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Study Design: A retrospective study of prospectively collected radiographic and clinical data. Objective: This study aims to investigate the relationship between endplate morphology parameters and the incidence of cage subsidence in patients with mini-open single-level oblique lateral lumbar interbody fusion (OLIF). Methods: We included 119 inpatients who underwent OLIF from February 2015 to December 2017. A total of 119 patients with single treatment level of OLIF were included. Plain anteroposterior and lateral radiograph were taken preoperatively, postoperatively, and during follow-up. The correlation between disc height, endplate concave angle/depth, cage position and cage subsidence were investigated. Functional rating index (Visual Analogue Scale for pain, and Roland Morris Disability Questionnaire) were employed to assess clinical outcomes. Results: Cage subsidence was more commonly seen at the superior endplates (42/119, 35.29%) than at the inferior endplates (6/119, 5.04%) (p < 0.01). More importantly, cage subsidence was significantly less in patients with superior endplates that were without concave angle (3/20, 15%) than with concave angle (37/99, 37.37%) (p < 0.05). Cage subsidence correlated negatively with preoperative anterior disc height (r = −0.21, p < 0.05), but positively with disc distraction rate (r = 0.27, p < 0.01). Lastly, the distance of cage to the anterior edges of the vertebral body showed a positive correlation (r = 0.26, p < 0.01). Conclusions: This study for the first time demonstrated that endplate morphology correlates with cage subsidence after OLIF. Since relatively flat endplates with smaller concave angle significantly diminish the incidence of subsidence, the morphology of cage surface should be taken into consideration when designing the next generation of cage. In addition, precise measurement of the disc height to avoid over-distraction, and more anteriorly placement of the cage is suggested to reduce subsidence. [ABSTRACT FROM AUTHOR]

Osteoporosis is characterized by a decrease in bone mass and destruction of the bone microarchitecture, and it commonly occurs in postmenopausal women and the elderly. Overactivation of osteoclasts caused by the inflammatory response or oxidative stress leads to osteoporosis. An increasing number of studies have suggested that intracellular reactive oxygen species (ROS) are strongly associated with osteoclastogenesis. As a novel angiotensin (Ang) II receptor blocker (ARB), azilsartan was reported to be associated with the inhibition of intracellular oxidative stress processes. However, the relationship between azilsartan and osteoclastogenesis is still unknown. In this study, we explored the effect of azilsartan on ovariectomy-induced osteoporosis in mice. Azilsartan significantly inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and downregulated the expression of osteoclast-associated markers (Nfatc1, c-Fos, and Ctsk) in vitro. Furthermore, azilsartan reduced RANKL-induced ROS production by increasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Mechanistically, azilsartan inhibited the activation of MAPK/NF-κB signaling pathways, while Nrf2 silencing reversed the inhibitory effect of azilsartan on MAPK/NF-κB signaling pathways. Consistent with the in vitro data, azilsartan administration ameliorated ovariectomy (OVX)-induced osteoporosis, and decreased ROS levels in vivo. In conclusion, azilsartan inhibited oxidative stress and may be a novel treatment strategy for osteoporosis caused by osteoclast overactivation. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to compare the radiological features of intravertebral clefts (IVC) between Kümmell disease (KD) and acute osteoporotic vertebral compression fracture (OVCF). Materials and Methods: This is a retrospective study. A total of 79 patients with IVC from January 2014 to December 2018 were included in this study. There were 22 men and 57 women, with an average of 73.5 years. Based on the exact time interval from injury to treatment and the pathological examination results, the patients were divided into KD group (44 patients) and acute OVCF group (35 patients). The two groups were compared by the margin sclerosis of IVC, vertebra and pedicle ossification, stress fracture of the spinous process, paravertebral callus, the shape of IVC, cleft in the adjacent disc, and flatness of IVC's margin from plain radiographs and computed tomography (CT). The two groups were compared by the IVC content, double‐line sign, and signal of fracture vertebral from their magnetic resonance imaging (MRI). Results: There were no significant differences in sex, age, and fracture distribution between the KD group and the acute OVCF group. IVC was present in both the KD group and the acute OVCF group. Six radiological features were only present in the KD group, including sclerosis of the cleft margin (95.5%, 42/44), ossification of the fractured vertebrae (100%, 44/44), ossification of the pedicle (31.8%, 14/44), double‐line sign (27.3%, 12/44), stress fracture of the spinous process (13.6%, 6/44), and even formation of paravertebral callus (18.2%, 8/44). Although there were statistical differences in the other four radiological features of content of IVC (P = 0.02), cleft sign in adjacent intervertebral disc (P < 0.01), margin of IVC (P = 0.02), and the shape of IVC (P = 0.01) between the KD group and acute OVCF group, these characteristics could be found in both groups. Conclusion: IVC could present in patients with both KD and acute OVCF; however, we found that marginal cleft sclerosis, vertebral and pedicle ossification, double‐line sign, spinous process fracture, and formation of paravertebral callus are unique radiological features of KD and could be used for differentiation of KD from acute OVCF with IVC. [ABSTRACT FROM AUTHOR]

Microfibrillar‐associated proteins (MFAPs) are extracellular matrix glycoproteins, which play a role in microfibril assembly, elastinogenesis, and tissue homeostasis. MFAPs consist of five subfamily members, including MFAP1, MFAP2, MFAP3, MFAP4, and MFAP5. Among these, MFAP2 and MFAP5 are most closely related, and exhibit very limited amino acid sequence homology with MFAP1, MFAP3, and MFAP4. Gene expression profiling analysis reveals that MFAP2, MFAP5, and MFAP4 are specifically expressed in osteoblastic like cells, whereas MFAP1 and MFAP3 are more ubiquitously expressed, indicative of their diverse role in the tropism of tissues. Molecular structural analysis shows that each MFAP family member has distinct features, and functional evidence reveals discrete purposes of individual MFAPs. Animal studies indicate that MFAP2‐deficient mice exhibit progressive osteopenia with elevated receptor activator of NF‐κB ligand (RANKL) expression, whereas MFAP5‐deficient mice are neutropenic, and MFAP4‐deficient mice displayed emphysema‐like pathology and the impaired formation of neointimal hyperplasia. Emerging data also suggest that MFAPs are involved in cancer progression and fat metabolism. Further understanding of tissue‐specific pathophysiology of MFAPs might offer potential novel therapeutic targets for related diseases, such as skeletal and metabolic disorders, and cancers. [ABSTRACT FROM AUTHOR]

Aim: We aimed to investigate the proteomics of primary chondrocyte exosomes and the effect of exosomes in osteoarthritis (OA) treatment. Materials & methods: We isolated exosomes from primary chondrocytes cultured in normal (D0) and inflammatory environments induced by IL-1β and determined the proteomics of these exosomes. Next, we investigated what effect and mechanism D0 chondrocytes exosomes have in OA treatment. Results: There were more proteins that belonged to mitochondrion and were involved in immune system processes in D0 exosomes. Notably, intra-articular administration of D0 exosomes successfully prevented the development of OA. D0 chondrocyte exosomes could restore mitochondrial dysfunction and polarize macrophage response toward an M2 phenotype. Conclusion: Our findings demonstrated that primary chondrocyte exosomes are efficient in OA treatment. [ABSTRACT FROM AUTHOR]

Osteoporosis (OP) is a serious metabolic disease that, due to the increased number or function of osteoclasts, results in increased bone brittleness and, therefore, fragile fracture. Some recent studies report the importance of the transforming growth factor β (TGFβ) pathway in bone homeostasis. RepSox is a small molecule inhibitor of TGFβRI that has a wide range of potential application in clinical medicine, except OP. The aim of our study is to evaluate the effects of RepSox on the differentiation and bone resorption of osteoclasts in vitro and in vivo in an ovariectomy (OVX)‐induced OP model. An initial analysis showed TGFβRI messenger RNA expression in both bone samples and bone cells. In the in vitro study, RepSox inhibited the receptor activator of nuclear factor κB ligand (RANKL)‐induced osteoclast differentiation and bone resorption activity. Real‐time polymerase chain reaction (PCR) analysis showed that RepSox suppressed osteoclastic marker gene expression in both dose‐dependent and time‐dependent manners. In addition, RepSox did not affect osteoblast differentiation, migration or osteoblastic‐specific gene expression in vitro. Furthermore, western blot analysis indicated the underlying mechanisms of the RepSox suppression of osteoclastogenesis via the Smad3 and c‐Jun N‐terminal kinase/activator protein‐1 (JNK/AP‐1) signaling pathways. Finally, our animal experiments revealed that RepSox prevented OVX‐induced bone loss in vivo. Together, our data suggest that RepSox regulates osteoclast differentiation, bone resorption, and OVX‐induced OP via the suppression of the Smad3 and JNK/AP‐1 pathways. Bone destruction or osteolysis, marked by excessive osteoclastic bone resorption, is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions, such as osteoporosis. In the present paper, we report that RepSox inhibits osteoclast formation in vitro and in vivo, suggesting that it is potentially valuable in the treatment of osteoclast‐related diseases. [ABSTRACT FROM AUTHOR]