Ligature induced peri‐implantitis: tissue destruction and inflammatory progression in a murine model

结扎 种植周围炎 破骨细胞 医学 牙科 吸收 植入 臼齿 骨吸收 肉芽组织 结扎 佩里 病理 伤口愈合 外科 内科学 受体
作者
Trang N. Nguyen Vo,Jia Hao,Joshua Chou,Masamitsu Oshima,Kazuhiro Aoki,Shinji Kuroda,Boosana Kaboosaya,Shohei Kasugai
出处
期刊:Clinical Oral Implants Research [Wiley]
卷期号:28 (2): 129-136 被引量:50
标识
DOI:10.1111/clr.12770
摘要

Abstract Objectives The aim of this study was to investigate tissue destruction and inflammatory progression of ligature‐induced peri‐implantitis in mice and to establish an alternative murine model of peri‐implantitis. Material and methods Sixty male C57 BL /6 NC rSlc mice (4‐week‐old) were used and the maxillary right first molars were extracted. Eight weeks after extraction, custom‐made pure titanium machined screw type implants (0.8 × 1.5 mm) were placed, one implant per animal. Four weeks later, 5‐0 silk ligatures were applied around implant necks to induce peri‐implantitis. Animals were sacrificed at 0 (before ligature), 7, 14, 21 and 28 days after ligature. Half of the samples were analyzed radiologically and histologically to measure bone level change, osteoclast number, density, and distribution. The rest of the samples was used to determine the relative mRNA expression levels of IL ‐1 and TNF ‐α with RT ‐ PCR analysis. Results Bone levels at all sites (buccal, palatal, mesial, distal) decreased 40–50% significantly 28 days after ligature ( P < 0.01). Osteoclast number at all post‐ligature time points increased significantly ( P < 0.05). However, their density at day 28 decreased significantly compared to that of day 21 ( P < 0.05). Accordingly, IL ‐1 and TNF ‐α mRNA expression increased significantly at the early time points but decreased significantly at day 28 after ligature ( P < 0.05). Conclusions Inflammatory response followed by significant peri‐implant bone resorption suggested 28 days ligation is sufficient to successfully induce peri‐implantitis in the current mice model. This model might open a new avenue to study the pathogenesis and mechanism of peri‐implantitis.
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