Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Welschnonnenstrasse 17, 53111, Bonn, Germany.
Department of Periodontology and Operative Dentistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Clin Oral Investig. 2022 Jan;26(1):171-181. doi: 10.1007/s00784-021-03988-4. Epub 2021 May 23.
The aim of this in vitro and in vivo study was to investigate the interaction of periodontitis and orthodontic tooth movement on interleukin (IL)-6 and C-X-C motif chemokine 2 (CXCL2).
The effect of periodontitis and/or orthodontic tooth movement (OTM) on alveolar bone and gingival IL-6 and CXCL2 expressions was studied in rats by histology and RT-PCR, respectively. The animals were assigned to four groups (control, periodontitis, OTM, and combination of periodontitis and OTM). The IL-6 and CXCL2 levels were also studied in human gingival biopsies from periodontally healthy and periodontitis subjects by RT-PCR and immunohistochemistry. Additionally, the synthesis of IL-6 and CXCL2 in response to the periodontopathogen Fusobacterium nucleatum and/or mechanical strain was studied in periodontal fibroblasts by RT-PCR and ELISA.
Periodontitis caused an increase in gingival levels of IL-6 and CXCL2 in the animal model. Moreover, orthodontic tooth movement further enhanced the bacteria-induced periodontal destruction and gingival IL-6 gene expression. Elevated IL-6 and CXCL2 gingival levels were also found in human periodontitis. Furthermore, mechanical strain increased the stimulatory effect of F. nucleatum on IL-6 protein in vitro.
Our study suggests that orthodontic tooth movement can enhance bacteria-induced periodontal inflammation and thus destruction and that IL-6 may play a pivotal role in this process.
Orthodontic tooth movement should only be performed after periodontal therapy. In case of periodontitis relapse, orthodontic therapy should be suspended until the periodontal inflammation has been successfully treated and thus the periodontal disease is controlled again.
本体外和体内研究旨在探讨牙周炎和正畸牙齿移动对白细胞介素(IL)-6 和 C-X-C 基序趋化因子 2(CXCL2)的相互作用。
通过组织学和 RT-PCR 分别研究了牙周炎和/或正畸牙齿移动(OTM)对牙槽骨和牙龈 IL-6 和 CXCL2 表达的影响。将动物分为四组(对照组、牙周炎组、OTM 组和牙周炎与 OTM 联合组)。还通过 RT-PCR 和免疫组织化学研究了人牙周健康和牙周炎受试者牙龈活检中 IL-6 和 CXCL2 的水平。此外,通过 RT-PCR 和 ELISA 研究了牙周病原体福赛斯坦纳菌和/或机械应变对牙周成纤维细胞中 IL-6 和 CXCL2 的合成。
牙周炎导致动物模型中牙龈 IL-6 和 CXCL2 水平升高。此外,正畸牙齿移动进一步增强了细菌诱导的牙周破坏和牙龈 IL-6 基因表达。在人类牙周炎中也发现了升高的 IL-6 和 CXCL2 牙龈水平。此外,机械应变增加了 F. nucleatum 对体外 IL-6 蛋白的刺激作用。
我们的研究表明,正畸牙齿移动会增强细菌诱导的牙周炎症,从而破坏,而 IL-6 可能在这一过程中发挥关键作用。
只有在牙周治疗后才能进行正畸牙齿移动。如果发生牙周炎复发,应暂停正畸治疗,直到成功治疗牙周炎症并再次控制牙周疾病。