生物材料相关钙化:病理、机制和预防策略。

F J Schoen, H Harasaki, K M Kim, H C Anderson, R J Levy
{"title":"生物材料相关钙化:病理、机制和预防策略。","authors":"F J Schoen,&nbsp;H Harasaki,&nbsp;K M Kim,&nbsp;H C Anderson,&nbsp;R J Levy","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Deposition of calcium-containing apatite mineral occurs widely in association with cardiovascular and noncardiovascular medical devices and biomaterials, is the leading cause of failure of contemporary bioprosthetic heart valves, and limits the functional lifetime of experimental (and potentially clinical) mechanical blood pumps and polymeric heart valves. Calcification of bioprosthetic tissue is primarily intrinsic, related to cuspal connective tissue cells and fragments, and collagen. In contrast, the predominant site of calcific crystals on flexing polymeric surfaces in blood pumps or valve prostheses is extrinsic, associated with adherent cells, thrombus, or pseudointima. Pathologic calcification shares key features with physiologic skeletal mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. This suggests a unified hypothesis for normal and abnormal mineralization. Several approaches are being studied experimentally for the inhibition of bioprosthetic heart valve calcification. Controlled-release diphosphonate therapy, perhaps in conjunction with an anticalcification cuspal pretreatment, appears most effective. Research objectives in biomaterial-associated calcification include (1) development of animal models, (2) determination of initial crystal nucleation events and sites, (3) elucidation of the relative roles of host, implant, and mechanical determinants, and (4) development of approaches for the inhibition of mineralization.</p>","PeriodicalId":15159,"journal":{"name":"Journal of biomedical materials research","volume":"22 A1 Suppl","pages":"11-36"},"PeriodicalIF":0.0000,"publicationDate":"1988-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Biomaterial-associated calcification: pathology, mechanisms, and strategies for prevention.\",\"authors\":\"F J Schoen,&nbsp;H Harasaki,&nbsp;K M Kim,&nbsp;H C Anderson,&nbsp;R J Levy\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Deposition of calcium-containing apatite mineral occurs widely in association with cardiovascular and noncardiovascular medical devices and biomaterials, is the leading cause of failure of contemporary bioprosthetic heart valves, and limits the functional lifetime of experimental (and potentially clinical) mechanical blood pumps and polymeric heart valves. Calcification of bioprosthetic tissue is primarily intrinsic, related to cuspal connective tissue cells and fragments, and collagen. In contrast, the predominant site of calcific crystals on flexing polymeric surfaces in blood pumps or valve prostheses is extrinsic, associated with adherent cells, thrombus, or pseudointima. Pathologic calcification shares key features with physiologic skeletal mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. This suggests a unified hypothesis for normal and abnormal mineralization. Several approaches are being studied experimentally for the inhibition of bioprosthetic heart valve calcification. Controlled-release diphosphonate therapy, perhaps in conjunction with an anticalcification cuspal pretreatment, appears most effective. Research objectives in biomaterial-associated calcification include (1) development of animal models, (2) determination of initial crystal nucleation events and sites, (3) elucidation of the relative roles of host, implant, and mechanical determinants, and (4) development of approaches for the inhibition of mineralization.</p>\",\"PeriodicalId\":15159,\"journal\":{\"name\":\"Journal of biomedical materials research\",\"volume\":\"22 A1 Suppl\",\"pages\":\"11-36\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1988-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biomedical materials research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical materials research","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

含钙磷灰石矿物的沉积与心血管和非心血管医疗器械和生物材料广泛相关,是当代生物假体心脏瓣膜失效的主要原因,并限制了实验性(和潜在的临床)机械血泵和聚合物心脏瓣膜的功能寿命。生物假体组织的钙化主要是内在的,与尖结缔组织细胞和碎片以及胶原蛋白有关。相反,在血泵或瓣膜假体的弯曲聚合物表面上,钙化晶体的主要部位是外源性的,与粘附细胞、血栓或假内膜有关。病理性钙化与生理性骨骼矿化具有共同的关键特征,包括通过细胞膜介导的晶体起始,通常以细胞外囊泡的形式出现。这为正常矿化和异常矿化提出了统一的假设。几种方法正在实验研究抑制生物人工心脏瓣膜钙化。控释二膦酸盐治疗,可能结合抗钙化尖端预处理,似乎是最有效的。生物材料相关钙化的研究目标包括:(1)建立动物模型;(2)确定初始晶体成核事件和位置;(3)阐明宿主、植入物和机械决定因素的相对作用;(4)开发抑制矿化的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Biomaterial-associated calcification: pathology, mechanisms, and strategies for prevention.

Deposition of calcium-containing apatite mineral occurs widely in association with cardiovascular and noncardiovascular medical devices and biomaterials, is the leading cause of failure of contemporary bioprosthetic heart valves, and limits the functional lifetime of experimental (and potentially clinical) mechanical blood pumps and polymeric heart valves. Calcification of bioprosthetic tissue is primarily intrinsic, related to cuspal connective tissue cells and fragments, and collagen. In contrast, the predominant site of calcific crystals on flexing polymeric surfaces in blood pumps or valve prostheses is extrinsic, associated with adherent cells, thrombus, or pseudointima. Pathologic calcification shares key features with physiologic skeletal mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. This suggests a unified hypothesis for normal and abnormal mineralization. Several approaches are being studied experimentally for the inhibition of bioprosthetic heart valve calcification. Controlled-release diphosphonate therapy, perhaps in conjunction with an anticalcification cuspal pretreatment, appears most effective. Research objectives in biomaterial-associated calcification include (1) development of animal models, (2) determination of initial crystal nucleation events and sites, (3) elucidation of the relative roles of host, implant, and mechanical determinants, and (4) development of approaches for the inhibition of mineralization.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
A comparative study of in vitro apatite deposition on heat-, H(2)O(2)-, and NaOH-treated titanium surfaces. Prophylaxis of implant-related staphylococcal infections using tobramycin-containing bone cement. Effects of geometry of hydroxyapatite as a cell substratum in BMP-induced ectopic bone formation. Well-defined sulfobetaine-based statistical copolymers as potential antibioadherent coatings. Platelet adhesion and procoagulant activity induced by contact with radiofrequency glow discharge polymers: roles of adsorbed fibrinogen and vWF.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1