Orthodontic forces have been reported to significantly increase
nicotine-induced
periodontal bone loss. At present, however, it is unknown, which further (side) effects can be expected during orthodontic treatment at a
nicotine exposure corresponding to that of an average European smoker. 63 male Fischer344 rats were randomized in three consecutive experiments of 21 animals each (A/B/C) to 3 experimental groups (7 rats, 1/2/3): (A) cone-beam-computed tomography (CBCT); (B) histology/serology; (C) reverse-transcription quantitative real-time polymerase chain reaction (RT-qPCR)/
cotinine serology-(1) control; (2)
orthodontic tooth movement (OTM) of the first and second upper left molar (NiTi closed coil spring, 0.25 N); (3) OTM with 1.89 mg·kg-1 per day s.c. of L(-)-
nicotine. After 14 days of OTM, serum
cotinine and
IL-6 concentration as well as orthodontically induced inflammatory
root resorption (OIIRR), osteoclast activity (histology),
orthodontic tooth movement velocity (CBCT, within 14 and 28 days of OTM) and relative gene expression of known inflammatory and osteoclast markers were quantified in the dental-periodontal tissue (RT-qPCR). Animals exposed to
nicotine showed significantly heightened serum
cotinine and
IL-6 levels corresponding to those of regular European smokers. Both the extent of
root resorption, osteoclast activity,
orthodontic tooth movement and gene expression of inflammatory and osteoclast markers were significantly increased compared to controls with and without OTM under the influence of
nicotine. We conclude that apart from increased
periodontal bone loss, a progression of dental
root resorption and accelerated
orthodontic tooth movement are to be anticipated during orthodontic
therapy, if
nicotine consumption is present. Thus patients should be informed about these risks and the necessity of
nicotine abstinence during treatment.