Red Wine Again?
第一作者:Moyo Chikondi Kruyt
2015-06-29 点击量:782 我要说
In their article, Hsu et al. describe how a specific constituent of cigarette smoke (dioxin) negatively influences bone morphogenetic protein (BMP)-2-mediated spinal fusion in rats. On the basis of their findings, they speculate on potential therapeutic options to improve fusion in spinal arthrodesis and bone-healing in other orthopaedic procedures in patients who continue smoking.
Recently, a detailed overview of the adverse effects of smoking on the musculoskeletal system was published in The Journal of Bone & Joint Surgery. These negative effects can be roughly summarized as (1) prothrombotic effects with, among others, an increased risk of osteonecrosis; (2) metabolic effects resulting in decreased bone strength with subsequent increased fracture risk; (3) anti-osteogenic effects with decreased healing capacity of fractures and osteotomy and arthrodesis sites; and (4) other general adverse effects increasing the risk of perioperative complications such as wound-healing disturbances.
Although the specific effects of many toxic substances in cigarette smoke, such as carbon monoxide and nicotine, have been established in terms of tissue oxygenation, carcinogenesis, and addiction, it is unclear which toxic substances specifically cause adverse musculoskeletal effects. The role of nicotine, the main addictive substance, is especially controversial regarding the often-reported positive effect on bone formation. Identifying the specific adverse mechanisms of tobacco smoking would aid in balancing the pros and cons of less optimal solutions compared with complete cessation. Realistically, failure to quit smoking should be accepted as the most probable scenario, even in dedicated cessation programs. Due to expected poor compliance, nicotine replacement therapy or use of e-cigarettes could be an alternative when these solutions elicit substantially less or no adverse effects. The knowledge of specific adverse pathways may also facilitate (pharmacological) inhibition of these mechanisms to mitigate the negative effects of smoking if cessation fails or is too late to reverse the deleterious effects already rendered on the musculoskeletal system.