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Novel Preosteoclast Populations in Obesity-Associated Periodontal Disease
Journal of Dental Research ( IF 5.7 ) Pub Date : 2021-10-12 , DOI: 10.1177/00220345211040729
K H Kwack 1 , L Zhang 1 , J Sohn 1, 2, 3 , V Maglaras 1 , R Thiyagarajan 2, 4 , K L Kirkwood 1, 5
Affiliation  

Although there is a clear relationship between the degree of obesity and periodontal disease incidence, the mechanisms that underpin the links between these conditions are not completely understood. Understanding that myeloid-derived suppressor cells (MDSCs) are expanded during obesity and operate in a context-defined manner, we addressed the potential role of MDSCs to contribute toward obesity-associated periodontal disease. Flow cytometry revealed that in the spleen of mice fed a high-fat diet (HFD), expansion in monocytic MDSCs (M-MDSCs) significantly increased when compared with mice fed a low-fat diet (LFD). In the osteoclast differentiation assay, M-MDSCs isolated from the bone marrow of HFD-fed mice showed a larger number and area of osteoclasts with a greater number of nuclei. In the M-MDSCs of HFD-fed mice, several osteoclast-related genes were significantly elevated when compared with LFD-fed mice according to a focused transcriptomic platform. In experimental periodontitis, the number and percentage of M-MDSCs were greater, with a significantly larger increase in HFD-fed mice versus LFD-fed mice. In the spleen, the percentage of M-MDSCs was significantly higher in HFD-fed periodontitis-induced (PI) mice than in LFD-PI mice. Alveolar bone volume fraction was significantly reduced in experimental periodontitis and was further decreased in HFD-PI mice as compared with LFD-PI mice. The inflammation score was significantly higher in HFD-PI mice versus LFD-PI mice, with a concomitant increase in TRAP staining for osteoclast number and area in HFD-PI mice over LFD-PI mice. These data support the concept that M-MDSC expansion during obesity to become osteoclasts during periodontitis is related to increased alveolar bone destruction, providing a more detailed mechanistic appreciation of the interconnection between obesity and periodontitis.



中文翻译:

肥胖相关牙周病中的新型破骨前细胞群

尽管肥胖程度与牙周病发病率之间存在明确的关系,但支持这些疾病之间联系的机制尚不完全清楚。了解骨髓来源的抑制细胞 (MDSCs) 在肥胖过程中会扩张并以特定的方式运作,我们探讨了 MDSCs 在导致肥胖相关牙周病方面的潜在作用。流式细胞术显示,与喂食低脂饮食 (LFD) 的小鼠相比,在喂食高脂肪饮食 (HFD) 的小鼠脾脏中,单核细胞 MDSCs (M-MDSCs) 的扩增显着增加。在破骨细胞分化试验中,从 HFD 喂养小鼠的骨髓中分离出的 M-MDSCs 显示出更大数量和面积的破骨细胞以及更多的细胞核。在 HFD 喂养小鼠的 M-MDSC 中,根据聚焦的转录组学平台,与 LFD 喂养的小鼠相比,几个破骨细胞相关基因显着升高。在实验性牙周炎中,M-MDSCs 的数量和百分比更大,HFD 喂养的小鼠与 LFD 喂养的小鼠相比显着增加。在脾脏中,M-MDSCs 的百分比在 HFD 喂养的牙周炎诱导 (PI) 小鼠中明显高于 LFD-PI 小鼠。与 LFD-PI 小鼠相比,实验性牙周炎的牙槽骨体积分数显着降低,并且在 HFD-PI 小鼠中进一步降低。HFD-PI 小鼠的炎症评分显着高于 LFD-PI 小鼠,同时 HFD-PI 小鼠破骨细胞数量和面积的 TRAP 染色比 LFD-PI 小鼠增加。

更新日期:2021-10-12
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