| It's well known that smoking is the major risk factor for chronic periodontal disease. Tobacco-related periodontal disease is characterized as the destruction of periodontal supporting tissues, bone loss, attachment loss, and pocket formation, which finally lead to loss of teeth. Nicotine, as the main alkaloid in tobacco, can cause a variety of damage on the periodontal tissue, but the exact mechanism is not yet fully understood. In recent studies,α7 nicotinic acetylcholine receptor (α7 nAChR) has been found connected with the tobacco-related toxicity.The objective of this study is to investigate the expression and function ofα7 nicotinic acetylcholine receptor (α7 nAChR) in the periodontal membrane of rat with experimental periodontitis. The main contents and results are described as follows.1. The effects of nicotine/mecamylamine on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.Experimental periodontitis was induced by ligaturing the cervix of the right second maxillary molar with 3-0 thread of 16 SD male adult rats. On the following day, the animals were assigned into 4 groups: control(C) group, saline(S) group, nicotine(NT)group and nicotine +mecamylamine(MEC) group(n=4). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and MEC group were intraperitonealy injected with mecamylamine (1mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical and histological examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.α7 nAChR was mainly found in the fibroblasts and osteoblast. Nicotine significantly increased the values of sulcular bleeding index (SBI) and probe depth (PD) (P<0.05), and enhanced the expression ofα7nAChR in periodontal membrane (P<0.05). But the MEC can block the effect of the nicotine (P<0.05).α7nAChR may play an important role in the development of tobacco-related periodontitis.2. The effects of nicotine/α-BTX on the expression ofα7nAChR in rat periodontal tissue and the development of experimental periodontitis.24 male SD rats were randomly assigned into 4 groups: control(C) group, saline(S) group, nicotine (NT) group and nicotine +α-BTX(BTX) group(n=6). On the following day, the cervixes of the both sides second maxillary molar were ligatured with 3-0 silk thread. The left sides of control group were not ligatured as the blank control (C), and right sides were ligatured as the positive control (L). NT group intraperitonealy injected with nicotine (1.7mg/kg/d), and BTX group were intraperitonealy injected withα-BTX (10mg/kg/d), followed 30 min later by injection of nicotine (1.7mg/kg/d). 14 and 28 days after ligation, half rats were sacrificed respectively in each group. Clinical, histological, and MicroCT examinations were used to evaluate the degree of the periodontitis.α7 nAChR in the periodontal membrane of rats was examined using immuno-histochemical techniques.Clinical examination and HE showed that nicotine can increase the thread ligation-induced periodontitis symptoms, and if given earlyα-BTX, the effects of nicotine would be obviously suppressed. MicroCT analysis showed that compared with the C group, the alveolar bone significantly decreased (P <0.05). L and S group showed no significant difference (P>0.05). NT group had significantly more alveolar bone loss than that of L and S group (P <0.05). BTX group compared with the NT group, showed less alveolar bone loss (P <0.05). BTX group and L, S group showed no significant difference (P> 0.05). Further BMD, BVF, TB.Sp, TB.Th also displayed similar results. Immunohistochemistry results revealed that nicotine enhanced the expression ofα7 nAChR in periodontal ligament tissue of rats.α-BTX pretreatment of nicotine-treated rats abrogated the increasedα7nAChR expression.The results indicate that nicotine enhances susceptibility to periodontitis viaα7 nAChR, which may act via suppressing protective immune responses through the cholinergic anti-inflammatory pathway. |
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