Overexpression of the receptor for resolvin E1 (ERV1) prevents early alveolar bone loss in leptin receptor deficiency‐induced diabetes

IF 4.2 2区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of periodontology Pub Date : 2024-06-21 DOI:10.1002/jper.24-0060
Lina J. Suárez, Hatice Hasturk, Vanessa Tubero Euzebio Alves, David Díaz‐Baez, Thomas Van Dyke, Alpdogan Kantarci
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Abstract

BackgroundThis study was designed to test the hypothesis that the leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the receptor for resolvin E1 (ERV1) prevents age‐ and diabetes‐associated alveolar bone loss.MethodsLepR‐deficient transgenic (TG) mice were cross‐bred with those overexpressing ERV1 (TG) to generate double‐TG mice. In total, 95 mice were divided into four experimental groups: wild type (WT), TG, LepR deficient (db/db), and double transgenic (db/db TG). The groups were followed from 4 weeks up to 16 weeks of age. The natural progression of periodontal disease without any additional method of periodontitis induction was assessed by macroscopic and histomorphometric analyses. Osteoclastic activity was measured by tartrate‐resistant acid phosphatase (TRAP) staining.ResultsAt 4 weeks, ERV1 overexpression prevented weight gain. From Week 8 onward, there was a significant increase in the weight of db/db mice with or without ERV1 overexpression compared to the WT mice, accompanied by an increase in glucose levels. By 8 weeks of age, the percentage of bone loss in the LepR deficiency groups was significantly greater compared to WT mice. ERV1 overexpression in the db/db TG mice prevented early alveolar bone loss; however, it did not impact the development of diabetic bone loss in aging mice after the onset of weight gain and diabetes.ConclusionsThe findings suggest that the overexpression of ERV1 prevents LepR‐associated alveolar bone loss during the early phases of periodontal disease by delaying weight gain, diabetes onset, and associated inflammation; however, LepR deficiency increases susceptibility to naturally occurring inflammatory alveolar bone loss as the animal ages, associated with excess weight gain, onset of diabetes, and excess inflammation.
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过表达溶血素 E1(ERV1)受体可预防瘦素受体缺乏症诱发的糖尿病患者早期牙槽骨流失
背景本研究旨在验证瘦素受体(LepR)调节牙周组织变化以及过表达溶血素E1(ERV1)受体可预防年龄和糖尿病相关牙槽骨丧失的假说。方法将LepR缺陷的转基因(TG)小鼠与过表达ERV1(TG)的小鼠杂交,产生双TG小鼠。总共 95 只小鼠被分为四个实验组:野生型(WT)、TG、LepR 缺陷(db/db)和双转基因(db/db TG)。实验组从 4 周龄开始随访至 16 周龄。通过宏观和组织形态学分析评估了牙周病的自然进展,而无需任何额外的牙周炎诱导方法。结果4周时,ERV1的过表达阻止了体重的增加。从第 8 周起,与 WT 小鼠相比,无论是否过表达 ERV1,db/db 小鼠的体重都有显著增加,同时血糖水平也有所上升。到8周龄时,与WT小鼠相比,LepR缺乏组的骨质流失比例明显增加。ERV1 在 db/db TG 小鼠中的过表达可防止早期牙槽骨流失;但在体重增加和糖尿病发生后,ERV1 的过表达并不影响老龄小鼠糖尿病骨流失的发展。结论研究结果表明,在牙周病的早期阶段,ERV1的过表达可通过延迟体重增加、糖尿病发病和相关炎症来防止与LepR相关的牙槽骨流失;然而,随着动物年龄的增长,LepR的缺乏会增加自然发生的炎症性牙槽骨流失的易感性,这与体重增加过多、糖尿病发病和炎症过多有关。
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来源期刊
Journal of periodontology
Journal of periodontology 医学-牙科与口腔外科
CiteScore
9.10
自引率
7.00%
发文量
290
审稿时长
3-8 weeks
期刊介绍: The Journal of Periodontology publishes articles relevant to the science and practice of periodontics and related areas.
期刊最新文献
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