Development and internal validation of a clinical prediction model for acute adjacent vertebral fracture after vertebral augmentation

Hijikata, Yasukazu; Kamitani, Tsukasa; Nakahara, Mikio; Kumamoto, Shinji; Sakai, Tsubasa; Itaya, Takahiro; Yamazaki, Hajime; Ogawa, Yoshihide; Kusumegi, Akira; Inoue, Takafumi; Yonetani, Takashi; Furue, Naoya; Fukuhara, Shunichi; Yamamoto, Yosuke

doi:10.1302/0301-620x.104b1.bjj-2021-0151.r3

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…2 Fractures caused by osteoporosis are becoming increasingly common in females over the age of 55 years, leading to a large number of fracture-related diseases and increased mortality and medical costs. [3][4][5][6][7] The pathogenesis of osteoporosis involves complex signalling pathway regulation and protein modification; however, little is currently known about this process. Osteoporosis is mainly caused by osteoclast-mediated bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Melatonin induces RAW264.7 cell apoptosis via the BMAL1/ROS/MAPK-p38 pathway to improve postmenopausal osteoporosis

Wang,

Jiang,

Pan

et al. 2023

Bone Joint Res

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AimsCurrently, the effect of drug treatment for osteoporosis is relatively poor, and the side effects are numerous and serious. Melatonin is a potential drug to improve bone mass in postmenopausal women. Unfortunately, the mechanism by which melatonin improves bone metabolism remains unclear. The aim of this study was to further investigate the potential mechanism of melatonin in the treatment of osteoporosis.MethodsThe effects of melatonin on mitochondrial apoptosis protein, bmal1 gene, and related pathway proteins of RAW264.7 (mouse mononuclear macrophage leukaemia cells) were analyzed by western blot. Cell Counting Kit-8 was used to evaluate the effect of melatonin on cell viability. Flow cytometry was used to evaluate the effect of melatonin on the apoptosis of RAW264.7 cells and mitochondrial membrane potential. A reactive oxygen species (ROS) detection kit was used to evaluate the level of ROS in osteoclast precursors. We used bmal1-small interfering RNAs (siRNAs) to downregulate the Bmal1 gene. We established a postmenopausal mouse model and verified the effect of melatonin on the bone mass of postmenopausal osteoporosis in mice via micro-CT. Bmal1 lentiviral activation particles were used to establish an in vitro model of overexpression of the bmal1 gene.ResultsMelatonin promoted apoptosis of RAW264.7 cells and increased the expression of BMAL1 to inhibit the activation of ROS and phosphorylation of mitogen-activated protein kinase (MAPK)-p38. Silencing the bmal1 gene weakened the above effects of melatonin. After that, we used dehydrocorydaline (DHC) to enhance the activation of MAPK-p38, and the effects of melatonin on reducing ROS levels and promoting apoptosis of RAW264.7 cells were also blocked. Then, we constructed a mouse model of postmenopausal osteoporosis and administered melatonin. The results showed that melatonin improves bone loss in ovariectomized mice. Finally, we established a model of overexpression of the bmal1 gene, and these results suggest that the bmal1 gene can regulate ROS activity and change the level of the MAPK-p38 signalling pathway.ConclusionOur study confirmed that melatonin promotes the apoptosis of RAW264.7 cells through BMAL1/ROS/MAPK-p38, and revealed the therapeutic effect and mechanism of melatonin in postmenopausal osteoporosis. This finding enriches BMAL1 as a potential target for the treatment of osteoporosis and the pathogenesis of postmenopausal osteoporosis.Cite this article: Bone Joint Res 2023;12(11):677–690.

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Section: Introductionmentioning

confidence: 99%

Melatonin induces RAW264.7 cell apoptosis via the BMAL1/ROS/MAPK-p38 pathway to improve postmenopausal osteoporosis

Wang,

Jiang,

Pan

et al. 2023

Bone Joint Res

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“…However, if the cement is not in close contact with the endplates, it does not increase endplate deformation in the adjacent vertebrae, thereby minimizing the risk of adjacent vertebral fracture [ 85 ]. Several studies have developed scoring systems to predict adjacent vertebral fracture based on the identified risk factors [ 82 , 86 , 87 ]. The usefulness of these scoring systems may be revealed in the future.…”

Section: Discussionmentioning

confidence: 99%

Risk of Revision After Vertebral Augmentation for Osteoporotic Vertebral Fracture: A Narrative Review

Takahashi,

Inose,

Tamai

et al. 2023

Neurospine

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Osteoporotic vertebral fractures (OVFs) can hinder physical motor function, daily activities, and the quality of life in elderly patients when treated conservatively. Vertebral augmentation, which includes vertebroplasty and balloon kyphoplasty, is a commonly used procedure for OVFs. However, there have been reports of complications. Although serious complications are rare, there have been instances of adjacent vertebral fractures, cement dislocation, and insufficient pain relief due to cement failure, sometimes necessitating revision surgery. This narrative review discusses the common risks associated with vertebral augmentation for OVFs, such as cement leakage and adjacent vertebral fractures, and highlights the risk of revision surgery. The pooled incidence of revision surgery was 0.04 (0.02–0.06). The risks for revision are reported as follows: female sex, advanced age, diabetes mellitus, cerebrovascular disease, dementia, blindness or low vision, hypertension, hyperlipidemia, split type fracture, large angular motion, and large endplate deficit. Various treatment strategies exist for OVFs, but they remain a subject of controversy. Current literature underscores the lack of substantial evidence to guide treatment strategies based on the risks of vertebral augmentation. In cases with a high risk of failure, other surgeries and conservative treatments should also be considered as treatment options.

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“…The presence of an IVC may indicate delayed tissue mineralization caused by decreased osteoblast activity and excessive tissue absorption due to increased osteoclast activity [25]. IVC has been reported as an independent risk factor and potential predictor for NVFs following VA [26,27]. A history of previous VFs is also an important risk factor for developing NVFs.…”

Section: Discussionmentioning

confidence: 99%

Preoperative Prediction of New Vertebral Fractures after Vertebral Augmentation with a Radiomics Nomogram

Jiang,

Zhang,

Huang

et al. 2023

Diagnostics

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The occurrence of new vertebral fractures (NVFs) after vertebral augmentation (VA) procedures is common in patients with osteoporotic vertebral compression fractures (OVCFs), leading to painful experiences and financial burdens. We aim to develop a radiomics nomogram for the preoperative prediction of NVFs after VA. Data from center 1 (training set: n = 153; internal validation set: n = 66) and center 2 (external validation set: n = 44) were retrospectively collected. Radiomics features were extracted from MRI images and radiomics scores (radscores) were constructed for each level-specific vertebra based on least absolute shrinkage and selection operator (LASSO). The radiomics nomogram, integrating radiomics signature with presence of intravertebral cleft and number of previous vertebral fractures, was developed by multivariable logistic regression analysis. The predictive performance of the vertebrae was level-specific based on radscores and was generally superior to clinical variables. RadscoreL2 had the optimal discrimination (AUC ≥ 0.751). The nomogram provided good predictive performance (AUC ≥ 0.834), favorable calibration, and large clinical net benefits in each set. It was used successfully to categorize patients into high- or low-risk subgroups. As a noninvasive preoperative prediction tool, the MRI-based radiomics nomogram holds great promise for individualized prediction of NVFs following VA.

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Development and internal validation of a clinical prediction model for acute adjacent vertebral fracture after vertebral augmentation

Cited by 8 publications

References 36 publications

Melatonin induces RAW264.7 cell apoptosis via the BMAL1/ROS/MAPK-p38 pathway to improve postmenopausal osteoporosis

Melatonin induces RAW264.7 cell apoptosis via the BMAL1/ROS/MAPK-p38 pathway to improve postmenopausal osteoporosis

Risk of Revision After Vertebral Augmentation for Osteoporotic Vertebral Fracture: A Narrative Review

Preoperative Prediction of New Vertebral Fractures after Vertebral Augmentation with a Radiomics Nomogram

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