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.

中文翻译：

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Resolvin E1 (ERV1) 受体的过度表达可预防瘦素受体缺乏引起的糖尿病的早期牙槽骨丢失


背景本研究旨在检验以下假设：瘦素受体 (LepR) 调节牙周组织的变化，以及 Resolvin E1 (ERV1) 受体的过度表达可预防与年龄和糖尿病相关的牙槽骨丢失。方法LepR 缺陷转基因 (TG) ）小鼠与过度表达 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缺陷型（db/db）和双转基因（db/db TG）。对各组从 4 周龄至 16 周龄进行随访。通过宏观和组织形态测量分析评估牙周病的自然进展，无需任何额外的牙周炎诱导方法。通过抗酒石酸酸性磷酸酶 (TRAP) 染色来测量破骨细胞活性。结果在 4 周时，ERV1 过度表达阻止了体重增加。从第8周开始，与WT小鼠相比，有或没有ERV1过表达的db/db小鼠的体重显着增加，并伴随着葡萄糖水平的增加。到 8 周龄时，LepR 缺陷组的骨质流失百分比明显高于 WT 小鼠。 db/db TG 小鼠中 ERV1 过度表达可预防早期牙槽骨丢失；然而，它并没有影响衰老小鼠体重增加和糖尿病发作后糖尿病性骨质流失的发展。结论研究结果表明，ERV1 的过度表达可通过延缓体重增加、糖尿病发病和相关炎症来预防牙周病早期阶段与 LepR 相关的牙槽骨丢失；然而，随着动物年龄的增长，LepR 缺陷会增加对自然发生的炎症性牙槽骨损失的易感性，与体重过度增加、糖尿病发作和过度炎症有关。