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Early intervention of peri‐implantitis and periodontitis using a mouse model

作者
Ryan L. Wong,Sarah Hiyari,Aline Yaghsezian,Mina Davar,Maísa Casarin,Yi‐Ling Lin,Sotirios Tetradis,Paulo M. Camargo,Flávia Q. Pirih
出处
期刊:Journal of Periodontology [Wiley]
卷期号:89 (6): 669-679 被引量:38
标识
DOI:10.1002/jper.17-0541
摘要

BACKGROUND: Peri-implantitis is an inflammatory response to bacterial biofilm resulting in bone loss and can ultimately lead to implant failure. Because of the lack of predictable treatments available, a thorough understanding of peri-implantitis's pathogenesis is essential. The objective of this study is to evaluate and compare the response of acute induced peri-implantitis and periodontitis lesions after insult removal. METHODS: Implants were placed in one-month-old C57BL/6J male mice eight weeks post extraction of their left maxillary molars. Once osseointegrated, ligatures were placed around the implants and contralateral second molars of the experimental groups. Controls did not receive ligatures. After one week, half of the ligatures were removed, creating the ligature-retained and ligature-removed groups. Mice were sacrificed at two time points, 5 and 14 days, from ligature removal. The specimens were analyzed via micro-computed tomography and histology. RESULTS: By 5 and 14 days after ligature removal, the periodontitis group experienced significant bone gain, whereas the peri-implantitis group did not. Histologically, all implant groups exhibited higher levels of cellular infiltrate than any of the tooth groups. Osteoclast numbers increased in peri-implantitis and periodontitis ligature-retained groups and decreased following insult removal. Collagen was overall more disorganized in peri-implantitis than periodontitis for all groups. Peri-implantitis experimental groups revealed greater matrix metalloproteinase-8 and NF-kB levels than periodontitis. CONCLUSIONS: Implants respond slower and less favorably to insult removal than teeth. Future research is needed to characterize detailed peri-implantitis disease pathophysiology.

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