Abstract
Introduction
Femoral head osteonecrosis (FHO) is a condition in which the inadequate blood supply disrupts osteogenic-angiogenic coupling that results in diminishment of femoral perfusion and ends up with FHO. The insufficient knowledge on molecular background and progression pattern of FHO and the restrictions in obtaining human samples bring out the need for a small animal trauma model to research FHO aetiology. Hence, this study aims to develop a mouse trauma model to elucidate the molecular mechanisms behind FHO.
Method
Left femoral head was dislocated from the hip joint, ligamentum teres was cut, and a slight circular incision was done around the femoral neck of 8-week-old male C57BL/6J mice to disrupt the blood supply to femoral head. Right hip joint was left unoperated as control. Animals (n=5 per time point) were sacrificed on 2-3-4-6-8-10-12 weeks, and ex-vivo µCT was taken to assess bone structural parameters. Haematoxylin/eosin (HE)- and immunohistochemical-staining (IHCS) for CD31 and EMCN were done to observe histology and marrow-specific H-type vascular structures, respectively.
Result
μCT assessment showed trabecular bone loss and decreased BV/TV from 2 to 8 weeks in FHO side. HE staining displayed the increased number of empty lacunae was observed in FHO side as early as 24h after operation. By 4th week, IHCS results displayed the invasion of the epiphyseal plate by H-type blood vessels in FHO side, while the epiphyseal plate was observed intact in control side. Also, by 6th week the HE-staining showed the presence of bone marrow necrosis and bone fat accumulation in FHO side.
Conclusion
Trabecular bone loss, increased number of empty lacunae, bone fat imbalance and bone marrow necrosis are reported as the signs of osteonecrosis. Thus, our results are coherent with the literature and indicated that we were able to effectively generate a trauma model for FHO in mice for the first time in literature.
