医学
骨愈合
多发伤
炎症
重症监护医学
生物信息学
免疫学
外科
生物
作者
Joseph Borrelli,Chris Pape,David J. Hak,Joseph R. Hsu,Sheldon S. Lin,Peter V. Giannoudis,Joseph M. Lane
标识
DOI:10.1097/bot.0b013e318274da8b
摘要
Summary: Bone healing after fracture occurs in a well-organized manner and involves a multitude of cell types, inflammatory cytokines, growth factors, prostaglandins, and certain vitamins. Some of the means by which alterations in these essential components affect bone repair are understood, whereas others still need to be delineated. Based on clinical experience and basic science research, certain clinical conditions have become associated with delays in bone repair after fracture. These conditions include chronic inflammation, diabetes, hypovitaminosis, aging, and polytrauma. This brief report reviews some of the ways by which these conditions have been shown to negatively influence bone repair.
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