Silva Davi N A, Monajemzadeh Sepehr, Casarin Maísa, Chalmers Jaclyn, Lubben Jacob, Magyar Clara E, Tetradis Sotirios, Pirih Flavia Q
Section of Periodontics, School of Dentistry, University of California, Los Angeles, California, USA.
School of Dentistry, Federal University of Pelotas, Pelotas, Brazil.
J Clin Periodontol. 2024 Nov;51(11):1511-1523. doi: 10.1111/jcpe.14051. Epub 2024 Aug 12.
To investigate the influence of diabetes mellitus (DM) in a murine model of peri-implantitis (PI).
Twenty-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 (mm) 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.
Gingival 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.
DM exacerbates PI-induced soft-tissue inflammation, matrix degradation and bone loss.
研究糖尿病（DM）对种植体周围炎（PI）小鼠模型的影响。
27只4周龄C57BL/6J雄性小鼠拔除上颌左侧第一和第二磨牙。8周后，每只小鼠植入一枚机械加工的种植体。骨整合4周后，将小鼠分为三组：（a）对照组（C）、（b）PI组和（c）DM + PI组。通过注射链脲佐菌素（STZ）诱导糖尿病。糖尿病诱导后，使用结扎线诱导PI 2周。收集半侧上颌骨进行显微CT和组织学分析。主要观察指标为线性（mm）和体积（mm）骨丢失。次要观察指标基于组织学分析，包括炎性浸润、破骨细胞活性、基质组织、组成和重塑。数据以平均值±标准误表示。采用单因素方差分析，随后进行Tukey检验进行统计分析。
PI组和DM + PI组检测到牙龈组织水肿。显微CT显示，与C组和PI组相比，DM + PI组的线性和体积骨丢失显著增加。苏木精-伊红染色显示，PI组和DM + PI组的炎症反应和骨吸收比C组更明显。DM + PI组的破骨细胞数量显著高于C组和PI组。苦味酸天狼星红染色显示，PI组和DM + PI组的I型和III型胶原蛋白染色比C组少。与C组和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）标记物水平显著增加，基质金属蛋白酶抑制标记物（TIMP-2）水平显著降低。
糖尿病会加剧种植体周围炎诱导的软组织炎症、基质降解和骨丢失。
