BoneKEy reports最新文献_第2页

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":null,"pages":null},"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

Ibandronate for the prevention of bone loss after allogeneic stem cell transplantation for hematologic malignancies: a randomized-controlled trial. 依班膦酸钠预防恶性血液病异体干细胞移植后骨质流失:一项随机对照试验。

BoneKEy reports Pub Date : 2016-10-19 DOI: 10.1038/bonekey.2016.72

Huifang Lu, R. Champlin, U. Popat, X. Pundole, C. Escalante, Xuemei Wang, W. Qiao, W. Murphy, R. Gagel

引用次数: 4

Tissue-engineered 3D cancer-in-bone modeling: silk and PUR protocols. 组织工程三维骨癌建模:丝绸和PUR协议。

BoneKEy reports Pub Date : 2016-10-19 DOI: 10.1038/BONEKEY.2016.75

U. Dadwal, C. Falank, H. Fairfield, Sarah Linehan, C. Rosen, D. Kaplan, J. Sterling, M. Reagan

引用次数: 15

How rare bone diseases have informed our knowledge of complex diseases. 罕见的骨病如何让我们了解复杂的疾病。

BoneKEy reports Pub Date : 2016-09-21 DOI: 10.1038/bonekey.2016.69

Mark L. Johnson

引用次数: 6

Osteocyte isolation and culture methods. 骨细胞分离和培养方法。

BoneKEy reports Pub Date : 2016-09-14 DOI: 10.1038/bonekey.2016.65

Karan M. Shah, M. Stern, A. Stern, J. Pathak, N. Bravenboer, A. Bakker

引用次数: 27

Intramembranous bone regeneration and implant placement using mechanical femoral marrow ablation: rodent models. 机械股骨骨髓消融的膜内骨再生和植入物放置:啮齿动物模型。

BoneKEy reports Pub Date : 2016-09-07 DOI: 10.1038/bonekey.2016.61

Meghan M. Moran, K. Sena, M. McNulty, D. R. Sumner, A. Virdi

引用次数: 10

Osteoporosis drug effects on cortical and trabecular bone microstructure: a review of HR-pQCT analyses. 骨质疏松药物对骨皮质和骨小梁微观结构的影响:HR-pQCT分析综述。

BoneKEy reports Pub Date : 2016-08-31 DOI: 10.1038/bonekey.2016.59

E. Lespessailles, R. Hambli, S. Ferrari

引用次数: 33

Post-yield and failure properties of cortical bone. 皮质骨的屈服后和破坏特性。

BoneKEy reports Pub Date : 2016-08-24 eCollection Date: 2016-01-01 DOI: 10.1038/bonekey.2016.60

Uwe Wolfram, Jakob Schwiedrzik

引用次数: 74

Skeletal implications and management of cystinosis: three case reports and literature review. 胱氨酸病对骨骼的影响及治疗:三例报告及文献回顾。

BoneKEy reports Pub Date : 2016-08-17 eCollection Date: 2016-01-01 DOI: 10.1038/bonekey.2016.55

Justine Bacchetta, Marcella Greco, Aurélia Bertholet-Thomas, François Nobili, Jozef Zustin, Pierre Cochat, Francesco Emma, Georges Boivin

{"title":"Skeletal implications and management of cystinosis: three case reports and literature review.","authors":"Justine Bacchetta, Marcella Greco, Aurélia Bertholet-Thomas, François Nobili, Jozef Zustin, Pierre Cochat, Francesco Emma, Georges Boivin","doi":"10.1038/bonekey.2016.55","DOIUrl":"https://doi.org/10.1038/bonekey.2016.55","url":null,"abstract":"Hypophosphatemic rickets and short stature are observed in nephropathic cystinosis, an orphan autosomal recessive lysosomal storage disease due to a deficiency of cystinosin (CTNS gene). Although bone impairment is not common, it nevertheless appears to be more and more discussed by experts, even though the exact underlying pathophysiology is unclear. Four hypotheses are currently discussed to explain such impairment: copper deficiency, bone consequences of severe hypophosphatemic rickets during infancy, cysteamine toxicity and abnormal thyroid metabolism. In murine models, the invalidation of the CTNS gene is associated neither with renal phosphate wasting nor with renal failure, but causes severe osteopenia and growth retardation, thus raising the hypothesis of a specific underlying bone defect in cystinosis. Moreover, the in vitro ability of mesenchymal stromal cells isolated from bone marrow to differentiate along the osteoblastic lineage is reduced in patients with cystinosis as compared with cells obtained from healthy controls, this cellular abnormality being reverted after cysteamine treatment. From our experience of three pediatric patients with cystinosis and severe bone deformations having undergone a thorough biochemical evaluation, as well as a bone biopsy, we conclude that even though copper deficiency, high-doses cysteamine regimens and abnormal thyroid metabolism may worsen the bone picture in cystinosis patients, the exact pathophysiology of such impairment remains to be defined. The role of chronic hypoparathyroidism due to chronic phosphate wasting could also be discussed. In the future, larger and prospective studies should focus on this topic because of the potential major impact on patients' quality of life. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988218/pdf/bonekey201655.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34350934","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: 17

Protein/amino-acid modulation of bone cell function 骨细胞功能的蛋白质/氨基酸调节

BoneKEy reports Pub Date : 2016-08-10 DOI: 10.1038/bonekey.2016.58

R. Macdonell, M. Hamrick, C. Isales

引用次数: 24