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肥胖对大鼠骨愈合的影响。

Effects of Obesity on Bone Healing in Rats.

机构信息

Department of Periodontology and Operative Dentistry, University Medical Center, University of Mainz, 55131 Mainz, Germany.

Center of Dento-Maxillo-Facial Medicine, Department of Orthodontics, University of Bonn, 53111 Bonn, Germany.

出版信息

Int J Mol Sci. 2021 Dec 11;22(24):13339. doi: 10.3390/ijms222413339.

DOI:10.3390/ijms222413339
PMID:34948136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8704371/
Abstract

Although the association between periodontitis and obesity is well explored, it is unclear whether obesity is associated with a worse therapeutic outcome after periodontal treatment. The aim of this study was to investigate the effects of obesity on bone healing with and without the application of regeneration-promoting molecules. A standardized bone fenestration-type defect was created over the root of the mandibular first molar in 15 Wistar rats. Ten animals received a high-fat, high-sucrose diet (HFSD), while the remaining five animals were fed a standard diet. During surgery, the fenestration defects from half of the HFSD-fed, i.e., obese animals, were treated with regeneration-promoting molecules (enamel matrix derivative; EMD). After four weeks, bone healing was evaluated by histomorphometry, TRAP staining and immunohistochemistry for RUNX2 and osteopontin. The analyses revealed that the spontaneous healing of the periodontal defects was compromised by obesity. Application of EMD partially compensated for the negative effect of obesity. Nevertheless, EMD-stimulated bone healing in obese animals was not better than the spontaneous healing in the obesity-free control group, indicating that obesity may also inhibit the stimulatory effects of regeneration-promoting molecules. Our results show that obesity can negatively influence bone healing and suggest that bone healing may be compromised in humans.

摘要

虽然牙周炎和肥胖之间的关联已经得到了充分的研究,但肥胖是否与牙周治疗后的治疗效果更差有关仍不清楚。本研究旨在研究肥胖对骨愈合的影响,无论是否应用促进再生的分子。在 15 只 Wistar 大鼠下颌第一磨牙的根部制造了一个标准化的骨开窗型缺损。其中 10 只动物给予高脂肪、高蔗糖饮食(HFSD),其余 5 只动物给予标准饮食。在手术过程中,HFSD 喂养的一半即肥胖动物的开窗缺陷用促进再生的分子(釉基质衍生物;EMD)进行治疗。四周后,通过组织形态计量学、TRAP 染色和 RUNX2 和骨桥蛋白的免疫组织化学评估骨愈合。分析表明,肥胖症会损害牙周缺损的自发愈合。应用 EMD 部分补偿了肥胖的负面影响。然而,在肥胖动物中,EMD 刺激的骨愈合并不优于无肥胖对照组的自发愈合,表明肥胖症也可能抑制促进再生分子的刺激作用。我们的研究结果表明,肥胖会对骨愈合产生负面影响,并表明骨愈合可能在人类中受到影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/65052563c83a/ijms-22-13339-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/b0c6f7010bb7/ijms-22-13339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/abb3d809e578/ijms-22-13339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/5e4b78073c0a/ijms-22-13339-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/87d6d04e47a3/ijms-22-13339-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/65052563c83a/ijms-22-13339-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/b0c6f7010bb7/ijms-22-13339-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/abb3d809e578/ijms-22-13339-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/5e4b78073c0a/ijms-22-13339-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6751/8704371/65052563c83a/ijms-22-13339-g005.jpg

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Metformin accelerates wound healing by Akt phosphorylation of gingival fibroblasts in insulin-resistant prediabetes mice.二甲双胍通过使胰岛素抵抗前期糖尿病小鼠牙龈成纤维细胞的Akt磷酸化来加速伤口愈合。
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Obesity and Bone Health: A Complex Link.肥胖与骨骼健康:复杂的联系。
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