AimTo investigate the influence of diabetes mellitus (DM) in a murine model of peri‐implantitis (PI).Materials and MethodsTwenty‐seven 4‐week‐old C57BL/6J male mice had their first and second maxillary left molars extracted. Eight weeks later, one machined implant was placed in each mouse. Four weeks after osseointegration, the mice were divided into three groups: (a) control (C), (b) PI and (c) DM + PI. DM was induced by streptozotocin (STZ) administration. After DM induction, PI was induced using ligatures for 2 weeks. The hemimaxillae were collected for micro‐CT and histological analyses. The primary outcomes consisted of linear (mm) and volumetric (mm3) bone loss. Secondary outcomes were based on histological analysis and included inflammatory infiltrate, osteoclastic activity, matrix organization, composition and remodelling. Data are presented as means ± SEM. Statistical analyses were performed using one‐way ANOVA, followed by Tukey's test.ResultsGingival tissue oedema was detected in the PI and DM + PI groups. Micro‐CT showed significantly increased linear and volumetric bone loss in the DM + PI group compared to the C and PI groups. H&E staining showed greater inflammatory response and bone resorption in the PI and DM + PI groups than in the C group. The DM + PI group had significantly higher osteoclast numbers than the C and PI groups. Picrosirius red stained less for types I and III collagen in the PI and DM + PI groups than in the C group. There was a significant increase in monocyte/macrophage (CD‐11b) counts and matrix metalloproteinases (MMP‐2 and MMP‐8) marker levels and a significant decrease in the matrix metalloproteinases inhibition marker (TIMP‐2) levels in the DM + PI group compared to the C and PI groups.ConclusionsDM exacerbates PI‐induced soft‐tissue inflammation, matrix degradation and bone loss.

中文翻译：

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糖尿病加剧了结扎诱导的种植体周围炎小鼠模型的炎症：一项组织学和显微断层扫描研究


目的 研究糖尿病 （DM） 对种植体周围炎 （PI） 小鼠模型的影响。材料与方法拔除 27 只 4 周龄 C57BL/6J 雄性小鼠的第一和第二上颌左磨牙。八周后，在每只小鼠中放置一个机加工植入物。骨整合后 4 周，将小鼠分为 3 组：（a） 对照 （C） 、 （b） PI 和 （c） DM + PI。DM 由链脲佐菌素 （STZ） 给药诱导。DM 诱导后，使用结扎线诱导 PI 2 周。收集半上颌骨用于 micro-CT 和组织学分析。主要结局包括线性 （mm） 和体积性 （mm3） 骨丢失。次要结局基于组织学分析，包括炎性浸润、破骨细胞活性、基质组织、组成和重塑。数据以均值表示± SEM。使用单因素方差分析进行统计分析，然后进行 Tukey 检验。结果PI 和 DM + PI 组检出牙龈组织水肿。显微 CT 显示，与 C 和 PI 组相比，DM + PI 组的线性和体积骨丢失显着增加。H&E 染色显示 PI 和 DM + PI 组的炎症反应和骨吸收比 C 组更大。DM + PI 组的破骨细胞数量显著高于 C 和 PI 组。PI 和 DM + PI 组中 I 型和 III 型胶原蛋白的 Picrosirius 红染色率低于 C 组。与 C 和 PI 组相比，DM + PI 组的单核细胞/巨噬细胞 （CD-11b） 计数和基质金属蛋白酶 （MMP-2 和 MMP-8） 标志物水平显著增加，基质金属蛋白酶抑制标志物 （TIMP-2） 水平显著降低。结论DM 加剧了 PI 诱导的软组织炎症、基质降解和骨质流失。