Trang N Nguyen Vo1, Jia Hao1, Josh Chou2, Masamitsu Oshima3, Kazuhiro Aoki4, Shinji Kuroda1, Boosana Kaboosaya1, Shohei Kasugai1. 1. Department of Oral Implantology and Regenerative Dental Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. 2. School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia. 3. Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan. 4. Department of Bio-Matrix (Pharmacology), Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
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 C57BL/6NCrSlc 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.
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 C57BL/6NCrSlc 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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