Treatment with hydrogen sulfide attenuates sublesional skeletal deterioration following motor complete spinal cord injury in rats

Treatment with hydrogen sulfide mitigates spinal cord injury-induced sublesional bone loss, possibly through abating oxidative stress, suppressing MMP activity, and activating Wnt/β-catenin signaling. Spinal cord injury (SCI)-induced sublesional bone loss represents the most severe osteoporosis and is resistant to available treatments to data.

Three-dimensional printing akermanite porous scaffolds for load-bearing bone defect repair: An investigation of osteogenic capability and mechanical evolution

Some Ca–Mg-silicate ceramics have been widely investigated to be highly bioactive and biodegradable, whereas their osteogenic potential and especially biomechanical response in the early stage in vivo are scarcely demonstrated.

Material properties of bone in the femoral head treated with ibandronate and BMP-2 following ischemic osteonecrosis

Bone morphogenetic protein (BMP)-2 and ibandronate (IB) decrease the femoral head deformity following ischemic osteonecrosis of the femoral head (ONFH). The purpose of this study was to determine the effects of BMP-2 and IB on the mineral content and nanoindentation properties of the bone following ONFH. ONFH was surgically induced in a femoral head of piglets.

BMP Signaling is Required for Adult Skeletal Homeostasis and Mediates Bone Anabolic Action of Parathyroid Hormone

Bmp2 and Bmp4 genes were ablated in adult mice (KO) using a conditional gene knockout technology. Bones were evaluated by microcomputed tomography (μCT), bone strength tester, histomorphometry and serum biochemical markers of bone turnover. Drill-hole was made at femur metaphysis and bone regeneration in the hole site was measured by calcein binding and μCT.

Thymidine phosphorylase exerts complex effects on bone resorption and formation in myeloma

Myelomatous bone disease is characterized by the development of lytic bone lesions and a concomitant reduction in bone formation, leading to chronic bone pain and fractures. To understand the underlying mechanism, we investigated the contribution of myeloma-expressed thymidine phosphorylase (TP) to bone lesions.

Association Between Progranulin and Gaucher Disease

Gaucher disease (GD) is a genetic disease caused by mutations in the GBA1 gene which result in reduced enzymatic activity of β-glucocerebrosidase (GCase). This study identified the progranulin (PGRN) gene (GRN) as another gene associated with GD.