Aims

Prior to the availability of vaccines, mortality for hip fracture patients with concomitant COVID-19 infection was three times higher than pre-pandemic rates. The primary aim of this study was to determine the 30-day mortality rate of hip fracture patients in the post-vaccine era.

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