Bone Abstracts

Bone regeneration and fracture healing processes are impaired in post menopausal osteoporosis which is induced by estrogen deficiency. Though agents like BMPs and PTH have been shown to promote bone regeneration but are associated with undesirable side effects. There is a need for new agents that enhance bone regeneration and repair.

The aim of this study was to evaluate the bone regenerative capacity of medicarpin in the osteoporotic rat model. Cortical bone defect was generated by a drill hole injury in femoral bones of adult osteopenic Sprague–Dawley rats. The treatment of medicarpin (at doses of 0.5, 1.0 and 5.0 mg/kg per day)was commenced the day after and continued for 15 days. PTH (10.0 μg/kg per day) was taken as a reference standard. Fifteen days post-treatment, the animals were sacrificed. Bones were collected for static and dynamic histomorphometry at the injury site by confocal microscopy and micro-computed tomography (μCT). RNA and protein from newly generated bone was harvested from the area adjoining the injury site. Using μCT and confocal microscopy it was found that medicarpin promotes bone healing at the injury site and was comparable to PTH in many aspects. Investigation by qPCR and protein expression studies indicated the up regulation of Notch and Wnt signalling components via increased expression of NICD, JAGGED-1, β-catenin and LRP5. Medicarpin treated group also showed predominant immunolocalization of β-catenin at injury site.

In conclusion, our data shows that medicarpin treatment repairs cortical bone defect by activating Notch and Wnt/canonical signalling pathway. These results are also suggestive of its promising role in fracture repair process.

Disclosure: The authors declared no competing interests.

Figure 1 (A) Confocal imaging of fracture callus. (B) MicroCT data of fracture callus.