Kirschneck Christian, Proff Peter, Maurer Michael, Reicheneder Claudia, Römer Piero
Department of Orthodontics, University Medical Center of Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, Germany,
J Orofac Orthop. 2015 May;76(3):195-212. doi: 10.1007/s00056-015-0283-7.
Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26% of adult and 12% of adolescent patients in orthodontic practice, we performed in vivo and in vitro studies as to whether orthodontic forces may add to the nicotine-induced loss of periodontal bone.
Fourteen male rats (Fischer 344 inbred) were used. Seven of these served as controls, while the other seven received daily subcutaneous injections of 1.89 mg L-nicotine per kg body weight. Both groups were exposed to orthodontic mesialization of the first two upper left molars using a NiTi closed-coil spring, the contralateral side serving as control. Periodontal bone loss was assessed by cone-beam computed tomography (CBCT). Human periodontal fibroblasts were stressed by compression (2 g/cm(2)) and/or nicotine (3/5/7.5 µmol), and the expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) was determined at the transcriptional level by quantitative real-time polymerase chain reaction (qRT-PCR) and at the translational level by enzyme-linked immunosorbent assay (ELISA). In addition, differentiation of co-cultured murine RAW264.7 cells to osteoclast-like cells was quantified by tartrate-resistant acid phosphatase (TRAP) staining.
Orthodontic force application in vivo led to a significant increase in nicotine-induced periodontal bone loss, and cell compression in vitro to increased COX-2, PGE2, IL-6, and RANKL expression, reduced OPG expression, and enhanced differentiation of RAW264.7 cells to osteoclast-like cells compared to nicotine alone.
Additional loss of periodontal bone must be expected during orthodontic treatment of smokers. Clinicians should inform their patients of this increased risk and refrain from performing tooth movements before cessation of smoking.
尼古丁被认为是牙周膜内慢性炎症现象的一个病因，这可能导致牙周附着丧失。鉴于在正畸治疗中，成年患者中有26%、青少年患者中有12%为吸烟者，我们进行了体内和体外研究，以探讨正畸力是否会加重尼古丁诱导的牙周骨丧失。
使用14只雄性大鼠（Fischer 344近交系）。其中7只作为对照，另外7只每天接受每千克体重1.89毫克L-尼古丁的皮下注射。两组均使用镍钛闭合曲弹簧对左上第一、二磨牙进行正畸近中移动，对侧作为对照。通过锥形束计算机断层扫描（CBCT）评估牙周骨丧失情况。对人牙周成纤维细胞施加压缩力（2克/平方厘米）和/或尼古丁（3/5/7.5微摩尔），通过定量实时聚合酶链反应（qRT-PCR）在转录水平以及通过酶联免疫吸附测定（ELISA）在翻译水平测定环氧化酶-2（COX-2）、前列腺素E2（PGE2）、白细胞介素-6（IL-6）、骨保护素（OPG）和核因子κB受体活化因子配体（RANKL）的表达。此外，通过抗酒石酸酸性磷酸酶（TRAP）染色对共培养的小鼠RAW264.7细胞向破骨细胞样细胞的分化进行定量。
体内施加正畸力导致尼古丁诱导的牙周骨丧失显著增加，与单独使用尼古丁相比，体外细胞压缩导致COX-2、PGE2、IL-6和RANKL表达增加，OPG表达降低，RAW264.7细胞向破骨细胞样细胞的分化增强。
在对吸烟者进行正畸治疗期间，预计会出现额外的牙周骨丧失。临床医生应告知患者这种增加的风险，并且在患者戒烟之前避免进行牙齿移动。
