University of Pennsylvania, Philadelphia, PA 19104, USA.
Curr Osteoporos Rep. 2011 Dec;9(4):202-9. doi: 10.1007/s11914-011-0068-x.
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.
吸烟是可预防的发病率和死亡率的最大原因，而吸烟的一个常常被低估的影响是严重的骨质流失。目前对吸烟的临床模式是低转换型骨质疏松症。这篇综述强调了最近的临床试验和动物研究的发现，这些发现支持或与现有模式相冲突。临床上，有研究表明吸烟者的骨形成标志物通常正常；这些临床发现与精心设计的动物研究相矛盾，这些研究表明，作用于芳基氢受体的致癌物质可显著减少成骨细胞的形成和功能。关于骨吸收，最近的临床研究强调吸烟可增加骨重塑。与这种增强的破骨细胞生成直接矛盾的是，几项动物研究都表明，暴露于吸烟的致癌物质可显著抑制破骨细胞的形成和功能。需要进一步的研究来阐明吸烟是否真的是一种低骨重塑骨质疏松症，还是一种破骨细胞驱动的骨破坏，伴有不适当的正常骨形成。
