Abstract
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.
Highlights
Deleterious effects of nicotine and tobacco smoke are often investigated and discussed regarding their interrelationship with cancer as well as chronic conditions of the cardiovascular system such as atherosclerosis and respiratory diseases such as chronic obstructive pulmonary disease (COPD), which can affect adults and children all the same.[1]
The rats remained in good health with gross body weight steadily increasing from day 10 over day 0, day 14 (M = 259 g; SD = 21 g) and day 28 (M = 272 g; SD = 24 g) of tooth movement: F = 46.655; df = 2.049; P ≤ 0.001
We suggest based on our observations that nicotine exposure during orthodontic tooth movement synergistically increased the release of proinflammatory cytokines and RANKL-mediated differentiation of osteoclasts within the compression areas of the periodontal ligament, resulting in increased resorption of both alveolar bone in direction of movement and formation of orthodontically induced inflammatory dental root resorptions (OIIRR)
Summary
Deleterious effects of nicotine and tobacco smoke are often investigated and discussed regarding their interrelationship with cancer as well as chronic conditions of the cardiovascular system such as atherosclerosis and respiratory diseases such as chronic obstructive pulmonary disease (COPD), which can affect adults and children all the same.[1]. Teeth are linked to their surrounding alveolar bone socket of the jaw via connective tissue, the periodontal ligament, known as dento-alveolar joint or gomphosis.[2] In the dental specialty of orthodontics, tooth movement—therapeutically induced by fixed or removable orthodontic intraoral appliances—is performed to enhance position and alignment of permanent teeth for improved masticatory and phonetic function, psychological and esthetic reasons To this end, a physiological, defined mechanical force is applied to the respective teeth, which results is the creation of tension and pressure zones within the periodontal ligament.[3] This triggers a pseudo-inflammatory, immunological, multicellular process instigated by periodontal fibroblasts,[4] resulting in increased osteoclast differentiation and bone resorption in direction of movement as well as bone formation by osteoblasts in zones of tension.[3] In some cases, osteoclast activity during orthodontic tooth movement turns against the tooth itself, causing orthodontically induced inflammatory dental root resorptions (OIIRR), which are a rather frequent and unpredictable side effect during orthodontic treatment of varying severity and unknown etiology.[5,6]
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