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单侧鼻腔阻塞致大鼠牙槽骨密度降低。

Alveolar Bone Density Reduction in Rats Caused by Unilateral Nasal Obstruction.

机构信息

Department of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China

Haiyuan College, Kunming Medical University, Kunming, Yunnan, China

出版信息

Balkan Med J. 2019 Oct 28;36(6):311-319. doi: 10.4274/balkanmedj.galenos.2019.2018.12.11. Epub 2019 Jul 10.

DOI:10.4274/balkanmedj.galenos.2019.2018.12.11
PMID:31290639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6835169/
Abstract

BACKGROUND

Oral breathing can cause morphological changes in the oral and maxillofacial regions.

AIMS

To investigate whether oral breathing affected structural changes in bone tissues.

STUDY DESIGN

Animal experimentation.

METHODS

A total of 48 8-day-old male Sprague−Dawley rats were divided into two groups: a breathing group and a sham (control) group. All Sprague−Dawley rats were killed at 7 weeks after unilateral nostril obstruction modeling. Then, structural changes in bone tissues were detected by micro-computed tomography, and the expression levels of receptor activator of nuclear factor-κB, osteoprotegerin, and receptor activator of nuclear factor-κB ligand in the signal pathway of bone metabolism within the local alveolar bone and serum of rats were detected by reverse transcription-quantitative polymerase chain reaction and Western blotting.

RESULTS

The results showed that receptor activator of nuclear factor-κB ligand and receptor activator of nuclear factor-κB levels in bone tissues and serum in the oral breathing group were higher than those in the control group [Maxillary alveolar bone: receptor activator of nuclear factor-κB ligand (pRNA=0.009, pprotein=0.008), receptor activator of nuclear factor-κB (pRNA=0.008, pprotein=0.009); Mandibular alveolar bone: receptor activator of nuclear factor-κB ligand (pRNA=0.047, pprotein=0.042), receptor activator of nuclear factor-κB (pRNA=0.041, pprotein=0.007); Serum: receptor activator of nuclear factor-κB ligand (pRNA<0.001, pprotein<0.001), receptor activator of nuclear factor-κB (pRNA<0.001, pprotein<0.001)], along with decreased osteoprotegerin expression (Maxillary alveolar bone: pRNA=0.038, pprotein=0.048; Mandibular alveolar bone: pRNA<0.001, pprotein<0.001; Serum: pRNA=0.009, pprotein=0.006) and elevated receptor activator of nuclear factor-κB ligand/osteoprotegerin. Micro-computed tomography analysis indicated a significant difference in the level of bone volume fraction, as well as trabecular thickness in maxillary alveolar bone between the experimental and control groups (p=0.049, p=0.047). Meanwhile, trabecular thickness, and cortical thickness levels in mandibular alveolar bone also differed significantly between the experimental and control groups (p=0.043, p=0.024).

CONCLUSION

Structural changes of the respiratory system affect the alveolar bone structure and unilateral nasal obstruction may lead to a change in regional specific bone density.

摘要

背景

口腔呼吸可引起口腔颌面部形态结构的改变。

目的

探讨口腔呼吸是否会影响骨组织的结构变化。

研究设计

动物实验。

方法

将 48 只 8 日龄雄性 Sprague-Dawley 大鼠随机分为两组:呼吸组和假手术(对照)组。所有 Sprague-Dawley 大鼠在单侧鼻孔阻塞建模后 7 周处死。然后,通过微计算机断层扫描检测骨组织的结构变化,通过逆转录-定量聚合酶链反应和 Western blot 检测局部牙槽骨和大鼠血清中骨代谢信号通路中核因子-κB 受体激活剂、骨保护素和核因子-κB 受体激活剂配体的表达水平。

结果

结果显示,呼吸组骨组织和血清中核因子-κB 受体激活剂配体和核因子-κB 水平高于对照组[上颌牙槽骨:核因子-κB 受体激活剂配体(pRNA=0.009,pprotein=0.008),核因子-κB(pRNA=0.008,pprotein=0.009);下颌牙槽骨:核因子-κB 受体激活剂配体(pRNA=0.047,pprotein=0.042),核因子-κB(pRNA=0.041,pprotein=0.007);血清:核因子-κB 受体激活剂配体(pRNA<0.001,pprotein<0.001),核因子-κB(pRNA<0.001,pprotein<0.001)],同时骨保护素表达降低[上颌牙槽骨:pRNA=0.038,pprotein=0.048;下颌牙槽骨:pRNA<0.001,pprotein<0.001;血清:pRNA=0.009,pprotein=0.006],核因子-κB 受体激活剂配体/骨保护素升高。微计算机断层扫描分析表明,实验组和对照组之间上颌牙槽骨的骨体积分数和骨小梁厚度有显著差异(p=0.049,p=0.047)。同时,实验组和对照组下颌牙槽骨的骨小梁厚度和皮质厚度也有显著差异(p=0.043,p=0.024)。

结论

呼吸系统结构的改变影响牙槽骨结构,单侧鼻阻塞可能导致局部特定骨密度的变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/ca08cf67c83a/BMJ-36-311-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/74480aaa735c/BMJ-36-311-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/4688adc19b33/BMJ-36-311-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/ff5f159db3d7/BMJ-36-311-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/9630030ea743/BMJ-36-311-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/ca08cf67c83a/BMJ-36-311-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/74480aaa735c/BMJ-36-311-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/4688adc19b33/BMJ-36-311-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/ff5f159db3d7/BMJ-36-311-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/9630030ea743/BMJ-36-311-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8211/6835169/ca08cf67c83a/BMJ-36-311-g5.jpg

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