| It is well know that tobacco smoking is the main risk factor associated with periodontal disease. The prevalence of periodontal disease is significantly more pronounced in smokers compared with non-smokers. The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the clinical symptoms of attachment loss, pocket formation, bone loss, and eventually tooth loss. Smoking, thus, considerably increases the risks for destructive periodontal disease. However, the mechanisms behind the destructive effects of smoking on the periodontal tissues are not well understood. It has been speculated that nicotine in tobacco smoke may be one potential mechanism.Previous studies considered that the acetylcholine receptors existed primarily on the neuronal or neuronal-related tissues. Recently, however, many studies had found that neuronal nAChRs (nicotinic Acetylcholine receptors) can be expressed on many different non-neuronal cell types throughout the body, including the oral epithelium tissues.The present study, in order to investigate the role ofα7 nAChR in tobacco smoking and its impacts on the development of periodontal disease, the effects of nicotine on the development of periodontitis was evaluated by animal experiments and Micro-CT assay. The expression ofα7 nAChR in periodontal tissues and the effects of nicotine administration onα7 nAChR expression were detected by immuno-histochemistry and in situ hybridization methods. The main contents and results are described as follows:1 The establishment of nicotine experimental periodontitis model in rats.36 adult male SD rats were received silk ligatures around the cervixes of the right second maxillary molars while the contralateral tooth was left untreated. Then the animals were randomly assigned into 3 groups, of daily intraperitoneal injections: group A (control), saline solution; group B, 0.83 mg of nicotine /kg/d; and group C, 1.67 mg of nicotine/kg/d. Animals were sacrificed at day 14 and 28 after ligature placement. Clinical and histological and Micro-CT (microcomputed tomography) examinations were used to evaluate the periodontal breakdown. The results showed that ligature significantly increased SBI (sulcular bleeding index), PD (periodontal depth) and ABL (alveolar bone loss) of the ligated molars. Nicotine administration enhanced the alveolar bone loss in a dose-dependent manner.2 The establishment of three-dimensional alveolar bone model of periodontitis rats by Micro-CT.To establish three-dimensional alveolar bone model of periodontitis rats by Micro-CT, linear measuring of ABL value in all groups were taken to evaluate the loss of alveolar bone, three-dimensional measuring of BMD\BVF\Tb.Th\Tb.N and Tb.Sp were carried out to assess the change of bone mass and bone trabecula. Paring t- test and correlation test showed that in all groups, BMD\BVF\TB.N and Tb.Th values of the ligated sides were significantly lower than that of non- ligated sides. With the nicotine dose increased, bilateral BMD\BVF and Tb.Th values were gradually reduced in a dose-dependent manner. Of all the three groups, however, the Tb.Sp of ligated sides was significantly higher than that of non-ligated sides. ANOVA showed that bilateral values of BMD\BVF\Tb.Th and Tb.Sp had significant differences between groups, indicated that ligation can decrease the BMD\BVF and Tb.Th, but increase the Tb.Sp of alveolar bone of the right second maxillary molars, and that ncotine administration further aggravated such changes. Therefore, ligature could successfully induced experimental periodontitis in rats, and daily administration of nicotine resulted in significantly greater alveolar bone loss in a dose-dependent manner.3 Expression ofα7 nAChR in periodontal tissues in rats.14 and 28 days after periodontitis induction, the animals were sacrificed; periodontal tissues were stained by immunohistochemically and in-situ hybridization methods. Results showed that, in the control group,α7 nAChR was positively stained in gingival epithelial cells and fibroblasts in periodontal ligament of the non-ligation sides.α7 nAChR was also positively stained in periodontal pocket epithelial cells and osteoclasts and vascular endothelial cells in periodontal ligament of the ligated sides. In nicotine administration group, the expressions ofα7 nAChR were gradually increased with dose increased. The results confirmed thatα7 nAChR was expressed in rat's normal periodontal tissues and the expression ofα7 nAChR could be gradually upregulated by nicotine administration in a dose depended manner, which indicates thatα7 nAChR may play an important role in development of periodontitis.
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