BoneKEy reports最新文献

Role of cortical bone in hip fracture. 皮质骨在髋部骨折中的作用。

BoneKEy reports Pub Date : 2017-01-13 eCollection Date: 2017-01-01 DOI: 10.1038/bonekey.2016.82

Jonathan Reeve

{"title":"Role of cortical bone in hip fracture.","authors":"Jonathan Reeve","doi":"10.1038/bonekey.2016.82","DOIUrl":"https://doi.org/10.1038/bonekey.2016.82","url":null,"abstract":"In this review, I consider the varied mechanisms in cortical bone that help preserve its integrity and how they deteriorate with aging. Aging affects cortical bone in two ways: extrinsically through its effects on the individual that modify its mechanical loading experience and 'milieu interieur'; and intrinsically through the prolonged cycle of remodelling and renewal extending to an estimated 20 years in the proximal femur. Healthy femoral cortex incorporates multiple mechanisms that help prevent fracture. These have been described at multiple length scales from the individual bone mineral crystal to the scale of the femur itself and appear to operate hierarchically. Each cortical bone fracture begins as a sub-microscopic crack that enlarges under mechanical load, for example, that imposed by a fall. In these conditions, a crack will enlarge explosively unless the cortical bone is intrinsically tough (the opposite of brittle). Toughness leads to microscopic crack deflection and bridging and may be increased by adequate regulation of both mineral crystal size and the heterogeneity of mineral and matrix phases. The role of osteocytes in optimising toughness is beginning to be worked out; but many osteocytes die in situ without triggering bone renewal over a 20-year cycle, with potential for increasing brittleness. Furthermore, the superolateral cortex of the proximal femur thins progressively during life, so increasing the risk of buckling during a fall. Besides preserving or increasing hip BMD, pharmaceutical treatments have class-specific effects on the toughness of cortical bone, although dietary and exercise-based interventions show early promise.","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":"6 ","pages":"867"},"PeriodicalIF":0.0,"publicationDate":"2017-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2016.82","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34798559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 18

Repeated irradiation from micro-computed tomography scanning at 2, 4 and 6 months of age does not induce damage to tibial bone microstructure in male and female CD-1 mice. 在2、4和6月龄时，反复进行微计算机断层扫描，不会对雄性和雌性CD-1小鼠的胫骨微结构造成损伤。

BoneKEy reports Pub Date : 2017-01-13 eCollection Date: 2017-01-01 DOI: 10.1038/bonekey.2016.87

Sandra M Sacco, Caitlin Saint, Amanda B Longo, Charles B Wakefield, Phil L Salmon, Paul J LeBlanc, Wendy E Ward

{"title":"Repeated irradiation from micro-computed tomography scanning at 2, 4 and 6 months of age does not induce damage to tibial bone microstructure in male and female CD-1 mice.","authors":"Sandra M Sacco, Caitlin Saint, Amanda B Longo, Charles B Wakefield, Phil L Salmon, Paul J LeBlanc, Wendy E Ward","doi":"10.1038/bonekey.2016.87","DOIUrl":"https://doi.org/10.1038/bonekey.2016.87","url":null,"abstract":"Long-term effects of repeated in vivo micro-computed tomography (μCT) scanning at key stages of growth and bone development (ages 2, 4 and 6 months) on trabecular and cortical bone structure, as well as developmental patterns, have not been studied. We determined the effect of repetitive μCT scanning at age 2, 4 and 6 months on tibia bone structure of male and female CD-1 mice and characterized developmental changes. At 2, 4 and 6 months of age, right tibias were scanned using in vivo μCT (Skyscan 1176) at one of three doses of radiation per scan: 222, 261 or 460 mGy. Left tibias of the same mice were scanned only at 6 months to serve as non-irradiated controls to determine whether recurrent radiation exposure alters trabecular and cortical bone structure at the proximal tibia. In males, eccentricity was lower (P<0.05) in irradiated compared with non-irradiated tibias (222 mGy group). Within each sex, all other structural outcomes were similar between irradiated and non-irradiated tibias regardless of dose. Trabecular bone loss occurred in all mice due to age while cortical development continued to age 6 months. In conclusion, repetitive μCT scans at various radiation doses did not damage trabecular or cortical bone structure of proximal tibia in male and female CD-1 mice. Moreover, scanning at 2, 4 and 6 months of age highlight the different developmental time course between trabecular and cortical bone. These scanning protocols can be used to investigate longitudinal responses of bone structures to an intervention.","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":"6 ","pages":"855"},"PeriodicalIF":0.0,"publicationDate":"2017-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2016.87","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34798560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21

Confocal/two-photon microscopy in studying colonisation of cancer cells in bone using xenograft mouse models. 用共聚焦/双光子显微镜研究癌细胞在异种移植小鼠骨模型中的定植。

BoneKEy reports Pub Date : 2016-12-07 DOI: 10.1038/bonekey.2016.84

Gloria Allocca, Anjali P. Kusumbe, Saravana K. Ramasamy, Ning Wang

引用次数: 9

Parathyroid hormone reflects adiposity and cardiometabolic indices but not bone density in normal men. 甲状旁腺激素反映正常男性的肥胖和心脏代谢指标，但不反映骨密度。

BoneKEy reports Pub Date : 2016-12-07 DOI: 10.1038/bonekey.2016.85

E. Billington, G. Gamble, I. Reid

引用次数: 6

Prophylactic augmentation of the osteoporotic proximal femur-mission impossible? 预防性增强骨质疏松的股骨近端-任务不可能?

BoneKEy reports Pub Date : 2016-12-07 DOI: 10.1038/bonekey.2016.86

P. Varga, L. Hofmann-Fliri, M. Blauth, M. Windolf

引用次数: 19

Erratum: The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation. 更正：骨重塑周期的逆转阶段：将吸收和形成结合起来的细胞先决条件。

BoneKEy reports Pub Date : 2016-11-30 eCollection Date: 2016-01-01 DOI: 10.1038/bonekey.2016.88

Jean-Marie Delaisse

引用次数: 0

Bone muscle crosstalk targets muscle regeneration pathway regulated by core circadian transcriptional repressors DEC1 and DEC2. 骨骼肌串以核心昼夜节律转录抑制因子DEC1和DEC2调控的肌肉再生途径为靶点。

BoneKEy reports Pub Date : 2016-11-16 DOI: 10.1038/BONEKEY.2016.80

J. Gorski, J. Price

引用次数: 9

Lessons on skeletal cell plasticity from studying jawbone regeneration in zebrafish. 斑马鱼颚骨再生对骨细胞可塑性的启示。

BoneKEy reports Pub Date : 2016-11-16 DOI: 10.1038/BONEKEY.2016.81

Sandeep Paul, J. G. Crump

引用次数: 10

Methodological considerations when studying the skeletal response to glucose intolerance using the diet-induced obesity model. 利用饮食诱发肥胖模型研究骨骼对葡萄糖不耐受的反应时的方法学考虑。

BoneKEy reports Pub Date : 2016-10-26 eCollection Date: 2016-01-01 DOI: 10.1038/bonekey.2016.71

Elizabeth Rendina-Ruedy, Brenda J Smith

{"title":"Methodological considerations when studying the skeletal response to glucose intolerance using the diet-induced obesity model.","authors":"Elizabeth Rendina-Ruedy, Brenda J Smith","doi":"10.1038/bonekey.2016.71","DOIUrl":"10.1038/bonekey.2016.71","url":null,"abstract":"The prevalence of obesity and type 2 diabetes mellitus (T2DM) continues to rise, and as a result, research aimed at understanding the molecular basis for the co-morbidities has become an area of much scientific interest. Among the more recently recognized chronic complications of T2DM is the increased risk of fracture, especially hip fracture, that has been reported independent of bone mineral density (BMD). A widely used animal model to study how the development and progression of impaired glucose tolerance affect the skeleton has been the diet-induce obesity (DIO) model. As the name implies, this model employs the use of a version of high-fat diets to induce obesity and the subsequent metabolic perturbations that occur with T2DM. Although the model offers a number of advantages, the literature reveals some inconsistent results. Upon further review, discrepancies in the choice of the experimental high-fat diets and the control diets have become a point of major concern. The variability between diets and study design has made it difficult to compare data and results across studies. Therefore, this review aims to provide guidelines that should be employed when designing studies using DIO models of T2DM.","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":"5 1","pages":"845"},"PeriodicalIF":0.0,"publicationDate":"2016-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58485435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The clinical contribution of cortical porosity to fragility fractures. 皮质多孔性对脆性骨折的临床影响。

BoneKEy reports Pub Date : 2016-10-26 eCollection Date: 2016-01-01 DOI: 10.1038/bonekey.2016.77

Åshild Bjørnerem

{"title":"The clinical contribution of cortical porosity to fragility fractures.","authors":"Åshild Bjørnerem","doi":"10.1038/bonekey.2016.77","DOIUrl":"10.1038/bonekey.2016.77","url":null,"abstract":"Cortical bone is not compact; rather it is penetrated by many Haversian and Volkmann canals for blood supply. The lining of these canals are the intracortical bone surfaces available for bone remodeling. Increasing intracortical bone remodeling increases cortical porosity. However, cortical bone loss occurs more slowly than trabecular loss due to the fact that less surface per unit of bone matrix volume is available for bone remodeling. Nevertheless, most of the bone loss over time is cortical because cortical bone constitutes 80% of the skeleton, and the relative proportion of trabecular bone diminishes with advancing age. Higher serum levels of bone turnover markers are associated with higher cortical porosity of the distal tibia and the proximal femur. Greater porosity of the distal radius is associated with higher odds for forearm fracture, and greater porosity of the proximal femur is associated with higher odds for non-vertebral fracture in postmenopausal women. Measurement of cortical porosity contributes to fracture risk independent of areal bone mineral density and Fracture Risk Assessment Tool. On the other hand, antiresorptive treatment reduces porosity at the distal radius and at the proximal femoral shaft. Thus, porosity is a substantial determinant of the bone fragility that underlies the risk of fractures and may be a target for fracture prevention.","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":"5 1","pages":"846"},"PeriodicalIF":0.0,"publicationDate":"2016-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58485242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0