Diabetes mellitus exacerbates inflammation in a murine model of ligature-induced peri-implantitis: A histological and microtomographic study

IF 5.8 1区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of Clinical Periodontology Pub Date : 2024-08-12 DOI:10.1111/jcpe.14051
Davi N. A. Silva, Sepehr Monajemzadeh, Maísa Casarin, Jaclyn Chalmers, Jacob Lubben, Clara E. Magyar, Sotirios Tetradis, Flavia Q. Pirih
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Abstract

Aim

To investigate the influence of diabetes mellitus (DM) in a murine model of peri-implantitis (PI).

Materials and Methods

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 (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.

Results

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.

Conclusions

DM exacerbates PI-induced soft-tissue inflammation, matrix degradation and bone loss.

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糖尿病会加剧小鼠结扎诱发的种植体周围炎模型中的炎症:组织学和显微解剖学研究。
目的:研究糖尿病(DM)对小鼠种植体周围炎(PI)模型的影响:27只4周大的C57BL/6J雄性小鼠拔除了上颌左侧第一和第二臼齿。八周后,为每只小鼠植入一颗加工好的种植体。骨结合四周后,小鼠被分为三组:(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 DM。DM 诱导后,使用结扎法诱导 PI 2 周。收集半月板进行显微 CT 和组织学分析。主要结果包括线性骨质流失(毫米)和体积骨质流失(立方毫米)。次要结果基于组织学分析,包括炎症浸润、破骨细胞活性、基质组织、成分和重塑。数据以均数 ± SEM 表示。统计分析采用单因素方差分析,然后进行 Tukey 检验:结果: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 组的线性骨质流失和体积骨质流失明显增加。H&E 染色显示,与 C 组相比,PI 组和 DM + PI 组的炎症反应和骨吸收更为严重。DM + PI 组的破骨细胞数量明显高于 C 组和 PI 组。与 C 组相比,PI 组和 DM + PI 组的 I 型和 III 型胶原的毕赤染色较少。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)标记物水平明显增加,基质金属蛋白酶抑制标记物(TIMP-2)水平明显下降:结论:DM会加剧PI诱导的软组织炎症、基质降解和骨质流失。
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来源期刊
Journal of Clinical Periodontology
Journal of Clinical Periodontology 医学-牙科与口腔外科
CiteScore
13.30
自引率
10.40%
发文量
175
审稿时长
3-8 weeks
期刊介绍: Journal of Clinical Periodontology was founded by the British, Dutch, French, German, Scandinavian, and Swiss Societies of Periodontology. The aim of the Journal of Clinical Periodontology is to provide the platform for exchange of scientific and clinical progress in the field of Periodontology and allied disciplines, and to do so at the highest possible level. The Journal also aims to facilitate the application of new scientific knowledge to the daily practice of the concerned disciplines and addresses both practicing clinicians and academics. The Journal is the official publication of the European Federation of Periodontology but wishes to retain its international scope. The Journal publishes original contributions of high scientific merit in the fields of periodontology and implant dentistry. Its scope encompasses the physiology and pathology of the periodontium, the tissue integration of dental implants, the biology and the modulation of periodontal and alveolar bone healing and regeneration, diagnosis, epidemiology, prevention and therapy of periodontal disease, the clinical aspects of tooth replacement with dental implants, and the comprehensive rehabilitation of the periodontal patient. Review articles by experts on new developments in basic and applied periodontal science and associated dental disciplines, advances in periodontal or implant techniques and procedures, and case reports which illustrate important new information are also welcome.
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