BONE 是一个跨学科论坛，用于快速发表有关骨和矿物质代谢的基础、转化和临床方面的原创文章和评论。该杂志还鼓励提交有关骨骼与其他器官系统相互作用的论文，包括软骨、内分泌、肌肉、脂肪、神经、血管、胃肠道、造血和免疫系统。特别注意将实验研究应用于临床实践。

BONE is an interdisciplinary forum dedicated to the rapid publication of original articles and reviews concerning the fundamental, translational, and clinical aspects of bone and mineral metabolism. The journal also encourages submissions on the interactions between bone and other organ systems, including cartilage, endocrine, muscle, fat, nerve, vascular, gastrointestinal, hematopoietic, and immune systems. Special emphasis is placed on applying experimental research to clinical practice.

BONE 是一个跨学科的论坛，旨在快速发表关于骨骼和矿物质代谢的基础研究、转化研究和临床研究的原创文章和评论。该杂志还鼓励提交关于骨骼与其他器官系统相互作用的论文，包括软骨、内分泌、肌肉、脂肪、神经、血管、胃肠道、造血和免疫系统。特别关注将实验研究应用于临床实践。

Bone

Research into the pathophysiology of osteoarthritis (OA) has focused on cartilage and peri-articular bone, but there is increasing recognition that OA affects all of the joint tissues, including the synovium (SM). Under normal physiological conditions the synovial lining consists of a thin layer of cells with phenotypic features of macrophages and fibroblasts. These cells and the underlying vascularized connective tissue stroma form a complex structure that is an important source of synovial fluid (SF) components that are essential for normal cartilage and joint function. The histological changes observed in the SM in OA generally include features indicative of an inflammatory "synovitis"; specifically they encompass a range of abnormalities, such as synovial lining hyperplasia, infiltration of macrophages and lymphocytes, neoangiogenesis and fibrosis. The pattern of synovial reaction varies with disease duration and associated metabolic and structural changes in other joint tissues. Imaging modalities including magnetic resonance (MRI) and ultrasound (US) have proved useful in detecting and quantifying synovial abnormalities, but individual studies have varied in their methods of evaluation. Despite these differences, most studies have concluded that the presence of synovitis in OA is associated with more severe pain and joint dysfunction. In addition, synovitis may be predictive of faster rates of cartilage loss in certain patient populations. Recent studies have provided insights into the pathogenic mechanisms underlying the development of synovitis in OA. Available evidence suggests that the inflammatory process involves engagement of Toll-like receptors and activation of the complement cascade by degradation products of extracellular matrices of cartilage and other joint tissues. The ensuing synovial reaction can lead to synthesis and release of a wide variety of cytokines and chemokines. Some of these inflammatory mediators are detected in joint tissues and SF in OA and have catabolic effects on chondrocytes. These inflammatory mediators represent potential targets for therapeutic interventions designed to reduce both symptoms and structural joint damage in OA. This article is part of a Special Issue entitled "Osteoarthritis".

Carla R Scanzello

Steven R Goldring

The role of synovitis in osteoarthritis pathogenesis.

滑膜炎在骨关节炎发病机制中的作用。

For many years, pharmaceutical therapies for osteoarthritis (OA) were focused on cartilage. However, it has been theorized that bone changes such as increased bone volume fraction and decreased bone matrix mineralization may play an important role in the initiation and pathogenesis of OA as well. The mechanisms behind the bone changes are subject of debate, and a better understanding may help in the development of bone-targeting OA therapies. In the literature, the increase in bone volume fraction has been hypothesized to result from mechanoregulated bone adaptation in response to decreased mineralization. Furthermore, both changes in bone volume fraction and mineralization have been reported to be highest close to the cartilage, and bone volume fraction has been reported to be correlated with cartilage degeneration. These data indicate that cartilage degeneration, bone volume fraction, and bone matrix mineralization may be related in OA. In the current study, we aimed to investigate the relationships between cartilage degeneration, bone matrix mineralization and bone volume fraction at a local level. With microCT, we determined bone matrix mineralization and bone volume fraction as a function of distance from the cartilage in osteochondral plugs from human OA tibia plateaus with varying degrees of cartilage degeneration. In addition, we evaluated whether mechanoregulated bone adaptation in response to decreased bone matrix mineralization may be responsible for the increase in bone volume fraction observed in OA. For this purpose, we used the experimentally obtained mineralization data as input for bone adaptation simulations. We simulated the effect of mechanoregulated bone adaptation in response to different degrees of mineralization, and compared the simulation results to the experimental data. We found that local changes in subchondral bone mineralization and bone volume fraction only occurred underneath severely degenerated cartilage, indicating that bone mineralization and volume fraction are related to cartilage degeneration at a local level. In addition, both the experimental data and the simulations indicated that a depth-dependent increase in bone volume fraction could be caused by decreased bone matrix mineralization. However, a quantitative comparison showed that decreased mineralization can only explain part of the subchondral sclerosis observed in OA.

L G E Cox

C C van Donkelaar

B van Rietbergen

P J Emans

K Ito

Decreased bone tissue mineralization can partly explain subchondral sclerosis observed in osteoarthritis.

骨组织矿化减少可部分解释骨关节炎中观察到的软骨下硬化。

Osteoarthritis (OA) is a disease that involves the entire joint, but its pathophysiology is not well described. Alterations in peri-articular bone are an integral part of the OA disease process and different aspects of bone changes have been described in different patient (sub)groups and animal models. In this review we will discuss the osteoarthritis pathophysiology from the perspective of periarticular bone changes, which can be considered at three hierarchical levels: the bone (or joint) shape, the subchondral bone architecture and its cellular and molecular phenotype. In this review we try to provide an overview of the current knowledge of peri-articular bone changes in OA and what it could possibly imply for the initiation of OA and its progression. This article is part of a Special Issue entitled "Osteoarthritis".

H Weinans

M Siebelt

R Agricola

S M Botter

T M Piscaer

J H Waarsing

Pathophysiology of peri-articular bone changes in osteoarthritis.

骨关节炎中关节周围骨改变的病理生理学

The prevalence of hip fracture and associated risk factors in China were evaluated in a Health and Retirement Longitudinal Study. There is an apparent geographic variation in the prevalence of hip fracture in China. Advanced age, West region, lower education, under-weight, having self-reported history of chronic lung diseases, heart diseases, stroke, and arthritis appear to be associated with risk of hip fracture.

Yan Ren

Jiang Hu

Bing Lu

Weijun Zhou

Bo Tan

Prevalence and risk factors of hip fracture in a middle-aged and older Chinese population.

中国中年及老年人群髋部骨折的患病率及危险因素。

The causes of excess cardiovascular mortality associated with chronic kidney disease (CKD) have been attributed in part to the CKD-mineral bone disorder syndrome (CKD-MBD), wherein, novel cardiovascular risk factors have been identified. New advances in the causes of the CKD-MBD are discussed in this review. They demonstrate that repair and disease processes in the kidneys release factors to the circulation that cause the systemic complications of CKD. The discovery of WNT inhibitors, especially Dickkopf 1 (Dkk1), produced during renal repair as participating in the pathogenesis of the vascular and skeletal components of the CKD-MBD implied that additional pathogenic factors are critical. This lead to the discovery that activin A is a second renal repair factor circulating in increased levels during CKD. Activin A derives from peritubular myofibroblasts of diseased kidneys, wherein it stimulates fibrosis, and decreases tubular klotho expression. Activin A binds to the type 2 activin A receptor, ActRIIA, which is variably affected by CKD in the vasculature. In diabetic/atherosclerotic aortas, specifically in vascular smooth muscle cells (VSMC), ActRIIA signaling is inhibited and contributes to CKD induced VSMC dedifferentiation, osteogenic transition and neointimal atherosclerotic calcification. In nondiabetic/nonatherosclerotic aortas, CKD increases VSMC ActRIIA signaling, and vascular fibroblast signaling causing the latter to undergo osteogenic transition and stimulate vascular calcification. In both vascular situations, a ligand trap for ActRIIA prevented vascular calcification. In the skeleton, activin A is responsible for CKD stimulation of osteoclastogenesis and bone remodeling increasing bone turnover. These studies demonstrate that circulating renal repair and injury factors are causal of the CKD-MBD and CKD associated cardiovascular disease.

Keith A. Hruska

Toshifumi Sugatani

Olga Agapova

Yifu Fang

The chronic kidney disease — Mineral bone disorder (CKD-MBD): Advances in pathophysiology

慢性肾脏病-矿物质骨异常（CKD-MBD）：病理生理学进展

Ping Li

Wensheng Zhang

Jie Zhang

Jie Liu

Jiaming Fu

Zhengnong Wei

Shiyong Le

Jiajia Xu

Liang Wang

Zhongmin Zhang

Corrigendum to “Macrophage migration inhibitory factor promotes heterotopic ossification by mediating ROS/HIF-1α positive feedback loop and activating Wnt/β-catenin signaling pathway” [Bone 190 (2025) 117331]

更正“巨噬细胞迁移抑制因子通过介导ROS/HIF-1α正反馈环路并激活Wnt/β-catenin信号通路促进异位骨化”[Bone 190 (2025) 117331]

Postmenopausal osteoporosis is a type of bone disease with bone loss and deterioration of skeletal function that occurs in women after menopause. Studies have found that early-life exercise can reduce the risk of fractures and decrease the occurrence of osteoporosis, making it a promising approach for preventing and reversing bone loss. In this study, to identify the optimal forms of exercise during early life to optimize bone health and provide suggestions for promoting bone health through exercise training during early life, we conducted different forms of exercise interventions including ladder climbing, treadmill running, combined training, and whole-body vibration (WBV) on adolescent mice for 8 weeks and observed the accumulation of bone mass and arrangement of bone microstructure in adult mice. After removing the ovaries bilaterally, the mice were resting for 22 weeks to simulate the bone loss condition observed in postmenopausal women. We examined the resistance of the bone microstructure to degradation in response to exercise during early life and characterized the specific effects of different forms of exercise on countering bone microstructure deterioration. Our findings demonstrate that early-life exercise exerts long-term beneficial effects on bone health. All four forms of early-life exercise can delay bone loss due to decreased estrogen and improve the bone microstructure to varying degrees, with resistance and vibration training demonstrating superior protective benefits.

Yuxuan Wang

Keping Zhang

Weiwei Gao

Haiqi Lin

Tingting Li

Timon Cheng Yi Liu

Xiquan Weng

Yu Yuan

The effects of different forms of exercise during the early life on the bone microstructure of ovariectomized mice

早期生活中不同形式运动对卵巢切除小鼠骨微结构的影响

This study aims to investigate the roles of the EXT1 and FGFR3 genes in the development of osteochondromas, focusing specifically on their potential interactions in chondrocyte proliferation, differentiation, and tumor formation.

Hongrong Zhang

Zhencun Tang

Shiying Shen

Lei Feng

Yunfa Qin

Liangchong Huang

Yanyan Chen

Yu Liu

Weihong Wang

Deficiency of EXT1 and FGFR3 genes promotes chondrocyte differentiation, leading to the induction of osteochondroma formation

EXT1和FGFR3基因缺陷促进软骨细胞分化，导致骨软骨瘤形成

Both trabecular and cortical bone undergo changes at multiple scales. We previously demonstrated the multi-scale changes in trabecular bone quality that contribute to bone fragility in type 2 diabetes (T2D). The link between increased fragility in T2D and multi-scale changes in cortical bone and their interaction with glycation remains unclear. This study presents, first-ever, multi-scale cortical bone quality parameters in T2D patients after their first hip fracture. The study objective was to determine the association between cortical porosity (Ct.Po.), mechanical, material, and bone compositional properties in T2D. Inferomedial femoral neck (FN) bone tissue specimens were collected from patients (n = 10 with T2D, n = 25 age- and sex-matched non-diabetes controls) who underwent hip replacement surgery following the first hip fragility fracture. Bone mineral density at FN was found to be similar between groups. In T2D, Ct.Po was higher (p = 0.038), while ultimate stress (p = 0.021), ultimate strain (p = 0.040), post-yield strain (p = 0.011), toughness (p = 0.005), yield energy (p = 0.003), and post-yield energy (p = 0.004) were notably lower. Tissue compositional differences included lower gravimetric mineral/matrix (p = 0.017), higher non-enzymatic collagen cross-link ratio (NE-xLR) (p = 0.049) and higher sugar/matrix ratio (p = 0.042) in T2D. Fluorescent advanced glycation end-product (fAGEs) content was higher in T2D bone (p = 0.043). At the mesoscale, the fAGEs in the bone matrix are inversely related to the yield- and ultimate strain of T2D bone, and NE-xLR is negatively correlated with yield- and ultimate- stress in the T2D group. In conclusion, study findings demonstrate that elevated glycation weakens the mechanical integrity of cortical bone by reducing its ability to absorb energy and resist deformation, thereby contributing to bone fragility in T2D. The strong association of fAGEs with lower yield strain, along with the association of NE-xLR with lower yield- and ultimate stress, establishes a causal link between AGEs and the deterioration of cortical bone mechanical properties. These findings underscore the need for strategies targeting glycation and collagen quality to mitigate fracture risk in T2D patients.

Praveer Sihota

Saroj Kumar

Ruban Dhaliwal

Piyush Uniyal

Ram Naresh Yadav

Vandana Dhiman

Deepak Neradi

Shailesh Karn

Mohin Sapara

Sidhartha Sharma

Sameer Aggarwal

Vijay G Goni

Vishwajeet Mehandia

Björn Busse

Deepak Vashishth

Sanjay Kumar Bhadada

Navin Kumar

Multi-scale inferomedial femoral neck bone quality in type 2 diabetes patients with fragility fracture

2型糖尿病伴脆性骨折患者股骨颈内侧多尺度骨质量研究

Managing osteoporotic patients at immediate fracture risk is challenging, in part due to the slow and localized effects of anti-osteoporotic drugs. Combining systemic anti-osteoporotic therapies with local bone augmentation techniques offers a promising strategy, but little is known about potential interactions. We hypothesized that integrating systemic treatments with local bone-strengthening biomaterials would have an additive effect on bone density and structure. This study investigated interactions and synergies between systemic therapies and injectable biomaterials, HA2 and HA2-ZOL, designed for local bone strengthening. HA2-ZOL incorporates Zoledronate, a bisphosphonate, to enhance anti-resorptive effects. These materials were tested in an in vivo rat model of osteoporosis using microCT and histology.

Vincent A Stadelmann

Estelle Gerossier

Ulrike Kettenberger

Dominique P Pioletti

Combining systemic and local osteoporosis treatments: A longitudinal in vivo microCT study in ovariectomized rats

结合系统性和局部骨质疏松治疗：卵巢切除大鼠体内微CT纵向研究

Abbreviation
Journal Impact	3.36
Quartiles(Global)	ENDOCRINOLOGY & METABOLISM(Q2)

ISSN	1873-2763, 8756-3282
h-index	224
Top Journals	Yes

Publication Information	Publisher: Elsevier Inc.，Publishing cycle: ，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1985，Proportion of original research papers: ，Self Citation Rate:， Gold OA Rate:

Bone

Journal Citation Format

A journal article with 1 author

A journal article with 2 authors

A journal article with 3 authors

A journal article with 5 or more authors

Books Citation Format

Thesis Citation Format

Web sites Citation Format

Patent Citation Format

Staying up late manually editing references? ivySCI automatically matches journals and helps you generate references with a single click.

Share Submission Experience