The Charles and Jane Pak Center for Mineral Metabolism and Clinical Research and Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8885, USA.
Osteoporos Int. 2012 Aug;23(8):2081-92. doi: 10.1007/s00198-012-1940-y. Epub 2012 Feb 21.
Osteoporosis is a common, morbid and costly disorder characterized by deterioration in bone strength. Cigarette smoking is associated with reduced bone mineral density (BMD) and increased fracture risk. There are basic, clinical, and observational studies that define several of the underlying pathophysiologic mechanisms that predispose smokers to bone loss. Such mechanisms include alterations in calciotropic hormone metabolism and intestinal calcium absorption, dysregulation in sex hormone production and metabolism, alterations in adrenal cortical hormone metabolism and in the receptor activator of nuclear factor kappa-B (RANK), receptor activator of nuclear factor kappa-B ligand (RANKL), and osteoprotegerin (OPG) system (RANK-RANKL-OPG system), and direct cellular effects of cigarette use on bone cells. In addition, there is evidence of reversibility in the aforementioned mechanisms with smoking cessation. In summary, cigarette smoking is a reversible risk factor for osteoporosis and osteoporotic fractures through diverse pathophysiologic mechanisms.
骨质疏松症是一种常见的、严重的和昂贵的疾病，其特征是骨强度恶化。吸烟与骨密度（BMD）降低和骨折风险增加有关。有基础、临床和观察性研究定义了几种使吸烟者易发生骨丢失的潜在病理生理机制。这些机制包括钙调节激素代谢和肠道钙吸收的改变、性激素产生和代谢的失调、肾上腺皮质激素代谢以及核因子 kappa-B（RANK）受体激活剂、核因子 kappa-B 配体（RANKL）和骨保护素（OPG）系统（RANK-RANKL-OPG 系统）的改变，以及香烟使用对骨细胞的直接细胞作用。此外，有证据表明戒烟可以使上述机制逆转。总之，吸烟通过多种病理生理机制成为骨质疏松症和骨质疏松性骨折的可逆转危险因素。
