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Abnormal subchondral bone remodeling and its association with articular cartilage degradation in knees of type 2 diabetes patients

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Bone Research 2017年第4期5卷 305-316页

作者： Yan Chen Yong-Can Huang Chun Hoi Yan Kwong Yuen Chiu Qingjun Wei Jingmin Zhao x edward guo Frankie Leung William W Lu Department of Bone and Joint Surgery The First Affiliated HospitalGuangxi Medical UniversityChina Department of Orthopaedics and Traumatology The University of Hong KongHong Kong Bone Bioengineering Laboratory Department of Biomedical EngineeringColumbia UniversityNew YorkNYUSA Shenzhen Engineering Laboratory of Orthopaedic Regenerative Technologies Orthopaedic Research CenterPeking University Shenzhen HospitalShenzhenChina

Type 2 diabetes （T2D） is associated with systemic abnormal bone remodeling and bone loss. Meanwhile, abnormal subchondral bone remodeling induces cartilage degradation, resulting in osteoarthritis （OA）. Accordingly, we investigated alterations in subchondral bone remodeling, microstructure and strength in knees from T2D patients and their association with cartilage degradation. Tibial plateaus were collected from knee OA patients undergoing total knee arthroplasty and divided into non-diabetic （n---70） and diabetes （n = 51） groups. Tibial plateaus were also collected from cadaver donors （n = 20） and used as controls. Subchondral bone microstructure was assessed using micro-computed tomography. Bone strength was evaluated by micro-finite-element analysis. Cartilage degradation was estimated using histology. The expression of tartrate-resistant acidic phosphatase （TRAP）, osterix, and osteocalcin were calculated using immunohistochemistry. Osteoarthritis Research Society International （OARSI） scores of lateral tibial plateau did not differ between non-diabetic and diabetes groups, while higher OARSI scores on medial side were detected in diabetes group. Lower bone volume fraction and trabecular number and higher structure model index were found on both sides in diabetes group. These microstructural alterations translated into lower elastic modulus in diabetes group. Moreover, diabetes group had a larger number of TRAP~ osteoclasts and lower number of Osterix~ osteoprogenitors and Osteocalcin~ osteoblasts. T2D knees are characterized by abnormal subchondral bone remodeling and microstructural and mechanical impairments, which were associated with exacerbated cartilage degradation. In regions with intact cartilage the underlying bone still had abnormal remodeling in diabetes group, suggesting that abnormal bone remodeling may contribute to the early pathogenesis of T2D-associated knee OA.

关键词： Th Abnormal subchondral bone remodeling and its association with articular cartilage degradation in knees of type 2 diabetes patients

Trabecular Plate Loss and Deteriorating Elastic Modulus of Femoral Trabecular Bone in Intertrochanteric Hip Fractures

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Bone Research 2013年第4期1卷 346-354页

作者： Ji Wang Bin Zhou Ian Parkinson C.David L.Thomas John G.Clement Nick Fazzalari x.edward guo Bone Bioengineering Laboratory Department of Biomedical EngineeringColumbia UniversityNew YorkNew York 10027USA Bone and Joint Research Lab SA Pathology and Discipline of Anatomy and PathologyUniversity of AdelaideAdelaideAustralia Section of Oral Anatomy and Surgery The Melbourne Dental SchoolUniversity of MelbourneVictoria 3010Australia

Osteoporotic hip fracture is associated with significant trabecular bone loss, which is typically characterized as low bone density by dual-energy x-ray absorptiometry （DxA） and altered microstructure by micro-computed tomography （pCT）. Emerging morphological analysis techniques, e.g. individual trabecula segmentation （ITS）, can provide additional insights into changes in plate-like and rod-like trabeculae, two major micro- structural types serving different roles in determining bone strength. Using ITS, we evaluated trabecular microstructure of intertrochanteric bone cores obtained from 23 patients undergoing hip replacement surgery for intertrochanteric fracture and 22 cadaveric controls. Micro-finite element （~FE） analyses were performed to further understand how the abnormalities seen by ITS might translate into effects on bone strength. ITS analyses revealed that, near fracture site, plate-like trabeculae were seriously depleted in fracture patients, but trabecular rod volume was maintained. Besides, decreased plate area and rod length were observed in fracture patients. Fracture patients also showed decreased elastic moduli and shear moduli of trabecular bone. These results provided evidence that in intertrochanteric hip fracture, preferential loss of plate-like trabeculae led to more rod-like microstructure and deteriorated mechanical competence adjacent to the fracture site, which increased our understanding of the biomechanical pathogenesis of hip fracture in osteoporosis.

关键词： hip fracture intertrochanteric microstructure individual trabecula segmentation finite element

Bone density, microarchitecture and stiffness in Caucasian and Caribbean Hispanic postmenopausal American women

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Bone Research 2014年第3期2卷 194-202页

作者： Bin Zhou Ji Wang Emily M Stein Zhendong Zhang Kyle K Nishiyama Chiyuan A Zhang Thomas L Nickolas Elizabeth Shane x edward guo Bone Bioengineering Laboratory Department of Biomedical Engineering Columbia University Division of Endocrinology Department of Medicine Columbia University Department of Orthopedic Surgery First Affiliated Hospital School of Medicine Shihezi University

Hispanic Americans of Caribbean origin are a fast-growing subset of the US population, but there are no studies on bone density, microstructure and biomechanical integrity in this minority group. In this study, we aimed to compare Caucasian and Caribbean Hispanic postmenopausal American women with respect to these characteristics. Thirty-three Caribbean Hispanics were age-matched to thirty-three Caucasian postmenopausal women. At the lumbar spine, the Hispanic women had significantly lower areal bone mineral density （aBMD）. At the radius by high-resolution peripheral quantitative computed tomography （HR-pQCT）, there were minimal differences between Hispanic and Caucasian women. At the tibia, Hispanic women had lower trabecular volumetric bone density and trabecular number, and higher trabecular separation. Individual trabecula segmentation （ITS） analyses indicated that at the tibia, Hispanic women not only had significantly lower bone volume fraction, but also had significantly lower rod bone volume fraction, plate trabecular number, rod trabecular number and lower plate-plate, plate-rod and rod-rod junction densities compared to Caucasian women. The differences in bone quantity and quality contributed to lower whole bone stiffness at the radius, and both whole bone and trabecular bone stiffness at the tibia in Hispanic women. In conclusion, Hispanic women had poorer bone mechanical and microarchitectural properties than Caucasian women, especially at the load-bearing distal tibia.

关键词： bone DxA Bone density microarchitecture and stiffness in Caucasian and Caribbean Hispanic postmenopausal American women

Mechanosignaling activation of TGFβmaintains intervertebral disc homeostasis

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Bone Research 2017年第1期5卷 27-40页

作者： Qin Bian Lei Ma Amit Jain Janet L Crane Khaled Kebaish Mei Wan Zhengdong Zhang x edward guo Paul D Sponseller Cheryle A Seguin Lee H Riley Yongjun Wang xu Cao Department of Orthopaedic Surgery Institute for Cell EngineeringJohns Hopkins UniversityBaltimoreMDUSA Institute of Spine Longhua HospitalShanghai University of Traditional Chinese MedicineShanghaiPR China Department of Pediatrics Johns Hopkins UniversityBaltimoreMDUSA Department of Biomedical Engineering Columbia UniversityNYUSA Departments of Physiology and Pharmacology University of Western OntarioLondonCanada

Intervertebral disc （IVD） degeneration is the leading cause of disability with no disease-modifying treatment. IVD degeneration is associated with instable mechanical loading in the spine, but little is known about how mechanical stress regulates nucleus notochordal （NC） cells to maintain IVD homeostasis. Here we report that mechanical stress can result in excessive integrin αvβ6-mediated activation of transforming growth factor beta （TGFβ）, decreased NC cell vacuoles, and increased matrix proteoglycan production, and results in degenerative disc disease （DDD）. Knockout of TGFβ type II receptor （TβRII） or integrin αv in the NC cells inhibited functional activity of postnatal NC cells and also resulted in DDD under mechanical loading. Administration of RGD peptide, TGFβ, and αvβ6-neutralizing antibodies attenuated IVD degeneration. Thus, integrin-mediated activation of TGFβ plays a critical role in mechanical signaling transduction to regulate IVD cell function and homeostasis. Manipulation of this signaling pathway may be a potential therapeutic target to modify DDD.

关键词： Mechanosignaling activation of TGF maintains intervertebral disc homeostasis IVD

Calcium signaling in osteocyte network

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医用生物力学 2010年第S1期25卷 22-24页

作者： x.Lucas Lu Andrew D.Baik Victor Chiang x.edward guo Bone Bioengineering Laboratory Department of Biomedical Engineering Columbia University

Introduction Osteocytes are interconnected through numerous intercellular processes,forming extensive cell networks throughout the bone tissue[1]. It has been shown that osteocyte density is an important physiological... 详细信息

关键词： AFM bone cell MEM MLO EMD

Mechanically induced Ca^(2+) oscillations in osteocytes release extracellular vesicles and enhance bone formation

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Bone Research 2018年第1期6卷 72-82页

作者： Andrea E.Morrell Genevieve N.Brown Samuel T.Robinson Rachel L.Sattler Andrew D.Baik Gehua Zhen xu Cao Lynda F.Bonewald Weiyang Jin Lance C.Kam x.edward guo Bone Bioengineering Laboratory Department of Biomedical Engineering Columbia University Center for Musculoskeletal Research Department of Orthopaedic Surgery Johns Hopkins University Indiana Center for Musculoskeletal Health Indiana University School of Medicine Microscale Biocomplexity Laboratory Department of Biomedical Engineering Columbia University

The vast osteocytic network is believed to orchestrate bone metabolic activity in response to mechanical stimuli through production of sclerostin, RANKL, and osteoprotegerin(OPG). However, the mechanisms of osteocyte mechanotransduction remain poorly understood. We've previously shown that osteocyte mechanosensitivity is encoded through unique intracellular calcium (Ca^(2+) ) dynamics. Here, by simultaneously monitoring Ca^(2+) and actin dynamics in single cells exposed to fluid shear flow, we detected actin network contractions immediately upon onset of flow-induced Ca^(2+) transients, which were facilitated by smooth muscle myosin and further confirmed in native osteocytes ex vivo. Actomyosin contractions have been linked to the secretion of extracellular vesicles(EVs), and our studies demonstrate that mechanical stimulation upregulates EV production in osteocytes through immunostaining for the secretory vesicle marker Lysosomal-associated membrane protein 1(LAMP1) and quantifying EV release in conditioned medium, both of which are blunted when Ca^(2+) signaling was inhibited by neomycin. Axial tibia compression was used to induce anabolic bone formation responses in mice, revealing upregulated LAMP1 and expected downregulation of sclerostin in vivo. This load-related increase in LAMP1 expression was inhibited in neomycin-injected mice compared to ***-computed tomography revealed significant load-related increases in both trabecular bone volume fraction and cortical thickness after two weeks of loading, which were blunted by neomycin treatment. In summary, we found mechanical stimulation of osteocytes activates Ca^(2+) -dependent contractions and enhances the production and release of EVs containing bone regulatory proteins. Further, blocking Ca^(2+) signaling significantly attenuates adaptation to mechanical loading in vivo, suggesting a critical role for Ca^(2+) -mediated signaling in bone adaptation.

关键词： OPG conditioned medium Ca2+-dependent

How does Mechanical Loading Make Bone Microstructure: Modeling vs. Remodeling

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医用生物力学 2019年第A1期34卷 11-11页

作者： Samuel T.Robinson Yizhong Hu x.edward guo Bone Bioengineering Laboratory Department of Biomedical EngineeringColumbia University

Bone modeling and remodeling are governed by distinct biochemical processes that may hold unique opportunities for optimizing bone mass[1,2].Remodeling refers to the coupled resorption and subsequent formation on the bone surface,while modeling represents uncoupled formation or *** loading is known to improve bone mass,though whether this occurs through modeling or remodeling(or by some combination)is *** in vivo morphometry utilizing high resolution micro-CT and image registration has only recently become feasible and thus holds an untapped and expanding potential for understanding bone metabolism by quantifying and localizing formation/resorption and modeling/remodeling events.16-week-old mice were given 2 baseline weekly micro-CT scans of both tibiae prior to the initiation of daily unilateral loading(contralateral limb for nonloaded control).Weekly scanning and daily loading continued for 5 *** images for each mouse in a global coordinate system revealed the time course of each voxel,and changes in bone mass were quantified as modeling or remodeling starting at the onset of *** cortical bone,after an initial response to loading in both regimes,modeling emerged as the dominant *** effects were largest in areas of mechanical *** example,anabolic modeling on the periosteal surface of the half of the tibia in compression under axial load presented a strong effect of loading,whereas the same measure on the endosteal surface in the area in tension showed no ***,in trabecular bone anabolic modeling was significantly increased with loading on trabecular plates but not rods(plates have been shown to be the major contributor to overall bone strength).The catabolic modeling response on the endosteal surface showed an interesting transition over *** initially led to a significant suppression of catabolic modeling,but over time increased it to levels significantly beyond tha

关键词： Mechanical Loading Make Bone Microstructure Modeling vs Remodeling

The roles of extracellular vesicles released by mechanically stimulated osteocytes in regulating osteoblast and osteoclast functions

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Mechanobiology in Medicine 2024年第2期2卷 71-78页

作者： Yumei Chen Runze Zhao Li Yang x.edward guo Bone Bioengineering Laboratory Department of Biomedical EngineeringColumbia UniversityNew YorkNYUSA Bioengineering College Chongqing UniversityChongqing CityChina Center of Translational Medicine and Clinical Laboratory The Fourth Affiliated Hospital of Soochow UniversitySuzhou215028China

Bone adapts to mechanical loading by changing its shape and ***,as major mechanosensors,are critical for bone modeling/remodeling in response to mechanical *** calcium oscillation is one of the early responses in osteocytes,and this further facilitates bone cell communication through released biochemical *** previous study has found that mechanically induced calcium oscillations in osteocytes enhance the release of extracellular vesicles(EVs),and those released EVs can elevate bone formation ***,the mechanism of mechanically stimulated EVs’regulation of bone formation and resorption is still ***,using in vitro studies,we exposed OCY454 cells,with relatively high sclerostin expression,to steady fluid flow(SFF)and characterized the functions of rapidly released EVs in osteoblast and osteoclast *** study demonstrates that SFF stimulates intracellular calcium response in OCY454 cells and further induces sclerostin,osteoprotegerin(OPG),receptor activator of NF-κB ligand(RANKL)inside or outside EVs to regulate osteoblast and osteoclast *** load-induced protein and EVs release is load-duration ***,stimulated osteocytes rapidly regulate osteoclast maturation through EVs capsulated *** contrast,other regulating proteins,OPG,and sclerostin,are mainly released directly into the medium without EV capsulation.

关键词： OCY454 Osteocyte Mechanotransduction Fluid flow Extracellular vesicles

Intracellular calcium oscillations in live osteocytes in ex vivo intact mouse long bones under dynamic mechanical loading

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Intracellular calcium oscillations in live osteocytes in ex ...