The effects of smoke carcinogens on bone

被引：29

作者：

Yan C. ^{[1
]}

Avadhani N.G. ^{[1
]}

Iqbal J. ^{[2
]}

机构：

[1] University of Pennsylvania, Philadelphia

[2] Mount Sinai School of Medicine, Annenberg Building Floor 5, New York, NY 10029

来源：

Current Osteoporosis Reports | 2011年 / 9卷 / 4期

关键词：

Bone; Bone remodeling; Carcinogens; Osteoporosis; Tobacco smoking;

D O I：

10.1007/s11914-011-0068-x

中图分类号：

学科分类号：

摘要：

The greatest cause of preventable morbidity and mortality is smoking, and one of the often-underappreciated effects of smoking is profound bone loss. The existing clinical paradigm for smoking is that there is a low turnover osteoporosis. This review highlights findings from recent clinical trials and animal research demonstrating either support or conflict with the existing paradigm. Clinically, it is noted that markers of bone formation are often normal in smokers; these clinical findings conflict with well-conducted animal research demonstrating that carcinogens acting on the aryl hydrogen receptor can significantly reduce osteoblast formation and function. Regarding bone resorption, highlights from recent clinical studies suggest that bone remodeling is increased in smokers. Directly contradicting this enhanced osteoclastogenesis are several animal studies all demonstrating significant inhibition of osteoclast formation and function upon exposure to smoke carcinogens. Future research is needed to clarify whether smoking is truly a low bone remodeling osteoporosis, or an osteoclast-driven bone destruction, with inappropriately normal bone formation. © 2011 Springer Science+Business Media, LLC.

引用

页码：202 / 209

页数：7

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