Smoking dependent alterations in bone formation and inflammation represent major risk factors for complications following total joint arthroplasty

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 followi
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-1β, IL-6, TNF-α, and IFN-γ 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.
show moreshow less

Export metadata

  • Export Bibtex
  • Export RIS
Metadaten
Author:Sabrina Ehnert, Romina Haydeé Aspera-Werz, Christoph Ihle, Markus Trost, Barbara Zirn, Ingo Flesch, Steffen Schröter, Borna Relja, Andreas Klaus Nussler
URN:urn:nbn:de:hebis:30:3-503591
DOI:http://dx.doi.org/10.3390/jcm8030406
ISSN:2077-0383
Pubmed Id:http://www.ncbi.nlm.nih.gov/pubmed?term=30909629
Parent Title (English):Journal of Clinical Medicine
Publisher:MDPI
Place of publication:Basel
Document Type:Article
Language:English
Year of Completion:2019
Date of first Publication:2019/03/24
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2019/06/24
Tag:bone metabolism; cigarettes; complications; delayed wound healing; infection; pack-years (PY); revision surgery; smoking; total joint arthroplasty (TJA)
Volume:8
Issue:3, Art. 406
Pagenumber:16
First Page:1
Last Page:16
Note:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
HeBIS PPN:450689115
Institutes:Medizin
Dewey Decimal Classification:610 Medizin und Gesundheit
Sammlungen:Universitätspublikationen
Licence (German):License LogoCreative Commons - Namensnennung 4.0

$Rev: 11761 $