Background: Bone homeostasis is mediated by osteoblast-related bone formation and osteoclast-related resorption. The imbalance of bone homeostasis due to excessive osteoclastogenesis or reduced osteogenesis can result in various disorders, such as postmenopausal osteoporosis (PMOP). The receptor activator of nuclear factor-κB ligand (RANKL)-induced nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) pathways are essential in osteoclastogenesis. In this study, we aimed to investigate the effects of rosavin, an alkylbenzene diglycoside compound from the traditional Chinese medicine Rhodiola Rosea L, on RANKL-induced osteoclastogenesis in vitro and in vivo.Methods: The effects of rosavin on osteoclastogenesis were assessed by TRAP staining of bone marrow monocyte cells (BMMCs) and RAW 264.7 cells. The effects of rosavin on osteogenesis were determined using alkaline phosphatase (ALP) and alizarin red staining, as well as real-time quantitative reverse transcription polymerase chain reaction. Actin ring formation and bone formation experiments were performed to evaluate osteoclast function. Western blotting was carried out to determine the expression of osteoclastogenesis-related genes, and the activation of the NF-κB and MAPK pathways was evaluated by performing western blotting and immunofluorescence staining. Ovariectomized mice were used to explore the effect of rosavin on bone loss.Results: Rosavin could inhibit osteoclastogenesis, suppress the function of osteoclasts, and decrease the expression of osteoclast differentiation-related genes, including tartrate-resistant acid phosphatase (TRAP), cathepsin K, matrix metalloproteinase-9 (MMP-9), calcitonin receptor (CTR), TNF receptor-associated factor 6 (TRAF-6), receptor activator of nuclear factor-κB (RANK), and colony-stimulating factor-1 receptor (c-fms). Rosavin inhibited RANKL-induced phosphorylation of p65 and inhibitory subunit of NF-κB alpha (IκBα), and suppressed p65 nuclear translocation. Rosavin was also found to inhibit the phosphorylation of extracellular-signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). Furthermore, rosavin promoted osteogenesis in bone marrow mesenchymal stem cells (BMSCs). In vivo experiments showed that treatment with rosavin could alleviate ovariectomy-induced osteoporosis in mice.Conclusions: Our results indicated that rosavin suppressed RANKL-induced osteoclastogenesis in vivo and in vitro by blocking the NF-κB and MAPK pathways. Rosavin treatment is a potential therapy for the clinical treatment of osteoclastogenesis-related disorders.
Idiopathic bone cavity (IBC) is a rare, asymptomatic, unilateral, oval-shaped radiolucent defect in the mandible. It is extremely rare that IBC occurs in the mandibular branch and condylar process. This article presents a 16-year-old male with IBC occuring in the mandibular branch.
Purpose
Neurovascular compression (NVC) is hypothesized to be the main pathogenic factor of trigeminal neuralgia (TN). Microvascular decompression (MVD) has become a popular surgery for TN, and the success rate depends on the degree of NVC. As the routine examination before MVD, magnetic resonance tomographic angiography (MRTA) shows high sensitivity for detecting NVC. However, there are no reports on the sensitivity of MRTA for assessing the degree of NVC.
Methods
This study aimed to evaluate the sensitivity of MRTA for determining the degree of NVC by comparing preoperative MRTA and intraoperative endoscopy findings. A total of 480 patients who suffered from TN and underwent MVD were included. Their preoperative MRTA and intraoperative endoscopy findings were reviewed. The kappa test was used to identify similarities between the MRTA and endoscopy findings.
Results
The degree of NVC on preoperative MRTA was similar to that on endoscopy (kappa = 0.770). The number of offending vessels according to preoperative MRTA was coincident with that according to endoscopy (kappa = 0.722).
Conclusion
MRTA had high sensitivity for detecting not only the presence of NVC but also the degree of NVC.
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