gms | German Medical Science

Objectives: Since 1976 there have been several studies describing a correlation between cigarette consumption and reduced bone mass. This not only increases fracture risk but also impedes reconstruction and fixation of fractures. Thus, an increased frequency of complications following surgery is expected. Aim of this study was to investigate the effect of smoking habits on the clinical outcome following total joint arthroplasty (TJA).

Methods: Patients receiving TJA (primary and secondary) at our level one trauma center have been randomly interviewed twice (pre- and 6 months post-surgery) on their lifestyle habits - smoking was reported in pack-years (PY). Patient and clinical data (e.g. complications: ±C) were obtained from the clinical documentation system in accordance with the ethical vote 538/2016BO2. Alterations in blood cytokine levels were screened with a RayBio® Human Cytokine Array and quantified with ELISA kits. Data sets were compared by Mann-Whitney U- or Kruskal Wallis H-test.

Results and conclusion: Of 817 patients interviewed 29 patients were lost to follow up. 159 patients developed complications (infections, disturbed wound healing, required revision surgery, thrombosis, and/or death) within 6 month following surgery. Considering smoking as risk factor for complications, it is notable that the mean age was significantly lower in smokers (59.2±1.0 a) than non-smokers (64.6±0.8; p< 0.001). Despite the younger age, number of comorbidities was comparable between smokers and non-smokers. Complication rate was even higher in smokers (23.1%) than non-smokers (17.3%). This was dose dependent, as with increasing PY the relative risk for complications increased: OR ≤20PY=1.62 (p=0.005) and OR >20PY=2.11 (p<0.001). Consequently, the mean hospital stay in heavy smokers was significantly longer (18.4±1.0 d) as compared to non-smokers (15.3±0.5 d; p=0.009) or moderate smokers (15.9±0.6 d). In line with delayed fracture healing, bone formation markers (BAP and CICP) were significantly lower in smokers than non-smokers 2 days following TJA. Although, regulators of osteoclastogenesis (OPG, sRANKL and osteopontin) were increased in heavy smokers, bone resorption markers (TRAP5b and CTX-I) were comparable between smokers and non-smokers, which is in clear contrast to reports on periodontitis patients. As expected, serum levels of MCP-1 (oxidative stress marker) increased with PY (p<0.05). Inversely, serum levels of 25OH vitamin D3 (immune-modulatory) decreased with PY (p<0.05). In line with this, serum levels of the pro-inflammatory IL-1β, IL-6, TNF-α, and IFN-γ were significantly lower in smokers than non-smokers (p<0.01) 2 days following surgery.

Our data clearly show that smoking not only affects bone formation following TJA, but also suppresses the inflammatory response in these patients. Thus, it is feasible that therapies favoring bone formation and immune response help to improve clinical outcome in smokers following TJA.