28 and 35 days in Nod-scidIL2Rγ^null mice. BV/TV of the callus of Nod-scidIL2Rγ^null mice was significantly decreased after 28 and 35 days (by 32% and 41%). The histological evaluation showed a significantly enhanced amount of cartilage in the fracture gap of Nod-scidIL2Rγ^null mice.

These data indicate an only moderate delay in fracture healing in Nod-scidIL2Rγ^null mice suffering on severe defects in innate and adaptive immune response.