A balance between bone formation by osteoblasts and bone resorption by osteoclasts is necessary to maintain bone health and homeostasis. As a cancer of plasma cells, multiple myeloma (MM) is accompanied with rapid bone loss and fragility fracture. Bortezomib has been used as a first-line for treating MM for decades. Recently, the potential protection of bortezomib on osteoporosis (OP) is reported; however, the specific mechanism involving bortezomib-mediated antiosteoporotic effect is undetermined. In the present study, we assessed the effects of in vitro bortezomib treatment on osteogenesis and osteoclastogenesis and the protective effect on bone loss in ovariectomized (OVX) mice. Our results indicated that bortezomib treatment increased osteogenic differentiation of MC3T3-E1 cells as evidenced by increased levels of matrix mineralization and osteoblast-specific markers. In bortezomib-treated bone marrow monocytes (BMMs), osteoclast differentiation was suppressed, substantiated by downregulated tartrate-resistant acid phosphatase- (TRAP-) positive multinucleated cells, areas of actin rings, pit formation, and osteoclast-specific genes. Mechanistically, bortezomib exerted a protective effect against OP through the Smad ubiquitination regulatory factor- (SMURF-) mediated ubiquitination pathway. Furthermore, in vivo intraperitoneal injection of bortezomib attenuated the bone microarchitecture in OVX mice. Accordingly, our findings corroborated that bortezomib might have future applications in the treatment of postmenopausal OP.
BackgroundEndplate fractures is an important factor affecting the curative effect of percutaneous kyphoplasty for spinal fracture. The purpose of this study is to investigate the effect of sealing endplate fracture with bone cement on minimally invasive treatment of spinal fracture.MethodsA total of 98 patients with osteoporotic vertebral fractures combined with endplate fractures treated with bone cement surgery in our hospital were retrospectively analyzed. They were grouped according to whether bone cement was involved in the endplate fractures. Group A: bone cement was not only distributed in the fractured vertebral body, but also dispersed into the endplate fractures. Group B: bone cement was confined to the fractured vertebra but did not diffuse into the cracks of the endplate. The basic information, imaging changes of the fractured vertebral body, VAS score, ODI score, bone cement distribution and postoperative complications of the two groups were analyzed and compared.ResultsThe height of the injured vertebra and the kyphotic Cobb angle in the two groups were significantly improved after surgery, but the anterior height of the vertebra in group B was lower than that in group A and the kyphotic Cobb angle was higher than that in group A at the last follow-up (P < 0.05). VAS score and ODI score in 2 groups were significantly improved after operation (P < 0.05), but the VAS score and ODI score in group A were lower than those in group B at the last follow-up (P < 0.05). The incidence of bone cement leakage and adjacent vertebral fracture in group A was higher than that in group B (P < 0.05).ConclusionDiffusion of bone cement into the cracks of the endplate may also restore and maintain the height of the injured vertebra, relieve pain and restore lumbar function. However, diffusion of bone cement into the cracks of the endplate can increase the incidence of cement leakage and adjacent vertebral fractures.
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