中国组织工程研究

中国组织工程研究 ›› 2022, Vol. 26 ›› Issue (20): 3117-3120.doi: 10.12307/2022.607

• 骨组织构建 bone tissue construction •    下一篇

烟熏与大鼠的骨骼密度

蔡振存，高振淮，任立宣，张泽林   

  1. 沈阳医学院附属中心医院骨科，辽宁省沈阳市   110024
  • 收稿日期:2021-05-17 修回日期:2021-05-18 接受日期:2021-08-07 出版日期:2022-07-18 发布日期:2022-01-18
  • 通讯作者: 蔡振存，主任医师，博士，硕士生导师，沈阳医学院附属中心医院骨科，辽宁省沈阳市 110024
  • 作者简介:蔡振存，男，1980年生，主任医师，博士，硕士研究生导师，主要从事骨关节创伤和四肢畸形研究。
  • 基金资助:
    沈阳医学院硕士研究生科技创新基金项目(Y20190517)，项目负责人：高振淮；辽宁省教育厅科学研究项目(2019-117-14)，项目负责人：蔡振存

Effect of smoking on bone mineral density in rats

Cai Zhencun, Gao Zhenhuai, Ren Lixuan, Zhang Zelin   

  1. Department of Orthopedics, the Affiliated Central Hospital of Shenyang Medical College, Shenyang 110024, Liaoning Province, China
  • Received:2021-05-17 Revised:2021-05-18 Accepted:2021-08-07 Online:2022-07-18 Published:2022-01-18
  • Contact: Cai Zhencun, Department of Orthopedics, the Affiliated Central Hospital of Shenyang Medical College, Shenyang 110024, Liaoning Province, China
  • About author:Cai Zhencun, MD, Chief physician, Master’s supervisor, Department of Orthopedics, the Affiliated Central Hospital of Shenyang Medical College, Shenyang 110024, Liaoning Province, China
  • Supported by:
    Science and Technology Innovation Fund for Graduates of Shenyang Medical College, No. Y20190517 (to GZH); Scientific Research and Development Project of the Educational Department of Liaoning Province, No. 2019-117-14 (to CZC)

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摘要：

文题释义：
吸烟与骨质疏松症：骨质疏松症是一种全身性骨骼系统密度下降、强度降低及微结构改变为特点的疾病，骨质疏松症的病因很多，吸烟可引起机体处于低氧状态，进而影响骨的代谢，可能是骨质疏松症发生的原因之一。
骨密度：全称是骨骼矿物质密度，是骨骼硬度及质量的一个重要指标，在临床通常使用骨密度检测仪测量骨密度，通过骨密度数值判断患者是否存在骨质疏松症。

背景：骨质疏松症是由多种原因引起骨代谢异常、骨密度下降的全身性疾病，临床研究发现多数骨质疏松患者有长期吸烟病史，但是吸烟是否与骨密度降低有直接关系目前尚没有定论。
目的：探讨烟熏与大鼠骨密度变化的关系，进而评价吸烟与骨质疏松的关联。 
方法：选择Wistar大鼠40只，随机分为2组，烟熏组大鼠20只作为实验组，模拟人类吸烟过程应用被动吸烟动物染毒系统烟熏，每次应用20支香烟熏40 min，2次/d，连续8周；未烟熏组20只作为对照组，仅饲养于被动吸烟动物染毒系统内8周，不予以烟熏，两组大鼠的自然实验环境、喂养饲料、供水量等其他方面完全相同。应用双能X射线骨密度仪分别于实验开始前、实验开始4，8周测量大鼠双侧股骨及L5腰椎的骨密度，取平均值；同时测量大鼠的体质量变化。
结果与结论：①两组大鼠在实验开始前骨密度和体质量比较差异均无显著性意义(P > 0.05)；②实验开始第4周，进行烟熏的实验组大鼠的骨密度值低于未烟熏的对照组[(225.50±10.11) mg/cm2 vs. (238.86±11.53) mg/cm2，P=0.002]；实验开始第8周，实验组大鼠的骨密度值进一步降低，低于对照组[(201.98±15.58) mg/cm2 vs. (240.26±13.69) mg/cm2，P=0.013]；③实验开始第4周，实验组大鼠的体质量低于对照组[(236.4±15.3) g vs. (258.8±19.6) g，P=0.026]；实验开始第8周，实验组大鼠的体质量仍低于对照组[(278.9±18.1) g vs. (339.5±13.3) g，P=0.008]；并且实验组后4周(5-8周)体质量增长量明显小于前4周(1-4周)，差异有显著性意义(P=0.006)，而对照组体质量增长则无明显差别(P=0.081)；④结果显示烟熏可以使大鼠的骨密度减低、体质量增长缓慢，说明吸烟与骨质疏松有密切的关系，临床上应注重对骨质疏松患者吸烟的控制，以达到有效治疗。

https://orcid.org/0000-0003-2778-4151 (蔡振存) 

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

关键词: 骨质疏松症, 吸烟, 骨密度, 烟熏, 大鼠, 体质量, 实验

Abstract: BACKGROUND: Osteoporosis is a systemic disease that causes abnormal bone metabolism and decreases bone mineral density due to various reasons. Clinical studies have found that most patients with osteoporosis have a long-term history of smoking, but whether smoking is directly related to bone mineral density reduction has not been determined yet.
OBJECTIVE: To explore the relationship between smoking and bone mineral density in rats, and to evaluate the association between smoking and osteoporosis.
METHODS: Forty Wistar rats were randomly divided into two groups (n=20 per group): non-smoking group and smoking group. Rats in the smoking group were subjected to passive cigarette smoking through a passive smoking animal exposure system that could simulate the process of human smoking. Each rat was fumigated with 20 cigarettes for 40 minutes, twice a day, for 8 weeks. Rats in the non-smoking group were used as controls and they were only raised in the passive smoking animal exposure system for 8 weeks without smoking. The natural experimental environment, feeding, water supply and other aspects of the two groups were completely the same. The bone mineral density of bilateral femurs and L5 lumbar vertebrae of rats were measured with dual-energy X-ray bone densitometer before the experiment and 4 and 8 weeks after the experiment, and the average value was taken. Body mass changes of rats were measured at the same time. 
RESULTS AND CONCLUSION: There was no significant difference in bone mineral density and body mass between the two groups before the beginning of the experiment (P > 0.05). In the 4th week of the experiment, the bone mineral density of the smoking group was lower than that of the non-smoking group [(225.50±10.11) mg/cm2 vs. (238.86±11.53) mg/cm2, P=0.002]. In the 8th week of the experiment, the bone mineral density of the smoking group was further reduced, which was lower than that of the non-smoking group [(201.98±15.58) mg/cm2 vs. (240.26±13.69) mg/cm2, P=0.013]. In the 4th week of the experiment, the body mass of the rats in the smoking group was lower than that of the non-smoking group [(236.4±15.3) g vs. (258.8±19.6) g, P=0.026]. In the 8th week of the experiment, the body mass of the rats in the experimental group was still lower than that of the non-smoking group [(278.9±18.1) g vs. (339.5±13.3) g, P=0.008].The body mass gain of the experimental group in the last 4 weeks (5-8 weeks) was significantly less than that in the first 4 weeks (1-4 weeks) (P=0.006), but there was no significant difference in the body mass gain of the non-smoking group (P=0.081). Therefore, smoking can reduce bone mineral density and slow body mass growth in rats, indicating that smoking is closely related to osteoporosis. Control of smoking should be clinically concerned in patients with osteoporosis in order to achieve effective treatments. 

Key words: osteoporosis, smoking, bone mineral density, fumigation, rat, body mass, experiment

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