A multicenter cross-sectional study on the correlation between sarcopenic obesity and primary osteoporosis of kidney-yang deficiency in young elderly people in Liaoning Province

开始日期2023-12-01

申办/合作机构-

100 项与原发性骨质疏松症相关的临床结果

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100 项与原发性骨质疏松症相关的转化医学

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0 项与原发性骨质疏松症相关的专利（医药）

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项与原发性骨质疏松症相关的文献（医药）

2024-12-01·Cellular and Molecular Life Sciences

Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss

Article

作者: Nga, Ha Thi ; Tian, Jingwen ; Yi, Hyon-Seung ; Lee, Ju Hee ; Shong, Minho ; Moon, Ji Sun ; Nguyen, Thi Linh ; Lee, Ho Yeop ; Jang, Hyo Ju ; Setoyama, Daiki

AbstractThis study examines the interplay between ambient temperature, brown adipose tissue (BAT) function, and bone metabolism, emphasizing the effects of cold exposure and BAT mitochondrial activity on bone health. Utilizing ovariectomized (OVX) mice to model primary osteoporosis and BAT-specific mitochondrial dysfunction (BKO) mice, we evaluated the impact of housing temperature on bone density, immune modulation in bone marrow, and the protective role of BAT against bone loss. Cold exposure was found to universally reduce bone mass, enhance osteoclastogenesis, and alter bone marrow T-cell populations, implicating the immune system in bone remodeling under cold stress. The thermogenic function of BAT, driven by mitochondrial oxidative phosphorylation, was crucial in protecting against bone loss. Impaired BAT function, through surgical removal or mitochondrial dysfunction, exacerbated bone loss in cold environments, highlighting BAT’s metabolic role in maintaining bone health. Furthermore, cold-induced changes in BAT function led to systemic metabolic shifts, including elevated long-chain fatty acids, which influenced osteoclast differentiation and activity. These findings suggest a systemic mechanism connecting environmental temperature and BAT metabolism with bone physiology, providing new insights into the metabolic and environmental determinants of bone health. Future research could lead to novel bone disease therapies targeting these pathways.

2024-10-01·Journal of Clinical Densitometry

Lumbar Osteoarthritis in Patients with Osteoporosis Evaluated with the Lane and Wilke Scale and its Effect on Dexa Scores

Article

作者: Melikoğlu, Meltem Alkan ; Taş, Nurmuhammet

OBJECTIVEThis study aimed to compare bone mineral density (BMD) values in patients with lumbar osteoarthritis (OA) with and without osteoporosis (OP). This study evaluated the effect of lumbar osteoarthritis in patients with osteoporosis on Dexa scores using the Lane and Wilke scale.METHODSA total of 51 individuals with OA, 20 with OP, and 31 without OP were included in the study. Lumbar osteoarthritis was assessed and recorded using the Lane and Wilke scale. BMD was measured by dual-energy X-ray absorptiometry (DEXA) at the waist and hip (femoral neck, lumbar vertebrae). Frax assessed the risk of osteoporosis and fracture risk.RESULTSThe mean age of patients with OP was 68.1±8.2 years, and the mean age of patients without OP was 68.6±9.4 years. There was a significant decrease between the lumbar vertebrae and femoral neck BMD values of the two groups in favor of the osteoporosis group. The t-scores of the OP group were significantly lower (p = 0.045). All variables showed a statistically significant difference between the group with OP and those without OP (p<0.05). The median values of L1-L2, L2-L3, L3-L4, and total L1-L4 were higher in absolute value in the group with OP. In frax hip and frax primary osteoporosis, the median values were higher in the group with OP than in the group without OP (p = 0.023/p = 0.020). All L1-L2, L2-L3, and L3-L4 dexa parameters with and without OP were not significantly different between the groups according to the Lane and Wilke classification (p > 0.05).CONCLUSIONThere was no statistically significant difference between DEXA parameters in osteoporosis and non-osteoporosis patients with low back osteoarthritis (according to the Lane and Wilke classification).

2024-09-01·Journal of Orthopaedic Translation

Emerging role of liver-bone axis in osteoporosis

Review

作者: Peng, Xing ; Ma, Peiqi ; Xu, Tao ; Gou, Liming ; Qin, Jian ; Qin, Xihu ; Li, Ning ; Wang, Yuqi ; Wu, Jing ; Xue, Bin ; Li, Shu ; Gao, Hongliang ; Liang, Hui

BackgroundIncreasing attention to liver-bone crosstalk has spurred interest in targeted interventions for various forms of osteoporosis. Liver injury induced by different liver diseases can cause an imbalance in bone metabolism, indicating a novel regulatory paradigm between the liver and bone. However, the role of the liver-bone axis in both primary and secondary osteoporosis remains inadequately elucidated. Therefore, exploring the exact regulatory mechanisms of the liver-bone axis may offer innovative clinical approaches for treating diseases associated with the liver and bone.MethodsHere, we summarize the latest research on the liver-bone axis by searching the PubMed and Web of Science databases and discuss the possible mechanism of the liver-bone axis in different types of osteoporosis. The literature directly reporting the regulatory role of the liver-bone axis in different types of osteoporosis from the PubMed and Web of Science databases has been included in the discussion of this review (including but not limited to the definition of the liver-bone axis, clinical studies, and basic research). In addition, articles discussing changes in bone metabolism caused by different etiologies of liver injury have also been included in the discussion of this review (including but not limited to clinical studies and basic research).ResultsSeveral endocrine factors (IGF-1, FGF21, hepcidin, vitamin D, osteocalcin, OPN, LCAT, Fetuin-A, PGs, BMP2/9, IL-1/6/17, and TNF-α) and key genes (SIRT2, ABCB4, ALDH2, TFR2, SPTBN1, ZNF687 and SREBP2) might be involved in the regulation of the liver-bone axis. In addition to the classic metabolic pathways involved in inflammation and oxidative stress, iron metabolism, cholesterol metabolism, lipid metabolism and immunometabolism mediated by the liver-bone axis require more research to elucidate the regulatory mechanisms involved in osteoporosis.ConclusionDuring primary and secondary osteoporosis, the liver-bone axis is responsible for liver and bone homeostasis via several hepatokines and osteokines as well as biochemical signaling. Combining multiomics technology and data mining technology could further advance our understanding of the liver-bone axis, providing new clinical strategies for managing liver and bone-related diseases.The translational potential of this article is as follows: Abnormal metabolism in the liver could seriously affect the metabolic imbalance of bone. This review summarizes the indispensable role of several endocrine factors and biochemical signaling pathways involved in the liver-bone axis and emphasizes the important role of liver metabolic homeostasis in the pathogenesis of osteoporosis, which provides novel potential directions for the prevention, diagnosis, and treatment of liver and bone-related diseases.

项与原发性骨质疏松症相关的新闻（医药）

2024-09-27

·Business Wire

Award-winning Study Confirms Medimaps Group New AI Software Accurately Assesses Bone Fragility From Routine X-rays

GENEVA--( BUSINESS WIRE )--Medimaps Group, a Swiss/Global med-tech company specializing in clinical bone microarchitecture image-processing software with deep-tech and Artificial Intelligence (AI) capabilities, announced today the presentation of new data on its AI deep learning software model to opportunistically detect bone fragility on conventional X-ray modalities, at the American Society for Bone and Mineral Research annual congress (ASBMR) in Toronto, Canada, September 27-30. “ We know that 70% of patients at high risk of fragility fracture have never been referred for a DXA scan to address their osteoporosis. By developing an opportunistic screening tool, our goal is to address this gap,” said Prof. Didier Hans, co-founder and CEO of Medimaps Group. “Our new software model uses patients’ routine X-ray scans for other pathologies to analyze their bone microarchitecture and density, requiring no further examination time for patients nor radiologists. It flags patients who might present high risk bone fragilities, enabling their referral for further DXA examination. This is a smart way to use AI for early detection and subsequent prevention of osteoporosis fractures. ” The new data will be presented by lead investigator Guillaume Gatineau, Ph.D. candidate in AI in the Interdisciplinary Center of Bone Diseases at Lausanne University Hospital, Switzerland, and Data Scientist at Medimaps Group, in the following sessions: Plenary Poster Session I Sept 27 I 5:30 - 7:30 PM Early Career Spotlight Rapid Fire Presentation I Sept 28, 2024 I 1:45 - 2:15 PM Poster Session 1 I Sept 28 I 2:15 - 3:45 PM Focused on minimizing false positives, the AI model underwent rigorous training and validation on over 25,000 lumbar-spine X-ray DICOM files. It demonstrated an impressive internal validation accuracy of 86% and external validation accuracy of 85%. These results demonstrate a significant reduction in false positives, which is important to prevent unnecessary referrals, addressing a common limitation of over-diagnosis often seen in some other AI diagnostic tools. For this study, Guillaume Gatineau will be awarded a Young Investigator Award from the ASBMR scientific committee in Toronto. “ Our opportunistic software’s robust specificity underscores its capacity to reduce false-positive rates, an important criterion for hospital centers and private practices when purchasing new AI applications. We expect to present further validation studies confirming the clinical relevance, generalizability and efficacy of our multi-modal software under development in the near future,” added Prof. Didier Hans. Globally, over 37 million fragility fractures occur annually due to osteoporosis. The challenge lies in the under-identification of individuals at risk, resulting in missed opportunities for preventive treatment. References G. Gatineau M. Degruttola, G. Nguyen, M. Davies, K. Hind, M. Kužma, J. Payer, G. Guglielmi, A. Fahrleitner-Pammer, D. Krueger, N Binkley, D. Hans; Artificial Intelligence-Based, Automatic and Explainable Bone Fragility Detection from X-ray: a Multi-National Cohort Study; Oral presentation, ASBMR annual congress 2024 About Medimaps Group Medimaps Group is a Swiss-based company developing and marketing deep-tech and AI imaging software to comprehensively assess bone microarchitecture and predict fracture risk in primary and secondary osteoporosis in clinical practice. By leveraging Trabecular Bone Score (TBS), our multimodal imaging software empower clinicians to improve detection of bone fragilities, initiate treatment plans, and monitor response over time. Our lead product TBS iNsight™ (Osteo) has been used for years in clinical practice worldwide in the field of osteoporosis, and is established as the gold standard for bone texture assessment in clinical practice. It benefits from 4 category 1 CPT codes for US reimbursement. Learn more at www.medimaps.ai

2024-09-09

·日健中外制药

骨头松松怎么办？骨科专家的 “绝招”，收藏！

导语随着年龄的增长，很多朋友都面临着骨质疏松的问题，但初识骨质疏松时，却不知如何是好？幸运的是，你及时看到了这篇文章，我们将骨科专家防治骨质疏松的“绝招”整理如下，帮你有效预防和改善骨质疏松，保持骨骼健康。破松一式——均衡饮食营养是骨骼健康的基石，均衡的饮食是预防骨质疏松的关键。首先，确保摄入足够的钙1，钙是构成骨骼的重要成分2，其拥有有广泛的食物来源，其中奶制品是钙摄入的最佳来源，250mL牛乳中约有250~300mg钙。其他含钙食物来源有: 蔬菜（如花茎甘蓝、卷心菜、大白菜）、豆腐、豆类、虾皮、小鱼、种子、坚果等。面食和谷类含钙虽低，但进食较多，也能提供不少的钙，提倡日常生活中多吃奶制品及富含钙的蔬菜食品3。维生素D有助于钙的吸收，食用富含维生素D的食物，如鱼肝油、蛋黄和蘑菇，可以帮助身体合成维生素D3。其次还需控制盐的摄入，建议低盐饮食（即每日摄入量不超过5g）1。此外，蛋白质也是骨骼健康不可或缺的营养素，低蛋白质摄入会提高骨量丢失，而高蛋白质摄入会增加钙流失，因此需控制蛋白质摄入量3，推荐每日摄入量为1.0~1.2g/kg，日常进行抗阻训练的老年人推荐为1.2~1.5g/kg1。小贴士地中海饮食有助于提高腰椎骨密度和肌肉质量，对预防骨质疏松和骨折有积极的影响4。破松二式——规律运动运动可促进骨代谢、促进骨形成和重建，使骨密度和骨的弹性增加，有利于减少骨折的发生3，良好的运动习惯需保持并贯穿于从儿童青少年到老年的整个生命周期2。活动类型：建议进行包括有氧运动、肌肉强化和平衡训练活动在内的多元身体活动2。有氧运动包括步行、慢跑、骑自行车等；肌肉强化训练包括推举杠铃、背部下拉、坐姿划船等；平衡活动可选择踏步走直线、从坐姿到站立的练习等；舞蹈、太极拳、园艺等多元身体活动可兼顾各种运动的优点，适合老年患者2。活动时间：对老年人或骨质疏松患者，建议减少久坐，每周至少进行150~300min 中等强度运动，或者每周 75～150 min 高强度有氧运动，或者效果相当的中等强度和高强度组合有氧运动。此外应进行中等强度或更高强度的肌肉强化活动，每周 2 天或更多时间以使主要肌肉群参与，获得更多的健康益处2。小贴士运动前应进行充分的热身，避免运动损伤。同时，根据个人体质和健康状况选择合适的运动方式和强度3。破松三式——健康生活保持健康的生活方式、避免不良习惯对骨骼健康十分重要。充足日照：维生素D的产生与日光中的紫外线密不可分3，建议上午11点到下午3点间尽可能多地暴露皮肤于阳光下晒15~30min，每周2次，以促进体内维生素D的合成，尽量不涂抹防晒霜，以免影响日照效果。但需注意避免强烈阳光照射，以防灼伤皮肤5。避免吸烟和过量饮酒：吸烟可影响钙的吸收，降低钙含量，降低骨密度并增加骨质疏松发病率；过量饮酒也会导致骨量快速流失、骨微结构破坏，增加骨折发生率6。避免碳酸饮料和咖啡，可饮用茶水：饮用碳酸饮料后的高糖环境会抑制成骨细胞分化成熟，低pH也会影响钙的吸收，咖啡中的咖啡因也会对生长板软骨和骨骼健康产生负面影响，引发骨质疏松。饮茶是一种健康的生活方式，红茶和绿茶含有丰富的类黄酮，会增加成骨细胞活性，抑制破骨细胞形成，拥有增加骨密度的作用4。合理的睡眠时间和时长：白天睡眠时间过长（＞1h）、晚上睡觉时间过晚（晚于10点）、过短或过长的睡眠时间（＜5h、≥9h）均会增加或加剧骨质疏松风险，因此需保证睡眠质量的前提下合理控制睡眠时间和时长6。小贴士保持积极乐观的心态，参与社交活动，也有助于身心健康，从而间接促进骨骼健康7。破松四式——营养补充剂仅靠饮食及生活方式的调整可能无法满足人体对于钙和维生素D的需要，因此，日常还需补充钙剂和维生素D来预防和治疗骨质疏松钙剂: 充足的钙摄入对获得理想峰值骨量、缓解骨丢失、改善骨矿化和维护骨骼健康有益。中国居民中青年推荐每日钙摄入量为800mg（元素钙），50 岁以上中老年、妊娠中晚期及哺乳期人群推荐每日摄入量为1000~1200mg，我国居民每日膳食约摄入元素钙400mg，故尚需补充元素钙约500~600mg/d1。维生素D：充足的维生素D可增加肠钙吸收、促进骨骼矿化、保持肌力、改善平衡和降低跌倒风险，对于维生素D缺乏或不足者，应给予维生素D补充剂，每日口服维生素D3 1000～2000 IU1。小贴士大剂量钙剂补充可能增加肾结石和心血管疾病风险，因此钙剂补充需适量1，维生素D同样不建议单次口服大剂量1。破松五式——药物治疗对于已经确诊患有骨质疏松症者、发生过肢体脆性骨折者、经骨密度测试骨量减少且有高骨折风险者，还需要遵医嘱联合抗骨质疏松症药物治疗药物3。目前可用于骨质疏松防治的药物种类繁多1：骨吸收抑制剂：包括双膦酸盐类、RANKL单抗、降钙素、雌激素和选择性雌激素受体调节剂类药物骨形成促进剂：主要为甲状旁腺素类似物双重作用药物：硬骨抑素单抗其他机制类药物：包括活性维生素D及其类似物和维生素K2 中成药：中药复方制剂等。小贴士活性维生素D及其类似物中的艾地骨化醇具有提高骨密度、减少跌倒、降低骨折风险的作用，而且在应用期间，可不必服用钙剂1。另外还需要注意，药物治疗应在医生的指导下进行，避免自行用药或过量用药。结语骨质疏松并不是不可避免的，通过均衡饮食、适当运动、健康的生活方式以及必要时的药物治疗，我们可以有效地预防和改善这一状况。请记住，保持骨骼健康是一个长期的过程，需要我们持之以恒的努力。参考文献（向上滑动阅览） 1. 中华医学会骨质疏松和骨矿盐疾病分会. 原发性骨质疏松症诊疗指南（2022）. 中国全科医学，2023，26(14):1671-1691. 2. 中国营养学会骨营养与健康分会,中华医学会骨质疏松和骨矿盐疾病分会. 原发性骨质疏松症患者的营养和运动管理专家共识[J]. 中华骨质疏松和骨矿盐疾病杂志,2020,13(5):396-410. 3. 杨红旗,赵欣,陈燕,等. 骨质疏松症的健康管理[J]. 中国临床保健杂志,2018,21(5):718-720. 4. 张永政,王荷晴,崔立敏. 骨质疏松防治中的膳食模式管理[J]. 中华骨质疏松和骨矿盐疾病杂志,2024,17(2):189-194. 5. 中华医学会,中华医学会杂志社,中华医学会全科医学分会,等. 原发性骨质疏松症基层诊疗指南（2019年）[J]. 中华全科医师杂志,2020,19(4):304-315. 6. 李想,毛立伟,邹军. 绝经后骨质疏松运动处方及生活方式影响因数的研究进展[J]. 中国骨质疏松杂志,2022,28(9):1390-1394. 7. 管晶晶,陈宇,汤华冬,等. 骨质疏松的健康管理发展现状及挑战[J]. 中华全科医学,2021,19(10):1729-1732. NP-DX-20240724-EXP202707 请阅读者留意材料有效期。本公司不对过期材料的准确性、完整性、及时性或其他任何方面做出明示或暗示的保证或声明。

2024-07-08

·复星医药

复星医药：药友阿仑膦酸钠片获批上市

2024年7月5日，国家药品监督管理局官网显示，药友制药的阿仑膦酸钠片（70mg）获批上市并视同通过仿制药质量和疗效一致性评价。阿仑膦酸钠片 1993年在意大利首次上市，后于1995年在美国上市，现已获批用于：治疗和预防绝经后妇女骨质疏松症治疗男性骨质疏松症以增加骨量治疗糖皮质激素诱导的骨质疏松症治疗Paget骨病阿仑膦酸钠片是首个获得FDA批准用于治疗绝经后骨质疏松症的双膦酸盐类药物，也是第一个被FDA批准用于治疗男性骨质疏松症的药物。双膦酸盐能够特异性结合到骨重建活跃的骨表面，抑制破骨细胞功能，从而抑制骨吸收，防止骨丢失，增加骨量。阿仑膦酸钠片用于骨质疏松症的治疗已有30年历史，其疗效和安全性得到了充分的临床认证和医患认可。目前，阿仑膦酸钠被国内外多指南推荐用于各类型骨质疏松症的初始治疗，如：《美国医师协会（ACP）临床指南：药物治疗成人原发性骨质疏松症或低骨量以预防骨折（2023）》：双膦酸盐应作为女性和男性原发性骨质疏松的一线治疗药物。《原发性骨质疏松症诊疗指南（2022）》：对于骨折高风险者建议首选口服双膦酸盐（如阿仑膦酸钠）。《老年脆性骨盆骨折临床诊疗指南（2022）》：双磷酸盐类药物是抗骨质疏松药物治疗的首选药物。所有老年脆性盆骨患者均应尽早、序贯、长期抗骨质疏松治疗。双磷酸盐类药物因安全、有效、依从性佳等而被临床广泛应用。《男性骨质疏松症诊疗指南（2020）》：无论是原发性骨质疏松症或部分继发性骨质疏松症，非转移性前列腺癌接受雄激素剥夺治疗、HIV相关性骨质疏松症、糖皮质激素诱导的骨质疏松症等，口服阿仑膦酸钠均有效增加腰椎、髋部或股骨颈骨密度。《欧洲绝经后妇女骨质疏松症诊断和治疗指南（2019）》：口服双膦酸盐（如阿仑膦酸钠等）可作为初始治疗，阿仑膦酸钠可以同时降低椎体骨折和非椎体（包括髋关节）骨折风险。 1999年，阿仑膦酸钠片在我国获批上市，用于治疗绝经后妇女的骨质疏松症，以预防髋部和脊柱骨折（椎骨压缩性骨折），还可用于治疗男性骨质疏松症以增加骨量。目前，阿仑膦酸钠片为国家医保乙类品种，国家基药。近年市场持续攀升，国内市场规模已达4亿元，市场容量1140万片（以70mg计）。数据来源：IQVIA 数据来源：RPDB 截至发稿，阿仑膦酸钠片已有5家企业通过或视同通过一致性评价，尚有6家企业正在审评审批中，可能纳入第十批国家带量采购。通过/视同通过一致性评价的企业正在审评审批的企业骨质疏松是药友制药重点布局的领域之一，核心产品“立庆®（阿法骨化醇片）”市场占有率处于全国第1位，全球第2位。（数据来源：IQVIA）此次阿仑膦酸钠片的获批，将进一步丰富药友制药骨质疏松产品管线，为患者提供全新的用药选择。相关链接关于药友制药药友制药成立于1939年中华民族危难时刻，10余名大学爱国师生以“谋医药之永远自给，药学之逐日昌明，分担建国复兴工作”的创始宗旨，创立了药友制药。经过80余年的发展，药友制药已成为一家拥有完整医药产业链的集团化、国家级重点高新技术企业。公司自主研发生产的原料药及制剂产品已先后在欧美市场上市，重点冻干产品荣获“国家科技进步二等奖”。

上市批准一致性评价CSCO会议