Smoking promotes the resorption of periodontal alveolar bone

doi:10.3969/j.issn.2095-4344.2014.20.011

Abstract

Abstract:

BACKGROUND: Various studies confirm that smoking can contribute to the resorption of periodontal alveolar bone.
OBJECTIVE: To observe the effect of smoking in alveolar bone resorption of periodontitis rat models.
METHODS: A total of 24 rats were randomly divided into three groups. Normal group: rats were normally fed without any other pre-treatment; Control group: experimental periodontitis model was established using wire ligation method in rats; Experimental group: rat models were given passive smoking during experimental modeling period. All rats were sacrificed after 8 weeks of modeling, periodontal tissue were removed. Hematoxylin-eosin staining was used for examining pathological changes in periodontal tissue, and immunohistochemical analysis was done for observing receptor activator of nuclear factor-κB ligand and osteoprotegrin expression.
RESULTS AND CONCLUSION: After 8 weeks of modeling, expression of receptor activator of nuclear factor-κB ligand factor was significantly higher in alveolar bone of rats from experimental group in comparison to control group (P < 0.05), whereas expression of osteoprotegerin in alveolar bone was significantly greater in rats from control group when compared to experimental group (P < 0.05). This finding suggests that smoking can increase the expression of receptor activator of nuclear factor-κB ligand protein and reduce osteoprotegrin expression in periodontal rats, thus increasing the resorption of periodontal alveolar bone.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

全文链接：

Key words: smoking, periodontitis, alveolar bone loss, NF-kappa B, osteoprotegrin

CLC Number:

R318

Zhu Jian-hua, Wang Ying, Zhao Zhong-nan, Liu Ji-guang. Smoking promotes the resorption of periodontal alveolar bone[J]. Chinese Journal of Tissue Engineering Research, 2014, 18(20): 3172-3177.

Figures/Tables 3

2.1 实验动物数量分析纳入Wistar大鼠数量为24只，进行造模的大鼠造模成功率为100%，1只大鼠死亡，原因为麻药过量，死亡后及时给予补充。共24只大鼠进入结果分析。 2.2 实验动物大体观察结果在造模成功后第6周，正常组大鼠牙周组织未出现明显异常，牙龈形态正常，呈粉红色，质地坚韧，无探诊出血，无牙周袋。对照组大鼠结扎丝处见食物残渣堆积，周围牙龈颜色鲜红，探诊出血，部分大鼠有浅牙周袋形成。实验组大鼠结扎丝处见软垢堆积，结扎处牙龈出现红肿，牙面色素沉着，牙龈质地松软，探诊出血，有牙周袋形成。在第7周时，正常组仍未见明显的牙周袋，对照组及实验组大鼠牙龈炎症均加重，牙周袋深度加深。在第8周时，正常组大鼠牙龈仍正常无炎症表现，而在对照组及实验组大鼠中结扎处牙龈炎症加重明显，探诊极易出血，有深牙周袋形成，且在实验组大鼠中部分牙龈明显退缩，根分叉区域暴露，为十分典型中重度牙周炎的表现。 2.3 探诊深度测定结果 3组大鼠牙周探诊深度的变化结果发现：正常组大鼠在实验过程中均无牙周袋形成，6周时，实验组牙周探诊深度高于对照组和正常组(P < 0.05)，对照组与正常组比较差异无显著性意义(P < 0.05)。8周时，实验组、对照组牙周探诊深度均高于正常组(P < 0.05)，且实验组、对照组牙周探诊深度分别较6周时升高(P < 0.05)，同时，实验组牙周袋深度对照组高(P < 0.05)。见表1。 2.4 苏木精-伊红染色观察在实验开始第8周时，显微镜下观察可见正常组大鼠下颌第1磨牙牙周组织标本，可见其结构正常，结合上皮位于釉牙骨质界处，牙龈纤维排列整齐，牙周膜纤维排列亦正常有序，牙槽骨边缘平整无吸收，牙槽嵴顶存。对照组可见上皮钉突明显伸长，结合上皮向根方增殖，结缔组织内可见较多淋巴细胞浸润，牙槽骨出现吸收，牙槽嵴顶形态不规则。实验组可见，结合上皮继续向根方增殖，结缔组织内可见密集的炎性细胞浸润，骨小梁稀疏，牙槽嵴顶消失，牙槽骨明显吸收(图1)。 2.5 免疫组织化学染色后各组大鼠灰度值的表达变化骨保护素蛋白免疫组织化学染色后显示：骨保护素活化的阳性表达为细胞的胞质、胞膜及核膜都被染色，呈弥漫成片的黄色或棕黄色颗粒状。在3组大鼠的牙周组织中均可见到骨保护素蛋白的表达。建模后8周各组大鼠平均灰度值比较：实验组灰度值高于对照组(P < 0.05)。且对照组高于假手术组(P < 0.05，表2，图2)。核因子κB受体活化因子配体蛋白免疫组织化学染色后显示：与骨保护素相比，各组大鼠均有核因子κB受体活化因子配体表达，且表达部位和骨保护素相似，主要位于骨小梁周围细胞的胞核，呈棕黄色，骨细胞胞质和胞膜中亦可见表达。在各组间大鼠平均灰度值比较：实验组灰度值低于对照组(P < 0.05)，且对照组低于假手术组(P < 0.05，表2，图3)。"

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