Kim Hyun Ju, Jung Bo Hyun, Yoo Ki-Yeon, Han Jin-Woo, Um Heung-Sik, Chang Beom-Seok, Lee Jae-Kwan
Department of Periodontology, Seoul National University School of Dentistry, Seoul, Korea.
Department of Periodontology and Research Institute of Oral Sciences, Gangneung-Wonju National University College of Dentistry, Gangneung, Korea.
J Periodontal Implant Sci. 2017 Oct;47(5):339-350. doi: 10.5051/jpis.2017.47.5.339. Epub 2017 Oct 30.
The purpose of this study was to determine the critical diabetes duration in a streptozotocin (STZ)-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration by evaluating the association between diabetes duration and bone healing capacity through histological and radiographic analyses.
Experimental diabetes was induced in 50 of 60 rats by an STZ injection. The rats were divided into 5 groups, including a control group (group 1), according to diabetes durations of 0, 2, 4, 6, and 8 weeks, respectively. Eighteen rats survived: 4 in group 1, 4 in group 2, 4 in group 3, 5 in group 4, and 1 in group 5. Calvarial defects were created at 0, 2, 4, 6, and 8 weeks after STZ injection in groups 1-5. Cone-beam computed tomography scanning was performed at baseline and at 5 and 7 weeks after surgery. The rats were sacrificed 7 weeks after surgery, followed by histological evaluation.
The voxel gray values (VGVs) of group 1 and group 2 increased, whereas the VGVs of group 3 and group 4 decreased starting 5 weeks after surgery, although this trend did not reach statistical significance between groups. On the reconstructed 3-dimensional images and based on an analysis of histological features, groups 1 and 2 showed apparent bone regeneration, while groups 3-5 showed very limited bone regeneration.
The critical diabetes duration in an STZ-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration was between 2 and 4 weeks. It is suggested that researchers who use STZ-induced diabetic rats wait for more than 2 weeks following diabetes induction before placing implants or conducting bone regeneration studies to allow definite disturbances in bone healing to emerge.
本研究的目的是通过组织学和影像学分析评估糖尿病病程与骨愈合能力之间的关联,从而确定链脲佐菌素(STZ)诱导的糖尿病大鼠颅骨缺损模型中进行骨再生实验的关键糖尿病病程。
60只大鼠中有50只通过注射STZ诱导实验性糖尿病。根据糖尿病病程分别为0、2、4、6和8周,将大鼠分为5组,包括一个对照组(第1组)。18只大鼠存活:第1组4只,第2组4只,第3组4只,第4组5只,第5组1只。在第1 - 5组中,于STZ注射后0、2、4、6和8周创建颅骨缺损。在基线以及术后5周和7周进行锥形束计算机断层扫描。术后7周处死大鼠,随后进行组织学评估。
第1组和第2组的体素灰度值(VGVs)增加,而第3组和第4组的VGVs在术后5周开始下降,尽管各组之间这种趋势未达到统计学意义。在重建的三维图像上并基于组织学特征分析,第1组和第2组显示出明显的骨再生,而第3 - 5组显示出非常有限的骨再生。
在STZ诱导的糖尿病大鼠颅骨缺损模型中进行骨再生实验的关键糖尿病病程在2至4周之间。建议使用STZ诱导的糖尿病大鼠的研究人员在诱导糖尿病后等待超过2周再植入或进行骨再生研究,以使骨愈合出现明确的干扰。