AN INVESTIGATION OF JOINT DEGENERATION

关节退化的研究

基本信息

  • 批准号:
    3151717
  • 负责人:
  • 金额:
    $ 17.29万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1979
  • 资助国家:
    美国
  • 起止时间:
    1979-09-30 至 1987-11-30
  • 项目状态:
    已结题

项目摘要

We plan to study the factors promoting progressive cartilage destruction in animal models of osteoarthrosis in order to understand the pathophysiology of this condition. The effectiveness of these models has been established by previous experimentation. The joint tissues are studied biochemically, metabolically, and biomechanically. Since the pathology of osteoarthrosis involves destruction of the articular cartilage and the remodeling of the bone adjacent to the joints, we must use in vivo preparations because osteoarthrosis mainly affects mature, older individuals and its development involves an inter-relationship between a variety of tissues, organ cultures utilizing fetal materials are inappropriate. This study, involving collaborative biochemical, biomechanical, anatomical, pathological, and clinical analyses of these models, should provide a better understanding of osteoarthrosis with the hope that the process can some day be halted and reversed. We propose utilizing poorly-protected-against repetitive impulsive loading of a physiologically reasonable amount to create osteoarthrosis in the right knees of rabbits. The left knee is used as a control. We want to establish the threshold levels at which articular cartilage is mechanically injured, the nature of the load which is most deleterious, and the mechanical factors responsible for progression of the joint deterioration. We will first predict the most deleterious force analytically by finite element analysis and test that hypothesis experimentally. We will also utilize stiffening, caused by remodeling of a local area of subchondral bone overlying an implanted plug just under the knee joint of a sheep to study the relationship of bone stiffening and progressive cartilage deterioration. Finite element analysis reveals that such remodeling achieved does increase the stress in the deep layers of the overlying cartilage. We plan to study this in long- and short-term animals to delineate the progression of changes. Experimental results coupled with an expansion of analytical understanding should help define the important mechanical parameters causing joint deterioration in osteoarthrosis.
我们计划研究促进进行性软骨破坏的因素。 骨关节病动物模型的建立及其病理生理意义 在这种情况下。这些模型的有效性已经被证实。 根据之前的实验。对关节组织进行生化研究, 在新陈代谢和生物力学方面。自骨关节病的病理学以来 涉及关节软骨的破坏和关节的重塑 骨与关节相邻时,必须使用体内制剂,因为 骨关节病主要影响成熟、老年个体及其发育 涉及各种组织、器官培养之间的相互关系 使用胎儿材料是不合适的。这项研究,涉及 协同生化、生物力学、解剖学、病理学和 对这些模型的临床分析,应该提供更好的理解 骨关节病,希望有一天这个过程可以停止和 颠倒了。我们建议使用保护不力的-防止重复 冲动地加载生理上合理的量来创造 兔右膝骨关节病。左膝被用作 控制力。我们想要确定关节的门槛水平 软骨是机械性损伤的,其性质是负荷最大 有害的,和机械因素导致的进展 关节恶化。我们将首先预测最有害的力量 通过有限元分析进行分析并验证假设 试验性的。我们还将利用由一个 软骨下骨覆盖在种植塞上的局部区域 绵羊膝关节骨僵硬与骨质疏松症关系的研究 进行性软骨退化。有限元分析表明, 这样的重塑确实增加了深层的应力。 覆盖着软骨。我们计划在长期和短期动物身上研究这一点。 勾勒出变化的进程。实验结果与 分析理解的扩展应该有助于确定重要的 导致骨关节病关节恶化的力学参数。

项目成果

期刊论文数量(23)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
[Synovial membrane and cartilage changes in an arthrosis model. Instability and impact stress model].
[关节病模型中滑膜和软骨的变化。
Hypothesis: joints can heal.
假设:关节可以愈合。
Bone and cartilage changes following experimental varus or valgus tibial angulation.
实验性胫骨内翻或外翻角度后骨和软骨发生变化。
Skeletal change in response to altered strain environments: is woven bone a response to elevated strain?
骨骼变化响应改变的应变环境:编织骨是对升高应变的响应吗?
  • DOI:
    10.1016/8756-3282(89)90057-4
  • 发表时间:
    1989
  • 期刊:
  • 影响因子:
    4.1
  • 作者:
    Burr,DB;Schaffler,MB;Yang,KH;Lukoschek,M;Sivaneri,N;Blaha,JD;Radin,EL
  • 通讯作者:
    Radin,EL
Early vascular changes in rabbit subchondral bone after repetitive impulsive loading.
重复脉冲载荷后兔软骨下骨的早期血管变化。
{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

ERIC L RADIN其他文献

ERIC L RADIN的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('ERIC L RADIN', 18)}}的其他基金

ACL LOSS AND KNEE DYNAMICS IN THE PATHOGENESIS OF OA
OA 发病机制中的 ACL 丢失和膝关节动力学
  • 批准号:
    2083619
  • 财政年份:
    1995
  • 资助金额:
    $ 17.29万
  • 项目类别:
ACL LOSS AND KNEE DYNAMICS IN THE PATHOGENESIS OF OA
OA 发病机制中的 ACL 丢失和膝关节动力学
  • 批准号:
    2517509
  • 财政年份:
    1995
  • 资助金额:
    $ 17.29万
  • 项目类别:
ACL LOSS AND KNEE DYNAMICS IN THE PATHOGENESIS OF OA
OA 发病机制中的 ACL 丢失和膝关节动力学
  • 批准号:
    2083620
  • 财政年份:
    1995
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155517
  • 财政年份:
    1990
  • 资助金额:
    $ 17.29万
  • 项目类别:
GORDON CONFERENCE ON BIOENGINEERING AND ORTHOPEDICS
戈登生物工程和骨科会议
  • 批准号:
    3433713
  • 财政年份:
    1986
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155513
  • 财政年份:
    1985
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155514
  • 财政年份:
    1979
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155512
  • 财政年份:
    1979
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155515
  • 财政年份:
    1979
  • 资助金额:
    $ 17.29万
  • 项目类别:
AN INVESTIGATION OF JOINT DEGENERATION
关节退化的研究
  • 批准号:
    3155516
  • 财政年份:
    1979
  • 资助金额:
    $ 17.29万
  • 项目类别:

相似海外基金

Pathophysiology of bone disorder in light of epigenetic alteration and comprehensive network of transcription factors
表观遗传改变和转录因子综合网络的骨病病理生理学
  • 批准号:
    20H03458
  • 财政年份:
    2020
  • 资助金额:
    $ 17.29万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Acute kidney injury-induced mineral and bone disorder: concept and characterization
急性肾损伤引起的矿物质和骨疾病:概念和特征
  • 批准号:
    20K08618
  • 财政年份:
    2020
  • 资助金额:
    $ 17.29万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Vitamin D Genetics and Racial Differences in Pediatric Chronic Kidney Disease-Mineral and Bone Disorder
儿科慢性肾脏病 - 矿物质和骨骼疾病的维生素 D 遗传学和种族差异
  • 批准号:
    10380577
  • 财政年份:
    2020
  • 资助金额:
    $ 17.29万
  • 项目类别:
Vitamin D Genetics and Racial Differences in Pediatric Chronic Kidney Disease-Mineral and Bone Disorder
儿科慢性肾脏病 - 矿物质和骨骼疾病的维生素 D 遗传学和种族差异
  • 批准号:
    10592364
  • 财政年份:
    2020
  • 资助金额:
    $ 17.29万
  • 项目类别:
Salt inducible kinases: novel therapeutic targets for chronic kidney disease mineral and bone disorder (CKD-MBD)
盐诱导激酶:慢性肾病矿物质和骨疾病 (CKD-MBD) 的新治疗靶点
  • 批准号:
    413021
  • 财政年份:
    2019
  • 资助金额:
    $ 17.29万
  • 项目类别:
    Fellowship Programs
Fluoride and Human Health: Assessing Novel Biomarkers in Detecting Bone Disorder
氟化物与人类健康:评估检测骨疾病的新型生物标志物
  • 批准号:
    9891065
  • 财政年份:
    2018
  • 资助金额:
    $ 17.29万
  • 项目类别:
Systems biology approach to the management of chronic kidney disease-mineral bone disorder
治疗慢性肾病-矿物质性骨病的系统生物学方法
  • 批准号:
    10310403
  • 财政年份:
    2018
  • 资助金额:
    $ 17.29万
  • 项目类别:
Chronic Kidney Disease-Mineral Bone Disorder (CKD-MBD) Syndrome in the Diabetic, Neuropathic Foot
糖尿病神经性足部的慢性肾病-矿物质骨紊乱 (CKD-MBD) 综合征
  • 批准号:
    10734640
  • 财政年份:
    2016
  • 资助金额:
    $ 17.29万
  • 项目类别:
Fluoride and human health: Assessing novel biomarkers in detecting bone disorder
氟化物与人类健康:评估检测骨疾病的新型生物标志物
  • 批准号:
    9057043
  • 财政年份:
    2015
  • 资助金额:
    $ 17.29万
  • 项目类别:
Beneficial effects of rice endosperm and bran protein on chronic kidney disease-mineral bone disorder
稻米胚乳和麸皮蛋白对慢性肾病-矿物质性骨病的有益作用
  • 批准号:
    15K21004
  • 财政年份:
    2015
  • 资助金额:
    $ 17.29万
  • 项目类别:
    Grant-in-Aid for Young Scientists (B)
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了