Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty
Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty
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DOI：
10.3390/jcm8030406
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发表时间：
2019-03-24
影响因子：
3.9
通讯作者：
Nussler, Andreas K.
中科院分区：
文献类型：
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作者：
Ehnert, Sabrina;Aspera-Werz, Romina H.;Nussler, Andreas K.
许多研究已经描述了吸烟和骨量减少之间的相关性。这不仅会增加骨折风险，还会阻碍骨骼的重建/固定。手术后并发症的频率增加是常见的。在这里，我们调查了吸烟对全关节置换术（TJA）后临床结果的影响。在我们的一级创伤中心接受初次或翻修（包括临床转移）TJA的817例患者随机接受了两次采访（术前和术后6个月）。我们发现159例患者发生并发症（感染、愈合不良、翻修、血栓形成和/或死亡）。考虑到营养状况、饮酒和吸烟是可能的危险因素，吸烟的OR最高。值得注意的是，吸烟者的平均年龄（59.2 +/- 1.0a）显著低于非吸烟者（64.6 +/- 0.8; p < 0.001）。然而，两组之间的合并症数量相当。与不吸烟者（17.8 +/- 1.9%）相比，并发症发生率随着吸烟量的增加而增加（1-20包-年（PY）：19.2 +/- 2.4%和>20 PY：30.4 +/- 3.6%; p = 0.002）。因此，重度吸烟者的平均住院时间（18.4 ± 1.0天）长于非吸烟者（15.3 ± 0.5天; p = 0.009）或中度吸烟者（15.9 ± 0.6天）。与延迟愈合一致，TJA后2天，吸烟者的骨形成标志物（BAP和CICP）显著低于非吸烟者。尽管吸烟增加了MCP-1、OPG、sRANKL和骨桥蛋白的血清水平，但骨吸收标志物（TRAP 5 b和CTX-1）未受影响。与感染率增加一致，吸烟降低了25 OH维生素D3（免疫调节）、IL-1 β、IL-6、TNF-α和IFN-γ血清水平。我们的数据清楚地表明，吸烟不仅影响TJA后的骨形成，而且还抑制了这些患者的炎症反应。因此，有利于骨形成和免疫应答的疗法有助于改善TJA后吸烟者的临床结局是可行的。
Numerous studies have described a correlation between smoking and reduced bone mass. This not only increases fracture risk but also impedes reconstruction/fixation of bone. An increased frequency of complications following surgery is common. Here, we investigate the effect of smoking on the clinical outcome following total joint arthroplasty (TJA). 817 patients receiving primary or revision (including clinical transfers) TJA at our level-one trauma center have been randomly interviewed twice (pre- and six months post-surgery). We found that 159 patients developed complications (infections, disturbed healing, revisions, thrombosis, and/or death). Considering nutritional status, alcohol and cigarette consumption as possible risk factors, OR was highest for smoking. Notably, mean age was significantly lower in smokers (59.2 +/- 1.0a) than non-smokers (64.6 +/- 0.8; p < 0.001). However, the number of comorbidities was comparable between both groups. Compared to non-smokers (17.8 +/- 1.9%), the complication rate increases with increasing cigarette consumption (1-20 pack-years (PY): 19.2 +/- 2.4% and >20 PY: 30.4 +/- 3.6%; p = 0.002). Consequently, mean hospital stay was longer in heavy smokers (18.4 +/- 1.0 day) than non-smokers (15.3 +/- 0.5 day; p = 0.009) or moderate smokers (15.9 +/- 0.6 day). In line with delayed healing, bone formation markers (BAP and CICP) were significantly lower in smokers than non-smokers 2 days following TJA. Although, smoking increased serum levels of MCP-1, OPG, sRANKL, and Osteopontin as well as bone resorption markers (TRAP5b and CTX-I) were unaffected. In line with an increased infection rate, smoking reduced 25OH vitamin D3 (immune-modulatory), IL-1 beta, IL-6, TNF-alpha, and IFN-gamma serum levels. Our data clearly show that smoking not only affects bone formation after TJA but also suppresses the inflammatory response in these patients. Thus, it is feasible that therapies favoring bone formation and immune responses help improve the clinical outcome in smokers following TJA.